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Elaina CV 2 > Clin Med CV 2 > Flashcards

Clin Med CV 2 Flashcards

1
Q

this etiology comprises 75% of all cases of heart failure

A

MI or ischemia superimposed on prior infarctions

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2
Q

systolic failure represents an abnormality in what?

A

contraction

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3
Q

diastolic failure represents and abnormality in what?

A

relaxation

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4
Q

where will the edema be in acute vs. chronic HF?

A

acute=pulmonary edema

chronic=peripheral edema

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5
Q

most common sxs of left side heart failure?

A

pulmonary congestion & edema

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6
Q

most common sxs of right side heart failure?

A

peripheral edema, hepatic congestion, elevated JVP

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7
Q

how do we raise our BP to compensate for low cardiac output?

A

renin-angiotensin system is activated when kidneys are poorly perfused; angiotensin II vasoconstricts & aldosterone makes us hold onto sodium

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8
Q

what system mediates the redistribution of cardiac output so that we can adequately perfuse our brain under stress?

A

the adrenergic system

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9
Q

what are the beta 1 effects of norepinephrine?

A

increases cardiac output b

1) increasing heart rate (positive chonotropic effect)
2) increasing conduction velocity (positive dromotropic effect)
3) increasing stroke volume by enhancing contractility (positive inotropic effect)

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10
Q

what are the alpha 1 effects of norepinephrine?

A

increased peripheral resistance for redistribution of blood flow! (good to some degree so our vital organs get blood)

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11
Q

what is the cost of our adrenergic system’s compensatory effect during CHF?

A

increases cardiac afterload & oxygen demands of the failing ventricle!

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12
Q

what does long term elevation of catecholamines lead to?

A

progressive myocardial damage and death

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13
Q

what symptom does excess aldosterone production ultimately lead to?

A

edema

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14
Q

what does long term activation of angiotensin II and aldosterone lead to?

A

myocardial thinning and fibrosis

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15
Q

at what functional classification of heart disease do we see marked limitation of ADLS?

A

class 3 (out of 4)

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16
Q

what does a pulmonary capillary wedge pressure of 20 signify?

A

fluid in the interstitial spaces of lungs

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17
Q

what does a pulmonary capillary wedge pressure of 25 signify?

A

fluid in the alveoli

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18
Q

what is the hepato-jugular reflex? when do we see it?

A

in CHF; you can gently push on the liver and by doing so it pushes some blood from the sinusoids BACK to the vena cava & to the jugular veins (they will bulge)

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19
Q

what causes cardiac cachexia in CHF?

A

increased levels of cytokines (like circulating TNF)

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20
Q

what heart sound is most common in CHF?

A

S3 gallop! occurs due to volume overload and a weak heart

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21
Q

what is it called when we see increased markings at the TOP of the lungs in CHF?

A

cephalization of the vessels; they are engorged with blood!

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22
Q

what is the name for the white linear markings in the lower lungs in a patient with CHF?

A

kerley b lines

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23
Q

what is an ECHO good for identifying in CHF?

A

ventricular dysfunction & ejection fraction!

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24
Q

which hormone is produced by the heart ventricles in response to stress & stretch of the heart wall?

A

BNP; a marker of decompensated heart failure in the blood

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25
Q

what two physiologic properties does BNP have?

A

it is a weak diuretic & weak venodilator

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26
Q

your patient with COPD and CHF presents with SOB. what test is best to order?

A

BNP; it will be elevated if its an exacerbation of their CHF and not elevated if its an exacerbation of their COPD

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27
Q

what drug do we give to improve contractility in systolic failure?

A

digoxin

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28
Q

which three drugs prevent remodeling of the heart?

A

ACE inhibitors, spironolactone, beta blockers

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29
Q

what is the sodium intake recommendation for someone with CHF?

A

less than 4 grams

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30
Q

what is the effect of biventricular pacing? who do we use it for?

A

simultaneously makes the right and left ventricle contract at the same time (like it normally should); good for people with WIDE QRS, heart blocks, scar tissue, end stage HF

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31
Q

does biventricular pacing decrease mortality?

A

NO; simply improves quality of life and ejection fraction

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32
Q

which cardiac device DOES decrease mortality in patients with LV dysfunction and sxs of HF?

