Medicine Quick Knows Flashcards
(136 cards)
1
Q
ASA Classification I
A
Class I – normal healthy patient (non-smoker; no or minimal alcohol use)
2
Q
ASA Class II
A
patient with mild systemic disease (well-controlled and no functional limitation. Examples: Current
smoker, social alcohol drinker, pregnancy, obesity (30<BMI<40), well controlled DM/HTN, mild lung disease)
3
Q
ASA Class III
A
patient with severe systemic diseases (moderately controlled and definite functional limitation.
Examples: poorly controlled DM or HTN, COPD, morbid obesity BMI >40), active hepatitis, alcohol
dependence or abuse, implanted pacemaker, moderately reduced EF, ESRD undergoing regularly scheduled
dialysis, history (>3 months) of MI, CVA, TIA, of CAD/stents.)
4
Q
ASA Class IV
A
Severe systemic disease that is a constant threat to life (Examples: recent (<3 mos.) MI, CVA, TIA,
or CAD/stents, ongoing cardiac ischemia or severe valve dysfunction, severe reduction of EF, sepsis, DIC,
ARD, or ESRD not undergoing regular dialysis)
5
Q
ASA Class V
A
Moribund patient unlikely to survive without operation (Examples: ruptured abdominal/thoracic
aneurysm, massive trauma, intracranial bleed with mass effect, ischemic bowel in the face of significant
cardiac pathology or multiple system organ dysfunction.
6
Q
How many ASA classifications are there
A
I-VI
7
Q
Mallampati Classification I
A
visualization of the soft palate, fauces, uvula, anterior and posterior pillars
8
Q
Mallampati Classification II
A
visualization of soft palate, fauces and uvula
9
Q
Mallampati Classification III
A
visualization of soft palate and base of uvula
10
Q
Mallampati Classification IV
A
soft palate is not visible at all
11
Q
Pediatric Airway Differences (17 Points)
A
Small Nares
▸ Large Tongue
▸ Head Large, Neck Small
▸ Limited Cervical Extension
▸ Adenoids/Tonsils – Largest
ages 4-10
▸ Long, Narrow, Higher
Epiglottis
▸ Higher, Funnel Shaped
Larynx
▸ Vocal Cords Inclined
▸ Compliant, Shorter Trachea
▸ Lower Airway Anatomy
▸ Narrower Airway
▸ Diaphragmatic Breathing
▸ Horizontal Ribs
▸ Poorly developed Accessory Muscles
▸ Decreased Alveoli
▸ Decreased FRC – lung size increases rapidly until age 6, then more slowly
▸ Lack of elastin causes collapse of terminal airways to occur earlier, decrease in
12
Q
Noted difference with heart on pediatric patient due to intubation.
A
Increased vagal tone, prone to bradycardia on intubation
13
Q
Diameter for pediatric patient
A
Diameter: (age + 16)/4 i.e 4y.o. = size 5
Length: (age/2) = 12
14
Q
Bagging a pediatric patient
A
Bag valve mask – tidal volume 10-15cc/kg
15
Q
3 important points about pediatric physiology
A
-Blood pressure mainly dependent on HR (vs adults where controlled by HR, SV, SVR)
-Cardiac output needs to be twice as high as adults due to increased metabolic rate and oxygen consumption
*Major determinant is Heart rate
*Bradycardia leads to sharp decrease in cardiac output and BP
-Decreased FRC – one of the reasons they desaturate faster than adults
16
Q
Laryngospasm - 1 Liner
A
Protective reflex to prevent foreign matter from entering the larynx, trachea, or lungs.
17
Q
Algorithm to break laryngospasm
A
-100% Oxygen
-Suction all blood and foreign/pack surgical site to prevent further bleeding into the hypopharynx
-Depress patient’s chest and listen for a rush of air to indicate patency
-If obstruction persists, break spasm with positive pressure via 100% O2 and full-face mask with good seal (appropriately sized for child vs. adult patient.)
-If obstruction persists - Succinylcholine (where is it kept in your office?)
