TrueLearn CA-3 Flashcards
____________ has the lowest pKa of all of the listed drugs with a pKa of 6.5. At a physiologic pH of 7.4, approximately 89% of the drug will be in its nonionized form.
Alfentanil has the lowest pKa of all of the listed drugs with a pKa of 6.5. At a physiologic pH of 7.4, approximately 89% of the drug will be in its nonionized form.
The duration of effect of opioids, unlike many other drugs, is not primarily determined by drug elimination, but more importantly, by______________.
The duration of effect of opioids, unlike many other drugs, is not primarily determined by drug elimination, but more importantly, by lipid solubility.
___________ has a longer onset time and duration of action because it has a more difficult time crossing and then leaving the blood-brain (or blood-spinal cord) barrier due to a lower lipid solubility. By contrast, the more lipid-soluble ___________has a shorter onset and duration of action since it readily crosses, and leaves, the blood-brain barrier.
Morphine has a longer onset time and duration of action because it has a more difficult time crossing and then leaving the blood-brain (or blood-spinal cord) barrier due to a lower lipid solubility. By contrast, the more lipid-soluble fentanyl has a shorter onset and duration of action since it readily crosses, and leaves, the blood-brain barrier.
The _____________ of an opioid is a prime determinant of the onset and duration of action of the drug as it affects how easily the drug is able to cross cellular (lipid) membranes.
The lipid solubility of an opioid is a prime determinant of the onset and duration of action of the drug as it affects how easily the drug is able to cross cellular (lipid) membranes.
___________has the lowest pKa and highest fraction of nonionized drug at physiologic pH.
Alfentanil has the lowest pKa and highest fraction of nonionized drug at physiologic pH.
What happens at first breath?
Fetal PVR is high due to lack of oxygen in the alveoli. With the first breath of life, alveoli fill with oxygen and the infant’s PVR decreases. As PVR decreases, SVR increases and the ductus arteriosus functionally closes within the first 12-24 hrs. As a result, more blood flows through the lungs and into the left atrium. This results in functional closure of the foramen ovale. It will take several months for the ductus arteriosus and the foramen ovale to close. Of note, 25-30% of adults have a patent foramen ovale.
What causes the ductus arteriousus to close?
Factors that contribute to closure of the ductus arteriosus include decrease in PVR, increase in SVR, increase in PaO2 > 50 mmHg (causes arterial smooth muscle of the ductus to contract), normocarbia, and euvolemia.
How do you treat a PDA?
A trial of medical closure is usually attempted with indomethacin and fluid restriction. Medical treatment also includes avoiding overhydration, hypoxemia, acidosis, hypercarbia, and increased pulmonary artery pressures. Indomethacin is a nonselective cyclooxygenase (COX) inhibitor and therefore inhibits prostaglandin synthesis. Prostaglandins typically aid in smooth muscle relaxation within the ductus arteriosus, thus preventing closure.
What is a PDA?
The ductus arteriosus is an essential component of fetal circulation. The diagnosis of persistent fetal circulation or persistent pulmonary hypertension of the newborn can be made by noting a > 20 mmHg difference in PaO2 between preductal and postductal arterial lines. A PDA may be required for survival against hypoxemia due to inadequate pulmonary or systemic blood flow, depending on the congenital cardiac lesion(s). Prostaglandin E1 helps maintain a PDA whereas indomethacin (nonselective COX inhibitor) is the standard medical treatment for closure of a PDA by inhibiting prostaglandin synthesis. Ligation of a PDA is the surgical treatment of choice if medical therapy has failed. Closure results in higher systemic pressures (especially higher diastolic pressures) and patients may require antihypertensive therapy postclosure.
Most common cause of jaundice in population?
Gilbert syndrome is the most common cause of jaundice in the adult population of the United States and is characterized by a decrease in the activity of the hepatic enzyme, bilirubin glucuronyltransferase. This enzyme is required for hepatocyte uptake of unconjugated bilirubin
What is specificity?
Specificity = TN / (TN+FP), the chance (%) to correctly rule in the disease or problem. Specificity “rules in” the disease.
What is sensitivity?
Sensitivity = TP / (TP+FN), the chance (%) to correctly detect the disease or problem. Sensitivity “rules out” the disease.
What is PPV?
Positive predictive value = TP / (TP+FP), the chance (%) that a positive test result means that the subject actually has the disease or problem
Mnemonic for sensitivity vs specificity?
A mnemonic to help recall specificity and sensitivity is: SpIn and SnOut, specificity rules in and sensitivity rules out. The denominator “false” value is P (FP) in the specificity equation and N (FN) in the sensitivity equation.
What are propofol’s CNS effects vs. Cardio effects?
Propofol’s effect on the CNS causes loss of consciousness very quickly (peak < 2 min) but its effects on the cardiovascular system are delayed, especially in older adults.
why is pregnancy a prothrombotic state?
Pregnancy is a prothrombotic state with increased levels of many clotting factors. Factors VII, VIII, IX, X, and XII levels are all increased. In addition there is a decrease in factor C & S levels. This causes shorter PT and PTT times. However, not all factors are increased during pregnancy with factors XI and XIII levels decreasing slightly.
Fibrinogen is also increased during pregnancy
What is warfarin induced paradoxical thrombosis?
When initiating warfarin therapy in the nonparturient, low molecular weight heparin is typically coadministered until the INR has reached a therapeutic level. This is done in order to prevent warfarin-induced paradoxical thrombosis. This may occur since warfarin also inhibits production of the anticoagulant protein C. Warfarin is contraindicated in the parturient due to teratogenicity.
What 6 things can cause perioperative sickiling?
A useful mnemonic to help remember perioperative conditions leading to sickling: SIX H's cause SICKling (HbS) 1. Hypothermia 2. Hyperthermia 3. Hypoxemia 4. Hypotension 5. Hypovolemia 6. H+ ions (acidosis)
What is a VAE? How is it treated?
A venous air embolism (VAE) can be a life-threatening complication. Along with immediate resuscitation measures (circulation, airway, breathing), management of a VAE is focused on preventing additional air from being entrained into the circulation. If a VAE is suspected, the surgeons should immediately be informed and instructed to flood the operative field with normal saline.
How much air needs to be intrained in order to cause a VAE?
As little as 100 mL of air entrained into the circulation can cause an airlock in the right ventricle, disrupt forward blood flow, and have devastating consequences for the patient including stroke, myocardial infarction, cardiac arrest, and/or death. Cardiovascular collapse typically occurs with 300 mL of entrained air. The fatal dose is around 300-500 mL of air, or 3-5 mL/kg. As an example, a 14 g IV with 5 cm H2O of pressure gradient would entrain 100 mL per second.
Even the slightest suspicion of a VAE should be acted on immediately. Treatment includes increasing FiO2, notifying the surgeons so that they can flood the field, and considering a position change to left lateral decubitus.
What position is ideal in vae?
Ideal positioning for a patient with a suspected VAE is left lateral decubitus position. In this position, the right ventricular outflow tract is placed inferiorly to the right ventricle in attempt to overcome an airlock in the right ventricle.
Retrobulbar vs. peribulbar block
Peribulbar blocks offer the advantage of a decreased risk of retrobulbar hemorrhage and optic nerve injury. Disadvantages include a longer onset time and a lower incidence of complete akinesia.
What is hyperkalemic periodic paralysis?
Hyperkalemic periodic paralysis is an autosomal dominant disease leading to intermittent weakness associated with hyperkalemia and often precipitated by a potassium-rich meal, rest after exercise, or stressful situations. The paralysis lasts up to an hour.
Caused (at least partly) by mutations in sodium channel NaV1.4
How do you treat hyperkalemic periodic paralysis?
Treat a hyperkalemic episode with glucose, insulin, epinephrine, and calcium. β-agonists may also be helpful.
What is hyperkalemic periodic paralysis? Etiology\_\_\_\_\_\_ TRiggers\_\_\_\_\_\_ Management\_\_\_\_\_\_\_\_\_\_ Treatment\_\_\_\_\_\_
Hyperkalemic Periodic Paralysis
Etiology: mutations in sodium channel NaV1.4
Precipitated By: hyperkalemia, potassium-rich meal, rest after exercise, stressful situations, possibly hypoglycemia
Anesthesia Management: avoid cholinesterase inhibitors, SCh, and potassium. Maintain normothermia and normoglycemia
Treatment: glucose, insulin, epinephrine, β-agonists, and calcium
**Hypothermia is associated with paralytic attacks of both hyperkalemic and hypokalemic periodic paralysis. Hypothermia leads to further impairment of the dysfunctional ion channel.
How do inhaled beta agonists affect K levels?
Serum potassium levels decrease because of transcellular shift in potassium. When beta agonists are used beta receptor are activated and intracellular cAMP levels rise and potassium is taken into cells. This transcellular shift lowers serum potassium levels, which could prevent or partially abort an attack in this patient.
What is carbaprost tromethamine?
Carboprost tromethamine is a uterotonic used to treat uterine atony after delivery of the infant(s). It produces uterine muscle contraction, rather than relaxation, and therefore may impede intrauterine fetal version or repositioning. The mechanism of action is an increase in myometrial free calcium concentration. Its use is contraindicated in patients with pulmonary hypertension and reactive airway disease, potentially causing bronchospasm, an increased intrapulmonary shunt fraction, and hypoxemia.
What are tocolytics?
Terbutaline and nitroglycerin are used as tocolytics in an effort to halt preterm labor through uterine muscle relaxation. Terbutaline is a relatively selective beta2-receptor agonist which acts directly on uterine myometrial cells to activate adenyl cyclase, thereby decreasing intracellular calcium levels with resultant myometrial relaxation. A side effect of terbutaline is tachycardia and pulmonary edema (beta1-agonist effects), thus some practitioners currently use nitroglycerin to produce uterine muscle relaxation for fetal version, vagina delivery of a breech infant, or removal of retained placental fragments.
What is neurogenic pulmonary edema?
Following neurologic insult, a massive sympathetic discharge from traumatic brain injury (TBI) and intracranial hypertension can lead to neurogenic pulmonary edema (NPE).
Neurogenic pulmonary edema is a relatively rare form of pulmonary edema. It typically occurs within a few hours after a neurologic insult and diagnosis requires exclusion of other causes of pulmonary edema (e.g. cardiogenic). Clinically, NPE presents with rapid onset, severe pulmonary vascular congestion, intra alveolar hemorrhage, and protein-rich edematous fluid. Treatment includes supportive care and aims at reducing intracranial hypertension. Typical treatment modalities for cardiogenic pulmonary edema are usually ineffective in treating NPE.
How does diabetes insipidus present?
Diabetes insipidus presents with polyuria, polydipsia, hypernatremia, high serum osmolality, and dilute urine.
How does SIADH present?
SIADH presents with hyponatremia, serum hypoosmolality, increased renal excretion of sodium, urine osmolality greater than serum osmolality, and normal renal function, and normal adrenal function.
What is cerebral salt wasting?
Cerebral salt wasting, unlike SIADH (which presents with euvolemia and hyponatremia), presents with hypovolemia and hyponatremia
How do you measure ventricular contractility on ECHO?
dP/dt (the rate of rise in ventricular pressure) is a good measure of cardiac contractility
What casues hemodilutionon ACT?
Factors that can result in variable ACT include: hemodilution, hypothermia, platelet counts below 30-50 k/mL, and concomitant administration of other medications which affect platelets (e.g. prostacyclin, aspirin, glycoprotein IIb/IIIa inhibitors).
HOw do you reduce the risk of intermint porphyria?
Certain things increase the risk of an acute exacerbation in patients with acute intermittent porphyria. These include stressful situations, prolonged fasting times, and certain medications. Trying to avoid or decrease the extent of these will help decrease the risk of exacerbation. This includes adequate hydration to decrease the risk of dehydration and supplementation with glucose to avoid starvation states. Additionally, avoidance of medications that are known to precipitate an exacerbation can help (in the perioperative period this includes barbiturates, sulfonamides, ethyl alcohol, and ergotamine).
WHat does activation of muscarinic receptors cause?
The muscarinic receptors are found at the peripheral target organs. Stimulation will cause bradycardia, bronchoconstriction, miosis, salivation, gastrointestinal hypermotility and increased gastric acid secretion.
Which nervous systems secrete which neurotrnasmitters?
For generalization, the terminals in the PNS postganglionic fibers release ACh, in the SNS, NE is the principle transmitter released (except for sweat glands which use ACh).
Muscarininc stimulation casuses…
Muscarinic stimulation is characterized by bradycardia, bronchoconstriction (wheezing), miosis, salivation, gastrointestinal hypermotility, and increased gastric acid secretion. Organophosphate poisoning leads to increased acetylcholine, which causes repeated receptor stimulation. Symptoms of this disorder follow muscarinic stimulation and are remembered with the mnemonic SLUDGE-Mi: salivation, lacrimation, urination, defecation, gastrointestinal upset, emesis, miosis.
Whata re muscarinic agonists? What are the two classes?
Muscarinic receptor agonists can act through two mechanisms, directly on the muscarinic receptor or indirectly by inhibiting the breakdown of ACh causing more ACh to be available to bind to the muscarinic receptor. The direct acting agents are choline esters (ACh, methacholine, carbachol, bethanechol) or alkaloids (pilocarpine, muscarine, arecoline). Some of the direct acting agents have few clinical applications due to their very short half and longer activity can be achieved by methylating the choline moiety. The indirect acting agents are acetylcholinesterase inhibitors (physostigmine, neostigmine, pyridostigmine, edrophonium, and echothiophate). These medications are often used to improve neuromuscular function in disease states where weakness occurs such as myasthenia gravis or to help reverse the action of nondepolarizing neuromuscular blocking agents.
What are anticholanergic drugs?
Anticholinergic drugs are used commonly in anesthesia practice. These medications inhibit the action of ACh by reversibly binding at the muscarinic receptor. Antimuscarinic drugs used in anesthesia practice are atropine, scopolamine, and glycopyrrolate. Both atropine and scopolamine cross the blood-brain barrier, which can result in inhibition of vagal outflow from the central nervous system. At low doses, vagal outflow can potentially be augmented.
What local anesthetic drug can be toxic to a baby in fetal distress?
Lidocaine crosses the placenta and may accumulate to toxic levels due to the effect of ion trapping from fetal acidosis.
How does the pH of a fetus compare to the that of a normal human?
A healthy fetus has a relatively low pH when compared to the mother. Normal fetal pH is between 7.32-7.38 while maternal pH is around 7.43 due to chronic respiratory alkalosis. In the setting of decreased uterine blood flow, such as from significant maternal blood loss, fetal pH will decrease further. The difference in pH can produce a phenomenon known as “ion trapping” that results in the accumulation of certain basic drugs in the fetus.
How does ion trapping work?
A basic drug, such as a local anesthetic, that crosses the placenta in the unionized form accepts a hydrogen ion in the more acidic environment and becomes ionized. This occurs because lidocaine has a pKa of 7.8, meaning more of the drug exists in its ionized fraction as pH decreases below 7.8. The drug can then accumulate since ionized drugs (charged, non-lipophilic) are less likely to cross over the placenta back into the maternal circulation.
WHat are the four main factors that determine drug transfer across the placenta?
Four main factors determine placental transfer of drugs:
1) Size: Drugs with a molecular weight < 500 Dalton’s more readily cross the placenta, while drugs >1000 Dalton’s do not (e.g. heparin, protamine, insulin).
2) Degree of lipid solubility: Drugs that are highly ionized do not easily cross the placenta (e.g., succinylcholine and non-depolarizing muscle relaxants). Lipophilic drugs cross readily (e.g. fentanyl).
3) Protein binding: Drugs that are highly bound to plasma proteins are less likely to cross the placenta. Unbound fractions may still cross, however, mothers have 50% more plasma proteins than the fetus and will maintain a higher concentration of protein bound drugs (e.g. bupivacaine and ropivacaine).
4) Maternal drug concentration: The higher the concentration of a drug in the maternal circulation, the greater the rate of transfer through the placenta.
Mnemonic for remembering which drugs do not cross the placenta?
He Is Going Nowhere Soon = Heparin, Insulin, Glycopyrrolate, Non-depolarizing muscle relaxants, Succinylcholine.
WHen reversing a NMB on a pregnant lady, what should you consider?
The inability of glycopyrrolate to cross the placenta is important to consider when reversing a pregnant woman from neuromuscular blockade. Neostigmine is also a quaternary structure but does cross the placenta to a small degree. If glycopyrrolate is administrated with neostigmine, the fetus will accordingly be exposed to more neostigmine than glycopyrrolate and can become bradycardic. For this reason, atropine may be preferred in combination with neostigmine to antagonize non-depolarizing neuromuscular blockade in pregnant patients.
What is the intial dose of dantrolene for MH?