A

implantable cardioverted defibrillated

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33
Q

who gets ICDs?

A

EF

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34
Q

what is the biggest issue with cardiac transplants?

A

not enough donors!

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35
Q

the presence of what four conditions make it so you cannot call ischemia or infarction?

A

left ventricular hypertrophy, LBBB, wolf-parkinson-white, and digoxin

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36
Q

what is the criteria for ischemia?

A

greater than 1 mm ST segment depression that is horizontal or downsloping for more than .08 seconds (2 little boxes)

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37
Q

3 criteria for diagnosing MI?

A

1) history consistent w/ MI (chest pain)
2) EKG changes
3) release of cardiac markers (creatine kinase or troponins)

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38
Q

what is the first change seen on EKG of an MI?

A

hyperacute peaking T waves; represent potassium being released from injured cells

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39
Q

what does the deep Q wave represent post MI?

A

zone of myocardial infarction; the dead myocardium does not conduct electricity so therefore the Q wave will be large and INVERTED (bc it sees electrical activity going AWAY from it)

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40
Q

what if the LAD is occluded?

A

changes in V1-V4

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41
Q

what if the left circumflex is occluded?

A

pure lateral infarction (1, AVL, V5, V6)

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42
Q

what is the right coronary artery is occluded?

A

inferior infarction (II, III, AVF)

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43
Q

what will we see with infarction of the posterior wall of the heart?

A

90% of the time its supplied by RCA; instead of ST elevation and peaking of T waves you see the OPPOSITE

in lead V1/V2 you will see:

1) ST depression, T wave inversion
2) tall R waves instead of Q waves

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44
Q

where will reciprocal changes be seen with anterior wall STEMI?

A

inferior leads (II, III, AVF)

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45
Q

where will reciprocal changes be seen with inferior wall STEMI?

A

lateral leads (I and AVL)

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46
Q

what is the criteria for calling a pathologic Q wave?

A

greater in .04 seconds in duration that are 1/3 the height of the R wave in the same QRS complex

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47
Q

how do we distinguish between ischemia and NSTEMI?

A

cardiac markers because both will have inverted T waves

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48
Q

what is the most common cause of young patients with HTN?

A

sympathetic nervous system hyperactivity

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49
Q

is HTN caused by an increased or decreased amount of estrogen?

A

increased estrogen! stimulates angiotensin system so we hold onto more water

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50
Q

your patient taking OCPs is at risk for what?

A

developing HTN

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51
Q

how do NSAIDS contribute to the development of HTN?

A

they inhibit renal prostalgandins which are our vasodilators

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52
Q

how does cigarette smoking contribute to development of HTN?

A

releases norepinephrine which produces vasoconstriction

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53
Q

is HTN in pregnancy primary or secondary HTN?

A

secondary

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54
Q

what are the two forms of renal artery stenosis?

A

fibromuscular hyperplasia & atherosclerosis

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55
Q

how does a young patient with fibromuscular hyperplasia develop HTN?

A

they have an excess production of smooth muscle that leads to discrete narrowing and the decreased blood supply to the kidney dramatically raises renin levels

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56
Q

why do we run into issues with TX in atherosclerosis in renal vascular HTN?

A

VERY difficult to treat; sometimes using catheters and stents causes more harm

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57
Q

left ventricular hypertrophy leads to what type of dysfunction?

A

diastolic

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58
Q

what is identified by EKG in 50% of hypertensives?

A

LVH

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59
Q

why do we develop pulmonary edema with LVH?

A

it takes higher pressures in diastole to relax the stiff LV, so the pressures are reflected backwards

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60
Q

what is our major predisposing cause of stroke?

A

HTN

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61
Q

what population more commonly develops nephrosclerosis? what is it?

A

black populations; a disease that narrows kidney arteries & eventually the glomeruli are damaged and your renal function tests decline (check creatinine, BUN)

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62
Q

how do we treat nephrosclerosis?

A

similar to HTN

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63
Q

what is a “pock marked” appearance consistent with?

A

nephrosclerosis! the kidney gets small and the surface of the kidney gets “pock marked”

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64
Q

what will we see on fundoscopic exam of HTN?

