Flashcards in Critical Care Deck (70):
What are the components of ARDS?
ARDS is a life-threatening condition associated with a severe oxygenation defect related to a noncardiogenic proteinaceous pulmonary edema.
1- Respiratory failure not explained by heart failure or volume overload
2- Decreased arterial PO2/FiO2 ratio:
mild ARDS: ratio is 201 - 300 mmHg (≤ 39.9 kPa)
moderate ARDS: 101 - 200 mmHg (≤ 26.6 kPa)
severe ARDS: ≤ 100 mmHg (≤ 13.3 kPa)
3- Lung injury of acute onset, within 1 week of an apparent clinical insult and with progression of respiratory symptoms
4- bilateral opacities on chest imaging not explained by other pulmonary pathology (e.g. pleural effusion, lung collapse, or nodules)
What is involved in LPV?
- 6 cc/kg tidal volume
- plateau pressure < 30 cm/H20
- sufficient PEEP (5-24 cm H2O) and FiO2 to maintain the SaO2 > 88%
- Note that sacrificing a higher PCO2 and therefore lower arterial pH for oxygenation is known as permissive hypercapnia
- bicarbonate infusions can be used to maintain pH > 7.2 if desired while allowing for elevated PCO2
- A disturbance of consciousness that is ACUTE in onset
- A FLUCTUATING course of impaired cognitive functioning so that a patient's ability to receive, process, and store information is impaired.
What is Beck's triad of cardiac tamponade?
1- Hypotension (2/2 decreased stroke volume)
2- JVD (2/2 impaired venous return)
3- Muffled heart sounds (2/2 fluid inside the pericardium)
What are negative effects associated with sodium bicarbonate therapy for the treatment of acidosis?
1- venous hypercapnia
2- decreased CSF pH
3- tissue hypoxia
5- hyperosmolality of the CSF
6- shift in the oxygen dissociation curve
T or F: as compared to diabetic ketoacidosis, hyperglycemic hyperosmolar state is associated with higher glucose levels (usually > 600), pH > 7.3, higher serum bicarbonate, osmolality greater than 320, no serum or urine ketones, and more dehydration.
True: treatment includes hydration, insulin, and repletion of profound potassium deficits.
Acute treatment of tension pneumothorax?
Needle decompression inserted into the second intercostal space in the midclavicular line using a 14 g needle. Should be placed on the side of the tension pneumothorax.
Acute treatment of pericardial drainage?
needle decompression inserted between the xiphoid and left costal margin, passed at 30-45 degrees and angled toward the left shoulder.
Treatment of tension pneumothorax AFTER it has been urgently decompressed.
Tume thoracostomy decompression placed in the right fifth intercostal space at the midaxillary line.
Case presentation: a 35 year old woman presents with complaints of fatigue, poor appetite, weight loss, and nausea. On exam, she appears tanned but denies sun exposure. She is moderately hypotensive. Lab studies show she is mildly hyperkalemic and hyponatremic. What endocrine disorder does she have?
What is Addison's disease?
Primary adrenal insufficiency and due to a lack of both glucocorticoid and mineralocorticoid activity. Characterized by weightloss, weakness and lethargy, hypotension, GI symptoms, hyperpigmentation, hyperkalemia, hyponatremia, and hypercalcemia. Autoimmune causes are the most common casue of Addison's today.
Secondary adrenal insufficiency is due to failure of the pituitary and lack of ACTH. Secondary adrenal insufficiency does not show the hyperpigmentation of Addisons.
How can the adverse effects of etomidate manifest itself acutely intraoperatively?
Etomidate inhibits adrenal steroidogenesis by interaction with 11 beta-hydroxylase enzyme. This can result in reduced cortisol production in response to ACTH. Loss of adrenal responsiveness in times of stress can lead to increased resuscitation needs and poor response to pressor agents in the face of hypotension.
The effects of etomidate were thought to last for 8-12 hours after dosing, but newer studies are showing that effects may linger for longer periods, perhaps up to 48 hours.
What does the "French" in a french catheter refer to?
A catheter of 1 French has a diameter of ⅓ mm, and therefore the diameter of a round catheter in millimeters can be determined by dividing the French size by 3:
D (mm) = Fr / 3
What two things affect the flow rate in a central line?
Tube diameter and length of tubing
The diameter of the tube has a magnified effect on flow rates, but length can adversely affect flow. Given that the length of a central venous catheter exceeds the diameter, catheter length plays an important role.