Adults 0.1-0.2mg/kg IV for adults (small dose 10-20mg IV for partial obstruction).
Pediatric dose 0.25-0.50mg/kg IV
In a complete spasm where smaller dose fails to break spasm, use 20-40mg IV
18
Q
Complications of succinylcholine (4)
A
▸ Myalgias
▸ Malignant hyperthermia
▸ Hyperkalemic cardiac arrest (in susceptible patients with myopathies)
▸ Masseter muscle spasm in pediatric patients (potential indicator of MH)
19
Q
Post-treatment concerns of succinylcholine after laryngospasm
A
Cardiac rhythm changes in response to hypoxia and hypercarbia in prolonged spasm
-NPPE
20
Q
Bronchospasm - 1 Liner
A
Constriction of the walls of the bronchioles often
caused by mast cell degranulation that can occur in response to allergic triggers or physical stimuli (secretions or ETT).
-Airway diameter decreases due to mucosa thickening and increased production of thick, viscous mucous.
21
Q
Signs and symptoms of bronchospasm: (4)
A
▸ Wheezing
▸ Diminished breath sounds
▸ Prolonged expiration
▸ Increase airway pressures (in ventilated patients)
22
Q
▸ Predisposing factors to Bronchospasm
A
▸ History of asthma
▸ Recent symptoms of Asthma
▸ Recent respiratory infection: wait several weeks for airway edema to resolve
▸ Anesthetic technique
23
Q
▸ Treatment of bronchospasm
Awake/cooperative patient
A
▸ Inhaled beta agonist via inhaler of nebulizer
▸ Oxygen
24
Q
Treatment of bronchospasm
Obtunded/Unconscious patient (without ETT)
A
▸ 100% Oxygen
▸ Epinephrine (1:1,000) 0.3 to 0.5mg SC/IM [Peds= 0.01mg/kg]
▸ 10 to 20 mcg of 1:10,000 solution in response to anaphylaxis
▸ Airway support
▸ Consider corticosteroids
▸ If situation deteriorates -> intubation
25
NPO guidelines
▸ Clear liquids = 2 hours
▸ Light solids = 6 hours
▸ Fatty solids = >6 hours
▸ Prolonged gastric emptying seen with apprehension, pain, narcotics, analgesics and opiate sedatives
26
High aspiration risk groups (8)
▸ Pregnant
▸ Diabetics
▸ Anxious
▸ Geriatric
▸ Obese
▸ Smokers
▸ GERD
▸ Hiatal Hernia
27
Signs/Symptoms of aspiration – may set-in rapidly (6)
▸ Rales
▸ Dyspnea
▸ Tachycardia
▸ Bronchospasm
▸ Cyanosis
▸ Progressive hypotension
28
Treatment in emerging aspiration patient
▸ Encourage coughing to clear airway
▸ Put chair in Trendelenburg (head down 15 degrees) with patient onto right side (stomach empties more rapidly in this position.
▸ Suction airway – remove any foreign material
▸ 100% oxygen
29
If patient fails to clear lungs from aspiration, what do you do?
▸ Activate EMS
▸ Clear airway again
▸ Intubate and manage bronchospasm with beta agonist
▸ Small volume tracheobronchial lavage
▸ No antibiotics and no steroids
30
Appropriate management of patient with airway complication
▸ Observe at least 2 hours in office
▸ Discharge criteria
▸ SpO2 > 94% on room air
▸ No wheezing, shortness of breath and minimal cough
▸ Consider hospital transfer if
▸ Aspiration of particulate matter
▸ Supplemental O2 needed to keep SpO2 in 90’s
31
Explain the capnograph to me?
32
Describe Asthma - 1 Liner
A chronic inflammatory disorder of the airways that causes recurrent episodes of wheezing, breathlessness, chest tightness and cough particularly at night or in early morning.
These symptoms are usually associated with widespread but variable airflow limitation that is at least partially reversible either spontaneously or with treatment.