The Malignant Hyperthermia Association of the United States (MHAUS) recommends an initial, rapid IV administration of 2.5 mg/kg of dantrolene as soon as a diagnosis of MH is suspected.
Describe the pathophysiology of MH
Normally, skeletal muscle depolarization leads to brief activation (opening) of the ryanodine-sensitive calcium channel receptor (RYR1) located on the sarcoplasmic reticulum. This causes a brief efflux of calcium that produces muscle contraction. Malignant hyperthermia-susceptible patients have RYR1 defects that, in the presence of a triggering agent (succinylcholine or any volatile anesthetic), cause prolonged opening of the channel which leads to sustained muscle contraction. This produces a generalized hypermetabolic state characterized by increased CO2, lactic acidosis, and heat production which can progress to muscle cell breakdown leading to hyperkalemia and rhabdomyolysis and their sequelae (arrhythmias; liver, kidney, and other end-organ damage; and death).
How does dantrolene work?
Dantrolene blocks calcium release from skeletal muscle sarcoplasmic reticulum by interfering with the ability of calcium and calmodulin to activate the voltage-gated ion channels (RYR1 and the L-type calcium channel).
How do VAEs occur?
It occurs because non-collapsible venous channels such as venous sinuses can be violated during surgery and air is entrapped in them due to the negative pressure gradient between the surgical site and the heart. VAEs generally travel to the heart and, if small, can be absorbed in the pulmonary vasculature. However, if large, they can cause pulmonary occlusion, increased pulmonary pressures, and even right heart failure with decreased cardiac output.
What is the metabolite of vecuronium? How is it cleared?
Vecuronium has an active metabolite, 3-desacetyl-vecuronium, that has 80% of the potency of vecuronium. Accumulation of this renally-cleared metabolite can significantly prolong the duration of action of the drug, particularly when an infusion is used in a patient with renal failure.
What is the law of LaPlace?
Wall tension (T) = (P * r) / (2 h) Where P is the pressure within the ventricle, r is the radius of the ventricle, and h is the thickness of the ventricular wall.
What is MAT?
Multifocal atrial tachycardia (MAT) is defined by a heart rate greater than 100 and three or more distinct morphologies of the P wave on an electrocardiogram or rhythm strip. It is commonly seen in patients with pulmonary and cardiac pathologies, especially those resulting in atrial distention and pulmonary HTN. COPD exacerbation is the most common cause.
What nerves are blocked by a LPB? which is spared?
A LPB reliably blocks the femoral, lateral femoral cutaneous, and obturator nerves. It spares the sciatic nerve, though the commonly-used posterior approach for a LPB allows for easy access to the sciatic nerve for a separate block.
What are the side effects fo a celiac plexus block?
Celiac plexus neurolytic blocks are performed for chronic, intractable abdominal pain originating from most of the viscera. Adverse effects include hypotension, diarrhea, hiccups, pleurisy, retroperitoneal bleeding, abdominal aortic dissection, transient motor paralysis, and paraplegia.
Where does the great radicular artery arrise?
The great radicular artery (aka arteria radicularis magna or artery of Adamkiewicz) originates from the aorta between the T9 and T12 vertebral segments in 75% of the population. The anterior spinal cord is perfused by a single ASA with collateralization from the radicular arteries. Interruption of the great radicular artery may result in ASA syndrome, which includes bilateral lower extremity paraplegia as well as bowel and bladder dysfunction. Sensation and proprioception are classically spared as the posterior portion of the spinal cord is supplied by two PSAs. SCPP = MAP - CSF pressure. CSF pressure is measured via a lumbar spinal drain. Arterial pressure augmentation and CSF pressure reduction are therefore the best methods by which SCPP may be optimized.
sulfhemaglobinemia shifts o2 curve to the:
Carboxyhemoglobin and methemoglobin shift the oxyhemoglobin curve to the left, sulfhemoglobin to the right.
Which metabolities in renal failure do you need to be mindful of?
The active metabolite in meperidine, normeperidine, causes seizure activity. Morphine’s primary active metabolite, M6G, has a 100-fold greater potency, but exhibits an equal or decreased affinity for μ-receptors compared to morphine. Accumulation of M6G can result in respiratory depression. Morphine’s inactive metabolite, M3G, may cause myoclonus and allodynia. As morphine and meperidine metabolites are typically excreted via the kidneys, their side effects are prolonged in the setting of renal failure. Barbiturates have decreased protein binding in renal failure which leads to higher concentrations of free active molecules.
What is the ideal amplitude for a nerve stimulator for a peripheral nerve block?
The ideal intensity for stimulation and successful peripheral nerve blockade is between 0.3 and 0.5 mA. Intensities less than 0.3 mA are associated with increased intraneural injections and intensities greater than 0.5 mA are often too far from the intended nerve.
What are the risks associated with transfusing plts?
Platelet transfusions actually carry a higher risk of TRALI compared with red blood cell transfusions. In fact they have a higher risk compared to PRBCs on all four of the following categories 1) TRALI 2) transfusion-associated sepsis 3) non-hemolytic febrile reactions and 4) allergic reactions.
Which nerves are blocked by a TAPs block?
A transversus abdominal plane block affects the intercostal, subcostal, ilioinguinal, and iliohypogastric nerves.
When should you start compressions in a newborn?
During neonatal resuscitation, positive pressure ventilation is indicated if the neonate’s heart rate drops below 100 bpm. If the heart rate falls below 60 bpm for more than 30 seconds despite adequate ventilation, chest compressions should be started. If the heart rate remains below 60 bpm despite adequate ventilation and chest compressions, epinephrine should be administered.
How do you dx a prerenal oliguria?
A UOSM : POSM ratio >1.5 is indicative of prerenal oliguria secondary to dehydration or hypovolemia. The UOSM : POSM evaluates the ability of the kidneys to concentrate urine and increase urine osmolality above normal plasma osmolality in the setting of prerenal oliguria.
Cannulation of the brachial artery puts you at risk for injury to which nerve?
Median
When is maternal CO the highest?
Cardiac output immediately following delivery often peaks at 2.5x prepregnancy cardiac output (i.e., an increase of 150%). There is a sudden increase in preload following delivery (delivery of the baby removes some vena cava compression and uterine contraction causes autotransfusion) and less demand for blood flow to the uterus and fetus
Breast milk NPO time:
4 hours
When is an epidural steroid injection indicated?
ESI involves injecting steroid into the epidural space to decrease inflammation and edema of nerve roots. Nerve roots often become compressed as they leave the spinal cord by a herniated disk or spondylosis. Edema of the nerve causes increased compression and more nerve damage. Symptoms of a compressed nerve include radicular pain. Radicular pain is more likely to respond favorably to ESI than other types of back pain.
How does pulse oximetry work?
The oxygen saturation read by a standard two-wave pulse oximeter depends on the differential absorption of red and infrared light in tissue. Red light at 660 nm and infrared light at 940 nm (some manufacturers use 905, 910, or 920 nm) is pulsed through the tissue. A ratio of the absorbance of red to infrared light is calculated and that calculated number is translated to the oxygen saturation reading. At red wavelengths, deoxyhemoglobin absorbs more light than oxyhemoglobin; at infrared wavelengths, oxyhemoglobin absorbs more.
What wave length is absorbed by deoxyhemoglobin?
A mnemonic to help recall light absorption by wavelength is SeXy DARLing: at SiX hundred wavelength, Deoxyhemoglobin Absorbs Red Light.
What are the absolute indications fore OLV?
Absolute indications for one-lung ventilation include:
- Protective isolation of each lung to prevent contamination of the healthy lung: infection (e.g. abscess, infected cyst), massive hemorrhage.
- Control of distribution of ventilation to only one lung: bronchopleural fistula, bronchopleural cutaneous fistula, unilateral cyst or bullae, major bronchial disruption, or trauma.
- Unilateral lung lavage (e.g. pulmonary alveolar proteinosis).
- Video-assisted thoracoscopic surgery (VATS).
Factors that increase MAC requirements
Factors Increasing MAC: Drug - Amphetamine (acute use) - Cocaine - Ephedrine - Ethanol (chronic use) Age - Highest at age 6 months Electrolyte disturbance - Hypernatremia Hyperthermia Red hair
Factors that decrease MAC requirements
Factors Decreasing MAC: Drugs - Propofol, etomidate, barbiturates, benzodiazepines, ketamine - Alpha2 agonists (clonidine, dexmedetomidine) - Ethanol (acute use) - Local anesthetics - Opioids - Amphetamines (chronic use) - Lithium - Verapamil Age - Elderly patients Electrolyte disturbance - Hyponatremia Others - Anemia (Hgb < 5 g/dL) - Hypercarbia - Hypothermia - Hypoxia Pregnancy
Furosemide can lead to what acid/base abnormality?
Furosemide administration can cause a hypokalemic-hypochloremic metabolic alkalosis secondary to potassium excretion and a contraction alkalosis.
What are the symptoms of propofol infusion syndrome?
Propofol infusion syndrome is a rare complication of prolonged, high-dose propofol administration. Signs may include metabolic lactic acidosis, cardiac failure, renal failure, rhabdomyolysis, hyperkalemia, hypertriglyceridemia, hepatomegaly, and pancreatitis.
Sudden drop in ETCO2 and SPO2 after tourniquet release suggests_________
A sudden decrease in EtCO2 and SpO2 after tourniquet release should raise suspicion for a pulmonary embolus from a preoperative DVT.
WHat is the BOhr effect?
The Bohr effect is a physiologic effect that describes hemoglobin’s affinity for oxygen at different conditions. During alkalotic conditions oxygen has a greater affinity for hemoglobin and during acidic conditions oxygen binds to hemoglobin less avidly. Therefore, in the lung, oxygen binds to hemoglobin with a greater affinity than when it reaches the periphery or tissues like the placenta.
transtrachial lidocaine blocks which nerve?
Recurrent laryngeal
___________________ commonly presents as a hypochloremic, hypokalemic, metabolic alkalosis with compensatory respiratory acidosis. Elevated serum bicarbonate is often present along with increased urine specific gravity and decreased urine chloride.
Pyloric stenosis commonly presents as a hypochloremic, hypokalemic, metabolic alkalosis with compensatory respiratory acidosis. Elevated serum bicarbonate is often present along with increased urine specific gravity and decreased urine chloride.
How does ketamine work?
Ketamine is primarily a potent NMDA receptor antagonist. The NMDA receptors are a class of excitatory glutamate receptor. Ketamine does have agonist effects on the gamma-aminobutyric acid (GABA) receptor, however, this is an indirect effect via NMDA antagonism.
altered mental status, hypothermia, and non-pitting edema
Myxedema coma is an extreme form of hypothyroidism that is classically characterized by altered mental status, hypothermia, and non-pitting edema. It is most commonly seen in patients with chronic hypothyroidism in the setting of a physiologic stressor such as infection and is considered a life threatening emergency.
How is CO2 transported in the blood?
Carbon dioxide is transported in the blood as dissolved CO2, bicarbonate, and carbamino compounds.
What happens in pre-eclampsia?
In preeclampsia, there is an elevation in thromboxane A2 levels and a decrease in prostacyclin levels leading to a primarily vasoconstricted state. Preeclampsia is characterized by global vascular hyperreactivity leading to intravascular volume depletion, high systemic vascular resistance, uterine vasoconstriction of the myometrium, and decreased uterine and placental blood flow.
What is cyclosporine’s effect on NDNMB?
Cyclosporine is an immunosuppressant drug that can prolong the action of NDNBDs. In addition, it has potentially neurotoxic effects, including generalized seizures, and is nephrotoxic.
What other blocks can you do during labor?
Pudendal block provides analgesia for the 2nd stage of labor. By blocking the pudendal nerve vaginal and perineal distention pain is blocked. A paracervical block provides analgesia for the 1st stage of labor especially cervical dilation. However, paracervical blocks are associated with a high rate of fetal bradycardia. The rate of fetal bradycardia is increased if fetal acidosis is present.
What is measured and what is calculated in ABG?
Arterial blood gas analysis directly measures pH, PaCO2, and PaO2. Other parameters such as base excess (or deficit), bicarbonate, and SaO2 are calculated or derived from the directly-measured parameters.
What can lead to elevated ammonia levels after a TURP?
Glycine metabolism to ammonia following absorption of glycine-containing irrigation solution during transurethral resection of the prostate (TURP) may lead to neurological complications including encephalopathy and coma lasting up to 48 hours following the procedure.
What is fetal ion trapping?
The term “ion trapping” refers to fetal drug accumulation due to pH differences between maternal and fetal blood, particularly in cases of fetal acidosis. Nonionized drug passes from maternal to fetal circulation. Since fetal blood pH is less than maternal blood pH, but the drug’s pKa remains constant, more of the drug will exist in the ionized form in fetal circulation. Once a local anesthetic becomes ionized in the fetus, it does not readily transfer back across the placenta to the maternal circulation.
What is the PNS. What neurotransmitters does it use?
The PNS is responsible for the “rest-and-digest” processes in the body, and activation of target receptors causes salivation, lacrimation, urination, digestion, and defecation. The preganglionic fibers are long compared to the SNS, and release ACh to act on nicotinic receptors. The shorter postganglionic fibers release ACh to muscarinic receptors resulting in the above effects.
What is the SNS? WHat NTs are used?
The SNS is responsible for the “fight-or-flight response”. The preganglionic fibers are short as compared to the PNS, and release ACh to nicotinic receptors. The longer postganglionic fibers release norepinephrine (NE) to the heart and blood vessels via alpha/beta receptors, ACh to sweat glands via muscarinic receptors and dopamine to renal vessels via dopamine receptors. The adrenal glands have no postganglionic fibers, and release NE and epinephrine directly into the blood stream.
What are the two types of sweat glands?
There are two different types of sweat glands in the body, eccrine and apocrine. Eccrine sweat glands are distributed all over the body (except for the lips, tip of penis, and clitoris), although their density varies from region to region. Humans utilize eccrine sweat glands as the primary form of cooling via sweating. They also function as a route of water and electrolyte excretion, and protection by preserving the acid mantle of the skin (skin is slightly acidic which serves as a barrier). Apocrine sweat glands are larger, have different mechanism of secretion, and are limited to armpits and perianal areas in humans. Apocrine glands contribute little to cooling in humans.
How can antichlinergics contribute to fever?
Anticholinergic agents interfere with the sweating mechanism, which may cause body temperature to increase (especially a child with a fever). This should be included in the differential in any patient with a fever of unknown etiology.
How do CDH patients need to be ventilated?
“Gentle ventilation” with permissive hypercapnia using a low tidal volume strategy, PIP < 25 cm H20, and FiO2 + PEEP adjustment to maintain preductal SpO2 of 90-95% has been shown to decrease mortality in patients with congenital diaphragmatic hernia (CDH) and is the management strategy of choice.
How does CDH impact pulmonary anatomy?
Pulmonary hypoplasia with CDH occurs as a resultant decrease in bronchiolar divisions and alveoli with thickened walls which further impair gas exchange. Alterations in pulmonary vasculature also occur with increased muscular development in smaller arterioles, decrease in the total number of vessels, and increased airway reactivity. There also appears to be an imbalance between vasodilatory (prostacyclin, NO) and vasoconstrictive (endothelin, thromboxane) mediators leading to maintenance of pulmonary hypertension. This is not to say that remodeling does not occur as thinning of the muscular layer and increased pulmonary arteriole size does occur over a process of 2-4 weeks.
How should CDH be handeld from an anesthetic perspective?
Newer “gentle ventilation” strategies minimizing volutrauma with permissive hypercapnia and lowering peak pressures is thought to be the primary determinant of decreases in mortality associated with CDH and should be used during surgery and in the ICU. Further anesthetic management should focus on preventing elevations in pulmonary pressures, such as with hypothermia or large sympathetic outputs, and decreasing oxygen consumption in attempts to maintain oxygen balance. If sudden hypotension or hypoxia ensues, determination of the cause must be sought promptly, with two being the most common. One is contralateral pneumothorax, treated with chest tube or needle thoracostomy, and the other is worsened pulmonary hypertension, which should be treated with nitric oxide (NO).
How does renal failure affect NMB?
The half-lives of vecuronium and pancuronium are significantly prolonged due to the accumulation of active metabolites that are renally excreted. In fact, 80% of pancuronium is renally excreted unchanged in the urine.
By contrast, the half-life of rocuronium is only slightly prolonged (1.2-1.6 hours in normal patients vs. 1.6-1.7 hours in patients with end stage renal disease) since there are no active metabolites (B). There is conflicting evidence as to whether the clearance of rocuronium is slightly reduced or unaffected by renal failure. Similarly, the duration to spontaneous recovery has been reported as both similar and prolonged compared to patients without renal failure. More importantly, rocuronium is primarily excreted through the hepatobiliary system and prolonged paralysis can be seen in patients with cirrhosis and liver failure.
How does methadone work? Is it good for neuropathic pain?
