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
2
Q
systolic failure represents an abnormality in what?
A
contraction
3
Q
diastolic failure represents and abnormality in what?
A
relaxation
4
Q
where will the edema be in acute vs. chronic HF?
A
acute=pulmonary edema
chronic=peripheral edema
5
Q
most common sxs of left side heart failure?
A
pulmonary congestion & edema
6
Q
most common sxs of right side heart failure?
A
peripheral edema, hepatic congestion, elevated JVP
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
8
Q
what system mediates the redistribution of cardiac output so that we can adequately perfuse our brain under stress?
A
the adrenergic system
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)
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)
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!
12
Q
what does long term elevation of catecholamines lead to?
A
progressive myocardial damage and death
13
Q
what symptom does excess aldosterone production ultimately lead to?
A
edema
14
Q
what does long term activation of angiotensin II and aldosterone lead to?
A
myocardial thinning and fibrosis
15
Q
at what functional classification of heart disease do we see marked limitation of ADLS?
A
class 3 (out of 4)
16
Q
what does a pulmonary capillary wedge pressure of 20 signify?
A
fluid in the interstitial spaces of lungs
17
Q
what does a pulmonary capillary wedge pressure of 25 signify?
A
fluid in the alveoli
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)
19
Q
what causes cardiac cachexia in CHF?
A
increased levels of cytokines (like circulating TNF)
20
Q
what heart sound is most common in CHF?
A
S3 gallop! occurs due to volume overload and a weak heart
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!
22
Q
what is the name for the white linear markings in the lower lungs in a patient with CHF?
A
kerley b lines
23
Q
what is an ECHO good for identifying in CHF?
A
ventricular dysfunction & ejection fraction!
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
25
what two physiologic properties does BNP have?
it is a weak diuretic & weak venodilator
26
your patient with COPD and CHF presents with SOB. what test is best to order?
BNP; it will be elevated if its an exacerbation of their CHF and not elevated if its an exacerbation of their COPD
27
what drug do we give to improve contractility in systolic failure?
digoxin
28
which three drugs prevent remodeling of the heart?
ACE inhibitors, spironolactone, beta blockers
29
what is the sodium intake recommendation for someone with CHF?
less than 4 grams
30
what is the effect of biventricular pacing? who do we use it for?
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
31
does biventricular pacing decrease mortality?
NO; simply improves quality of life and ejection fraction
32
which cardiac device DOES decrease mortality in patients with LV dysfunction and sxs of HF?
implantable cardioverted defibrillated
33
who gets ICDs?
EF
34
what is the biggest issue with cardiac transplants?
not enough donors!
35
the presence of what four conditions make it so you cannot call ischemia or infarction?
left ventricular hypertrophy, LBBB, wolf-parkinson-white, and digoxin
36
what is the criteria for ischemia?
greater than 1 mm ST segment depression that is horizontal or downsloping for more than .08 seconds (2 little boxes)
37
3 criteria for diagnosing MI?
1) history consistent w/ MI (chest pain)
2) EKG changes
3) release of cardiac markers (creatine kinase or troponins)
38
what is the first change seen on EKG of an MI?
hyperacute peaking T waves; represent potassium being released from injured cells
39
what does the deep Q wave represent post MI?
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)
40
what if the LAD is occluded?
changes in V1-V4
41
what if the left circumflex is occluded?
pure lateral infarction (1, AVL, V5, V6)
42
what is the right coronary artery is occluded?
inferior infarction (II, III, AVF)
43
what will we see with infarction of the posterior wall of the heart?
