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Pass Machine - CV Flashcards

1
Q

Blood supply to:

  • SA node
  • AV node
  • Bundle of HIS
A

SA: 60% RCA, 40% LAD
AV: 90% RCA, 10% LCx
HIS: dual PDA + LAD

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2
Q

Most sensitive EKG leads for ischemia

A

V5: 75%

II + V5: 80%

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3
Q

Best TEE view to look for ischemia - why?

A

Transgastric short axis - view areas of perfusion of all 3 major coronaries (RCA, LAD, Cx)

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4
Q

R-sided vagus/stellate ganglion –> which cardiac node

L-sided?

A 
R = SA
L = AV
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5
Q

Describe how cardiac muscle contraction is triggered/released by calcium

What protein accounts for the phenomenon of lusitropy?

A
  • 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)

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6
Q

How do beta-1 receptors molecularly lead to increased heart rate?

A

Gs -> increase cAMP -> protein kinase -> T-type Ca channels and funny Na channels more open -> faster SA node depolarization

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7
Q

How do muscarinic receptors molecularly lead to decreased heart rate?

A

Gi -> inhibit T-type Ca channels and open K channels -> slower depolarization of SA node

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8
Q

What is reynold’s number? Equation?

A

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

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9
Q

Digoxin MOA

A

Inhibited Na/K pump -> increased intracellular Na -> decreased Na/Ca pump action (less Na gradient) -> more intracellular Ca

Result: decreased AV nodal conductance

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10
Q

Digoxin cardiac side effects

A
  • Bradycardia
  • AV block
  • Paroxysmal atrial tachycardia w/ AV block (like WPW)
  • Bi-directional v-tach
  • Regular a fib (regular R-R interval)
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11
Q

Digoxin toxicity symptoms

A
  • N/V/D
  • AMS
  • Blurred vision / green-yellow halos / color misperception
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12
Q

Digoxin is potentiated by what electrolyte abnormalities

A

Hyper/hypokalemia and hypercalcemia

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13
Q

MC EKG abnormality w/ digoxin

A

PVCs w/ hockey-stick QT interval

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14
Q

Treatment options of ventricular arrhythmias while on digoxin

A
  • Lidocaine
  • Phenytoin
  • Amio
  • Keep K upper-normal
  • Digoxin Fab
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15
Q

Digoxin and cardioversion/DCCV?

A
  • Preferred: low-energy synchronized cardioversion

- Danger: may lead to shock-refractory VFib

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16
Q

Adenosine: MOA

Uses?

Enhanced by what?

Antagonized by what?

A

Suppressed AV conductance

SVT, WPW – narrow-complex

Dipyridamole

Caffeine, theophylline, amrinone (methylxanthines)

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17
Q

Advantages of vasopressin

A
  • Cerebrovascular dilator despite systemic vasoconstrictor
  • Works well in acidosis
  • H2O reabsorption
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18
Q

Disadvantages of vasopressin

A
  • Thrombocytopenia
  • Lactic acidosis
  • Unpleasant symptoms in awake patients (abdominal, uterine contractions, skin pallor, bronchoconstriction)
19
Q

Epi: first line for what type of shock

A

Anaphylactic

20
Q

Levo: first line for what type(s) of shock

A

Vasodilatory (sepsis, neurogenic) w/o heart failure

21
Q

Dopa: first line for what type of shock

A

Vasodilatory + bradycardia

22
Q

Dobs: first line for what type(s) of shock

A

Cardiogenic + hypertension/high SVR

Sepsis + myocardial dysfunction (+ Levo)

23
Q

Vaso: second line for what type of shock

A

Vasodilatory (+ levo)

24
Q

Milrinone: second line for what type of shock

A

Cardiogenic + hypertension (may require pressor if causing hypotension)

25
Q

Milrinone MOA

A

Inhibit PDE3 -> increased cAMP -> increased pKa -> increased L-type Ca channel phosphorylation and expression -> increased inotropy/lusitropy/dromotropy/chronotropy, and vasodilation

26
Q

Mostly arterial dilators

A

CCBs, hydralazine, minoxidil

27
Q

Mostly venous dilators

A

Nitrates (+coronary dilation)

28
Q

Equal AV dilators

A

ACEIs, alpha-1 blockers, nitroprusside

29
Q

Hydralazine MOA

Side effect?

Rare side effects?

A

K channel activator on arterial smooth muscle -> dilation

Reflex tachycardia -> bad in CAD

Agranulocytosis, lupus-like syndrome

30
Q

Pure tachycardia CCB drug

31
Q

Pure peripheral vasodilating CCV drug

A

Nifedipine

32
Q

BEST vasodilator CCB drug

A

Nicardipine

33
Q

What NOT to use w/ beta blockers generally?

34
Q

Diltiazem - anti-tachy or anti-HTN?

35
Q

Hypokalemia - symptoms

A
  • Muscle weakness
  • Myalgia
  • Constipation
  • Flaccid Paralysis
  • Hyporeflexia
  • Respiratory weakness
36
Q

Hypokalemia - EKG finding

A

Peaked P, prolonged PR, ST depression, shallow T-wave, prominent U-wave

37
Q

Hyperkalemia - EKG finding progression

A

Peaked T, long PR

  • > long QRS, loss of P, ST elevation
  • > wide QRS/sine, asystole, blocks, etc
38
Q

Hypocalcemia - symptoms

A
  • AMS
  • Seizures/hyperreflexia (Chvostek/Trousseau)
  • Cararacts
  • Laryngospasm/bronchospasm/stridor
39
Q

Hypocalcemia - EKG findings

A

Long QT, T-wave changes

40
Q

Hypercalcemia - symptoms

A

Bones, stones, moans, groans, psych overtones

41
Q

Hypercalcemia - EKG findings

A

Bradycardia, short QT, arrhythmias

42
Q

EKG summary:

A 
HyperK: peaked T, long QRS
HypoK: shallow T, U-wave
HyperCa: short QT
HypoCa: long QT
HyperMg: tall T, depressed ST
43
Q

Hypo-Mg symptoms

Hyper-Mg symptoms

A

Fasciculations, tetany, tremor, others

Slow reflexes, hypotension, bradycardia, paralysis

44
Q

Hyper-Mg EKG

Tx?

A

Tall T, depressed ST

Calcium, dialysis, diuretic

Basic Exam (7 decks)

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