Methadone is an opioid analgesic with concurrent N-methyl-D-aspartate (NMDA) antagonistic properties, which makes it beneficial for patients with neuropathic pain.
Methadone, which has good efficacy for the treatment of chronic pain, has a high oral bioavailability, high potency, and long duration of action. It also lacks active metabolites. Furthermore, the NMDA antagonism and serotonin reuptake inhibition make methadone an effective choice for chronic neuropathic pain as well as modulation of some of the psychological concerns of patients living with chronic pain.
What is CMT disease?
Charcot-Marie-Tooth disease is a class of hereditary motor/sensory neuropathy caused by mutations in myelin and axonal genes. Most frequent manifestations include distal extremity weakness and sensory loss. Although concrete anesthetic management is hard to obtain given the limited amount of cases, caution should be taken when using neuromuscular blockade and utilizing regional anesthesia techniques.
HOw does milrinone work?
Milrinone is a second generation phosphodiesterase III (PDE III) inhibitor. Both PDE I and PDE II hydrolyze all cyclic nucleotides, but PDE III acts on cAMP specifically. Milrinone, therefore, increases cAMP levels which causes its inodilator properties.
Do what to dose of milrinone in renal fialure?
REduce it–it is renaly cleared
Most common side effects of ondansetron?
Common side effects of ondansetron include QTc prolongation (20%, very rarely clinically significant), headache (11%), transient AST/ALT increases (5%), constipation (4%), rash (1%), flushing/warmth (< 1%), and dizziness (< 1%).
MOA of ondansetron
Ondansetron is a serotonin (5-hydroxytryptamine type 3, 5-HT3) receptor antagonist commonly used perioperatively as prophylaxis against and treatment of postoperative nausea and vomiting. One of the major locations for processing of emetogenic stimuli is the chemoreceptor trigger zone (CTZ) located near the base of the fourth ventricle. The CTZ includes a number of different receptor classes including 5-HT3, dopamine, and opioid. The GI mucosa also has numerous 5-HT3 receptors. Accordingly, 5-HT3 antagonists are very effective at treating and preventing (non-motion related) nausea and vomiting.
Why do patients in renal failure have trouble with hemostasis?
Uremia interferes with platelet activation and aggregation (primarily via effects on vWF and GPIIb-IIIa) and leads to increased production of platelet inhibitors (e.g. prostacyclin and nitric oxide).
What is PGE1 and when is it used?
PGE1 is a direct-acting vasodilator via prostanoid receptors on the vascular smooth muscle of the ductus arteriosus. It can dilate and improve flow through the ductus arteriosus or even reopen a mechanically closed ductus arteriosus. It is relatively selective for the ductus arteriosus, but may decrease both pulmonary vascular resistance (PVR) and systemic vascular resistance (SVR). Hypotension is a side effect, especially in the setting of hypovolemia. Fever, flushing, bradycardia, gastric outlet obstruction, and CNS irritability are additional side effects.
What is the role of the ductus arteiousis?
In utero, the ductus arteriosus shunts blood from the pulmonary artery past the deflated lungs and directly into the descending aorta. At birth, lung expansion, increased alveolar oxygen tension, and several chemical mediators lead to a decrease in PVR. A combination of decreased PVR and increased SVR result in flow reversal in the ductus arteriosus. The flow reversal exposes the ductus arteriosus to oxygenated blood. A combination of exposure to oxygenated blood and decreasing prostaglandin E2 levels lead to mechanical closure of the ductus arteriosus within 1-2 days in full term neonates. True anatomic closure occurs over several weeks and requires fibrosis.
What condistions woudl you want the DA to be patent?
There are a variety of congenital heart diseases in neonates that require the patency of the ductus arteriosus. A neonate presenting with cyanosis and clinical suspicion of congenital heart disease within the first two weeks of life is likely to have a “ductal dependent lesion”. In this scenario, an empiric PGE1 infusion is often started as it is assumed progressive closure of the ductus arteriosus in the first few weeks of life is the inciting factor. For example, a neonate with a right-sided obstructive lesion preventing blood flow into the lungs, such as pulmonary atresia or critical pulmonary stenosis, is dependent on the ductus arteriosus to send blood from the aorta into the pulmonary vasculature for oxygenation. Closure of the ductus arteriosus would compromise ability to oxygenate the blood. An infusion of PGE1 will typically improve oxygenation in these neonates due to increased left to right shunting into the pulmonary vasculature. The infusion can be continued for maintenance of patency of the ductus arteriosus until surgical correction is possible.
What are the normal FRC adn oxygen consumption in a healthy adult?
Oxygen consumption in an adult is approximately 3-4 mL/kg/min and functional residual capacity (FRC) is 30 mL/kg.
What is statiscal power?
Power = 1-β. Practically speaking, the power tells us the chance that the null hypothesis (e.g. no treatment effect from a particular drug) will be rejected when an alternative hypothesis is actually true (e.g. a drug does have a treatment effect). The larger the sample population (usually denoted as “n = some number”), the greater the power.
What happens in AFE?
Amniotic fluid embolism is characterized by an early stage with pulmonary vasospasm and right heart dysfunction or failure leading to a second stage with pulmonary edema and left heart dysfunction or failure. Maternal coagulopathy (consumptive) occurs in the majority of cases. Emergency cesarean section is required if uterine hypertonus leads to fetal bradycardia and distress.
What ventilatory changes are seen in obesity?
Obesity is characterized by a marked decrease in expiratory reserve volume, leading to a decrease in lung compliance and FRC. Decreased FRC also leads to airway closure and decreased PaO2.
What is seen in hepatopulmonary syndrome?
Hepatopulmonary syndrome is defined as intrapulmonary vascular dilatations and increased alveolar-arterial (A-a) oxygen gradient, in the setting of end-stage liver disease. Hypoxia is improved when the patient lies flat (platypnea) and is worsened when the patient stands (orthodeoxia). The intrapulmonary vascular dilations cause increased perfusion relative to ventilation. Standing further worsens this ventilation-perfusion mismatch since gravity causes increased perfusion and pooling in the less-ventilated lower lung segmen
When is uterine relaxation indicated?
Nitroglycerin is a preferred agent for uterine relaxation. Other options include potent volatile anesthetics, inhaled amyl nitrite, and IV beta-adrenergic agonists. Indications for uterine relaxation include vaginal delivery of a twin in an abnormal position, breech presentations to deliver the fetal head, cesarean delivery of a fetus with an abnormality (such as hydrocephalus), inverted uterus, removal of retained placenta, and oxytocic overdose.
Difference between MELD and Childs-Pugh
Mnemonics to help differentiate MELD from Child-Pugh:
MELD: “I Crush Several Beers Daily” for INR, creatinine, sodium, bilirubin, dialysis
Childs-Pugh: “Pour Another Beer At Eleven” for PT, Ascites, Bilirubin, Albumin, Encephalopathy
Hypocarbia 2/2 hyperventilation can lead to what electrolyte abnormality?
Respiratory alkalosis, such as from hyperventilation, can cause electrolyte abnormalities such as hypocalcemia, hypokalemia, and hypophosphatemia. Hypocalcemia is caused by increased calcium binding to negatively charged plasma proteins as the proteins release hydrogen ions to restore physiologic pH.
what electrolyte abnormalities do you see in SIADH?
The SIADH is typically associated with the following electrolyte abnormalities:
1) Urine osmolality > 100 mOsm (often > 200-300 mOsm)
2) FENa > 1%
3) Urine Na+ >20 mEq/L
4) Low serum uric acid and BUN
5) Dilutional, euvolemic hyponatremia (serum Na+ < 135 mEq/L)
What hematologic changes do you see in pregnancy?
Serum albumin concentration decreases during pregnancy because of plasma expansion. Many other serum constituents such as fibrinogen, transferrin, and globulins increase, most likely due to the hormonal changes secondary to the pregnant state.
How does closing capacity change with age?
Increased chest wall stiffness, loss of muscle mass, flattening of the diaphragm, and increased compliance of lung parenchyma lead to several physiologic changes in elderly respiration. The volume at which small airways collapse increases with aging, such that by the mid-60s, closing capacity surpasses functional residual capacity and will eventually surpass tidal volume.
Where does GABApentin work?
Gabapentin is an anticonvulsant effective in several neuropathic pain conditions including post-herpetic neuralgia and painful diabetic neuropathy. Gabapentin has efficacy at the α2-delta subunit of calcium channels.
WHAT THINGS INCREASE MAC?
Hyperthermia, hypernatremia, chronic ethanol abuse, and increased central neurotransmitter levels (e.g. MAOIs, amphetamine, cocaine, ephedrine, and levodopa use) increase MAC requirements for anesthetic agents.
What is the BOHR effect?
The Bohr effect refers to the shift in the oxygen dissociation curve caused by changes in the concentration of carbon dioxide or the pH of the environment.
What is the Haldane effect?
The Haldane effect described hemoglobin’s ability to carry increased amounts of CO2 in the deoxygenated state as opposed to the oxygenated state. This is due to the fact oxygenated hemoglobin reduces the amount of CO2 bound to hemoglobin in addition to the histidine amino acid of hemoglobin being an important hydrogen ion buffer at physiologic pH.
Where do cardiac myxomas typically arise?
The most common primary tumor of the heart is a cardiac myxoma, which is typically located in the left atrium. However, metastatic disease to the heart is not uncommon from adjacent lung or renal cancer. Cardiac tumors have the potential to cause arrhythmias, ventricular obstruction, heart failure, pulmonary edema, pulmonary hypertension, arterial hypoxemia, dyspnea, positional hemodynamic compromise and embolism.
What is prolonged in pseudocholiesterase deficincy?
Pseudocholinesterase deficiency prolongs the actions of succinylcholine and mivacurium which can lead to prolonged neuromuscular blockade and apnea.
Echothiophate….
Echothiophate is an anticholinesterase used to treat refractory glaucoma by causing miosis. Since it inhibits BCHE, systemic absorption can cause up to a 95% decrease in BCHE function, thereby potentiating the effects of succinylcholine.
What do yuo see in Cushing Diesease
Cushing syndrome is characterized by a group of signs and symptoms resulting from prolonged exposure to excess cortisol. Classic symptoms include moon facies, buffalo hump, abdominal weight gain, thinning of the extremities, hirsutism, elevated blood sugar, and mood changes.
How does PTH increase calcium?
Parathyroid hormone (PTH) is released in response to decreasing serum calcium levels. PTH stimulates osteoclasts, increasing bone resorption and raising serum calcium. PTH also stimulates reabsorption of calcium from the distal renal tubule.
HOw does fenoldopam affect
Fenoldopam is a selective dopamine-1 agonist that increases renal blood flow despite decreased systemic arterial blood pressure. Fenoldopam has little to no alpha, beta, or dopamine-2 receptor agonist activity.
What causes a right shift on the oxyhemoglobin dissosciation curve?
Hypercarbia, acidosis, hyperthermia, and high 2,3-DPG levels, all shift the oxygen-hemoglobin dissociation curve to the right and increase oxygen unloading to tissues.
What is the mechanism of metaclopramide?
Metoclopramide is a dopamine antagonist centrally and a cholinergic agonist peripherally. It is used perioperatively as an antiemetic. By promoting gastric emptying and increasing gastroesophageal sphincter tone, it may decrease the risk of pulmonary aspiration. It is typically given in doses of 5-10 mg IV 15-30 minutes prior to induction to allow sufficient time for drug onset. However, drug combinations involving metoclopramide are not found to reduce PONV to a greater extent than monotherapy.
What effect does metaclopramide have on SUX?
Metoclopramide inhibits plasma cholinesterase and can increase the duration of action of succinylcholine.
What are the CV effects of milrinone?
The cardiovascular effects of milrinone can be summarized as: increased inotropy, increased lusitropy, increased ejection fraction, increased stroke volume, increased cardiac output, decreased afterload, decreased preload, pulmonary vasodilation, and systemic vasodilation.
What is the MOA of milrinone?
Milrinone is a phosphodiesterase III (PDE3) inhibitor which increases inotropy.
Both milrinone and inamrinone (formerly known as amrinone) act by inhibiting the PDE3 isoenzyme which is responsible for the cleavage of intracellular cyclic adenosine monophosphate (cAMP). This allows for greater diastolic storing of calcium (which is facilitated by cAMP) by the sarcoplasmic reticulum which improves diastolic relaxation, a physiologic effect known as lusitropy. Lusitropy may be depicted on the myocardial pressure-volume loop as a rightward shift of the diastolic filling phase
How is the cricothyroid muscle innervated?
The cricothyroid muscle is innervated by the external branch of the SLN. All other laryngeal muscles are innervated by the RLN. Bilateral RLN palsy or injury results in respiratory distress but unilateral injury or palsy typically does not.
What is the MOA of nicardipine and where is it metabolised?
The liver extensively metabolizes nicardipine and, as a result, hepatic insufficiency can result in prolonged half-life
Nicardipine is a calcium-channel blocker; more specifically, it is an antagonist of calcium influx through the slow channels of cell membranes. It is an effective coronary and peripheral arterial dilator. Nicardipine can be used to relieve angina, especially those due to coronary artery spasms. It is also useful as an anti-hypertensive drug, particularly in neurosurgical patients. However, the advantage of nicardipine is that it does not decrease cardiac function.
What effect does nicardipine have on CO and SVR?
Nicardipine decreases systemic vascular resistance, but also increases cardiac contractility (C). The exact mechanism of this positive inotropic effect is unknown.
HOw do the various volatiles affect hepatic blood flow?
Preservation of THBF amongst volatile anesthetics at 1 MAC, from greatest to least, is sevoflurane > isoflurane > halothane.
What do you need to watch out for with administration of flumazenil?
The duration of action of midazolam (half-life 1.7-2.6 hours) exceeds that of flumazenil (half-life 0.7-1.3 hours). This makes recrudescence of benzodiazepine-induced somnolence after metabolism of flumazenil likely in this context. Repeated dosing of flumazenil or flumazenil infusion may be necessary to prevent recrudescence after an initial bolus of flumazenil.
What is one of the potenital side effects of large bolusses of naloxone?
pulmonary edema
Which inhaled anesthetic is most affected by OLV?
One-lung ventilation (OLV) creates a right to left pulmonary shunt, which has the greatest effect on the less soluble inhalational anesthetics, such as desflurane.
What is the effect of solubilty on uptake of inhaled agents?
Inhalational anesthetics reach equilibrium when the anesthetic partial pressures of the alveolus, blood, and CNS become equal. The faster the alveolar fraction (FA) of inhaled agent approaches the fraction of inspired (FI) agent, the faster the agent will reach equilibrium. Insoluble agents (e.g. desflurane, nitrous oxide) have a low blood to gas partition coefficient. Therefore, their partial pressures quickly build in the alveoli. More soluble anesthetics (e.g. halothane, isoflurane) will diffuse across the alveoli and into the alveolar capillary bed more readily, thereby increasing the time needed reach this equilibrium.
What two factors determine impedence on US?
Acoustic impedance is the product of the density of a medium and the propagation speed of sound through that medium. Ultrasound reflections that occur at the interface of different mediums are due to the changes in acoustic impedance. Since propagation speed changes slightly between biological mediums, acoustic impedance is primarily dependent upon density.
Time to non-cardiac surgery after MI?
After an MI wait 14 days after balloon angioplasty, 30 days after BMS, 60 days if no coronary intervention, and 180 days after DES for elective noncardiac surgery.
Papilary rupture–most liekly blood supply?
Bottom Line: In the setting of non-ST elevation myocardial infarction and acute mitral regurgitation, there is high suspicion for papillary muscle rupture. The posteromedial papillary muscle receives a single blood supply from the right coronary artery in about two-thirds of patients. It is more susceptible to infarct than the anterolateral papillary muscle, which receives dual blood supply from the left anterior descending artery and left circumflex coronary artery.
How does an NMDA receptor work?
The NMDA receptor is an inotropic glutamate receptor that functions as a nonspecific ion channel when activated. Activation only occurs when glutamate is bound to the receptor AND the cell is depolarized. The receptor’s effects are primarily mediated via increased intracellular calcium.
Administration of magnesium along with ketamine can ___________ the effects of ketamine.
Administration of magnesium along with ketamine can potentiate the effects of ketamine.
What are the targets in DHCA?
Full flow CPB is maintained 20-30 minutes after reaching goal temperature to ensure adequate cerebral cooling prior to stopping circulation. Operative time is aimed at 45-60 minutes or less and is the only factor shown to improve outcomes.
WHat is pousille’s law?
The Poiseuille Law states that: Q = ΔP(π * radius4) / (8 * viscosity * length) Where: Q = flow, Δ = change in, P = pressure, π = 3.14159… (the mathematical constant). Notice the radius is taken to the fourth power in Poiseuille equation. Equivalent changes in the radius as compared to other parameters, will make the most impact on overall flow through the vessel. The radius of the vessel is directly proportional to flow and inversely proportional to resistance.