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
44
where will reciprocal changes be seen with anterior wall STEMI?
inferior leads (II, III, AVF)
45
where will reciprocal changes be seen with inferior wall STEMI?
lateral leads (I and AVL)
46
what is the criteria for calling a pathologic Q wave?
greater in .04 seconds in duration that are 1/3 the height of the R wave in the same QRS complex
47
how do we distinguish between ischemia and NSTEMI?
cardiac markers because both will have inverted T waves
48
what is the most common cause of young patients with HTN?
sympathetic nervous system hyperactivity
49
is HTN caused by an increased or decreased amount of estrogen?
increased estrogen! stimulates angiotensin system so we hold onto more water
50
your patient taking OCPs is at risk for what?
developing HTN
51
how do NSAIDS contribute to the development of HTN?
they inhibit renal prostalgandins which are our vasodilators
52
how does cigarette smoking contribute to development of HTN?
releases norepinephrine which produces vasoconstriction
53
is HTN in pregnancy primary or secondary HTN?
secondary
54
what are the two forms of renal artery stenosis?
fibromuscular hyperplasia & atherosclerosis
55
how does a young patient with fibromuscular hyperplasia develop HTN?
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
56
why do we run into issues with TX in atherosclerosis in renal vascular HTN?
VERY difficult to treat; sometimes using catheters and stents causes more harm
57
left ventricular hypertrophy leads to what type of dysfunction?
diastolic
58
what is identified by EKG in 50% of hypertensives?
LVH
59
why do we develop pulmonary edema with LVH?
it takes higher pressures in diastole to relax the stiff LV, so the pressures are reflected backwards
60
what is our major predisposing cause of stroke?
HTN
61
what population more commonly develops nephrosclerosis? what is it?
black populations; a disease that narrows kidney arteries & eventually the glomeruli are damaged and your renal function tests decline (check creatinine, BUN)
62
how do we treat nephrosclerosis?
similar to HTN
63
what is a "pock marked" appearance consistent with?
nephrosclerosis! the kidney gets small and the surface of the kidney gets "pock marked"
64
what will we see on fundoscopic exam of HTN?
narrowing of arterioles, AV nicking, silver/copper wiring, hemorrhages, papilledema
65
what do bruits indicate on PE?
atherosclerotic disease
66
when giving thiazide diuretics, what two things do we need to rule out before prescribing?
1) high uric acid levels (these drugs can cause gout)
| 2) electrolyte abnormalities (because we anticipate hypokalemia)
67
BP goal for elderly vs. everyone else?
elderly=
68
im not going to add a bunch of TX stuff because a lot of other people have already made flashcards with that
:)
69
what is present in >50% of cases of infective endocarditis?
underlying valve abnormality; typically aortic & mitral
70
what is the most common cause, location & infective organism of normal valve endocarditis?
IV drug using; staph aureus w/ vegetation on tricuspid valve (rarely goes to L heart)
71
prosthetic heart valves contribute to endocarditis; which two cardiac surgeries do NOT predispose?
bypass surgery & permanent pacemaker placements
72
what are the likely organisms in prosthetic valve endocarditis early on?
staph aureus (#1), staph epidermitis, gram negative organisms and fungi
73
what are the likely organisms in prosthetic valve endocarditis over 2 months out?
streptococci & staph
74
how do we diagnose endocarditis? what is the classic lesion?
TEE echo; we see a vegetation
75
which part of the valve gets infected during endocarditis?
the valve infections occur on the LOW pressure side of the valve!
1) mitral valve=left atrium side
2) aortic valve=LV side
76
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?
endocarditis (associated with fever and new murmur)
77
what may you find on PE of a patient with endocarditis?
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
what is the major complication of endocarditis?
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
staph aureus (and other virulent organs) will cause what type of course of endocarditis?
ACUTE course with rapid progression
rapid valve destruction, early embolization, REGURGITATION within 1-2 weeks
80
strep viridans & enterococcus will cause what type of course of endocarditis?
SUB-ACUTE course that takes weeks to come to a head (5-8)
SLOW destruction of valve; systemic and peripheral manifestations predominate
81
how do we diagnose and treat endocarditis?
blood cultures; 3 sets one hour apart and then RX ABX depending on culture
82
what are the 3 major criteria for dx of endocarditis?
