Cardio 1

Question 1

What is use-dependence phenomenon in regards to Class I antiarrhythmics?

Answer 1

Na channels in rapidly depolarizing tissue (inc. HR) spend more time in activated and inactivated state, thus allowing more binding time for class I antiarrhythmics, w/c dissociate during resting state of the channel. This allows for the blocking effects of the class I antiarrhythmics to intensify, and the slow conduction speed terminates tachyarrhythmias.

Question 2

What is the order of Na channel binding strength by class I antiarrhythmics? How is this significant for class IC and IB in particular?

Answer 2

Binding strength: 1C > 1A > 1B
>Class IC has the most pronounced use-dependence due to its slower dissociation – allows for accumulation of blocking effects over several cardiac cycles (inc. HR).
>Class IB has most rapid dissociation and least use-dependence – selective for ischemic myocardium cuz the dec. resting potential delays Na channel transition from inactivated to resting state.

Question 3

How are class IC antiarrhythmics useful for supraventricular tachycardia?

Answer 3

A patient with supraventricular tachycardia (A-fib) has an irregularly irregular rhythm. Class IC drugs can prolong QRS duration, and their pronounced use-dependence can further prolong QRS to greater extents at higher heart rates.

Question 4

What ion channels does Ivabradine act on and what is the effect?

Answer 4

Ivabradine is the only drug that decreases HR w/ no effect on cardiac contractility or relaxation – slows rate of SA node firing by selective inhibition of funny Na channels (If) – prolongs slow depolarization phase (phase 4)

Question 5

How does constrictive pericarditis present on CT scan and JVP tracing?

Answer 5

> CT scan: thickening and calcification of pericardium.
JVP tracing: rapid y-descent (atrial emptying) both steeper and deeper during inspiration – paradoxical rise in JVP (Kussmaul sign) due to RV not able to accommodate inspiratory inc. venous return.

Question 6

What is the significance of bicuspid aortic valves on the normal aging process?

Answer 6

Bicuspid aortic valves is one of the most common congenital heart defects. It accelerates the normal aging process by increasing hemodynamic stress – premature atherosclerosis and calcification of aortic valve.
Aortic stenosis occurs in >50% of affected pts (early, around age 50 vs age 60).

Question 7

How do transmural MI, Unstable angina, and Stable angina present in regards to degree of obstruction of coronary lumen?

Answer 7

> Transmural MI: ruptured plaque w/ fully obstructive thrombus.
Unstable angina: lesser degree of thrombus occlusion superimposing acute plaque change (ex. ulceration).
Stable angina: atheromatous plaque obstructing >75% lumen, no thrombus.

Question 8

What are the absolute contraindications to using OCPs? (6)

Answer 8

1) Prior hx of thromboembolic event or stroke
2) Hx of estrogen-dependent tumor
3) Women >35 y.o, heavy smokers
4) Hypertriglyceridemia
5) Decompensated or active liver dse (impair steroid metab)
6) Pregnancy

Question 9

What are the 2 ways in w/c B-blockers decrease BP?

Answer 9

> Dec. contractility and HR.

>Dec. renin release (sympa stimulation of B1-receptors on JG cells).

Question 10

What is the pathogenesis for cellular swelling and loss of contraction in the setting of myocardial ischemia?

Answer 10

Since blood flow can’t meet myocardial demands, heart cells transition from aerobic to anaerobic metabolism. Anaerobic metabolism can’t maintain ATP levels needed for Na/K-ATPase on membrane and Ca-ATPase of SR. This leads to inc. intracellular Na and Ca – free H2O drawn into cell – swelling, loss of contraction in ischemic zones.

Question 11

What are the cardiovascular and renal manifestations of SLE?

Answer 11

> CV: accelerated atherosclerosis, inc. risk of MI, vasculitis w/ fibrinoid necrosis of small arteries, pericarditis, Libman-Sacks endocarditis (vegetations on both sides of valve).
Renal: diffuse proliferative GN (“wire loop” capillaries)

Question 12

How do you dx Kawasaki disease?

Answer 12

Fever for 5+ days and 4 of the ff (MERCC):

1) Mucositis: strawberry tongue, fissured red lips
2) Extremity changes: edema, erythema of palms/soles, desquamation
3) Rash (starts at limbs, spreads to trunk)
4) Conjunctival injection (bilateral, nonexudative)
5) Cervical lymphadenopathy

Question 13

MOA of Fenoldopam

Answer 13

Peripheral D1 receptor agonist w/ virtually no effect on alpha/beta-receptors.
>For HTN emergency.
>Vasodilator of most arterial beds (dec. Systemic BP), renal vasodilation (benefit pts w/ AKI).

Question 14

Subclavian steal syndrome

[Px, ssx]

Answer 14

Significant stenosis of subclavian artery just before vertebral artery – dec. pressure in subclavian artery distal to stenosis – reverse blood flow from contralateral vertebral artery to ipsilateral vertebral artery to ipsilateral subclavian artery.
>Sx: arm ischemia; dizziness, vertigo, drop attacks

Question 15

Isolated systolic HTN

[BP, significance in aging patients]

Answer 15

Elevated SBP w/ normal DBP.

Pts. >60 y.o; aging is assctd w/ increased arterial stiffness – dec. compliance of aorta and major peripheral arteries.

Question 16

How does taking ACE inhibitors induce first-dose hypotension?

Answer 16

Significant hypotension will most likely occur in pts w/ high plasma renin activity, like with volume depletion (diuretic use) or heart failure. With dec. ATII from taking ACEi, there is peripheral vasodilation and thus dec. BP. Therapy should start in low doses then titrated upward.