Within which muscle does the musculocutenaous nerve run?
The musculocutaneous nerve travels within the belly of the coracobrachialis muscle. The nerve may therefore be neglected during an axillary brachial plexus block for distal upper extremity surgery since it is not contained within the axillary sheath. The median, ulnar, and radial nerves (as well as the axillary artery) are contained within the sheath.
Which vasoactive medications can be given IM?
Examples of cardiovascular medications that can be given IM include, but are not limited to: atropine, glycopyrrolate, ephedrine, epinephrine, phenylephrine, and hydralazine.
MOA of epinephrine
Epinephrine is a direct agonist at α1, α2, β1, and β2 adrenergic receptors. It increases contractility, heart rate, and cardiac output.
MOA ephedrine
Ephedrine is an indirect-acting sympathomimetic. It stimulates α and β adrenergic receptors primarily by triggering release of norepinephrine.
mOA norepeipnephrine
Norepinephrine is a direct α1, α2, and β1 agonist. It significantly increases blood pressure but its effects on heart rate and cardiac output are dependent on systemic vascular resistance. Adrenergic stimulation is α»_space; β leading to potent vasoconstriction.
MOA phenylephrine
Phenylephrine is a direct-acting α1 agonist. It improves blood pressure via increased preload and afterload but typically causes a reflexive bradycardia. Although phenylephrine mimics many of the effects of norepinephrine, it is less potent and causes venoconstriction > arterial constriction
R->L shunt induction
Inhalational induction is delayed in the setting of a right-to-left intracardiac shunt.
faster with IV induction
Where is ang 1 cleaved?
Angiotensin I (AI) is cleaved and converted to Angiotensin II (AII) in the pulmonary circulation by angiotensin converting enzyme (ACE).
HOw does hyperventilation alter CBF?
Hyperventilation leads to decreased CBF by decreasing PaCO2. CBF changes 1-2 mL/100 g/min per every 1 mmHg change in PaCO2.
What effect does increased FiO2 have on shunt flow?
Pulmonary shunt is increased by increased oxygen concentrations, which leads to blunting of hypoxic pulmonary vasoconstriction and microatelectasis.
How can high fio2 lead to decreased FRC?
Additionally, high concentrations of oxygen decrease functional residual capacity through development of microatelectasis. This occurs because of alveolar collapse – when higher concentrations of oxygen are used, less nitrogen is part of the alveolar gas. Nitrogen helps keep alveoli ‘stented’ open, helping to decrease the amount of micro collapse. Less nitrogen results in more alveolar collapse and what is called microatelectasis. Some of this effect can be blunted by using certain maneuvers such as positive end expiratory pressure or recruitment maneuvers. It should be mentioned that the verdict on oxygen concentration in the intraoperative period is still debated and further studies are needed to really determine the optimal concentration.
What are the second line uterotonics and their contraindications?
Several second-line therapies exist to help control postpartum hemorrhage due to uterine atony. Being aware of these contraindications - methylergonovine in coronary artery disease and preeclampsia/eclampsia, and carboprost in asthma - is essential to providing appropriate anesthetic care.
What si the role of prostaglandins on pain?
NSAIDs lead to a decrease in the production of prostaglandins. Prostaglandin E2 is the key mediator of both peripheral and central pain sensitization. Peripherally, prostaglandins do not directly mediate pain; rather, they contribute to hyperalgesia by sensitizing nociceptors to other mediators of pain sensation such as histamine and bradykinin. Centrally, prostaglandins enhance pain transmission at the level of the dorsal horn by increasing the release of substance P and glutamate from first-order pain neurons, increasing the sensitivity of second-order pain neurons, and inhibiting the release of neurotransmitters from the descending pain-modulating pathways.
Where is dexmetedomidine metabolised?
Dexmedetomidine undergoes extensive hepatic metabolism including conjugation, n-methylation, and hydroxylation followed by conjugation before being excreted in urine and feces. Its elimination half-life is 2-3 hours.
MOA od dexmeditomidien
Dexmedetomidine is a selective α2-adrenergic agonist (α2:α1 = 1600:1) that causes inhibition of presynaptic norepinephrine release from peripheral and central nervous system neurons (particularly those in the spinal cord and locus ceruleus in the brainstem). This results in analgesia, anxiolysis, sedation, and sympatholysis.
What is one fo the dangers of ESWL? How is it prevented?
During immersion extracorporeal shock wave lithotripsy (ESWL), a mechanically generated shock wave is passed through water toward the area of calculus. When the wave encounters a different density (such as the renal calculus), energy is released, which will break up the stone. If the shock travels through the heart, it may disrupt normal conduction, and cause dysrhythmias, and in the worst case scenario, the shock will reach the heart during repolarization (the T wave on the ECG), and cause ventricular fibrillation. For this reason, the shocks are timed to the R wave on the ECG (the refractory period of the cardiac cycle).
Mechansims of hypoxemia during OLV
Hypoxemia primarily occurs during OLV due to perfusion of the non-dependent (non-ventilated) lung, even in the setting of appropriate hypoxic pulmonary vasoconstriction. This leads to a right-to-left intrapulmonary shunt and mixing of deoxygenated blood into the systemic circulation. Except in the case of severe, acute hypoxemia, the first steps for management of hypoxemia during OLV are to confirm proper positioning of the double-lumen endotracheal tube and ensure 100% oxygen is being delivered.
Non-dependent lung in OLV
Non-ventilated lung
Dependent lung
the ventilated lung; the one that is generally lower to gravity
What potentiates NMB?
: Potentiation of neuromuscular blockade is seen with volatile anesthetics, local anesthetics, aminoglycosides, lithium, calcium channel blockers, acute phenytoin, and magnesium.
What is metaclopramide’s effect on NMB?
Metoclopramide has inhibitory effects upon plasma cholinesterase, therefore it may prolong the duration of mivacurium and succinylcholine by means of reduced degradation.
What is one of the most common side effects of sux?
Succinylcholine is a commonly used muscle relaxant. One of the most commonly reported side effects of succinylcholine administration is muscle pain or myalgia. Myalgia occurs in roughly 50% of patients who receive succinylcholine alone. Pain is often considered inconvenient and lasts 1-2 days. Pain is more likely in females of child-bearing age. Additionally, patients who are in better physical condition are less likely to experience myalgia.
What do you see in a phase 1 block?
Phase 1 block is the normal response to succinylcholine where the train-of-four (TOF) ratio stays >70% (subjectively, all four twitches feel equal) and is associated with fasciculations (though an absence of post tetanic fasciculations), a decreased response to single twitch stimuli, absence of fade to tetanus, enhancement of neuromuscular blockade (NMB) by anticholinesterases, and rapid recovery.
What are the categories on a dibucaine number?
Dibucaine is a local anesthetic that was found to inhibit normal pseudocholinesterase activity by 80%, meaning a normal patient has a dibucaine number of 80. This number is proportional to the amount of normal pseudocholinesterase.
A dibucaine number of 20 indicates a homozygous patient, a dibucaine number of 40-70 indicates a heterozygous patient.
What si the difference betweena phase 1 and a phase 2 block?
Both phase 1 and phase 2 blockades of succinylcholine administration display decreased contraction with single twitch stimulus. Phase 1 blockade is associated with fasciculations, minimal fade to TOF (TOF ratio >70%), and enhancement of neuromuscular blockade (NMB) by anticholinesterases. Phase 2 blockade is associated with repeated doses or an infusion of succinylcholine, resembles NDNMB, and can be partially reversed with anticholinesterases. The degree of pseudocholinesterase deficiency is established by the dibucaine number, which is proportional to the amount of normal pseudocholinesterase.
When is vasospasm most likely to occur after SAH?
Cerebral vasospasm is most likely to develop between days 2-10 or 3-15 (depending on source) after a subarachnoid hemorrhage (SAH) and the exact reasons why this interval is the peak time period is not well understood.
How is intracrancial vasospasm monitored and treated?
Transcranial Doppler (TCD) may also be performed every 24-48 hours to screen for cerebral vasospasm. This study assesses the flow velocity (FV) of the middle cerebral artery (MCA) and the internal carotid artery (ICA) and compares FVMCA to FVICA. Generally, vasospasm is considered if the FVMCA >120 cm/s or the FVMCA:FVICA ratio is larger than 3. The most efficacious form of treatment and prevention of cerebral vasospasm was thought to be the use of hypervolemia, hypertension, and hemodilution (“Triple H” therapy). However, no human studies have ever shown improved outcomes and there are detriments to this treatment including edema, anemia, and possibly worsening outcomes. Newer treatments focus on euvolemia and management of blood pressure with vasopressor support if needed to maintain CPP.
How is transcranial Doppler ultrasound used?
Transcranial Doppler is used during the perioperative period for CEA procedures to measure blood flow velocities, detect embolization to the brain, identify shunt function or malfunction, and detect asymptomatic carotid artery occlusion and/or hyperperfusion syndrome. The technique involves assessment of the middle cerebral artery.
Which coronary vessel supplies the anterior wall?
The anterior wall is supplied by the left anterior descending artery
What deos the RCA supply?
Right coronary supplies portions of the interventricular septum and the inferior wall.
What does the PDA supply
the inferior wall
What supplies the lateral wall
Circumflex artery
organsophosphate toxicity
SLUDGE
•Acetylcholine is the neurohumoral mediator at the cholinergic junctions. Since acetylcholinesterase is the enzyme that degrades acetylcholine following stimulation of a nerve, by inhibiting acetylcholinesterase, organophosphates allows acetylcholine to accumulate and result in initial excessive stimulation followed by depression.
What is norepinephrine’s role in sepsis?
Norepinephrine restores perfusion pressure, improves organ function, and corrects splanchnic ischemia in hypotensive patients and is thus the first-line vasopressor in patients with septic shock. This is assuming adequate fluid resuscitation has already occurred. Norepinephrine increases systemic arterial pressure with variable effects on cardiac output and heart rate through both α- and β-adrenergic receptor agonism. Increased systemic vascular resistance improves end-organ perfusion, accompanied by a decrease in lactate levels. In volume-resuscitated, hypotensive patients in septic shock, norepinephrine improves renal function. Norepinephrine can decrease organ perfusion in under-resuscitated patients, especially when high-dose infusions are used.
Need to palce emergent cervical cerlage–what is the best anesthetic choice that will also releax the uterus?
GA
Prophylactic cervical cerclage is usually performed under neuraxial anesthesia. When cervical dilation and bulging membranes are present, general anesthesia may be preferable if acceptable to the patient. In the absence of studies showing fetal outcomes, no technique is contraindicated, however, general anesthesia has the advantage of causing uterine relaxation which facilitates replacement of membranes.
How do you perform a Bier Block?
Briefly, it is performed by 1) placing a small IV in the operative extremity, 2) placing a double tourniquet proximally on the extremity, 3) exsanguinating the extremity with an Esmarch bandage, 4) inflating the proximal tourniquet cuff, and 5) injecting local anesthetic (commonly 40-50 ml 0.5% lidocaine, though some recommend smaller volumes of a higher concentration). If the patient experiences tourniquet pain, the distal cuff is inflated then the proximal cuff is deflated. Following the procedure (or after 20-30 minutes after the local anesthetic was injected if the procedure is short), the tourniquet is then released. Although a dorsal hand vein is most commonly used, the site of IV placement and injection does not affect the block efficacy (D)1.
What is the MOA of a Bier Block?
The mechanism of action of an upper extremity Bier block is believed to be diffusion of the local anesthetic from the veins into the capillaries surrounding peripheral nerves and then into the vasa nervora, which will then produce the nerve conduction block. Local anesthetic also diffuses extravascularly into the small nerves supplying the skin
HOw do yoiu treat WPW in an acute setting?
Supraventricular tachycardia in patients with WPW can be safely managed with procainamide.
IN a pateitn with asthma, what should be avoided to treat SVT?
In a patient with asthma, nonspecific (beta1 and beta2) beta-blockade can exacerbate bronchospasm thus it should only be given after all other causes of sinus tachycardia have been ruled out.
What is the relationship between epidurals and spinals and MS exacerbation?
Epidural anesthesia has been used safely in patients with MS and is not associated with exacerbations or worsening symptoms of MS. However, spinal anesthetics are often avoided because of risk of demyelinated nerves being sensitive to local anesthetics, which may cause a local toxicity to the nerve. Spinal anesthesia can be performed safely, though it is controversial. There is little evidence to either support or refute the use of subarachnoid block in patients with MS.
What is the relationship between sux and MS?
Succinylcholine is not associated with exacerbations of MS. Although, succinylcholine is associated with hyperkalemia and should be avoided in patients with MS. Succinylcholine induced hyperkalemia results from denervated muscle with upregulated immature acetylcholine receptors.
change in pitch after thyroid surgery?
DAMAGE TO SLN (INNERVATES CRICOTHYROUD MUSCLE)
WHat is antiphospholipid disease?
Antiphospholipid syndrome is a prothrombotic disorder resulting in both venous and arterial thrombosis. It is characterized by the presence of two autoantibodies, lupus anticoagulant and anticardiolipin antibody. Lupus anticoagulant has no true anticoagulant activity; instead, the anticoagulant activity is a laboratory artifact that affects the phospholipid-dependent coagulation assays. In the absence of an underlying coagulation deficit or anticoagulant therapy, the prolonged aPTT does not suggest a bleeding tendency and neuraxial anesthesia may be administered in this setting.
WHat are the first and second line vasopressors for sepsis?
1st: Norepiniephrine
2nd: Vaso OR EPI
The Surviving Sepsis Campaign guidelines have changed several times. All versions have included norepinephrine as the first-line agent. The first iteration recommended vasopressin as the second-line drug of choice. The second iteration lowered the dose of vasopressin and also suggested epinephrine as the second-line drug of choice instead of vasopressin. The Sepsis-3 guidelines then changed to either vasopressin or epinephrine as the second-line agent.
What does dopamine do?
Has it a role in sepsis?
Increases CO and SVR
NO–increased mortality
Dopamine raises mean arterial pressure by increasing cardiac output and, to a lesser extent, systemic vascular resistance. Dopamine effectively improves urine output by either improving overall hemodynamics, exerting a direct diuretic effect, or by decreasing the release of antidiuretic hormone via baroreceptor responses. The α-agonistic dosage of dopamine varies but may empirically begin at 10 mcg/kg/min and be titrated to effect. However, studies have shown an increased rate of morbidity including cardiac arrhythmias when dopamine is used in sepsis.
What are the key points of the latest sepsis guidelines?
Norepinephrine is the first-line vasopressor for treatment of septic shock after adequate intravascular volume expansion. Steroids may be helpful in resistant hypotension, but do not have any mortality benefits. Early administration of empiric antibiotics is recommended. The use of low-dose dopamine for renal protection confers no mortality benefit.
What effects do you see in Downs Syndrome?
Down syndrome patients frequently have cardiovascular defects. The most common of these is endocardial cushion defects. Down syndrome is associated with atlantoaxial instability, hypotonia, and gastrointestinal, genitourinary, respiratory, vascular, and metabolic defects.
Common features of DI?
Diabetes insipidus (DI) is characterized by a deficiency of antidiuretic hormone and can be caused by pituitary disease, trauma, infiltrative disease, brain tumors, and neurosurgical procedures. A patient with diabetes insipidus would likely present with polyuria, hypernatremia, a high plasma osmolality, and a low urine osmolality. Management includes administration of DDAVP and isotonic intravenous fluids to maintain euvolemia.
What do you commonly see in SIADH?
The syndrome of inappropriate release of antidiuretic hormone (SIADH) is characterized by water retention and hyponatremia due to overactive ADH. Oliguria would likely be seen
What is the treatment for MS?
Treatment for MS includes beta-interferon treatment, monoclonal antibody treatment (e.g. natalizumab), or immunosuppression. Steroids are not commonly used for chronic treatment but may be used to shorten an exacerbation.
what os GBS?
Guillain-Barré syndrome (GBS) is associated with SIADH, which causes hyponatremia. SIADH develops when ADH is released inappropriately. SIADH was detected in nearly 50% of patients who developed GBS. The severity of hyponatremia was associated with the severity of GBS.
GBS is an autoimmune demyelinating polyneuropathy that often develops following gastrointestinal or respiratory illnesses. GBS has also been weakly linked to vaccinations. GBS often begins with sensory changes (paresthesias) which lead to progressively ascending weakness. Many patients experience autonomic dysfunction which can become quite severe manifesting as hypotension, hypertension, cardiac dysrhythmias, and ileus. Dysrhythmias can be severe such that arterial catheterization may be necessary.
What are the changes seen in laparscopy?