What is Hagen-Poiseuille equation?
Flow through a rigid tube (ie catheter) is governed by this equation:
Q = DP x ( Pr^4/8mL)
Q = rate of flow
DP = the change in pressure through the tube
Pr^4 = size of the tube
m = viscosity of the fluid
L = length of the tube
Some key points with carbon monoxide poisoning:
- can be difficult to detect unless the diagnosis is suspected.
- CO has a higher affinity for hemoglobin than oxygen does --> displaces oxygen and diminishes the oxygen carrying capacity.
- Standard pulse oximetry does not differentiate between oxyhemoglobin and carboxyhemoglobin, so pulse oximetry readings are NOT helpful.
- headache and dizziness are common signs of mild CO poisoning.
- Classically described cherry-red pigmentation does NOT appear until high concetrations of carbon monoxide are present.
What are standard medications for the treatment of an anaphylactic reaction?
- anaphylactic reactions are characterized by IgE mediated release of histamine, leukotrienes, chemotactic factors, platelet aggregatng factor, prostaglandins.
- release of the above triggers capillary permeability leading to loss of circulating volume, hypotension, and tachycardia.
- Wheezing occurs secondary to bronchoconstriction
- skin manifestations and GI complaints may accompany the hemodynamic and pulmonary complications
- Standard therapy: epinephrine (inhibits mediator release by increasing levels of cAMP and affects symptoms by relaxing bronchoconstriction and improving hemodynamics)
- H1 blockers such as diphenydramine and H2 blockers such as famotidine blunt the response to histamine, including capillary permeability and cardiac dysfunction.
- corticosteroids increase tissue response to epinephrine and inhibit histamine synthesis.
- albuterol can help with pulmonary complications of anaphylaxis.
How does racemic epinephrine work?
- Works by stimulation of 1) the α-adrenergic receptors in the airway with resultant tightening of the mucosa (mucosal vasoconstriction) and decreased fluid in the airway (subglottic edema) and by stimulation of the 2) β-adrenergic receptors causing relaxation of the bronchial smooth muscle
- Commonly used in croup and when stridor is present after removal of an endotracheal tube (extubation).
- Side effects include increased heart rate, nausea, anxiety, heart palpitations and headache.
What is the RIFLE criteria for acute kidney injury?
In 2002, the Acute Dialysis Quality Initiative (ADQI) was created with the primary goal of developing consensus and evidence-based guidelines for the treatment and prevention of acute kidney injury (AKI). The first order of business was to create a uniform, accepted definition of AKI; hence, the RIFLE criteria were born:
End-stage renal disease
Note: Patients can be classified either by GFR criteria or by UO criteria. The criteria that support the most severe classification should be used.
Name treatments for hyperkalemia.
1- Albuterol: moves K out of serum and into intracellular space for 1-2 hours
2- Insulin/glucose: moves K intracellularly
3- Furosemide: triggers K loss in the urine
4- Sodium polystyrene sulfonate: potassium exchange resins in the GI tract
5- Calcium gluconate: changes the threshold potential of the myocardium conducting cells, blunting the ability of hyperkalemia to trigger myocardial arrhythmias
What is the progression of EKG changes in the setting of hyperkalemia?
1- T waves initially get taller and more peaked
2- PR interval lengthens
3- P wave flattens out
4- QRS widens
5- EKG assumes a sine-wave pattern
What are EKG changes in the setting of hypokalemia?
Development of a prominent U wave and is generally accompanied by flattening of the T waves and ST depression
True or false: intraoperative urine output is not a predictor of perioperative renal failure.
What is tPA used for?
As an enzyme, it catalyzes the conversion of plasminogen to plasmin, the major enzyme responsible for clot breakdown. Because it works on the clotting system, tPA is used in clinical medicine to treat embolic or thrombotic stroke.
What is the most effective method for reversing the effect of tPA?
- cryoprecipitate or fibrinogen concentrates replace fibrinogen and represent the accepted method for treating acute life-threatening bleeding after the administration of fibrinolytics.
T or F: ARDS network trial demonstrated a decrease in mortality from about 40% to 31% with the use of low tidal volume and controlling plateau pressures to less than 30 cm H2O.
True: this improved survival was accompanied by an increase in the RR, increased arterial CO2, and decrease in oxygenation.
What is a known side effect in the administration of nitric oxide?
Nitric oxide is a potent pulmonary vasodilator.