33
Asthma-Classic triad of symptoms
▸ Wheeze (high-pitched upon expiration)
▸ Cough – may be dry of productive (mucoid or pale yellow sputum)
▸ Shortness of breath or difficulty breathing
34
Triggers of Asthma
▸ Exercise – 5-15 minutes after brief exertion
▸ Cold air
▸ Exposure to allergens (dust, mold, pollen)
35
Classifications of Asthma (4)
Intermittent
Mild Persistent
Moderate Persistent
Severe Persistent
36
Intermittent Asthma
▸ Symptoms 2 or fewer days per week
▸ No interference of normal activity
▸ FEV1 between exacerbations are normal range
37
Mild Persistent Asthma
▸ Symptoms more than 2x weekly
▸ Minor interference with normal activity
▸ FEV1 within normal range
38
Moderate Persistent Asthma
▸ Daily symptoms and need for short acting beta agonist
▸ Some limitation of normal activity
▸ FEV1 60-80% of predicted
39
Severe Persistent Asthma
▸ Symptoms throughout the day
▸ Extreme limitation of normal activity
▸ Nocturnal wakening nightly
▸ FEV1<60% of predicted
40
▸ Perioperative Management of Asthma
▸ Peak Flow rate (PEFR)
▸ Reduce exposure to triggers
▸ Prophylactic use of bronchodilator
41
Drugs used to treat Asthma
▸ Short –acting beta-2-selective adrenergic agonist
▸ Low dose inhaled glucocorticoid
▸ Alternatives – Leukotiene receptor agonists, theophylline, and
cromoglycates
42
What should you expect an asthmatic patient to have post-operatively
Expect patient to have bronchospasm intra-op and follow management guidelines
43
Angina-1 Liner
Chest pain that Presents due to inadequate coronary blood flow to the myocardium
Most common sign of an acute coronary syndrome (70-80% of affected patients)
44
CONGESTIVE HEART FAILUIRE - 1 Liner
Complex clinical syndrome that can result from any structural or functional CV disorder causing systemic perfusion inadequate to meet the body’s metabolic demands without excessively increasing the left ventricular filling pressures
45
What is CHF characterized by. ( 3 symptoms)
fatigue, dyspnea and fluid retention
46
CONGESTIVE HEART FAILUIRE common causes (4)
Ischemic heart disease;
valvular heart disease;
idiopathic dilated cardiomyopathy;
chronic HTN
47
What helps determine severity of CHF?
Exercise tolerance (distance traveled on level ground before SOB);
ability to climb flights of stairs without stopping;
sleep position
(supine?);
lower extremity edema?;
most recent hospitalization
48
Cardiomyopathy - 1 Liner
Enlargement, thickening or increasing rigidity of heart muscle
49
Type of Cardiomyopathy and causes (6)
Dilated; hypertrophic; restrictive; arrhythmogenic; right ventricular
Ischemia;
EtOH;
viral illness;
atrial fibrillation/SVT;
ESRD;
poorly controlled HTN
50
Angina -
Classic Angina
Dull substernal discomfort/pressure/tightness that may radiate to left arm, neck and/or jaw. Associated shortness of breath
-
51
Angina -
Anginal Equivalent
No pain or discomfort, but sudden or decompensated ventricular
failure (dyspnea) or ventricular arrhythmias.
52
Angina
▸ Atypical chest pain:
Pain and discomfort that is localized to the precordial area and has
positional, musculoskeletal, or pleuritic features.
53
How is angina classified?
-Stable
Unstable-
Prinzmetal
54
Stable Angina - 1 Liner
poorly localized deep chest pain that is associated with physical exertion and relieved by rest or sublingual nitro
55
Unstable Angina - 1 liner
Pain with more random pattern of appearance – no physical exertion and unrelieved by rest.