Laparoscopic surgery is typically achieved through intraperitoneal insufflation with carbon dioxide (CO2). Intraperitoneal insufflation produces significant hemodynamic changes secondary to increased abdominal pressure (“pneumoperitoneum”), including a decrease in right heart filling pressures, decreased renal and splanchnic blood flow, and arrhythmias. CO2 is absorbed into the vasculature, producing hypercarbia and a resultant vasodilation. CO2 absorption produces an overall sympathetic response. In addition, the renin-angiotensin system is activated with resultant vasopressin release. Increased SVR and MAP is primarily the result of increased vasopressin levels and, to some degree, a CO2-induced sympathetic response plus a compressed intra-abdominal arterial tree.
What labs would you see in renal insuffecncy in a pregnant lady?
A serum creatinine concentration greater than 0.8 mg/dL or a blood urea nitrogen concentration greater than 13 mg/dL (which are normal values for the nonpregnant patient) suggests renal insufficiency in the pregnant woman.
What is vasogenic edema?
Vasogenic edema is caused by disruption of the blood brain barrier resulting in cerebrovascular permeability and leakage of serum proteins into the brain parenchyma. It is the escape of fluids and proteins from the vascular system into the parenchyma.
What is cytotoxic edema?
Cytotoxic brain edema occurs following ischemic conditions; the blood brain barrier remains intact however disturbance of osmoregulatory functions of the brain occurs. In other terms, cell membranes become more permeable most often due to disruption of ion channels following cellular injury.
What labs do you see in primary hyperthyroidsim?
Primary hyperthyroidism is characterized by elevated T3, T4 (free and total), and thyroid hormone binding ratio, and a low or normal TSH.
What do you see in anticholinergic toxicity?
Anticholinergic symptoms include: tachycardia, altered level of consciousness, hyperthermia (“atropine fever”), flushing, dry mouth, mydriasis, constipation, and urinary retention. Recall: “dry as a bone, mad as a hatter, blind as a bat, and hot as a hare.”
What is the deal with hetrastarches/tetrastarcehs?
Hydroxyethyl starches are synthetic colloids useful for volume resuscitation due to prolonged intravascular half-lives. Hetastarches are traditionally associated with a higher risk of coagulopathies (platelet adhesion interference, reduced factor VIII:C and vWF levels, and PTT prolongation) than the newer, lower molecular weight tetrastarches.
What is suggestive og discogenic pain?
discogenic pain is often described as decreased with standing and increased with bending/sitting. With acute disc herniation there is often a positive straight leg test and there may be associated weakness.
What are the constilation of symptoms in hyperparathyroidsim?
Chronic hypercalcemia from hyperparathyroidism leads to the constellation of symptoms of nephrolithiasis, abdominal discomfort, osteopenia, bone pain, and psychological depression.
What is carcinoicd syndrome?
Carcinoid syndrome is a constellation of symptoms that occurs from the release of serotonin from metastatic carcinoid tumors into the systemic circulation. Carcinoid tumors are usually slow-growing, benign, tumors that arise from neuroendocrine cells, usually in the small intestine, and evolve to secrete an excess amount of the neurotransmitter 5-hydroxytryptamine (5-HT), better known as serotonin. The GI tract is the most common site of origin for these tumors.
Carcinoid tumors are usually asymptomatic; patients may have vague symptoms of abdominal pain, intestinal obstruction, diarrhea, and GI bleeding. Once carcinoid tumors have metastasized, either into the hepatic or pulmonary circulation, they release vasoactive peptides into the systemic circulation, which causes patients to have signs and or symptoms of carcinoid syndrome. Symptoms of carcinoid syndrome include cutaneous flushing, vomiting, diarrhea, hypotension or hypertension, abdominal pain, dizziness, palpitations, and bronchoconstriction.
What are the arrangements of the acxillary sheath?
When performing an axillary brachial plexus block, three of the four major nerve branches to the arm are contained within the axillary sheath and surround the axillary artery. The radial nerve is the most posterior and is closest to the humerus and is commonly described as being in the six o’clock position relative to the artery when viewed on ultrasound. The median nerve is anterolateral to the artery and is often found in the nine or ten o’clock position. The ulnar nerve is anteromedial to the artery and typically located in the three o’clock position.
What is ACT?
ACT is a functional assessment of the intrinsic and final common pathway of the coagulation system. Whole blood is added to a tube that contains an activator substance (celite or kaoline) and time to clot formation is measured. The normal ACT is around 107 seconds. The ACT is commonly used in cardiac surgery to evaluate the anticoagulant effect of heparin. A value between 400-480 seconds is typically required to initiate cardiopulmonary bypass.
How does age affect opioid metaboslism in kids?
Neonates are more sensitive to morphine due to opioid receptor immaturity and inability to metabolize morphine into its metabolites. CYP2D6, UGT2B7, and CYP3A4 are all decreased at birth, and these enzymes allow codeine activation, morphine inactivation, and fentanyl inactivation, respectively.
DEscribe the RAAS pathway
The renin-angiotensin-aldosterone system (RAAS) is one of the primary regulators of volume and blood pressure. Angiotensinogen circulates in the plasma until cleaved by renin to form angiotensin I. Renin is released by the juxtaglomerular apparatus in response to β1 activation, decreased renal perfusion pressure (glomerulus), or decreased NaCl concentration at the macula densa (distal convoluted tubule). Angiotensin I is cleaved to form the active angiotensin II by angiotensin-converting enzyme (ACE) in the lungs.
What does BNP do?
Brain natriuretic peptide (BNP) is released from the heart in response to myocardial stretch receptors in the right and left ventricles similarly to atrial natriuretic peptide (ANP) released from the atria. Both ANP and BNP cause vasodilation, natriuresis/diuresis, and inhibition of the renin-angiotensin-aldosterone system in response to volume overload states (CHF, cirrhosis, renal failure, right heart failure). BNP causes inhibition of the sodium-potassium ATPase in the collecting ducts to promote sodium excretion.
Where are platelelts made?
Platelets are synthesized and released by megakaryocytes, which are produced in the bone marrow. Of note, thrombopoietin (TPO) is produced by the liver and stimulates bone marrow release of megakaryocytes. Thrombocytopenia is a common finding in cirrhosis given a deficiency of TPO and hypersplenism.
Where is VWF made?
VWF is synthesized from the Weibel-Palade bodies and subendothelium. Desmopressin (or DDAVP) is sometimes used to facilitate the release of vWF in coagulopathic patients or in patients with von Willebrand disease via activation of the V2 receptor.
What is the critical temperature?
The critical temperature of a given gas is the temperature above which it is not possible to convert said substance into liquid form by pressure alone. For nitrous oxide, this temperature is 36.5 degrees Celsius. Below this temperature, nitrous oxide can be liquefied when stored under pressure, as in the case of an E-cylinder being utilized in a typical operating room environment.
Drugs metabolised by red blood cell plasma esterases
Plasma and red blood cell esterases = clevidipine, esmolol, remifentanil
Drugs metabolized by pseudocholinesterases
Pseudocholinesterase = succinylcholine, mivacurium, ester local anesthetics
What is clevedipine?
Clevidipine is an intravenous, ultra-short acting, dihydropyridine calcium channel antagonist with selectivity for arteriolar vasodilation that is rapidly metabolized by plasma and red cell esterases providing its short duration of action. The other calcium channel blockers are metabolized by the cytochrome P450 system in the liver.
What is the MOA of an inhaled beta agonist?
The mechanism of beta-agonist induced bronchodilation is via Gs effects, cAMP generation, decreased intracellular calcium, and resulting airway muscle relaxation.
WHat are the nerves that inneravte the carotid bodies and carotid sinus?
Both CN IX and CN X carry signals generated in response to arterial hypoxia from the carotid and aortic bodies. The primary target for signals generated by carotid bodies is the chemosensitive area of the medulla, and an increase in signal generates an increase in minute ventilation. Aortic body activation results in a parasympathetic response throughout the body due to stimulation of the vagus nerve. Opioids, benzodiazepines, and inhaled anesthetics all attenuate the hypoxic ventilatory drive as a result of decreased signal production in the carotid bodies.
What is one of the major complicationes of a carotid endarterectomy?
Carotid body denervation following carotid endarterectomy can occur. Loss of a unilateral carotid body function may result in a decreased response to mild hypoxemia, with a lower threshold (PaO2 about 50 mmHg) generating an equivalent ventilatory response. Bilateral loss of carotid body function following bilateral carotid endarterectomy results in a complete loss of normal ventilatory response to acute hypoxia, and the patient becomes dependant on the hypercarbic respiratory drive. These patients have a baseline elevated PaCO2, and profound respiratory depression may result from administration of either opioids or benzodiazepines.
Muscarinic effects of choliergics
Muscarinic effects of cholinergic drugs include bradycardia, bronchospasm, miosis, salivation, lacrimation, defecation, urination, and sweating
Nicotinic effects of cholinergics
Nicotinic effects of cholinergic drugs include muscle fasciculations, weakness, paralysis, and tachycardia.
Cholinergic effects
Drugs that act on the parasympathetic nervous system are called cholinergic or cholinomimetic because their effects mimic acetylcholine. They do so either directly as agonists or indirectly by inhibiting acetylcholinesterase
Mneomoinic for muscarinc effects
Mnemonic devices for muscarinic effects:
SLUDGE-Mi “Sludge Me”: Salivation, Lacrimation, Urination, Defecation, GI upset, Emesis, Miosis
DUMBELS: Defecation/Diaphoresis, Urination, Miosis, Bradycardia/Bronchospasm, Emesis, Lacrimation, Salivation
Which agents are most affected by Fi/Fa and increased MV
The rate of inhaled anesthetic induction (FA/FI) is increased with increased minute ventilation. This effect is greatest with the agents with high solubility, including halothane and isoflurane.
WHich NT is released in preganglion sympathetic cleft?
Acetylcholine (ACh) is the primary neurotransmitter released by the preganglionic neurons of the sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS). ACh is released from vesicles near the presynaptic membrane to activate nicotinic acetylcholine receptors (nAChR) in the synapse.
SNS
Sympathetic outflow occurs from T1 to L2. The sympathetic nervous system is composed of a two-neuron system including:
1) Preganglionic: short, myelinated, release acetylcholine (nicotinic receptors), runs to paravertebral ganglia, prevertebral ganglia, and the adrenal medulla
2) Postganglionic: long, unmyelinated, release norepinephrine (most locations), ATP (vascular smooth muscle), or acetylcholine (eccrine sweat glands via muscarinic receptors)
ACLS and pregnant peopel
American Heart Association guidelines recommend beginning perimortem cesarean (resuscitative hysterotomy) at four minutes and completing delivery of the fetus by five minutes following cardiac arrest. Manual left uterine displacement should be performed during resuscitation, including during the performance of perimortem cesarean until the fetus is delivered.
HOw should a preannt lady be positioned for chest compressions?
the patient should be placed supine for chest compressions (Class I; Level of Evidence C) and continuous manual left uterine displacement (pushing uterus to the left) should be performed. This specific guideline change occurred in 2015.
WHat is physiostigmine?
Physostigmine is an acetylcholinesterase inhibitor that can cross the BBB and counteract the sedative effects of scopolamine.
parts of the scotty dog
parts of the scotty dog Transverse process: nose Pedicle: eye Pars interarticularis: neck Superior articular facet: ear Inferior articular facet: front leg
What is andexanet?
Andexanet alfa is a recombinant derivative of factor Xa, and acts as a “decoy receptor”, effectively binding factor Xa inhibitors (such as rivaroxaban, apixaban, and edoxaban) with higher affinity than factor Xa itself. Its approval represents an important step forward in anticoagulation management, as direct factor Xa inhibitors (like rivaroxaban and apixaban) continue to grow in popularity. Direct factor Xa inhibitors have oral bioavailability, do not require laboratory monitoring or have special dietary requirements (unlike warfarin), and have relatively attractive side effect profiles.
What is apixiban?
Apixaban is an oral direct factor Xa inhibitor, like rivaroxaban. While some anticoagulation agents, such as dabigatran, can at least be partially removed with the help of hemodialysis, apixaban (and, in fact, rivaroxaban) are notable in that they are NOT dialyzable.
What is bivalrudin?
Bivalirudin is a direct thrombin inhibitor with a relatively short half-life (25 minutes in patients with normal renal function; up to three hours in dialysis-dependent individuals). Its primary application is in patients undergoing percutaneous coronary intervention (PCI). As of 2018, there is no known antidote. Given its short half-life, treatment of hemorrhage is primarily supportive. Idarucizumab is a monoclonal antibody fragment that binds to the active site of dabigatran, a direct thrombin inhibitor with oral bioavailability. It is used for the management of serious bleeding caused by dabigatran but does not appear to be effective against bleeding caused by other direct thrombin inhibitors (such as bivalirudin or argatroban).
Where does inspiration occur and where does expiration occur?
The respiratory centers in the brain are located in the cerebral medulla, including both dorsal (inspiration) and ventral (expiration) respiratory groups.
Mnemonic: “DIVE” for dorsal = inspiration, ventral = expiration.
Which AB abnormablity leads to the biggest change in CBF?
respiratory acidosis
Carbon dioxide readily crosses the blood-brain barrier, while hydrogen ions do not. Thus respiratory acid-base derangements have a much greater effect on cerebrospinal fluid pH and therefore cerebral blood flow than do metabolic acid-base derangements. These effects are short-lived, however, as bicarbonate levels will normalize cerebrospinal pH in the setting of sustained respiratory acidosis or alkalosis over the course of 6 to 8 hours.
How does pyloric stenosis affect respiratpry rate?
In children with pyloric stenosis, serum alkalosis leads to CSF alkalosis. Even with correction of serum alkalosis (pH and bicarbonate), the CSF acid-base imbalance can persist. This CSF alkalosis can lead to postoperative apnea via the central control of ventilation.
What are the high, medium, and low pressure zones of the anesthesia workstation?
The high-pressure section includes auxiliary E cylinders, which are drawn from when there is pipeline failure.
Intermediate-pressure includes the hospital pipeline supply and portions of the anesthesia machine with pressures reduced by secondary pressure regulators in the 15-30 psig range.
The low-pressure section begins at the flow control valves and includes the flowmeters, vaporizers, and fresh gas supply line.
MAOI + meperidine =?
The combination of MAOIs with meperidine can precipitate serotonin syndrome.
What are the signs of serotinin syndrome?
Signs of serotonin syndrome include clonus, hyperreflexia, tachycardia, hyperpyrexia, diaphoresis, ataxia, and confusion. The most accurate diagnostic criteria currently are the Hunter Toxicity Criteria Decision Rules. Criteria are met when the patient has one of the following:
- Spontaneous clonus
- Inducible clonus plus agitation or diaphoresis
- Ocular clonus plus agitation or diaphoresis
- Tremor plus hyperreflexia
- Hypertonia plus temperature > 38 °C plus ocular clonus or inducible clonus
Note that diaphoresis is more common with serotonin syndrome. In contrast, xeroderma (dry skin) is more common with central anticholinergic syndrome (CAS).
What do you see in NMS?
Neuroleptic malignant syndrome occurs in patients taking antipsychotic medication. It is characterized by muscle rigidity and altered consciousness. Both first-generation neuroleptic medications, such as haloperidol, and newer atypical antipsychotics have been implicated in neuroleptic malignant syndrome.
During a carotid endarterectomy, the patient suddenly becomes bradycardic and hypotensive. which strucutre is affected?
Carotid sinus
….Surgical stimulation cannot always be stopped in the event that bradycardia and hypotension occur during carotid procedures. Consider the minimally invasive transcarotid artery revascularization (TCAR) procedure. During this procedure, a balloon is inflated within the carotid artery and blood flow is reversed to reduce the risk of stroke during carotid stenting. If bradycardia occurs, deflating the balloon to stop the stimulus would significantly increase the risk of stroke. Additionally, flow reversal is dependent on blood pressure and therefore hypotension that occurs during this process can also increase the risk of stroke. Thus, prophylactic glycopyrrolate is commonly given before balloon inflation. Atropine is another option, but it typically avoided as it crosses the blood-brain barrier and can affect post-procedure neurologic examination
What is lost on CVP waveform during afib?
loss of a wave
The central venous pressure tracing contains three systolic components (c wave, v wave, x descent) and two diastolic components (a wave, y descent). In patients with atrial fibrillation, two characteristic findings are the loss of the a wave and a prominent c wave.
What is Boyle law?
The Boyle law says changes in gas volume is inversely related to the pressure on the gas. As the pressure increases, then the volume will decrease. If the pressure doubles, then the volume will decrease by half.
What is Charle’s law?
The Charles law explains the relationship between volume (V) and temperature (T), where V1 / T1 = V2 / T2.
What is guy-Lussac law?
relates pressure (P) with temperature (T), where P1 / T1 = P2 / T2.
What is th corneal reflex?
The corneal reflex involves the ophthalmic branch of the trigeminal nerve (afferent limb) and the temporal and zygomatic branches of the facial nerve.