Known side effects:
What can cause negative pressure pulmonary edema? What is the treatment for this? How quickly does it resolve?
Negative pressure pulmonary edema is caused by a closed glottis in the spontaneously ventilating patient, with generation of significant negative intrathoracic pressure due to rib retraction from an inspiration attempt. This can also happen when an ETT becomes occluded, most commonly by a mucus plug, clot, or biting on the ETT. It follows releif of acute upper airway obstruction (postobstructive pulmonary edema) caused by postextubation laryngospasm, epiglottitis, tumors, obesity, hiccups, or OSA in spontaneously breathing patients.
The generation of significant negative intrathoracic pressure can cause increased left ventricular preload and afterload, altered pulmonary capillary permeability, a hyperadrenergic state, right ventricular dilatation, and increased hydrostatic pressure. The negative pleural pressure can result in fluid entry into the lung. Relief of the obstruction leads to decreased airway pressures, increased venous return, increase in pulmonary hydrostatic pressure, and ultimately pulmonary edema.
The time to the development of symptoms after relief of airway obstruction ranges from a few minutes to as long as 2-3 hours. Typical signs are tachypnea, cough, and failure to maintain oxygen saturation above 95%. Hypoxemia is accompanied by bilateral fluffy infiltrates on CXR, but radiographic evidence of pulmonary edema resolve within 12-24 hours.
Treatment: supportive with continuous PPV with PEEP. Typically resolves in 6-12 hours, transient and self-limited.
Acalculous cholecystitis is a surgical emergency. What are three risk factors for it?
Regarding conditions requiring GI prophylaxis, what are two independent risk factors?
Prolonged ventilation greater than 48 hours
Coagulopathy (Plt < 50,000, INR > 1.5, PTT > 2x control)
Other high risk conditions include head trauma, hypotension, renal failure, liver failure, > 30% burns. Stress related injury causes decreased mucosal blood flow.
T or F: hypophosphatemia in the setting of TPN administration is associated with respiratory failure.
What is the negative inspiratory force needed for extubation?
-20 to -25
What is RSBI?
Rapid shallow breathing index = respiratory rate / tidal volume
Values less than 105 are indicative of successful extubation.
T or F: increasing FiO2 > 60% for 48 hours can result in oxygen toxicity and free radicals.
T or F: pneumonia and sepsis are the most common triggers for ARDS.
Describe organophosphate poisoning.
Organophosphate poisoning occurs from exposure to pesticides, which block acetylcholinesterase, thereby increasing the amount of Ach in the body, resulting in cholinergic toxicity.
Clinical manifestations of organophosphate toxicity are secondary to increased Ach and not secondary to the organophosphate itself.
What are the main pharmacologic therapies for the treatment of organophosphate poisoning?
Atropine and pralidoxime are the main pharmacologic therapies for treatment of cholinergic toxicity from organophosphate poisoning.
What are the four types of shock?
What are causes of hypovolemic shock?
2/2 inadequate cardiac output from a decreased intravascular volume. It is most commonly due to hemorrhage, gastrointestinal or urinary tract fluid losses, or "third-space" losses into the interstitium.
What are causes of cardiogenic shock?
2/2 inadequate cardiac output from ventricular (left, right, or both) failure. Isolated right-side heart failure can be differentiated from isolated left-side heart failure because right-side heart failure will present with an elevated central venous pressure (CVP) with low or normal pulmonary artery occlusion pressure (PAOP). Biventricular failure is associated with elevations of both CVP and PAOP. Cardiogenic shock is most commonly due to myocardial infarction.
What are causes of distributive shock?
Distributive shock occurs due to significantly reduced peripheral vasomotor tone. It is most commonly due to septic shock, anaphylaxis, spinal cord injury, or corticosteroid insufficiency.
What are causes of obstructive shock?
Obstructive shock occurs from mechanical compression of the heart or outlet obstruction and results in inadequate stroke volume and cardiac output. Examples of causes of obstructive shock include cardiac tamponade, tension pneumothorax, and pulmonary embolism. The equalization of diastolic pressures and filling pressures is consistent with cardiac tamponade.
On an ABG, which of the following are measured and which are calculated? PaO2, PaCO2, HCO3, pH
Of these, only the HCO3 is calculated using the Henderson-Hasselbach equation. The remaining are measured.
Describe the CVP waveform.