56
Prinzmetal Angina - 1 Liner
cyclic vasospasm of coronary vessels frequently seen in
women
57
Describe Angina cause to me - 1 Liner
Myocardial oxygen demand > supply
58
Management of Angina Intraop
stop procedure, supplemental oxygen, morphine, aspirin, nitroglycerine
▸ Monitors (if not already on) BP/EKG — watch for decompensation and arrhythmias/ dysrhythmias
59
Differential for Angina (13 possibilities)
Aortic dissection,
myocarditis,
pericarditis,
costrochondritis,
neuropathic pain,
pneumothorax,
pulmonary embolism,
pleuritic pain,
cholecystitis,
GERD,
esophageal spasm,
anxiety,
panic attack
60
Management of Angina
▸ Vitals, CBC, BMP, cardiac enzymes, 12-lead EKG, CXR, oxygen, ASA, morphine
▸ Cardiac enzymes
▸ Creatine kinase, CK-MB, troponin T, troponin I
▸ Cardiac catheterization
▸ Revascularization procedures
61
STEMI Heart Attack ( 1 Liner)
transmural infarction of the myocardium, thus the entire thickness of the myocardium undergoes necrosis, resulting in ST elevation
****Usually indicates blockage of an artery
62
NSTEMI Heart Attack
non-occlusive thrombus of a coronary artery, or an occlusive thrombus in a minor artery. No ST elevation or Q waves
Causes troponin elevation
63
Management of patients with known frequent angina attacks
▸ Prophylactic Nitroglycerin 0.4mg SL prior to stressful procedure
▸ 100% O2
▸ Anxiolytics – IV sedation to control stress response
▸ Psychological support – stress reduction
64
Algorithm for treatment of an angina event in a t with documented angina attacks.
▸ Terminate procedure
▸ Administer O2 @ 4L via mask or nasal canula
▸ Monitor vitals
▸ Sublingual nitro if SBP >90mmHg
▸ CP >5 minutes -> administer second dose of nitro
▸ IV morphine 1-3mg increments at 5 minute intervals
▸ ASA 160-325mg -> chew
▸ If patient unresponsive to 3 doses of nitro in 10 minutes, assume AMI and activate EMS
65
Acute Myocardial Infarction
Most frequent presentation is sudden onset of severe, prolonged (>15 minutes)
substernal chest pain and pressure occurring usually at rest.
66
Diagnosis of MI in a 12-Lead eKG
▸ S-T segment elevations in leads II, III, and aVF (acute inferior)
▸ Q waves represent scarred heart tissue from prior MI
67
Diagnosis of an MI with Cardiac Enzymes
CK and CK-MB elevated – MB predominant more specific for heart
▸ Troponins (subunits I &T) – most specific and diagnostic if seen in conjunction with EKG findings
▸ Angiogram (cath through femoral artery)
▸ visually identifies narrowed artery
▸ Allows ability of stent or angioplasty for treatment
68
Management of AMI ( same as angina)
▸ EMS
▸ Stop surgery, clear mouth and 100% O2
▸ Morphine
▸ ASA
▸ Nitroglycerine – take BP first, do not give if hypotensive
▸ Vitals – watch for decompensation (hypotension, hypoxemia, bradycardia, or ventricular dysrhythmia
and cardiac arrest)
Institute ACLS protocol
69
Mnemonic for External Carotid
Branches
Some Anatomists Like Freaking Out Poor Maxillofacial Surgeons
* S: superior thyroid artery
* A: ascending pharyngeal artery
* L: lingual artery
* F: facial artery
* O: occipital artery
* P: posterior auricular artery
* M: maxillary artery
* S: superficial temporal artery
70
What is an allergic reaction - (1 Liner)
The union of an antigen and antibody causes a reaction that forms or liberates chemical mediators. These mediators exert certain pharmacologic responses that determine the nature and extent of a
hypersensitivity or allergic reaction.
71
What are the initial response of allergic reactions?
▸ Smooth muscle contraction
▸ Dilation and increased permeability of arterioles
▸ Increased glandular secretion
72
What chemical mediators are involved?
Histamine, slow-reacting substance
(lung),
eosinophil chemotactic factor,
kinins,
prostaglandins, and
complement.
73
What are manifestations of an allergic response?
▸ Cutaneous reaction – most common in drug reactions
▸ Angioedema
▸ Respiratory and ocular reactions
▸ Hypotension
▸ Anaphylaxis – most severe/least common (but most likely tested)
74
What is angioedema?