What is more potent T3 or T4? Why?
T3 is more potent than T4 due to its higher serum concentration on account of its decreased protein binding. Most circulating T3 is formed peripherally by the conversion of T4 by partial deiodination via the enzyme 5’-deiodinase.
WHERE IS TSH MADE?
Thyroid hormone production is regulated by thyroid-stimulating hormone (TSH), which is secreted by the anterior pituitary. TSH secretion is regulated by the hypothalamus and its secretion of thyrotropin-releasing hormone (TRH). These hormones feed back to control the serum level of T3 and T4.
What is secreted fromt he neurohypophysis (PP)?
Oxytocin and vasopressin (secreted, but not produced from the PP)
How does PTU work?
The process of peripheral T4-to-T3 conversion is targeted in treating hyperthyroidism with the drug propylthiouracil (PTU). In addition to central thyroid inhibition by inhibiting thyroperoxidase, PTU decreases peripheral conversion by inhibiting 5’-deiodinase.
What effect does etomidate have on SSEPs?
increases the amplitude…like ketamine
What are the three acetylchline muscarinic agonists?
Bethanechol, carbachol, and pilocarpine are examples of direct muscarinic acetylcholine agonists. These drugs are resistant to breakdown by acetylcholinesterase.
Which inhaled agent should be avoided in asthmatics?
Desflurane should be avoided in children with preexisting pulmonary disease as it increases airway resistance and can lead to bronchospasm. Treatment of bronchospasm includes positive airway pressure, increasing FiO2, inhaled bronchodilators, and intravenous epinephrine for resistant bronchospasm.
Which adrenergic agonists can bind centrally?
Endogenous adrenergic agonists (epinephrine, norepinephrine, dopamine) cannot cross the blood-brain barrier. However, alpha-2 agonists like dexmedetomidine and clonidine can cross and bind to central receptors.
Most signimfant casue for loss of temperature in an anesthetized indivcual
Radiation describes heat loss via photons, given off to the surrounding atmosphere. This type of heat transfer accounts for up to 60% of heat lost in the operating room setting, representing the most significant source of heat loss;
convection is 15%
Conduction is 10%
Evalopration is 5%–though higher in kids
What is the reticular activating system?
The reticular activating system is a collection of brain pathways that affect consciousness and wakefulness. The thalamus is responsible for transmission of signals from the reticular activating system to the cerebral cortex. Almost all anesthetics directly depress the RAS, thereby altering consciousness. Conversely, ketamine affects the thalamus, preventing fluid transmission of signals to the limbic cortex and producing its distinct dissociative effects, while also causing hyperexcitability and functional disorganization within the RAS.
How do antifibrimolytics work?
The antifibrinolytic agents TXA and aminocaproic acid are both lysine analogs which bind to activated plasmin in the place of fibrin, and in doing so prevent fibrin breakdown. TXA has been utilized effectively for the control of hemorrhage following the administration of tPA for both ischemic stroke and pulmonary embolism due to this mechanism of action.
How does protamine work?
Protamine is a large, positively charged molecule that is given as an antidote to heparin. It chelates the large, negatively charged heparin molecule and prevents its binding with antithrombin 3 and its subsequent anticoagulant effect
What are the TEG normal values?
Normal values for thromboelastography can be remembered by the rule of 6’s:
- R time around 6 minutes
- Alpha angle around 60 degrees
- Maximal amplitude around 60 mm
- LY30 of around 6%
These are rough estimates but are helpful as an approximation of normal values when interpreting TEG results.
Most resiliant monitoring form to anesrthetics
: Brainstem auditory evoked potentials, also known as brainstem auditory evoked responses (BAERs), are the most resistant to the effects of volatile anesthetics.
Which monitoring techniques are least to most effectied by volatile anesthetics?
Brainstem potentials are Barely affected, Sensory potentials are Somewhat affected, Motor potentials are Mostly affected, and Visual potentials are Very affected.
Why are the adrenals important?
The adrenal cortex secretes different steroids from three distinct layers; each secretes a unique substance. The outer layer, zona glomerulosa, produces mineralocorticoids (aldosterone). The middle layer, zona fasiculata, produces glucocorticoids (cortisol). The innermost layer, zona reticularis, produces gonadocorticoids. Throughout the adrenal cortex, the cells contain lipid droplets made of cholesterol that form the basis of the steroids. The adrenal medulla is comprised of chromaffin cells that synthesize and secretes catecholamines. The predominant catecholamine is adrenaline, accounting for approximately 80%. Noradrenaline is also produced and secreted from the medulla, accounting for approximately 20%.
How do the adrenals affect kidney function
The mineralocorticoid aldosterone acts to retain sodium and water in response to stimulation of the renin-angiotensin system. The primary site of action is the distal convoluted tubules and collecting ducts of the kidney. Aldosterone acts on numerous other epithelial tissues and the intestine. In all these places, it acts to promote excretion of potassium in exchange for sodium. Water follows the sodium.
What is yhe role of cortisol?
Cortisol is the body’s primary glucocorticoid. It is released from the zona fasciculata of the adrenal cortex, principally following ACTH secretion from the anterior pituitary. Cortisol levels typically follow a diurnal pattern, related to sleep patterns, with a peak in the early morning around wakening and a dip at midnight. Cortisol levels can be raised in response to several stimuli such as trauma, sepsis, heavy exercise, hypoglycemia, and acute anxiety. Glucocorticoids act to maintain blood glucose levels by promoting gluconeogenesis and fat metabolism.
REview the RAAS system
Renin is secreted from the juxtaglomerular apparatus in response to a decrease in renal perfusion pressure. Angiotensinogen is a protein secreted from the liver into the blood. It is converted by renin to angiotensin I. In the lungs angiotensin I is converted to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II acts on the zona glomerulosa of the adrenal cortex to release the mineralocorticoid, aldosterone. Angiotensin II also acts on other systems – in the blood vessels it stimulates smooth muscle contraction, in the brain, it activates thirst centers, and in the posterior pituitary it stimulates the release of antidiuretic hormone. Angiotensin II and aldosterone both act to maintain fluid balance and blood pressure. Conn syndrome is mineralocorticoid excess. It results in potassium depletion, sodium retention, polyuria, tetany, and weakness. In adrenal medulla tumors (pheochromocytoma), the ratio of catecholamines produced is reversed with 80% of noradrenaline and 20% of adrenaline.
APL valve “closed”
greater than 0; open means 0 . “0pen”
What is the activie metabolite of codeine?
morphine
metabolized via CYP2D6 (six letters + one D in codiene)
poor metabolizers get little effect from drug
fast metabolizers easily overdose
Sites where you can reliably measure core body temperature
The sites at which core temperature can be measured are the pulmonary artery, distal aspect of the esophagus, tympanic membrane, and nasopharynx.
How do the systolic and diastolic BP change as you move the NIMBP cuff more distally?
The pulse pressure increases as the cuff is moved more distally. Pulse pressure is equal to the systolic minus the diastolic pressure (PP = SBP - DBP). Hence, the SBP increases and DBP decreases more distally. In fact, in cardiac cases when measuring both the aortic root and radial artery pressures, they should have the same MAP, but the radial artery will have an increased SBP and decreased DBP.
Risk factors for breech presentation
Many factors predispose to breech presentation. Abnormalities of the fetus or the maternal pelvis or uterus may play a role. Factors associated with breech presentation include multiparty, multiple gestations, hydramnios, macrosomia, pelvic tumors, uterine anomalies, pelvic contracture, hydrocephalus, anencephaly, previous breech delivery, preterm gestation, oligohydramnios, cornual-fundal placenta, and placenta previa.
A 26-year-old female is undergoing an ultrasound-guided interscalene nerve block for a total shoulder arthroplasty. Upon injection of the local anesthetic, the patient immediately starts to seize. Accidental intravascular injection is suspected. What vessel was the local anesthetic MOST likely injected into?
The vertebral arteries most commonly originate from the subclavian arteries and are divided into four segments depending on their anatomic location. They traverse the neck anterior to the scalene muscle and enter the vertebral foramina of the sixth cervical vertebra. It can be a site for inadvertent arterial injection when performing an interscalene nerve block.
Absolute contraindications to BPAP
Absolute contraindications to the use of BPAP in the postoperative period include:
- Cardiac or respiratory arrest
- Severe agitation
- Voluminous secretions/vomiting/GI bleeding
- Inability to protect airway
- Facial trauma
- Hemodynamic instability
Specifically, recent upper gastrointestinal stapling is not a contraindication to the use of BPAP assuming that standard precautions are taken (peak airway pressures 25 cmH2O and PSV below 6-8 cmH2O). In such cases, a nasogastric tube may be in place which can be leveraged to assess for abdominal insufflation. If this tube is placed on a bag instead of to constant suction, insufflation of the bag will indicate insufflation of the stomach and upper gastrointestinal tract during BPAP ventilation, and would likely indicate a need for conversion to endotracheal intubation in this patient population.
How does gabapentin work?
Gabapentin reduces the release of glutamate by binding to the α2-δ subunit of voltage-gated calcium channels.
Decreased glutamate release decreases the production of the pain mediator substance P, thereby decreasing neuronal transmission of pain signals. There is also decreased activation of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptors on noradrenergic synapses, which attenuates the sympathetic response to pain.
MOA of ketamine
NMDA receptors are antagonized by ketamine. NMDA antagonism reduces the release of glutamate. Magnesium is another NMDA antagonist.
What is the most common cause of fetal bradycardia?
The primary cause of fetal bradycardia is increased parasympathetic activity via the vagus nerve in the setting of fetal hypoxia
What most determines fetal HR?
parasympathetic tone (which increases with term age) Variability of FHR is a subjective measure of the FHR tracing but is defines as cyclical fluctuation of the FHR at least twice per minute. This is primarily influenced by the parasympathetic tone, with increasing tone exerting an increased effect on the heart rate, and therefore increasing variability.
What effect does beta blocker have on fetus?
How about atropine?
LIttle–not mature sympathetics NS;
Atropine decreases variablity (less parasympathetic tone)
maternal administration of atropine, which effectively eliminated the vagal tone in the fetus as it readily crosses the placenta, causes a decrease in FHR variability. Conversely, maternal administration of a beta-blocker which also readily crosses the placenta has minimal effect on the FHR variability. This is due to the minimal impact of the immature fetal sympathetic nervous system on regulating FHR.
Decreases in FHR variablity
hypoxia
CNS injury/ Anacephaly
maternal opioid use
fetal sleep state
What is an early deceleration?
Early decelerations are defined as a decrease in FHR of typically no less than 20 bpm below baseline and occur simultaneously with contractions. These are thought to be due to reflex vagal stimulation and are in general considered to be a benign finding.
What is a late deceleration?
Late decelerations are also associated with uterine contractions but are slightly delayed in their onset (10-30 seconds following the onset of contractions). These are thought to represent a response to fetal hypoxemia, with traditional teaching implicating some form of placental insufficiency. By themselves, late decelerations are of uncertain clinical significance, but in combination with decreased variability, this finding may point towards fetal compromise.
What are variable decelerations?
Variable decelerations are variable in their presentation but typically result in a more profound deceleration of FHR than the other two. These are thought to be due to occlusion of the umbilical cord during contractions. While healthy fetuses can typically tolerate transient variable decelerations, prolonged fetal bradycardia impairs the ability of the fetus to maintain cardiac output and is an indication to consider emergent operative delivery.
Which medications cross the placenta?
The following medications cross the placenta following maternal administration and may impact the physiology of the fetus seen on monitoring: morphine, fentanyl, benzodiazepines, ephedrine, local anesthetics, atropine, beta-blockers.
What is the gold standard for platelet function assessment?
The gold standard laboratory analysis of platelet function is optical aggregometry, though viscoelastic monitoring of coagulation is a reasonable surrogate if the appropriate assays are utilized. Other point-of-care measures of platelet function are limited in their use to predict an increased risk of intraoperative bleeding.
Flow volume loop:
variable INTRAthoracic obstruction
Plateaued EXPIRation (flat top) A variable INTRAthoracic airway obstruction (e.g. distal tracheal tumor or mediastinal mass) produces a flow-volume loop with a plateaued EXPIRATORY curve and the flow rate is usually decreased. During expiration, intrathoracic pressure becomes positive which further decreases the airway diameter, enhances the degree of obstruction, and impairs airflow. The inspiratory curve is usually normal since the negative intrathoracic pressure generated during inspiration helps keep the airway open.
Flow volume loop:
variable EXTRAthoracic obstruction
Plateued INSPIRation (flat bottom) A variable EXTRAthoracic airway obstruction (e.g. proximal tracheal tumor, external compression from a goiter) produces a flow-volume loop with a plateaued INSPIRATORY curve, and the flow rate is usually decreased. During inspiration, the negative inspiratory pressure causes the obstruction to increase. The expiratory curve is usually normal since the positive airway pressure generated during expiration helps keep the airway open
Flow volume loop:
fixed obstruction
Plateued top and bottom
A fixed upper airway obstruction or fixed large airway obstruction (e.g. foreign body, tracheal stenosis, large airway tumor) impairs BOTH inspiration and expiration leading to a flow-volume loop with plateaued and decreased inspiratory and expiratory flows.
FVL:
COPD
SCooped out expiration portion (top)
(COPD) is characterized by an expiratory phase with a quick peak followed by a much lower than normal plateau phase. This is representative of the dynamic, intrapulmonary airway obstruction that occurs with COPD during exhalation. The inspiratory phase is usually normal
Common tocolytics:
Common tocolytics include magnesium, terbutaline, and ritodrine (not available in the United States).
PResentation of hypermagnesimia
Treatment
Common early symptoms include nausea, headache, lightheadedness, and muscle weakness. Hyporeflexia or lack of deep tendon reflexes, sedation, and hypotension suggest higher levels of magnesium. Marked levels of hypermagnesemia can lead to respiratory arrest and cardiac arrest.
Treatment includes discontinuation of the magnesium infusion/intake and administrating intravenous calcium. Loop diuretics and intravenous fluids can also be used to enhance excretion of magnesium.
What are p450s?
The cytochrome P450 (CYP) superfamily of enzymes is responsible for most of the phase one biotransformation reactions in the liver. The phase one reactions include oxidation (primary), reduction, and hydrolysis. The enzymes are highly concentrated in hepatocytes and in the small intestines but also are found in small amounts in the lungs, kidneys, and skin. There are multiple subtypes of CYP enzymes, including 3A4, 2D6, 2C9, 2C19, and 2E1.
What does fluoxetine do to midazolam metabolism
slows it down (p450 inhibitor)
Fluoxetine is a selective serotonin reuptake inhibitor (SSRI) that is used in the treatment of both generalized anxiety disorder and major depressive disorder. Fluoxetine and its metabolite norfluoxetine inhibit CYP 3A4, which is responsible for the metabolism of many anesthetic drugs, including midazolam
What side effects go with which uterotonics?
methylergometrine make the blood pressure go HYER (higher): HY ER: metHYlERgometrine HYpERtension
Also, the double O’s go together: OOS: carbOprOSt brOnchOSpasm
What is methylergometrine?
Uterine atony is a common cause of post-delivery hemorrhage. In patients who have a diagnosis of preeclampsia (as this patient is presumed to have), administration of methylergometrine should occur only after all other options are exhausted and with extreme caution. Methylergometrine is an ergot alkaloid that is typically given intramuscularly. It has an effect within 10 minutes and lasts 3-6 hours. It can lead to intense vasoconstriction, especially if accidentally given intravenously. This can cause significant morbidity (e.g. stroke) in patients with preexisting hypertension or preeclampsia.
What is carbaprost?
Carboprost is a prostaglandin, which increases the force and frequency of uterine contractions. It is typically given intramuscularly and can be repeated at 15-90 minute intervals for a maximum of 8 doses.
morphine vs fentably injected in epidural
One of the most important factors in determining the clinical pharmacology for a particular opioid is its degree of lipophilicity versus hydrophilicity. Cephalad movement of opioids in the CSF principally depends on lipid solubility. Highly lipid-soluble opioids are limited in their cephalad migration by uptake into the spinal cord, whereas less lipid-soluble opioids remain in the CSF and transfer to more cephalad locations. Hydrophilic opioids, like morphine, have the potential to produce a delayed, but longer duration of analgesia, along with a generally higher incidence of side effects because of cephalic or supraspinal spread.
What are vascular rings
Vascular rings should be considered in the differential diagnosis for airway compression, wheezing, stridor, respiratory distress, apnea, cyanosis, and dysphagia. MRI or CT should be employed to assess the level of branching, which will affect surgical planning. Mirror branching consists of a right-sided aortic arch that gives rise to a left brachiocephalic artery, which then gives rise to a left subclavian artery and left carotid artery. These patients should be extubated with caution and vocal cord paralysis may be seen.