Diastolic components: y descent, end-diastolic a wave
Systolic components: c wave, x descent, v wave
a-wave: represents atrial contraction in systole
c wave: reflects closure of the tricuspid valve with isovolumic ventricular contraction and motion of the valve toward the right atrium
x descent: represents fall in right atrial pressure following atrial contraction in systole
v wave: occurs during late systole and is generated by filling of the atrium
y-descent: fall in right atrial pressure after the tricuspid valve opens and the initiation of passive filling of the right ventricle
T or F: if HIT is strongly suspected, anticoagulation should be initiated using a direct thrombin inhibitor. Coumadin must be avoided in the setting of HIT as it may lead to warfarin necrosis.
T or F: the two main side effects from administration of amiodarone are bradycardia and hypotension.
True- these can be lessened by slowing the rate of administration, providing a fluid bolus, supporting with a vasopressor during the infusion, or temporary pacing if bradycardia is profound.
Amiodarone is a class III antiarrhythmic agent used to treat both atrial and ventricular arrhythmias. It prolongs repolarization and lengthens the cardiac action potential, providing negative chronotropy in nodal tissue, blocking cardiac potassium and calcium channels, thereby slowing conduction at the SA node.
What defines SIRS?
The presence of 2 or more of the following parameters:
1- body temperature > 38
2- Heart rate > 90 bpm
3- RR > 20 bpm or PaCO2 < 32
4- Leukocytosis > 12 or < 4
T or F: Regarding paralysis in the ICU, there is an increased incidence of polyneuropathy and myopathy, but it is potentially useful in severe ARDS patients.
True- there may occasionally be compelling reasons to administer paralytics in the setting of ARDS, where paralytics may lower the consumption of oxygen and allow for ultra-low tidal volumes.
What are causes for anion-gap metabolic acidosis?
Infection, iron, Isoniazid, inborn errors of metabolism
What is a normal anion gap? What is the calculation for an anion gap?
Anion gap = Na - (Cl + HCO3)
What are causes for non-anion gap metabolic acidosis?
Think USED CRAP
Ureteroenterostomy/ureterosigmoid connection, either because of surgical ureteral sigmoidostomy or a ureterosigmoid fistula as may occur in Crohn's disease
Small bowel fistula, steroid excess (addison's disease, iatrogenic)
Carbonic anhydrase inhibitors, CaCl ingestion, cholestyramine ingestion
RTA types I (distal). II (proximal), and IV (hyporeninemic hypoaldosteronism)
Adrenal insufficiency, alimentation, ammonium chloride ingestion
Pancreatic fistula, parenteral nutrition, hyperPTH, post-hypocapnia
T or F: left atrial collapse is a very sensitive sign for cardiac tamponade.
What is the CHADS2 score?
The CHADS2 score is a clinical prediction rule for estimating the risk of stroke in patients with non-rheumatic atrial fibrillation. It is used to determine whether or not treatment is required with anticoagulation therapy or antiplatelet therapy.
Congestive heart failure (1)
Hypertension consistently > 140/90 (1)
Age > 75 years (1)
Prior Stroke or TIA or thromboembolism (2)
CHADS > 2 --> warfarin therapy
Describe the triad of symptoms present in serotonin syndrome?
Many cases of serotonin toxicity occur in patients who have ingested drug combinations that synergistically increase synaptic serotonin.
The clinical triad of abnormalities are as follows:
1- Cognitive- headache, agitation, mental confusion, hallucinations, coma
2- Autonomic- shivering, sweating, hyperthermia, hypertension, tachycardia, nausea, diaphoresis
3- Somatic- myoclonus, hyperreflexia, tremor
TCAs are highly protein bound, lipophilic, and have a large volume of distribution, making them resistant to forced diuresis or hemodialysis. The treatment of choice for cardiac dysrhythmia or QRS complex duration greater than 100 ms in the setting of TCA poisoning is sodium bicarbonate. The administered sodium bicarbonate increases the gradient of sodium across neuronal membranes helping to overcome the blockade of sodium channels produced by the TCA, and the elevation in pH helps keep the TCA in its neutral form, which is less available to bind cardiac sodium channels.
Describe the phenomenon and etiology of neurogenic pulmonary edema.
Neurogenic pulmonary edema (NPE), reported in up to 20% of patients with severe head injury, commonly occurs within the first hours of the injury. An increase in intracranial pressure results in cerebral ischemia that stimulates intense sympathetic output with the release of vasoconstrictors (eg, norepinephrine) and other mediators. This results in an increase in vasoconstriction of the pulmonary and systemic circulations. In addition to an increase in systemic vascular resistance, venoconstriction results in an increase in venous return and pulmonary artery occlusion pressure. Echocardiographic assessment generally reveals a decrease in left ventricular contractility, left ventricular output, and aortic flow.