▸ Slight swelling of eyelids and lips
▸ Severe, life-threatening in mouth and upper airway
75
What is anaphylaxis?
-An allergic reaction in two or more systems?
▸ Progressive cardiovascular collapse due to increased capillary permeability refractory to treatment, smooth muscle spasm, and acute pulmonary edema.
▸ Additional pulmonary compromise due to upper airway edema causing obstruction
76
How do you manage mild allergic reactions?
urticarial, mild angioedema
▸ Identification and discontinuation of offending agent
▸ 50mg Diphenhydramine IV, IM or PO
77
Urticaria?
Hives-itchy welts that rise up on the skin.
78
How do you manage sever allergic reactions?
▸ Stop administration of any causative agent
▸ ABC’s
▸ Support circulation with IV fluids – Adult = rapid infusion of 1L lactated Ringer’s
▸ Epinephrine IV 1:10,000 (1mg in 10mL)
79
What is the dose of epi for severe allergic reactions?
▸ Adults: titrate 0.2mg (2mL) to 0.5mg (5ml) to affect every 2-5 minutes
▸ Children: 0.01mg/kg
80
What is Epi for allergic reactions if IM?
▸ Adults: 0.3 to 0.5mg of a 1:1,000 concentration repeated in 10-20 minute intervals
▸ Children: 0.01 mg/kg repeated in 10-20 minute intervals
81
For allergic reactions, can epi be delivered through the ETT
Yes, it is administered at twice the IV dose
82
After epi is delivered, what other methods are used to manage allergic reactions?
▸ Antihistamine administration – Diphenhydramine 50g (adults); 25mg (child 6-12)
▸ Corticosteroids – slow action, but important in regaining homeostasis
▸ Dexamethasone 4-12mg IV/IM given slowly
▸ Continue airway monitoring for edema and upper obstructions necessitating
intubation.
▸ Beware of seizures due to circulatory or respiratory inadequacy
▸ Hospital admission for 24h observation
83
COMPLICATIONS OF SUCCINYLCHOLINE (4 pts)
▸ Myalgias
▸ Malignant hyperthermia
▸ Hyperkalemic cardiac arrest (in susceptible patients with myopathies)
▸ Masseter muscle spasm in pediatric patients (potential indicator of MH)
84
Is rocuronium a depolarizing or non-depolarizing NMBA?
Alternative non-depolarizing NMBA
▸ Dose 1.0 - 1.2mg/kg IV
▸ Longer duration of action - be prepared for prolonged airway management
85
What is malignant hyperthermia ( 1 - Liner)
Pharmacogenetic disorder of skeletal muscle that presents as a hypermetabolic response and it causes a progressive hyperthermia
86
What causes malignant hyperthermia?
▸ Potent volatile anesthetic gases (halothane, servo, desflurane)
▸ Depolarizing Muscle relaxant (Succinylcholine)
▸ Stress such as vigorous exercise
87
What are the 7 clinical signs of malignant hyperthermia?
▸ Increasing ETCO2
▸ Trunk or total body rigidity
▸ Masseter spasm or trismus
▸ Tachycardia/tachypnea
▸ Mixed respiratory and metabolic acidosis
▸ Increased temperature (may be late sign)
▸ Myoglobinuria
88
How do you manage malignant hyperthermia?
▸ Stop all triggering agents
▸ Hyperventilate
▸ Halt procedure
▸ Place ET tube
▸ Dantrolene 2.5mg/kg IV; repeat every 5-10 minutes until fall in HR, normal rhythm decline in muscle tone
▸ Treat acidosis 1-2mEq/kg sodium bicarb
▸ Monitor temp
▸ Hyperkalemia - treat with hyperventilation
▸ Transport to ICU
▸ Follow EtCO2, electrolytes, blood gases, temp, UA, coagulation studies
▸ Malignant Hyperthermia Association of the United States (MHAUS) hotline (1-800-MH-HYPER)
89
What is the dosage of dantrolene for malignant hyperthermia management?