1) 2+ BC with typical organism
2) abnormal echo with vegetation
3) new regurgitant murmur
83
who do we treat with ABX prophylactically to prevent endocarditis?
prosthetic hear valves, prior episodes of endocarditis, complex cyanotic heart disease, cardiac transplant with valve disease
84
what two drugs do we give while waiting culture results for endocarditis?
vancomycin and ceftriaxone both IV
85
where are our two major sources of endogenously derived cholesterol?
liver and intestines
86
what is the rate limiting step of forming cholesterol?
converting HMG CoA to mevalonic acid by HMG CoA reductase in the liver
87
what needs to happen to LDL in order for it to damage endothelium?
oxidation
88
is a low HDL a risk factor for CHD even when LDL and total cholesterol are low?
YES
89
what are the three skin manifestations we may find in someone with hyperlipidemia?
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
what is VLDL?
a particle that carries triglycerides; when it is broken down LDL is formed
91
what two factors are INVERSELY related in terms of lipid disorders?
triglycerides & HDL
92
being born with a heterozygous form of familial hypercholesterolemia does what?
decreases amount of LDL receptors by 50%; you will be born with 350 total cholesterol
93
what nine factors are included in the risk score calculator for hyperlipidemia?
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
how much does high intensity statin therapy decrease your LDL by? what drugs do we use?
50%; atorvastatin, rousuvastatin
95
how much does moderate intensity statin therapy decrease your LDL by? what drugs do we use?
30-50%; simvastatin, pravastatin, lovastatin
96
where is the cutoff for medium vs. high intensity statin therapy?
greater than 7.5 percent 10 year risk of ASCVD
97
a coronary calcium score of >300 indicates you should do what?
prescribe high intensity statin therapy
98
an ABI less than .9 indicates you should do what?
prescribing high intensity statin therapy
99
CRP of >2mg (inflammation) should make you consider what?
prescribing high intensity statin therapy
100
what is the most common cause of sinus node dysfunction?
simple wear and tear
101
characterized by PR interval >.20 seconds
first degree AV block
102
characterized by progressive lengthening of PR interval until drop of QRS complex
Mobitz type I (Wenckebach)
103
where is the block typically in mobitz type 1?
the AV node
104
characterized by p waves followed by abrupt drop of one or more QRS complexes without PR prolongation
mobitz type II
105
where is the block typically in mobitz type II?
bundle of his; can potentially extend into bundle branches
106
how do we differentiate PAC from the heart blocks?
PAC will have a P wave that looks different
107
if you see WIDE QRS in which conduction starts in sinus node (we have p waves) think...
bundle branch block
108
something that may help you distinguish between mobitz I and mobitz II...
mobitz 1 NEVER gives you multiple dropped beats in a row, mobitz II can!
109
third degree AV block is characterized by what?
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
RSR' rabbit ear morphology in V1 most indicates...
RBBB
111
what will the late depolarization of the RV result in on EKG in RBBB?
WIDE S waves in V5, V6, 1, and AVL representing delayed RV depolarization
112
a notched, wide R wave in V6 most indicates...
LBBB
113
what will we see in V1 in a patient with LBBB?
downward wide QRS (either rS or wide Q) because the LV is depolarizing slowly from cell-to-cell
114
left ANTERIOR hemiblock leads to what type of deviation? which direction does the signal go in?
LEFT axis deviation; depolarization occurs inferior to superior, right to left
115
left POSTERIOR hemiblock leads to what type of deviation? which direction does the signal go in?
RIGHT axis deviation; depolarization occurs from superior to inferior, left to right
116
the key to hemiblocks is that they cause what?
axis deviation!
know that the QRS is usually narrow
117
what are the two types of dilated cardiomyopathy?
primary (idiopathic) and secondary (toxic/post partum/post-infectious/endocrine/ischemic)
118
what types of symptoms will your patient with dilated cardiomyopathy present with?
similar to HEART FAILURE w/ systolic dysfunction predominating
119
what type of murmur will occur with dilated cardiomyopathy?