What is omalizumab?
Omalizumab is a monoclonal anti-IgE antibody. It is used as an antihistamine anti-inflammatory for patients with severe asthma.
montelukast
leukotriene modifier
Burn resussitation
The Parkland formula calls for 4 mL of crystalloid / kg / % burn in the first 24 hours. The modified Brooke formula calls for 2 mL of crystalloid / kg / % burn in the first 24 hours. For both of these, half of the calculated predicted volume is given over the first eight hours, 25% is given over the next eight hours, and the last 25% is given during the final eight hours. The Joint Trauma Service rule of tens calls for an initial hourly rate of 10 * % burn (for patients 40-80 kg; for every 10 kg over 80 kg, an additional 100 ml/hr is added). In each case, the infusion rate should be regularly titrated (e.g. hourly) based on clinical response.
Describe diffusion hyopxia
Diffusion hypoxia (“Fink effect”) is a well-documented effect since the 1950s that can be observed following the cessation of an inhaled anesthetic involving the use of high concentrations of nitrous oxide. The relatively higher concentrations of nitrous oxide (up to 70%) required to maintain general anesthesia compared to other more potent inhaled anesthetics, and its low blood solubility result in the rapid alveolar elimination of large amounts of nitrous oxide following cessation of the anesthetic. This flooding of nitrous oxide results in the displacement of oxygen and carbon dioxide in the alveoli, leading to a temporary hypoxia. This diffusion hypoxia typically lasts for 5-10 minutes immediately after emergence, and can be prevented by the use of supplemental oxygen while the nitrous oxide is being eliminated.
Why is nitropuis oxide fast on and off
Nitrous oxide has a relatively low blood:gas coefficient of 0.47, which explains its property as a quick onset/offset inhaled anesthetic. This is in contrast to isoflurane, which has a much slower onset of action and elimination with its blood:gas coefficient of 1.4. In other words, isoflurane is nearly 3 times more soluble in blood compared to nitrous oxide. This results in a slower increase in alveolar isoflurane concentration because the anesthetic is rapidly removed from the alveoli into the bloodstream. In contrast, a less blood soluble anesthetic like nitrous oxide or desflurane results in a faster increase in alveolar concentration because the anesthetic is removed less quickly from the alveoli into the bloodstream. Similarly, less blood soluble anesthetics are eliminated faster from the blood into the alveoli when the anesthetic is discontinued. While it may appear counter-intuitive at first, it is important to understand this relationship between an inhaled anesthetic’s blood:gas coefficient as it relates to the speed of onset/offset.
What is diffusion hypoxia?
Diffusion hypoxia is a well-known phenomenon that can occur following administration of nitrous oxide as part of general anesthesia. The low blood solubility of nitrous oxide, coupled by relatively low potency leads to large amounts of nitrous oxide being eliminated into the alveoli over a short period of time following cessation of anesthesia. This leads to displacement of oxygen and carbon dioxide in the alveoli. Supplemental oxygen should be provided to mitigate this effect.
Which organisms are most commonly implicated in aspiration events?
Lung abscesses are most commonly a result of primary lung infections, such as aspiration pneumonia, leading to further necrosis and abscess formation. Organisms that are commonly implicated include anaerobes (Bacteroides, Peptostreptococcus), as well as some aerobes (Staphylococcus, Klebsiella, and Pseudomonas).
What is the MOA of etomidate
At clinical doses, etomidate exerts its effect at the γ-aminobutyric acid type A (GABAA) receptor by binding to specific sites on the receptor which enhances the affinity for GABA binding.
The principle inhibitory neurotransmitter in the central nervous system is GABA. GABA-A receptors are included in a class of receptors known as cys-loop ligand-gated ion channels composed of five subunits (two α, two β, one γ) and selectively conduct chloride ions. The activation of GABAA receptors leads to hyperpolarization of the neuron significantly below the resting Nernst potential of -70 mV and the sedative-hypnotic effects of the GABAA agonists. Other inhibitory neurotransmitters include glycine, adenosine (A2A receptor), norepinephrine (α2), and opioids. Other GABAA agonists include benzodiazepines, barbiturates, propofol, and volatile agents.
What is the pharmacology of etomidate?
Etomidate is a potent GABAA receptor agonist that leads to neuron hyperpolarization via positive modulation of the receptor for GABA binding. Etomidate is highly protein bound (~75%) and metabolized by liver ester hydrolysis to inactive metabolites that are primarily excreted by the kidneys. It does not inhibit sympathetic tone or myocardial function to a significant degree, and does not blunt the sympathetic response to laryngoscopy and intubation. Infusions are typically avoided due to adrenal suppression. Cerebral perfusion pressure is maintained. However, like other GABAA agonists, it does reduce the cerebral metabolic rate of oxygen and cerebral blood flow (and therefore intracranial pressure).
NMDA receptor antagomists (4)
Ketamine, nitrous oxide, methadone, and memantine are examples of NMDA receptor antagonists.
ALpha2 agonists (2)
Clonidine and dexmedetomidine are examples of α2 agonists.
Describe a needle thoracostomy
If the chest wall or pleura are violated, air can escape into the pleural space, resulting in a pneumothorax. Occasionally, a “one-way valve” effect may occur, resulting in a gradual build-up of pressure in the pleural space and compression of the great vessels leading to hemodynamic collapse. Patients may present with progressively worsening tachycardia, tachypnea, hypoxia, and hypotension. Late findings include a deviated trachea and a mediastinal shift away from the side of the tension pneumothorax. Without immediate treatment, the patient may develop pulseless arrest. Either the 5th intercostal space in the anterior axillary line or the 2nd intercostal space in the mid-clavicular line may be used for needle decompression. Needle insertion should be at the superior border of the rib to avoid the intercostal neurovascular bundle, and successful placement should result in a hiss of escaping air and improvement in patient hemodynamics.
Grey rami communicantes
Gray rami communicantes originate from adjacent paravertebral ganglia of the sympathetic trunk and contain postganglionic nerve fibers of the sympathetic nervous system. Gray rami are composed largely of unmyelinated neurons. White rami communicantes, on the other hand, are heavily myelinated neurons and give the rami their white appearance.
Helpful mnemonic: whIte on the way Into the sympathetic trunk, grEy Exiting the sympathetic trunk.
What is the central respiratory system?
The medulla is known to house the central respiratory system, which is chemically sensitive to dissolved carbon dioxide as bicarbonate does not permeate the blood-brain barrier.
Two groups of neurons in the medulla control basic respiratory rhythm. These are categorized as the dorsal and ventral respiratory group. The ventral respiratory group is active during expiration. Meanwhile, the dorsal respiratory group is active during inspiration and is regulated by the pons.
What is the equation for cerebral perfusion pressure/
Cerebral perfusion pressure is equal to mean arterial pressure - intracranial pressure (CPP = MAP - ICP). Cerebral autoregulation is typically compromised during brain injury. Cerebral perfusion pressure then becomes directly dependent on MAP and inversely dependent on ICP.
Non-shivering thermogensusis in adults (2 ways)
Brown fat tissues and skeletal muscles are the major sources of nonshivering thermogenesis in adults.
WHen do you use a chi square test?
The Chi-square test is a statistical option to determine the probability of an observed distribution occurring due to chance alone. It is often referred to a “goodness of fit” measurement because it evaluates how well the observed distribution of data fits with what the expected distribution would be if variables were truly independent.
Categorical data is well suited for analysis by a Chi-square test.
What is dead space ventialtion?
What is the Bohr equation?
Dead space is the proportion of tidal ventilation that does not participate in gas exchange because it does not come in contact with the pulmonary capillary blood flow. It is divided mainly into anatomical dead space and alveolar dead space. The sum of these makes up the physiologic dead space, which is calculated using the following formula known as the Bohr equation.
Vd = Vt*(PACO2-PECO2)/PACO2
(Vd: dead space, Vt: tidal volume, PACO2: mean alveolar partial pressure of CO2, PECO2: mixed expired partial pressure of CO2)
New onset actue afib in stable pt
Beta blockers and the calcium channel blocker diltiazem are the current drugs of choice for the pharmacologic management of new-onset AF in hemodynamically stable patients. Patient co-morbidities can help the provider determine which agent (beta blocker or calcium channel blocker) to choose. Additionally, amiodarone is not considered a first-line agent in the management of atrial fibrillation.
Dont give BB to peopel with COPD or DM
Abdominal compartment syndrome
Abdominal compartment syndrome is diagnosed by observing a tense, distended abdomen and by obtaining bladder pressure readings > 20-25 mm Hg via a urinary catheter. Abdominal compartment syndrome has a high rate of morbidity and mortality and therefore necessitates prompt recognition and surgical decompression to avoid multiorgan failure and death.
What are the line isolation monitors
The following are characteristics of Line isolation Monitors (LIM):
1) Monitors the integrity of the ungrounded power source in the operating room.
2) The primary circuit is attached to ground, but the secondary circuit is not.
3) The LIM alarms when the leakage current is greater than 5 milliamps.
4) A first fault is not a shock hazard, but a second fault is a hazard to operating room personnel.
If there is an alarm after the procedure has begun, the most appropriate next step is to unplug the electrical device which was most recently plugged in.
What is ethosuxamide?
A variety of antiepileptic agents are currently used for management of seizure disorders. However, only ethosuximide is used exclusively for the treatment of absence seizures. Its mechanism involves blockade of T-type calcium channels (which possess a corticothalamic distribution), resulting in a reduction in excessive excitatory activity.
Does water move freely across the BBB>
Yes
The BBB protects the CNS from pathogens and rapid fluctuations in its electrolyte-fluid balance. Water moves freely across the blood-brain barrier (BBB) based on the tonicity of intravascular fluid. With the pathologic disruption of the BBB, hydrostatic pressure becomes more central to intracranial fluid movement.
WhT DOES MANNITOL DO IN BRAIN SURGERY
Mannitol is a sugar alcohol with osmotically active properties. It is given to promote diuresis in situations such as the oliguric phase of acute renal failure, elevated intraocular pressure, and elevated intracranial pressure. Mannitol is also useful in flushing out harmful toxins. Its utility in elevated intracranial pressure stems from its large molecular weight, which makes it unable to penetrate the BBB. Mannitol then draws fluid from the brain into the intravascular space, which is then excreted as urine.
Does atropine cross the BBB?
YES
Certain drugs with the same function may differ in CNS permeability because of the BBB such as in the case of anticholinergic medications glycopyrrolate (does not cross BBB, does not cause sedation) and atropine (does cross BBB, does cause sedation).
Which benzo has the shortest t1/2
Flumazenil has the shortest elimination half-life of all currently used benzodiazepines, which makes recrudescence of sedation after a single administration of flumazenil likely.
What casues granulation formation on a intrathecal catheter?
Fentanyl has NOT been shown to cause intrathecal (IT) granuloma formation when chronically administered via an intrathecal drug delivery (ITDD).
Administration of both hydromorphone and morphine in ITDD systems is associated with the formation of IT granuloma which causes pump malfunction, neurologic deficits, and may require surgical excision.
Sleep stages
BATS Drink Blood
- Beta waves (awake)
- Alpha waves (drowsy)
- Theta waves (stage 1)
- Spindles and K complexes (stage 2)
- Delta waves (stage 3 and 4)
- then back to Beta waves (awake)
Note that the oscillation frequency starts high then progresses lower.
Spectrum of waves
Name Frequency Range (Hertz, Cycles per Second) Slow < 1 Delta 1 to 4 Theta 5 to 8 Alpha 9 to 12 Beta 13 to 25 Gamma 26 to 80
Where is acetylchoine made?
Acetylcholine (ACh) is synthesized in the presynaptic terminal by acetylation of choline with acetyl-CoA via choline acetyltransferase in the cytoplasm.
HOW IS ACETLY CO-A RELEASED INTO THE CLEFT?
Acetylcholine (ACh) is synthesized in the presynaptic terminal by acetylation of choline with acetyl-CoA via choline acetyltransferase in the cytoplasm. Large amounts of ACh molecules are then stored together within vesicles near the cell membrane. After propagation of an action potential (via sodium channels), there is activation of voltage-gated calcium channels at the nerve terminal and calcium influx leading to “docking” of the ACh vesicles to SNARE proteins. The two fuse and ACh is released via exocytosis. A portion of the ACh molecules activate the nicotinic acetylcholine receptors, although a large amount of ACh is rapidly metabolized by acetylcholinesterase to form acetate and choline. Choline is recycled back into the nerve terminal.
HOW IS ACETLY CO-A BROKEN DOWN?
Acetylcholine is rapidly broken down by acetylcholinesterase in the synapse into acetate and choline. Choline is recycled back into the presynaptic neuron. Unlike norepinephrine, there is no reuptake of acetylcholine and it must be synthesized constantly.
ARE ALL PLACES REQUIRED TO HAVE MH stuff?
No
As described in the American Society of Anesthesiologists (ASA) Guidelines for Office-Based Anesthesia, all locations that utilize triggering agents (succinylcholine and volatile anesthetics) for the administration of anesthesia are required to maintain on-site medications, protocols, and procedures for the effective management of malignant hyperthermia. If these agents are not utilized, then the office is not required to maintain these resources.
What is the pathophysiology of periphrial neuropahthy?
The hyperglycemia of diabetes leads to the non-enzymatic glycosylation of small vessel endothelium, which leads to ischemia in axonal nerve tissue (microangiopathy) and elsewhere.
What is the deadspace equation?
Physiologic dead space equation: VD/VT = (PaCO2 - PECO2) / PaCO2
What is hexamethonium?
Hexamethonium is an example of a ganglionic blocking drug which acts as an antagonist at the neuronal-type nicotinic receptors.
What is the role of trnscranial doppler?
Transcranial Doppler (TCD) ultrasound monitoring measures two parameters during carotid vascular surgical procedures: blood flow velocity in major arteries (normally the middle cerebral artery [MCA]) that lead to the cerebral cortex, as well as the number of atherosclerotic emboli detected in the same vessel.
When CO is low, which anesthetic has the most dramtic increase in FA/FI
Reduced cardiac output leads to an increased speed of inhaled anesthetic induction (FA/FI), particularly for the soluble anesthetics like isoflurane or halothane.
What layer of the heart are pacemaker leads placed?
endocardium
What KG change is most reliable in a intravascualr injection?
Cardiac effects of bupivacaine with epinephrine include an increase in the PR interval, increased duration of the QRS complex, increase in T-wave amplitude, ST-segment changes, sinus bradycardia, and sinus arrest. Bupivacaine-induced T-wave elevation is a sign of impending cardiac toxicity, especially during fast injection
Intravascualr injection of bupiviacine casues what EKG changes?
Injection of bupivacaine with epinephrine can cause QRS complex widening, PR interval lengthening, and QTc interval lengthening.
Static copmliance measure
Tissues possess both static and dynamic compliance. Compliance, in general, can be thought of as ΔV/ΔP. The Cstat of a tissue can be measured during an inspiratory hold. The formula uses plateau airway pressures since the value is measured during periods of no flow. The formula is Cstat = VT/(Pplat-PEEP).
What is dynamic compliance?
Dynamic compliance refers to compliance of lung tissue during gas flow. It can be calculated using the formula: Cdyn = VT/(PIP - PEEP). Decreases in dynamic compliance are observed in a variety of obstructions, such as obstruction of the endotracheal tube, mucous plugging, or airway narrowing. Keep in mind: because PIP is always higher than Pplat, the Cdyn for any given lung tissue is always lower than the Cstat.
What are the opioid receptors?
Opioid receptors remain a topic of continued research. It is known that they are G protein-coupled receptors with several subtypes, some of which are still being elucidated. The µ-, κ-, and δ-receptor subtypes are well-characterized. Each is found throughout the body in variable distribution and are responsible for the many effects exerted by both endogenous and exogenous opioids.
µ1: supraspinal analgesia, physical dependence
µ2: respiratory depression, miosis, euphoria, reduced gastrointestinal motility, physical dependence
κ: Spinal analgesia, sedation, miosis, inhibition of antidiuretic hormone release
δ: Analgesia, euphoria, physical dependence
What is almivopan?
Alvimopan is a potent µ-receptor antagonist which does not cross the blood-brain barrier. It is used to help prevent postoperative ileus while allowing continuation of pain management with opioids.
What do you see in HFpEF?
Patients with heart failure with preserved ejection fraction (HFpEF) have EF greater 50% with a normal left ventricular end-diastolic volume and an elevated left ventricular end-diastolic pressure. Concentric remodeling and left ventricular hypertrophy from long-standing hypertension contribute to abnormalities in diastolic function such as a delayed and slowed relaxation, decreased recoil, slow and incomplete early filling, increased filling during atrial contraction, and decreased distensibility.
At the neuromuscular junction, which of the following postjunctional acetylcholine receptor subunits contains the binding site of acetylcholine?