Factors contributing to the development of pulmonary edema include increased capillary permeability due to release of inflammatory mediators stimulated by disruption of the blood–brain barrier increased transmural capillary pressures due to increased pulmonary artery pressures impaired left ventricular function.
What is the treatment of neurogenic pulmonary edema?
Reducing ICP- The primary treatment of neurogenic pulmonary edema (NPE) following head injury is reduction of intracranial pressure (ICP). Surgical evacuation of a hematoma, ventriculostomy with drainage of cerebrospinal fluid, or decompressive craniectomy have all been used to accomplish this goal. Other treatments that lower ICP (eg,
administration of an osmotic diuretic such as mannitol) are also warranted, especially prior to definitive surgical care.
What is refeeding syndrome?
Refeeding syndrome may occur when parenteral nutrition is initiated in chronically malnourished individuals, such as chronic alcoholics and chronic malnutrition. The syndrome is defined by characteristic electrolyte abnormalities that may be life threatening.
These electrolyte abnormalities include hypophosphatemia, hypokalemia, hyperglycemia, and hypomagnesemia. Basically the electrolyte levels are low and glucose levels are high.
In high risk patients, electrolyte abnormalities must be identified and nutrition advanced slowly.
T or F: critical illness myopathy is associated with increased serum creatine phosphokinase concentrations.
True: in addition to prolonged weakness, CIM is associated with increased serum creatine phosphokinase concentration.
CIM also results in the following findings:
• Normal nerve conduction studies
• Absent compound muscle action potentials consistent with a diagnosis of unexcitable muscle on electromyographic testing
• Myosin filament loss with preservation of actin on muscle biopsy
T or F: ACE inhibitors have been associated with the development of life-threatening angioedema.
Angioedema is a term used to describe nonpitting mucocutaneous swelling that occurs in the skin or mucous membranes, primarily of the respiratory tract and bowel. When the larynx is involved, angioedema may be life threatening.
Angioedema may be hereditary and caused by C1 esterase deficiency.
Angioedema related to angiotensin-converting enzyme (ACE) inhibitors has been reported to be the cause of 17% to 38% of all patients presenting to the emergency room with angioedema. In 20% of these cases, the angioedema is described as life threatening.
Approximately half of patients who develop angioedema associated with ACE inhibitors manifest the problem in the first week after therapy is initiated. There are, however, case reports of patients developing angioedema for the first time after months of uncomplicated therapy with ACE inhibitors. Involvement of the bowel can result in severe abdominal pain that may be difficult to distinguish from a surgical abdomen. Angiotensin receptor blockers (ARBs) also are reported to cause angioedema, albeit much less frequently than ACE inhibitors.
Treatment of NSAID-, ACE inhibitor-, or ARB-related allergic or pseudoallergic angioedema that involves the airway includes epinephrine, diphenhydramine, and corticosteroids. Tracheal intubation may be indicated and occasionally tracheostomy may be necessary in cases of severe laryngeal involvement. Because patients may relapse after apparent initial stabilization, observation for 24 hours is generally recommended.
T or F: TPN should not be initiated in the first 7 days of ICU admission. Also, what are absolute indications to TPN?
True- absolute indications for TPN include short gut syndrome, small bowel obstruction, active GI bleeding, pseudoobstruction with complete intolerance to food, and high output enterocutaneous fistulas.
Chemo toxicities: cisplatin, carboplatin
acoustic nerve damage, nephrotoxicity
Chemo toxicities: vincristine
Chemo toxicities: bleomycin, busulfan
Chemo toxicities: doxorubicin
Chemo toxicities: trastuzumab
Chemo toxicities: cyclophosphamide
Chemo toxicities: 5-fluorouracil, 6-mercaptopurine, methotrexate
What is the formula for the amount of bicarbonate that should be administered to an acidotic patient?
Sodium bicarbonate (mEq) = 0.2 * pt weight in kg * base deficit
T or F: placement of a left-sided central line is associated with increased complications. There is an increased incidence of arterial puncture because the left IJ is often smaller and overlays the left internal carotid artery more often than on the right.
True- in addition, carotid artery cannulation can lead to embolization. Carotid embolization on the left poses a greater risk as the left cerebral hemisphere is dominant in the majority of the population.