Cardiology Flashcards
Do betablockers increase contractility?
Decrease contractility, digoxin increases contractility (increasing intracellular calcium)
When could you hear a fixed split of P2?
ASD- regardless of inspiration or expiration you have increased filling pressures because of ASD
What causes a late crescendo murmur with midsystolic click?
Mitral valve prolapse (can be to myxomatous degeneration) secondary to marfans or ehlers danlos, rheumatic fever, or chordae rupture
What gives you a U wave?
hypokalemia
What kind of block can lyme disease cause?
third degree heart block
What is a good measure of LA pressure?
PCWP (pulmonary capillary wedge pressure) it’s measured in the pulmonary artery with a Swan Ganz catheter, if you have PCWP> LV end diastolic pressure then you have mitral stenosis
What is unique about pulmonary vasculature?
it vasoconstricts in response to alveolar hypoxia (get blood to ventilated areas), other tissues will vasodilate
What is Eisenmenger syndrome?
when you have an unrepaired left to right shunt for too long and you get RVH and then right to left shunting develops and you get cyanosis, polycythemia, clubbing
what is cor pulmonale?
isolated right sided heart failure from pulmonary cause
What are the pathology findings in Rheumatic fever?
Aschoff bodies (granuloma with giant cells) and Anitschkow cells (enlarged macrophages with ovoid, wavy, rod like nucleus)
What type of hypersensitivity reaction is caused by Rheumatic fever?
Type 2- antibodies to M cells cross react with self-antigens (molecular mimicry)
What is Beck’s triad?
hypotension, distension of neck veins, , distant heart sounds
(happens in cardiac tamponade- can also get pulsus paradoxus, tachycardia, low voltage QRS)
What gives you the tree bark appearance of the aorta?
tertiary syphilis-disrupts vasa vasorum of the aorta, atrophy and dilation, csn get aneurysm
What is Osler-Weber-Rendu syndrome?
hereditary hemorrhagic telangiectasia, hereditary disorder of the blood vessels, skin, mucous membranes, recurrent epistaxis, AVMs, GI bleeding, hematuria
Which drugs are first line for HTN with diabetes?
ACEI (better for diabetic nephropathy)
how does hydralazine work? what is the side effect?
inc cGMP, gets smooth muscle relaxation, dec afterload, side effect is reflex tachycardia
what is the side effect of nitrates?
reflex tachycardia
What is the mechanism of digoxin?
inhibits Na/K ATPase and NA/Ca exchanger so you get build up of Ca in cell and increased ionotropy (contractility), stimulates the vagus nerve to give you increased HR, side effects are HF and a-fib, cholinergic, hyperkalemia
What are the class 1 of arrhythmics?
Class 1=sodium channel blockers
- 1A (inc AP duration, refractory period, prolong qt) quinidine, procainamide
- 1B (dec AP duration, best post MI for ischemic tissue) lidocaine
- 1C (inc ERP in AV node, but not below)- ideal for SVT, not VT (flecainide, propafenone)
What are the class 2 antiarrhythmics?
b-blockers- block SA and AV node by dec cAMP. Good for SVT, A fib anf A flutter, but can worsen asthma, COPD, cause impotence
What are the class 3 anti-arrhythmics?
K channel blockers- inc AP duration, ERP, good for A fib, A flutter and VT (amiodarone)- but amiodarone can cause pul fibrosis, hyper/hypothyroid, hepatotoxicity
What are the class 4 anti-arrhythmics?
Ca channel blockers (verapamil, diltiazem)-slow conduction velocity, inc ERP and PR interval, good for SVT and rate control in A fib. Can cause constipation, flushing, edema, HF
What does adenosine do?
causes K to flush out of cells, so Ca out too, dec AV node conduction, acts fast like 15sec-flushing, hypotension, chest pain, sense of impending doom, bronchospasm