Dantrolene 2.5mg/kg IV;
repeat every
5-10 minutes until fall in HR, normal
rhythm decline in muscle tone
90
How to mix dantrolene?
Preparation. Each vial of Dantrolene Sodium for Injection should be reconstituted by adding 60 mL of sterile water for injection USP (without a bacteriostatic agent), and the vial shaken until the solution is clear.
91
What should be done during MH management?
Active cooling with ice packs and chilled IVFluids
▸ Continue to monitor acidosis and treat with Bicarb
92
What is the mortality of MH even with proper management?
5-10%
93
Why is MH have a mortality rate?
Severe or untreated cases of acute rhabdomyolysis may result in lifethreatening hyperkalemia, myoglobinuria, renal failure, and multiorgan system failure
94
What manifestation may indicated MH?
Increase in masticatory muscle tension following succinylcholine administration
may provide the first sign that an individual may be susceptible to MH
95
What is needed to test for mH?
A muscle biopsy
96
Malignant Hyperthermia ( 1- Liner)
Hypermetabolic crisis due to an inherited muscle disorder that
can result in elevated levels of Ca+ in the myoplasm of muscle
cells resulting in activation of muscle contraction. In MH crisis,
the muscular contraction is sustained and heat, lactic acid, and
carbon dioxide are produced.
97
What happens to the liver and vitals during MH?
▸ Liver can’t clear lactate and severe metabolic acidosis occurs
▸ Increased CO2 -> tachycardia -> tachypnea
98
Name 3 risk factors for MH?
▸ Personal or family history of MH
▸ Personal or family history of muscle of neuromuscular disorders
(Duchene’s or Becker’s)
▸ History of dark of cola-colored urine following previous anesthesia of
exercise
99
What triggers MH? ( 2 substances)
▸ Succinylcholine (don’t be surprised if laryngospasm case leads to MH)
▸ Volatile anesthetic inhalation agents
100
Safe agent for MH
▸ Local anesthetics
▸ Benzodiazepines
▸ Opioids
▸ Barbituates
▸ Propofol
▸ Ketamine
▸ Nitrous oxide
▸ Etomadate
101
Primary signs and symptoms of impending MH
▸ Increased EtCO2 (double or triple over 10-20 minutes)
▸ Unexplained tachycardia, tachypnea, or hypercarbia
▸ Generalized muscle rigidity
▸ Hyperthermia (often late)
▸ Respiratory and/or metabolic acidosis.
▸ Cardiac arrest
102
MH management after stability is obtained
▸ Administer bicarbonate in order to correct the metabolic acidosis
(1-2mEq/kg)
▸ Active cooling with cold IV saline 15mL/kg every 15 minutes x 3
▸ Treat hyperkalemia with hyperventilation and IV glucose and insulin.
Consider calcium chloride (2-5mg/kg) if hyperkalemia is life threatening.
▸ ICU observation for 24hours because MH may recur.
▸ Continue dantrolene administration 1mg/kg every 4-6 hours.
103
Diabetes - 1 Liner
Diabetes is a chronic endocrine/metabolic disease that occurs either when the pancreas does not produce enough insulin or when the body cannot effectively use the insulin it produces.
104
Type I vs Type II Diabetes
Type I -An autoimmune disease—The immune system mediates the destruction of β-
cells which leads to a lack of insulin.
Type II - Obesity is associated with increased plasma levels of free fatty acids, which
make muscles more insulin resistant, reducing glucose uptake. Therefore,
obesity exacerbates insulin resistance.