A

narrowing of arterioles, AV nicking, silver/copper wiring, hemorrhages, papilledema

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65
Q

what do bruits indicate on PE?

A

atherosclerotic disease

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66
Q

when giving thiazide diuretics, what two things do we need to rule out before prescribing?

A

1) high uric acid levels (these drugs can cause gout)

2) electrolyte abnormalities (because we anticipate hypokalemia)

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67
Q

BP goal for elderly vs. everyone else?

A

elderly=

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68
Q

im not going to add a bunch of TX stuff because a lot of other people have already made flashcards with that

A

:)

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69
Q

what is present in >50% of cases of infective endocarditis?

A

underlying valve abnormality; typically aortic & mitral

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70
Q

what is the most common cause, location & infective organism of normal valve endocarditis?

A

IV drug using; staph aureus w/ vegetation on tricuspid valve (rarely goes to L heart)

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71
Q

prosthetic heart valves contribute to endocarditis; which two cardiac surgeries do NOT predispose?

A

bypass surgery & permanent pacemaker placements

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72
Q

what are the likely organisms in prosthetic valve endocarditis early on?

A

staph aureus (#1), staph epidermitis, gram negative organisms and fungi

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73
Q

what are the likely organisms in prosthetic valve endocarditis over 2 months out?

A

streptococci & staph

74
Q

how do we diagnose endocarditis? what is the classic lesion?

A

TEE echo; we see a vegetation

75
Q

which part of the valve gets infected during endocarditis?

A

the valve infections occur on the LOW pressure side of the valve!

1) mitral valve=left atrium side
2) aortic valve=LV side

76
Q

your patient comes in febrile and you are doing your regular cardio exam. you note a murmur that she claims has never been there before…what should you begin to work up?

A

endocarditis (associated with fever and new murmur)

77
Q

what may you find on PE of a patient with endocarditis?

A

1) oslers nodes (painful on fingers/toes)
2) janeway lesions (painless on palms or soles)
3) roth spots (exudative lesions on retina)

additional petechiae in palate, conjunctiva, subungual splinter hemorrhages

78
Q

what is the major complication of endocarditis?

A

emobili can break off and go to our organs; cause stroke, renal infarction, bowel infarction, ischemia (be curious in pt with flank pain, abdominal pain)

79
Q

staph aureus (and other virulent organs) will cause what type of course of endocarditis?

A

ACUTE course with rapid progression

rapid valve destruction, early embolization, REGURGITATION within 1-2 weeks

80
Q

strep viridans & enterococcus will cause what type of course of endocarditis?

A

SUB-ACUTE course that takes weeks to come to a head (5-8)

SLOW destruction of valve; systemic and peripheral manifestations predominate

81
Q

how do we diagnose and treat endocarditis?

A

blood cultures; 3 sets one hour apart and then RX ABX depending on culture

82
Q

what are the 3 major criteria for dx of endocarditis?

A

1) 2+ BC with typical organism
2) abnormal echo with vegetation
3) new regurgitant murmur

83
Q

who do we treat with ABX prophylactically to prevent endocarditis?

A

prosthetic hear valves, prior episodes of endocarditis, complex cyanotic heart disease, cardiac transplant with valve disease

84
Q

what two drugs do we give while waiting culture results for endocarditis?

A

vancomycin and ceftriaxone both IV

85
Q

where are our two major sources of endogenously derived cholesterol?

A

liver and intestines

86
Q

what is the rate limiting step of forming cholesterol?

A

converting HMG CoA to mevalonic acid by HMG CoA reductase in the liver

87
Q

what needs to happen to LDL in order for it to damage endothelium?

A

oxidation

88
Q

is a low HDL a risk factor for CHD even when LDL and total cholesterol are low?

A

YES

89
Q

what are the three skin manifestations we may find in someone with hyperlipidemia?

A

1) eruptive xanthomas on the buttocks (due to high triglycerides)
2) tendinous xanthomas (very high LDL nodules on achilles, back of hand, patella)
3) xanthelasma (plaques around eyes)

90
Q

what is VLDL?

A

a particle that carries triglycerides; when it is broken down LDL is formed

91
Q

what two factors are INVERSELY related in terms of lipid disorders?