S3 gallop
120
what type of valve murmur are we likely to get with dilated cardiomyopathy?
regurgitation murmur
121
what is the main difference between tricuspid regurg murmur and mitral regurg murmur?
tricuspid gets louder with inspiration!
122
what will EKG look like with dilated cardiomyopathy?
non-specific ST-T changes, wide QRS, PVC
123
how do we treat dilated cardiomyopathy?
EXACTLY like heart failure; afterload reduction (ACE inhibitors), beta blockers (decrease remodeling), preload reduction (diuretics)
124
what type of genetic mutation is hypertrophic cardiomyopathy?
autosomal dominant; VERY important to do ECG on siblings & offspring
125
aside from genetic mutations, how else may hypertrophic cardiomyopathy develop?
DE NOVO mutations of the genes that code for proteins that lead to excessive hypertrophy
126
where is the problem most focused in hypertrophic cardiomyopathy?
the interventricular septum
127
how is systolic vs. diastolic function in hypertrophic cardiomyopathy?
systolic function NORMAL or HYPERDYNAMIC early on
DIASTOLIC function decreased because ventricle can't relax
128
what are the two forms of hypertrophic cardiomyopathy?
obstructive & non-obstructive; sometimes the hypertrophy leads to narrowing right near the aortic valve
129
what may happen to the mitral valve in hypertrophic cardiomyopathy?
the mitral valve is often thickened and moves abnormally towards the interventricular septum; obstructing the left ventricular outflow tract (SEE ON ECHO)
130
what is one of the most common causes of sudden death in athletes?
hypertrophic cardiomyopathy; be sure to ask if they have hx of family member with sudden death
131
aside from sudden death, what is a major complication that occurs with hypertrophic cardiomyopathy?
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
what will the patient's pulse be like with hypertrophic cardiomyopathy?
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
what will the murmur be like with hypertrophic cardiomyopathy?
S4,S3 gallops. loud HARSH aortic outflow murmur (crescendo-decrescendo) best heard along LEFT STERNAL BORDER (sounds a lot like aortic stenosis)
134
what is unique about the murmur of hypertrophic cardiomyopathy in regards to body position?
it gets louder when you make the heart SMALL (valsalva, standing up)
135
what happens to most murmurs when you squat & bring more blood to the heart, making it bigger?
they usually increase!
applies to MS, AS, MR, AR
does NOT apply to MVP, hypertrophic cardiomyopathy
136
how do we treat hypertrophic cardiomyopathy?
minimize strenuous activity & beta blockers to slow HR, increase filling time, and prevent arrythmias
137
if we are going to surgically treat hypertrophic cardiomyopathy, what do we do?
myomectomy, alcohol ablation of septal branches, or dual chamber pacemaker or ICD
138
what type of dysfunction is restrictive cardiomyopathy?
diastolic
139
differentiating between restrictive vs. hypertrophic cardiomyopathy
1) restrictive=ventricular walls rigid
| 2) hypertrophic=ventricular septum rigid
140
what are some causes of restrictive cardiomyopathy?
amyloidosis, hemochromatosis (only reversible), fabry disease, gaucher disease, endomyocardial fibrosis w/ hypereosinofilia
141
do we normally have findings of left or right heart failure with restrictive cardiomyopathy?
RIGHT failure; stuff gets stuck.
JVD, edema, hepatomegaly
142
what is kussmaul's sign? what is it indicative of?
when you inhale your neck veins get big; seen with restrictive cardiomyopathy
143
which two valve disorders are most common with restrictive cardiomyopathy?
tricuspid and mitral regurgitation
144
how do we treat restrictive cardiomyopathy?
90% dead at 10 years; symptomatic treatment...calcium channel blocks MAY improve diastolic function in some individuals to help ventricles relax
145
what does tako-tsubo cardiomyopathy mimic?