ALPHA-1
The postjunctional nicotinic acetylcholine receptor is a pentamer consisting of 2 alpha-1 subunits, a beta-1 subunit, a delta-7 subunit, and an epsilon subunit (gamma subunit instead of epsilon subunit in the fetal receptor). The acetylcholine binding site is on the alpha-1 receptors.
What is the EEG cut off for brain death?
EEG monitoring is a reliable and widely used method of confirming brain death, but can only be used as an ancillary test after standard criteria have been met. Although EEG confirmation is reliable and widely used, it is an ancillary test and not mandatory. Electrocerebral silence on EEG (< 2 uV/mm activity) is confirmatory, especially when combined with evoked responses, but a false positive may occur with high doses of anesthetics such as barbiturates.
What is one of the effects seen sometimes from a cerberal AVM repair?
acute cerebral edema
Tight hemodynamic control is paramount in AVM embolization procedures. Cerebral dysautoregulation can result in rapid and profound cerebral edema in the downstream vascular distributions. This edema may require rapid action on the part of the anesthesiologist consisting of therapeutic hypotension, hypocapnia, hypothermia, or administration of sedative-hypnotic agents such as barbiturates or propofol.
zones fo the adrenal cortex
Adrenal cortex layers are GFR: glomerulosa (mineralocorticoids, “salty”), fasciculata (glucocorticoids, “sweet”), reticularis (reticularis, “sex”). Mnemonic: the deeper you go, the better it gets.
What do glucocortocoids do?
Glucocorticoids, primarily cortisol, acts to increase energy substrates. When stressed, the body needs a surge of energy available to handle the stress response. Cortisol is the primary glucocorticoid that will mobilize energy. Cortisol diffuses through the cell membrane to alter gene transcription. It mobilizes fatty acids, protein catabolism products, and glucose by increasing glucose substrates and impairing insulin sensitivity to decrease the amount of glucose taken up for storage.
What is a claims made policy?
A professional liability insurance policy that covers malpractice claims reported during the year the policy is active is known as a claims made policy.
WHAT IS THE RISK FACTOR FOR POCD?
No anesthetic best practice currently exists to prevent POCD. Age greater than 65 years old has been independently shown to predict the development of POCD. No other risk factors for POCD have been definitively identified. No difference in POCD has been seen with a regional versus general anesthetic technique, nor is there any single anesthetic drug that has been identified as either causative or protective.
A patient sustains an injury after laryngeal mask airway placement resulting in tongue motor palsy. Which of the following was MOST LIKELY injured?
Motor innervation of the tongue arises nearly entirely from the hypoglossal nerve (CN XII). The hypoglossal nerve innervates all the extrinsic and intrinsic muscles of the tongue, except for the palatoglossus which is innervated by the vagus nerve. It is a nerve with a solely motor function. The hypoglossal nerve controls the tongue movements required for speech, swallowing, and moving the tongue side to side. Damage to the nerve can affect the tongue’s ability to move.
The ___________ nerve provides both taste and sensory innervation to the posterior 1/3 of the tongue.
The glossopharyngeal nerve provides both taste and sensory innervation to the posterior 1/3 of the tongue.
What does the recurrent laryngeal nerve do?
The recurrent laryngeal nerve innervates the larynx below the vocal cords and the trachea. The recurrent laryngeal nerve provides the motor supply to all intrinsic laryngeal muscles except for the cricothyroid muscle.
The cricothyroid muscle receives motor innervation from the external branch of the superior laryngeal nerve. Because the recurrent laryngeal nerves supply all of the intrinsic muscles of the larynx (with the exception of cricothyroid muscle), trauma to these nerves can result in vocal cord dysfunction.
What does the superior laryngeal nerve do?
The superior laryngeal branch of the vagus nerve divides into an external (motor) nerve and an internal (sensory) laryngeal nerve that provide sensory supply to the larynx between the epiglottis and the vocal cords. The cricothyroid muscle receives motor innervation from the external branch of the superior laryngeal nerve.
What would happen if you poured iso into a sevo vaoprizer? Why?
Overdose
Pouring isoflurane into a sevoflurane vaporizer is most likely to lead to an overdose of volatile anesthetic. This is due to (1) the larger vapor pressure of isoflurane, and (2) the increased potency of isoflurane compared to sevoflurane. Sevoflurane has a relatively low vapor pressure of 160 mmHg at 20 °C compared to 240 mmHg for isoflurane. Therefore, there will be proportionally more molecules of isoflurane in the vapor phase and the output concentration of isoflurane will be greater than what is set on the “sevoflurane” vaporizer concentration dial. The use of an anesthetic agent analyzer (e.g. infrared absorption spectrophotometry) would alert the provider to such an error.
An increase in P50 corresponds with what?
Increased P50 values actually correspond with a decreased affinity of hemoglobin for oxygen. More oxygen offloading occurs in this situation.
The P50 (normally 27 mm Hg) is the partial pressure of oxygen (PO2) at which the hemoglobin (Hgb) molecule is 50% saturated with oxygen at 37 degrees Celsius and a pH of 7.4. Factors influencing the P50 are directly related to those parameters that shift the oxygen-hemoglobin dissociation curve to the “left” or to the “right”. The P50 is reduced when the curve is shifted to the left for the following reasons: hypothermia, alkalosis, decreased DPG. A decreased P50 results in an increased Hgb affinity for oxygen, leading to a release of oxygen to the tissues at a lower PO2. The P50 is increased when the curve is shifted to the right due to: hyperthermia, acidosis, increased DPG. An increased P50 results in a decreased Hgb affinity for oxygen and release of the oxygen to the tissues at a higher PO2.
What is normal P50?
What causes a left shift?
A right shift?
P50 is normally ~27 mm Hg and corresponds to the PO2 at which 50% of Hgb is saturated at normal physiologic pH and temperature. A left shift (due to hypothermia, alkalosis, decreased DPG) causes a decreased P50 and an increased Hgb affinity for oxygen. A right shift (due to hyperthermia, acidosis, increased DPG) causes an increased P50 and a decreased Hgb affinity for oxygen, meaning more offloading of oxygen.
Decreasing VT to 6-8mL/kg has what effect on kidneys?
Decreasing the tidal volume to 6 mL/kg (lung protective strategy) could decrease the risk of renal injury related to positive pressure in this patient by decreasing cytokine release.
How does PPV effect kidneys?
Renal effects from mechanical ventilation involve three broad categories: hemodynamic, neurohormonal, and biochemical. Induction of positive pressure ventilation affects hemodynamics by decreasing preload and increasing right ventricular afterload (both of which decrease cardiac output and renal blood flow), while promoting increased venous pressure, all of which have deleterious effects on the kidneys.
Positive pressure ventilation also results in an increase in sympathetic nervous system output which secondarily results in an increase in renin release through beta-1 receptor stimulation with resultant release of angiotensin-2 and aldosterone. This results in vasoconstriction with salt and water retention which can decrease urine output. There is also an increase in the release of ADH (also seen with surgical stress) which increases free water reabsorption and decreases urine output, however this is a minor component. Lastly, there is a decrease in atrial natriuretic peptide which decreases natriuresis and vasodilation.
Biochemically, positive pressure ventilation induces cytokine release which can cause endothelial activation, increase vascular permeability, and result in apoptosis of renal epithelial cells. The pattern of ventilation can have alterations in the amount of cytokine release and resultant renal injury as described earlier with the ARDSnet trial. There is also evidence that positive pressure ventilation increases the release of nitric oxide and enhances nitric oxide synthase activity. The breakdown products of nitric oxide cause oxidative damage, increased vascular permeability and can result in cellular apoptosis.
What are the contrainducations to retrograde intubation?
Contraindications:
- Coagulopathy.
- Inability to identify landmarks (obesity, thyroid goiter, distorted anatomy).
- Laryngeal disease (such as laryngeal stenosis directly at the puncture site. Retrograde intubation has successfully been used in epiglottitis, laryngeal trauma, laryngeal cancer).
- Local infection (such as pre-tracheal abscess).
What HD cahnges do you expect in a normal pregnancy?
The following table lists approximate changes with pregnancy.
Cardiac Output Increased 40-50%
Heart Rate Increased 15-25%
Stroke Volume Increased 30%
Intravascular Volume Increased 35%
Central Venous Pressure No Change
Plasma Volume Increase 45%
Red Blood Cell Mass Increased 20%
Systemic Vascular Resistance Decreased 15-20%
Describe uncoupling with respect to inhaled anesthetics
Both increased carbon dioxide tension and volatile agents increase cerebral blood flow (CBF), while the latter also decreases cerebral metabolic rate (CMR). Volatile agents delivered at levels greater than 1 MAC decrease CMR but increase CBF, known as uncoupling. This decreased neuronal metabolic demand with increased metabolic supply is called luxury perfusion. Although this can be beneficial during global ischemia, the excess blood flow to certain regions steals from other regions which can be detrimental during focal ischemia.
How much CO does the brain receive?
The brain receives 10-15% of the total cardiac output, or blood flow of approximately 50 mL/100 g/min. At rest, the cerebral metabolic rate of oxygen (CMRO2) is approximately 3.5 mL/100 g/min.
What does N2O do to CBF? and CBM?
Nitrous oxide (N2O) increases CBF, CMR, and subsequently ICP, though these effects differ depending on whether it is administered alone or with other agents.
What is the robin-hood phenomoenon?
Hypocapnia causes cerebral vasoconstriction, which was thought to be able to redirect blood flow from normal regions to ischemic regions: the so-called “Robin Hood phenomenon” or inverse steal.
Why does CSF tend to diffuse into the venous system?
Cerebrospinal fluid (CSF) lacks protein, which allows flow of fluid into the protein-rich systemic venous system.
How does CSF flow?
CSF flows from the ventricles of the brain into the subarachnoid space to provide buoyancy, clear waste, and protect the central nervous system (CNS) from trauma. Adult humans produce 21 mL/hr of CSF, which amounts to 500 mL a day. Most of this is completed by the choroid plexus although the lateral ventricles also produce a significant amount. CSF movement is pulsatile, driven by the arterial pulsations of the brain in a non-unidirectional flow.
Treatment for TCA overdose
Sodium bicarbonate is the standard initial therapy for tricyclic antidepressant (TCA) toxicity.
The primary mechanism of action of TCAs is the inhibition of presynaptic neurotransmitter uptake (mostly norepinephrine and serotonin). Side effects are mainly related to the antimuscarinic properties and include dry mouth, dry nose, blurry vision, constipation, and urinary retention. Overdose, however, can lead to serious cardiovascular and neurological consequences.
TCA overdose can lead to severe cardiotoxicity manifesting with ECG changes such as QRS widening with the possibility of degenerating into a lethal arrhythmia. After evaluating the patient’s airway, breathing, and circulation, sodium bicarbonate is the standard initial therapy for TCA toxicity.
Where does dexamethasone’s anti nausea effects occur?
While the mechanism of action of dexamethasone’s antiemetic effects remain unclear, it likely involves central inhibition of the nucleus tractus solitarii.
Who is at most risk of emergence delirium? How ca this be pre-treated?
Emergence delirium is most common in children aged 2-5 years who undergo a painful surgical procedure under general inhalational anesthesia. It is characterized by inconsolability, incoherence, thrashing, screaming, and/or crying. The incidence of emergence delirium can be decreased by prophylactic administration of clonidine, dexmedetomidine, fentanyl, ketamine, nalbuphine, or propofol.
What is seen in re-feeding syndrome?
Refeeding syndrome causes hypophosphatemia, hyponatremia, hypocalcemia, hypomagnesemia, hypokalemia, and hyperglycemia.
What causes premature fetal ductus arteriousis closure?
Maternal NSAID use is associated with premature closure of the ductus arteriosus. Prostaglandins keep the ductus open, PGE-1 is used after birth to keep ductus open in ductus-dependent congenital cardiac conditions. Because of the potential for premature ductus arteriosus closure, NSAIDs are discontinued several weeks before term gestation.
What causes persistent fetal circulation?
Hypoxemia, hypothermia, and acidosis are all associated with persistent fetal circulation. This is due to increased pulmonary pressures, which favors flow through shunts that are only functionally closed and not yet anatomically closed.
What produces surfactant?
Type II pneumocytes in the alveolus have a primary function of producing surfactant, which helps to prevent atelectasis. Secondarily these cells may also differentiate into Type I pneumocytes, which then contribute to gas exchange at the alveolar surface.
REasons for emergent dialysis
Reasons for emergent dialysis include AEIOU: Acidosis, Electrolytes, Ingestions (toxins), Overload, Uremia.
What is the DLCO? When is it high? When is it low?
The DLCO uses carbon monoxide diffusion to assess the parenchymal function of the lungs. DLCO is effected by cardiac output and hemoglobin concentration. The DLCO is elevated in conditions like: asthma, polycythemia, pulmonary hemorrhage, exercise, and left to right shunts. It is decreased in pulmonary embolism.
4T test for HITT
The 4T clinical scoring system is used to clinically diagnose HIT prior to laboratory confirmation. The 4Ts include:
1) Thrombocytopenia
2) Timing of the reduced platelet count
3) Presence of Thrombosis
4) The exclusion of other causes for thrombocytopenia
Signs of hypercalcemia
Hypercalcemia leads to “stones, bones, abdominal groans, thrones, and psychiatric overtones”
Stones: kidney stones
Bones: bone-related complications
Groans: gastrointestinal symptoms
Thrones: polyuria, constipation (throne = toilet)
Overtones: central nervous system effects
MOA of common aspiration prophylaxis
Mechanisms of action of medications for aspiration prophylaxis:
Metoclopramide - increases LES tone and gastric emptying.
Ranitidine and other H2 antagonists - decreases both the amount and acidity of gastric secretions.
Sodium citrate - decreases the acidity of gastric contents.
ST elevation vs depression
Acute ST elevation represents transmural myocardial injury whereas ST depression represents subendocardial ischemia. Recognition is important as treatment strategies between the two are different.
What can lead to hypochloremic metabolic alkalosis?
A hypochloremic metabolic alkalosis is classically found in newborns with pyloric stenosis due to significant acid and chloride loss from emesis.
Other etiologies include, but are not limited to: cystic fibrosis, diuretic-induced alkalosis or diuretic abuse (namely loop or thiazide diuretics), laxative abuse, recurrent vomiting, excessive gastric acid loss (such as with prolonged nasogastric tube suctioning), and post-hypercapnic metabolic alkalosis.
What are ideal leak pressures in apediartic ETT?
The ideal leak pressure of an uncuffed ETT in pediatric patients is 20-30 cm H2O. If a leak pressure >40 cm H2O is measured, the ETT should be replaced with a smaller size.
What should you not give to a MTHFR?
Nitrous oxide (C) should be avoided in patients with MTHFR deficiency. Nitrous oxide directly inhibits methionine synthetase. The MTHFR gene encodes a protein used in the folate pathway and synthesis of purines for DNA. When this pathway is inhibited homocysteine levels rise. Use of nitrous oxide further increases the homocysteine level because of impaired mechanisms of metabolism. Elevated homocysteine increases incidence of thrombosis and adverse coronary events.
High-dose oxytocin therapy is MOST likely to result in
hyponatremia
Oxytocin is structurally similar to vasopressin and at high doses can decrease urine excretion via antidiuresis independent of volume status. The resultant volume overload is sensed by the atria, which then release atrial natriuretic peptide that promotes natriuresis. In addition, high-dose oxytocin itself stimulates renal natriuresis. Combined, these effects can lead to hyponatremia
Fun fact about vasopression and glyco
Due to structural similarities between oxytocin and vasopressin, high-dose vasopressin administration can cause uterine contractions.
What will you see on an ABG for CO pointining>
Due to structural similarities between oxytocin and vasopressin, high-dose vasopressin administration can cause uterine contractions.
Whata re the effects of carbon onoxide?
Carbon monoxide reversibly binds to hemoglobin (Hgb) with 200-300 times greater affinity than oxygen. Accordingly, CO reduces oxyhemoglobin (oxyHgb) concentration by displacing oxygen from the hemoglobin molecule and creates carboxyhemoglobin (COHgb). This leads to a leftward shift of the Hgb-oxygen dissociation curve and reduction in oxygen availability to tissues. This then produces a lactic acidosis due to anemic hypoxia.
Looking at an ECHO of aortic vlave–what is what?
Right ventricle is an anterior structure, as is the right coronary cusp. The non-coronary cusp is always located next to the inter-atrial septum.
What heart changes are seen as we age?
Resting systolic function is not altered by aging, but exercise-induced increases in cardiac output, stroke volume, and heart rate are reduced. There is an increase in circulating catecholamines with a corresponding desensitization of the β-receptor. Diastolic dysfunction results in a reduction and delay in left ventricular relaxation and therefore reduced passive filling during early diastole. There is an increased reliance on atrial kick for adequate cardiac output.