A

triglycerides & HDL

92
Q

being born with a heterozygous form of familial hypercholesterolemia does what?

A

decreases amount of LDL receptors by 50%; you will be born with 350 total cholesterol

93
Q

what nine factors are included in the risk score calculator for hyperlipidemia?

A

1) age
2) sex
3) race
4) total cholesterol
5) HDL cholesterol
6) BP level
7) BP treatment status
8) diabetes status
9) smoking status

*NOTE THIS DOES NOT INCLUDE FAMILY HISTORY

94
Q

how much does high intensity statin therapy decrease your LDL by? what drugs do we use?

A

50%; atorvastatin, rousuvastatin

95
Q

how much does moderate intensity statin therapy decrease your LDL by? what drugs do we use?

A

30-50%; simvastatin, pravastatin, lovastatin

96
Q

where is the cutoff for medium vs. high intensity statin therapy?

A

greater than 7.5 percent 10 year risk of ASCVD

97
Q

a coronary calcium score of >300 indicates you should do what?

A

prescribe high intensity statin therapy

98
Q

an ABI less than .9 indicates you should do what?

A

prescribing high intensity statin therapy

99
Q

CRP of >2mg (inflammation) should make you consider what?

A

prescribing high intensity statin therapy

100
Q

what is the most common cause of sinus node dysfunction?

A

simple wear and tear

101
Q

characterized by PR interval >.20 seconds

A

first degree AV block

102
Q

characterized by progressive lengthening of PR interval until drop of QRS complex

A

Mobitz type I (Wenckebach)

103
Q

where is the block typically in mobitz type 1?

A

the AV node

104
Q

characterized by p waves followed by abrupt drop of one or more QRS complexes without PR prolongation

A

mobitz type II

105
Q

where is the block typically in mobitz type II?

A

bundle of his; can potentially extend into bundle branches

106
Q

how do we differentiate PAC from the heart blocks?

A

PAC will have a P wave that looks different

107
Q

if you see WIDE QRS in which conduction starts in sinus node (we have p waves) think…

A

bundle branch block

108
Q

something that may help you distinguish between mobitz I and mobitz II…

A

mobitz 1 NEVER gives you multiple dropped beats in a row, mobitz II can!

109
Q

third degree AV block is characterized by what?

A

complete dissociation of the atria and ventricles;

1) atrial rate=60-100
2) either ventricular escape rhythm (30-50 wide QRS) or junctional rhythm (40-60 narrow QRS)

110
Q

RSR’ rabbit ear morphology in V1 most indicates…

A

RBBB

111
Q

what will the late depolarization of the RV result in on EKG in RBBB?

A

WIDE S waves in V5, V6, 1, and AVL representing delayed RV depolarization

112
Q

a notched, wide R wave in V6 most indicates…

A

LBBB

113
Q

what will we see in V1 in a patient with LBBB?

A

downward wide QRS (either rS or wide Q) because the LV is depolarizing slowly from cell-to-cell

114
Q

left ANTERIOR hemiblock leads to what type of deviation? which direction does the signal go in?

A

LEFT axis deviation; depolarization occurs inferior to superior, right to left

115
Q

left POSTERIOR hemiblock leads to what type of deviation? which direction does the signal go in?

A

RIGHT axis deviation; depolarization occurs from superior to inferior, left to right

116
Q

the key to hemiblocks is that they cause what?

A

axis deviation!

know that the QRS is usually narrow

117
Q

what are the two types of dilated cardiomyopathy?

A

primary (idiopathic) and secondary (toxic/post partum/post-infectious/endocrine/ischemic)

118
Q

what types of symptoms will your patient with dilated cardiomyopathy present with?

A

similar to HEART FAILURE w/ systolic dysfunction predominating

119
Q

what type of murmur will occur with dilated cardiomyopathy?

A

S3 gallop

120
Q

what type of valve murmur are we likely to get with dilated cardiomyopathy?

A

regurgitation murmur

121
Q

what is the main difference between tricuspid regurg murmur and mitral regurg murmur?

A

tricuspid gets louder with inspiration!

122
Q

what will EKG look like with dilated cardiomyopathy?

A

non-specific ST-T changes, wide QRS, PVC

123
Q

how do we treat dilated cardiomyopathy?