STEMI; chest pain, ECG changes with modest elevations of troponins!
146
what will echo of tako-tsubo cardiomyopathy show?
LV dysfunction with anterior, apical, and inferior ballooning...maybe decreased ejection fraction because only part of the ventricle is contracting
147
what is the mechanism of tako-tsubo?
stressful events (90% women) lead to outpouring of catecholamines
148
how do we treat tako-tsubo?
SAME AS HEART FAILURE
149
what is the most common cause of myocarditis?
viral infection; coxsackie virus most common
150
symptoms of myocarditis?
prodromal viral syndrome followed by chest pain, fatigue, dyspnea, palpitations
151
what will PE of myocarditis look like?
muffled heart sounds, signs of HF in severe cases, temp, tachy
152
how do we diagnose myocarditis?
difficult! NSST-T changes; we may need to do acute and convalescent viral titers
153
how do we treat myocarditis?
supportive! AVOID NSAIDS
154
most common cause of pericarditis?
coxsackie B! viral infections
155
what are some other causes of pericarditis?
CANCER, POST MI, TRAUMA, DRUG INDUCED, AUTOIMMUNE (RA, SLE), UREMIA
156
what aggravates the sharp pain of pericarditis?
laying down, with inspiration, coughing, swalling
157
what will see see on PE with pericarditis?
pericardial friction rub when patient is sitting, leaning forward
158
what will EKG of pericarditis look like?
ST SEGMENT ELEVATION EVERYWHERE; don't develop Q waves like an MI
159
how to treat pericarditis?
NSAIDS
160
symptoms of pericardial effusion without cardiac compression?
dyspnea, hiccups, nausea, abdominal fullness, cough
161
what does an EKG with extremely low voltage and inverted T waves lead you to think?
pleural effusion
162
what will happen to our stroke volume with effusion?
pressure on the heart leads to limitation in diastolic filling leading to REDUCTION IN STROKE VOLUME
163
what is pathognomonic of cardiac tamponade?
pulsus paradoxus ; we get a systolic BP drop of more than 10 mm vs 2-4 mm
164
how do we treat cardiac tamponade?
pericardiocentesis
165
when you think kent bundle, what do you think of?
wolf-parkinson-white
166
what will EKG of WPW look like?
short PR interval, wide QRS, delta waves (slurring on upstroke of QRS), wide base of QRS & thin tip
167
what can you no longer rule in if you see WPW on EKG?
ischemia or infarction or LVH
168
what arrythmia is most common with WPW?
PSVT due to reentry
169
what will AFIB look like in a patient with WPW?
VTACH; if patient goes into AFIB they start conducting mostly by way of kent bundle
170
what does digoxin toxicity look like on EKG?
non-specific ST changes with SCOOPING of ST segment and shortening of QT interval
171
what are the most common arrythmias seen in digoxin toxicity?
multifocal PVC, accelerated junctional rhythm, and atrial tachycardia with AV block
172
what is digoxin's effect on the AV node?
it slows conduction through the AV node
173
common finding on EKG of hypokalemia?
ST segment depression, flattening of T wave, UPWARD U WAVES!
174
what will we see on EKG of a patient with hyperkalemia?
peaked T waves across ENTIRE 12 lead EKG
175
what is the sign wave? where do we see it?
in hyperkalemia; the QRS gets very wide followed by peaked T wave that lead to VFIB arrest
176
common causes of QT prolongation?
hypOcalemia, macrolides, anti-arrythmics, CNS lesions, bradyarrythmias, congenital syndromes (jervell & lange nielsen, romano-ward)
177
what is our diagnostic criteria of QT prolongation?
QT interval is greater than 50% of the R-R interval
178
upward U waves are seen in...
hypokalemia, digoxin toxicity, LVH, amiodarone
179
negative U waves are seen in....
HTN, mitral disease, ischemia
180
what is QT prolongation associated with?
VFIB and sudden death
