Pass Machine - CV Flashcards
(44 cards)
Blood supply to:
- SA node
- AV node
- Bundle of HIS
SA: 60% RCA, 40% LAD
AV: 90% RCA, 10% LCx
HIS: dual PDA + LAD
Most sensitive EKG leads for ischemia
V5: 75%
II + V5: 80%
Best TEE view to look for ischemia - why?
Transgastric short axis - view areas of perfusion of all 3 major coronaries (RCA, LAD, Cx)
R-sided vagus/stellate ganglion –> which cardiac node
L-sided?
R = SA L = AV
Describe how cardiac muscle contraction is triggered/released by calcium
What protein accounts for the phenomenon of lusitropy?
- Ca into muscle cell through L-type Ca channels (phase 2 plateau of AP)
- Ca opens ryanodine receptor on SR -> more Ca release
- Ca binds troponin which exposes myosin binding sites on actin to allow for contraction
- Ca is removed by Na/Ca ATPase (to outside of cell) and SERCA (into SR) and relaxation occurs
Lusitropy: phospholamban is either un-phosphorylated (inhibits SERCA -> less relaxation) or phosphorylated (no SERCA inhibition -> more relaxation)
How do beta-1 receptors molecularly lead to increased heart rate?
Gs -> increase cAMP -> protein kinase -> T-type Ca channels and funny Na channels more open -> faster SA node depolarization
How do muscarinic receptors molecularly lead to decreased heart rate?
Gi -> inhibit T-type Ca channels and open K channels -> slower depolarization of SA node
What is reynold’s number? Equation?
Equation to determine the likelihood of laminar vs turbulent flow within a given vessel
R = 2rvd/visc
Radius, velocity, and density favor turbulence
Viscosity favors laminar flow
R < 2000 = laminar flow
R > 2000 = turbulent flow
Digoxin MOA
Inhibited Na/K pump -> increased intracellular Na -> decreased Na/Ca pump action (less Na gradient) -> more intracellular Ca
Result: decreased AV nodal conductance
Digoxin cardiac side effects
- Bradycardia
- AV block
- Paroxysmal atrial tachycardia w/ AV block (like WPW)
- Bi-directional v-tach
- Regular a fib (regular R-R interval)
Digoxin toxicity symptoms
- N/V/D
- AMS
- Blurred vision / green-yellow halos / color misperception
Digoxin is potentiated by what electrolyte abnormalities
Hyper/hypokalemia and hypercalcemia
MC EKG abnormality w/ digoxin
PVCs w/ hockey-stick QT interval
Treatment options of ventricular arrhythmias while on digoxin
- Lidocaine
- Phenytoin
- Amio
- Keep K upper-normal
- Digoxin Fab
Digoxin and cardioversion/DCCV?
- Preferred: low-energy synchronized cardioversion
- Danger: may lead to shock-refractory VFib
Adenosine: MOA
Uses?
Enhanced by what?
Antagonized by what?
Suppressed AV conductance
SVT, WPW – narrow-complex
Dipyridamole
Caffeine, theophylline, amrinone (methylxanthines)
Advantages of vasopressin
- Cerebrovascular dilator despite systemic vasoconstrictor
- Works well in acidosis
- H2O reabsorption
Disadvantages of vasopressin
- Thrombocytopenia
- Lactic acidosis
- Unpleasant symptoms in awake patients (abdominal, uterine contractions, skin pallor, bronchoconstriction)
Epi: first line for what type of shock
Anaphylactic
Levo: first line for what type(s) of shock
Vasodilatory (sepsis, neurogenic) w/o heart failure
Dopa: first line for what type of shock
Vasodilatory + bradycardia
Dobs: first line for what type(s) of shock
Cardiogenic + hypertension/high SVR
Sepsis + myocardial dysfunction (+ Levo)
Vaso: second line for what type of shock
Vasodilatory (+ levo)
Milrinone: second line for what type of shock
Cardiogenic + hypertension (may require pressor if causing hypotension)