A

EXACTLY like heart failure; afterload reduction (ACE inhibitors), beta blockers (decrease remodeling), preload reduction (diuretics)

124
Q

what type of genetic mutation is hypertrophic cardiomyopathy?

A

autosomal dominant; VERY important to do ECG on siblings & offspring

125
Q

aside from genetic mutations, how else may hypertrophic cardiomyopathy develop?

A

DE NOVO mutations of the genes that code for proteins that lead to excessive hypertrophy

126
Q

where is the problem most focused in hypertrophic cardiomyopathy?

A

the interventricular septum

127
Q

how is systolic vs. diastolic function in hypertrophic cardiomyopathy?

A

systolic function NORMAL or HYPERDYNAMIC early on

DIASTOLIC function decreased because ventricle can’t relax

128
Q

what are the two forms of hypertrophic cardiomyopathy?

A

obstructive & non-obstructive; sometimes the hypertrophy leads to narrowing right near the aortic valve

129
Q

what may happen to the mitral valve in hypertrophic cardiomyopathy?

A

the mitral valve is often thickened and moves abnormally towards the interventricular septum; obstructing the left ventricular outflow tract (SEE ON ECHO)

130
Q

what is one of the most common causes of sudden death in athletes?

A

hypertrophic cardiomyopathy; be sure to ask if they have hx of family member with sudden death

131
Q

aside from sudden death, what is a major complication that occurs with hypertrophic cardiomyopathy?

A

arrythmias

it is REALLY bad if we get afib because we need our atria to contract to maintain decent cardiac output! our ventricles are messed up too

132
Q

what will the patient’s pulse be like with hypertrophic cardiomyopathy?

A

pulse is brisk; bisferiens carotid pulse; double or triple apical impulse due to atrial filling wave and early and late systolic impulses (sometimes you get double contraction of ventricles with every systole)

133
Q

what will the murmur be like with hypertrophic cardiomyopathy?

A

S4,S3 gallops. loud HARSH aortic outflow murmur (crescendo-decrescendo) best heard along LEFT STERNAL BORDER (sounds a lot like aortic stenosis)

134
Q

what is unique about the murmur of hypertrophic cardiomyopathy in regards to body position?

A

it gets louder when you make the heart SMALL (valsalva, standing up)

135
Q

what happens to most murmurs when you squat & bring more blood to the heart, making it bigger?

A

they usually increase!

applies to MS, AS, MR, AR

does NOT apply to MVP, hypertrophic cardiomyopathy

136
Q

how do we treat hypertrophic cardiomyopathy?

A

minimize strenuous activity & beta blockers to slow HR, increase filling time, and prevent arrythmias

137
Q

if we are going to surgically treat hypertrophic cardiomyopathy, what do we do?

A

myomectomy, alcohol ablation of septal branches, or dual chamber pacemaker or ICD

138
Q

what type of dysfunction is restrictive cardiomyopathy?

A

diastolic

139
Q

differentiating between restrictive vs. hypertrophic cardiomyopathy

A

1) restrictive=ventricular walls rigid

2) hypertrophic=ventricular septum rigid

140
Q

what are some causes of restrictive cardiomyopathy?

A

amyloidosis, hemochromatosis (only reversible), fabry disease, gaucher disease, endomyocardial fibrosis w/ hypereosinofilia

141
Q

do we normally have findings of left or right heart failure with restrictive cardiomyopathy?

A

RIGHT failure; stuff gets stuck.

JVD, edema, hepatomegaly

142
Q

what is kussmaul’s sign? what is it indicative of?

A

when you inhale your neck veins get big; seen with restrictive cardiomyopathy

143
Q

which two valve disorders are most common with restrictive cardiomyopathy?

A

tricuspid and mitral regurgitation

144
Q

how do we treat restrictive cardiomyopathy?

A

90% dead at 10 years; symptomatic treatment…calcium channel blocks MAY improve diastolic function in some individuals to help ventricles relax

145
Q

what does tako-tsubo cardiomyopathy mimic?

A

STEMI; chest pain, ECG changes with modest elevations of troponins!

146
Q

what will echo of tako-tsubo cardiomyopathy show?