105
DKA- Acute Complications and Treatment
▸ Hyperglycemia (>500), anion gap metabolic acidosis, and ketonemia
▸ Treatment
▸ IV fluids 0.9% NS (1L over 30 minutes)
▸ Replace K – measure K+ and replace 10-20 meq/hour IV
▸ IV regular insulin (15 units ) then sliding scale
▸ Correct pH with bicarb if <7
106
Hypoglycemia due to Diabetes - Symptoms
▸ Signs/symptoms
▸ fatigue, malaise, trembling, cold sweats, confusion, coma
107
Treatment for Diabetes Hypoglycemic episodes
▸ Treatment
▸ If alert – snack of glucose tabs
▸ If unconscious –
▸ dextrose IV 50% (D50) 1mL/kg IV up to 50mL
▸ OR D5W 10mL/kg IV up to 500mL
▸ OR Glucagon 0.025 0.1 mg/kg IV/IM/SC up to 1 mg
108
HTN - 1 Liner
A condition in which the force of the blood against the artery walls is too high
The current definition of hypertension (HTN) is systolic blood pressure (SBP) values of 130 mm Hg or more and/or diastolic blood pressure (DBP) of more than 80 mm Hg.
109
What causes HTN?
Primary hypertension, also called essential hypertension
For most adults, there's no identifiable cause of high blood pressure. This type of high blood pressure is called primary hypertension or essential hypertension. It tends to develop gradually over many years. Plaque buildup in the arteries, called atherosclerosis, increases the risk of high blood pressure.
Secondary hypertension
This type of high blood pressure is caused by an underlying condition. It tends to appear suddenly and cause higher blood pressure than does primary hypertension. Conditions and medicines that can lead to secondary hypertension include:
-Adrenal gland tumors
-Blood vessel problems present at birth, also called congenital heart defects
-Cough and cold medicines, some pain relievers, birth control pills, and other prescription drugs
-Illegal drugs, such as cocaine and amphetamines
-Kidney disease
-Obstructive sleep apnea
-Thyroid problems
110
HTN Stages and Classifications
111
HTN - Defer your limits
Preoperative Management
▸ Defer treatment for elective procedures (have in mind your own BP limits that you use
– i.e. >180/110)
▸ Optimize patient and ensure they adhere to routine medical management.
▸ Consider pre-operative medical assessment for uncontrolled/untreated hypertensive
patients
112
Hypertensive urgency
When BP >220/120 and no signs or symptoms
113
▸ Hypertensive crisis - 6 symptoms to look for
▸ When evidence of:
▸ Myocardial ischemia
▸ Neurological dysfunction
▸ Significant bradycardia
▸ Pulmonary edema
▸ Visual disturbances
Activate EMS
114
6 causes of HTN
▸ Anxiety
▸ Pain
▸ Cardiovascular disease
▸ Drug interaction
▸ Full bladder
▸ Hypoxia
115
Management of HTN - Esmolol
▸ A cardioselective B1 receptor blocker with rapid onset and short duration
of action
▸ 10-30 mg IV q5minutes
▸ Good choice if tachycardia present
▸ Good in asthmatics (no B-2 blockage)
116
Management of HTN - Labetalol
▸ An alpha- and ß-adrenergic blocker, given as an intravenous bolus or
infusion.
▸ 5-20 mg initially, followed by 20 to 80 mg every 10 minutes to a total dose
of 300 mg. Infusion: 0.5 to 2 mg/min.
***it doesn't slow down cardiac output
117
Management of HTN-Hydralazine
▸ An arteriolar dilator, given as an intravenous bolus. Initial dose:
▸ 5-10 mg given every 20 to 30 minutes; maximum dose: 20 mg.
▸ Good for pregnant women or if bradycardia present
118
What meds can you use to treat HTN
-Esmolol
-Labetalol
-Hydralazine
119
Hypertensive Crisis May Include...
▸ Nitroprusside — a rapidly acting arteriolar and venous dilator, given as an intravenous infusion. Initial
dose: 0.25 to 0.5 mcg/kg per min; maximum dose: 8 to 10 mcg/kg per min which should be
continued for no more than 10 minutes.
▸ Propranolol — a ß-adrenergic blocker, given as an intravenous infusion and then followed by oral
therapy. Dose: 1 to 10 mg load, followed by 3 mg/h.
▸ Nitroglycerin — a rapidly acting venous and, to a lesser degree, arteriolar dilator, given as an
intravenous infusion. Initial dose: 5 mcg/min; maximum dose: 100 mcg/min.
▸ Nicardipine — a calcium channel blocker, given as an intravenous infusion. Initial dose: 5 mg/h;
maximum dose: 15 mg/h.