A

LV dysfunction with anterior, apical, and inferior ballooning…maybe decreased ejection fraction because only part of the ventricle is contracting

147
Q

what is the mechanism of tako-tsubo?

A

stressful events (90% women) lead to outpouring of catecholamines

148
Q

how do we treat tako-tsubo?

A

SAME AS HEART FAILURE

149
Q

what is the most common cause of myocarditis?

A

viral infection; coxsackie virus most common

150
Q

symptoms of myocarditis?

A

prodromal viral syndrome followed by chest pain, fatigue, dyspnea, palpitations

151
Q

what will PE of myocarditis look like?

A

muffled heart sounds, signs of HF in severe cases, temp, tachy

152
Q

how do we diagnose myocarditis?

A

difficult! NSST-T changes; we may need to do acute and convalescent viral titers

153
Q

how do we treat myocarditis?

A

supportive! AVOID NSAIDS

154
Q

most common cause of pericarditis?

A

coxsackie B! viral infections

155
Q

what are some other causes of pericarditis?

A

CANCER, POST MI, TRAUMA, DRUG INDUCED, AUTOIMMUNE (RA, SLE), UREMIA

156
Q

what aggravates the sharp pain of pericarditis?

A

laying down, with inspiration, coughing, swalling

157
Q

what will see see on PE with pericarditis?

A

pericardial friction rub when patient is sitting, leaning forward

158
Q

what will EKG of pericarditis look like?

A

ST SEGMENT ELEVATION EVERYWHERE; don’t develop Q waves like an MI

159
Q

how to treat pericarditis?

A

NSAIDS

160
Q

symptoms of pericardial effusion without cardiac compression?

A

dyspnea, hiccups, nausea, abdominal fullness, cough

161
Q

what does an EKG with extremely low voltage and inverted T waves lead you to think?

A

pleural effusion

162
Q

what will happen to our stroke volume with effusion?

A

pressure on the heart leads to limitation in diastolic filling leading to REDUCTION IN STROKE VOLUME

163
Q

what is pathognomonic of cardiac tamponade?

A

pulsus paradoxus ; we get a systolic BP drop of more than 10 mm vs 2-4 mm

164
Q

how do we treat cardiac tamponade?

A

pericardiocentesis

165
Q

when you think kent bundle, what do you think of?

A

wolf-parkinson-white

166
Q

what will EKG of WPW look like?

A

short PR interval, wide QRS, delta waves (slurring on upstroke of QRS), wide base of QRS & thin tip

167
Q

what can you no longer rule in if you see WPW on EKG?

A

ischemia or infarction or LVH

168
Q

what arrythmia is most common with WPW?

A

PSVT due to reentry

169
Q

what will AFIB look like in a patient with WPW?

A

VTACH; if patient goes into AFIB they start conducting mostly by way of kent bundle

170
Q

what does digoxin toxicity look like on EKG?

A

non-specific ST changes with SCOOPING of ST segment and shortening of QT interval

171
Q

what are the most common arrythmias seen in digoxin toxicity?

A

multifocal PVC, accelerated junctional rhythm, and atrial tachycardia with AV block

172
Q

what is digoxin’s effect on the AV node?

A

it slows conduction through the AV node

173
Q

common finding on EKG of hypokalemia?

A

ST segment depression, flattening of T wave, UPWARD U WAVES!

174
Q

what will we see on EKG of a patient with hyperkalemia?

A

peaked T waves across ENTIRE 12 lead EKG

175
Q

what is the sign wave? where do we see it?

A

in hyperkalemia; the QRS gets very wide followed by peaked T wave that lead to VFIB arrest

176
Q

common causes of QT prolongation?

A

hypOcalemia, macrolides, anti-arrythmics, CNS lesions, bradyarrythmias, congenital syndromes (jervell & lange nielsen, romano-ward)

177
Q

what is our diagnostic criteria of QT prolongation?

A

QT interval is greater than 50% of the R-R interval

178
Q

upward U waves are seen in…

A

hypokalemia, digoxin toxicity, LVH, amiodarone

179
Q

negative U waves are seen in….

A

HTN, mitral disease, ischemia

180
Q

what is QT prolongation associated with?

A

VFIB and sudden death

Elaina CV 2 (2 decks)

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