120
Hypotension - 1 Liner
Blood pressure is the force of blood pushing against the walls of the arteries as the heart pumps out blood. This is low leading to inadequate perfusion of vital organs.
121
Hypootension
A reduction of arterial blood pressure of 15-20% from baseline
122
Cardiac symptoms accompanying reduced blood pressure:
▸Bradycardia (early) or tachycardia (late)
▸ Decreased cardiac output and tissue perfusion
123
Preoperative Hypotension Causes (8)
▸ Psychological factors - anxiety/syncope
▸ Premedication overdose
▸ Postural change
▸ Coexisting disease
▸ Hypovolemia from dehydration, infection or fasting
▸Drugs, hypercarbia, hypoxia
124
Hypotension-How to manage? (4 steps)
▸ Patient positioning – supine with legs elevated
▸ 100% O2
▸ Monitors (BP, pulse-ox, EKG)
▸ Look for specific cause and treat
125
Drug choices for Hypotension management (3)
▸ 0.01 mg/kg of atropine (up to 0.5mg if bradycardia)
▸ 5-10mg of ephedrine q5 minutes
▸ 0.1mg phenylephrine q 5 minutes – if tachycardia
-Consider Reversal
EMS activation
126
Von Willebrand Disease
▸ Factor VIII deficiency and von Willebrand factor deficiency
▸ Most common inherited bleeding disorder (up to 1%) (autosomal dominant/recessive)
-Bleeding disorder where there are low levels of clotting protein in the blood
▸ VWF serves to stabilize platelet adhesion and is produced by endothelial cells and monocytes
127
How many types of Vw disease are there?
-Type 1 - Partial quantitative deficiency of VWF (most common)
-Type 2 - Qualitative abnormalities (subtypes)
-Type 3 - Total deficiency of VWF (severe)
128
Hemophillia A
▸ Sex-linked factor VIII deficiency
▸ Clinical manifestations appear when deficiency >80%
▸ Severity
▸ <1% of Factor VIII = severe disease with spontaneous hemarthrosis
▸ >5% Factor VIII activity = mild disease, but significant bleeding from surgery
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How do you treat Von Willebrands and Hemophilia A?
Desmopressin-clotting promoter that ↑ release vWF (req >5% active factor VIII to release stores)
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Von Willebrand's Disease
▸ Moderate: cryoprecipitate (VIII, XII, vWF + fibrinogen)
▸ Severe: Factor VIII conc (often does not help w/ VWD alone → + cryo)
▸ Post-op: Amicar (inhibits fibrinolysis), 6g PO qid
▸ Note: can give pre-op: 5g IV 30 min before (= loading dose) for hemophilia, bleeding,
rebleeds (intracranial aneurysms), GI bleeds
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▸ Hemophilia B
▸(Christmas Disease) -Bleeding disorder that leads to prolonged oozing after trauma, surgical procedures
Factor IX deficiency
▸ Treatment
▸ Mild-Moderate: FFP(factors II, VII, IX, X)
▸ Severe: IV Proplex (contains concentrate factors II, VII, IX, X)
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Sickle Cell Anemia
▸ Autosomal recessive disorder of change in chemical composition of HgB with
valine substitution for glutamic acid
▸ Diagnosis is by Hgb electrophoresis
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What causes Sickling?
Sickling (change in shape of RBC’s) is exacerbated by
dehydration and hypoxia (decreases in O2 concnetration).
Amnormal RBS’c lead to:
▸ Vessel damage and associated tissues
▸ Thrombosis/microvascular occlusion
▸ Pain
▸ Ischemic damage to surrounding tissues
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Life span of RBCs in sickle cell disease
▸ Shortened life span of RBCs
▸ Normal = 120 days
▸ Sickle Cell trait = 29 days
▸ Sickle Cell Dz = 17 days
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Labs of sickle cell anemia would show (3 things)
▸ CBC – shows decreased Hgb, increased WBCs and creatinine
▸ Peripheral smear – shows sickle cells
▸ U/A – may show hematuria and casts
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