Step Up to medicine - Cardiovascular Flashcards

1
Q

stable angina pectoris is due to __________ narrowing of _________ vessels

A

fixed

atherosclerotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the top 5 risk factors for stable angina pectoris

A
DM
HLD
HTN
Cigarette smoking
age
FHx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the two prognostic indicators for CAD

A

Left ventricular function

vessels involved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

which of the vessels involved in CAD purports the worst prognosiss

A

left main

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

T/F multiple vessel disease is worse that single vessel

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

T/F ischemic pain changes with changes in body positioning and breathing

A

F ( does not change with these changes, these would indicate a different pathology for the pain)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Any combination of Hypercholesterolemia
Hypertriglyceridemia impaired glucose tolerance
diabetes hyperuricemia
HTN
Key underlying factor is insulin resistance

A

Metabolic syndrome X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

exertional angina with normal coronary arteriogram

exercise testing and nuclear imaging show evidence of myocardial ischemia

A

syndrome X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

T/F physical exam in patients with CAD is often normal

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the typical outcome of resting ecg in patients with stable angina

A

normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Q waves present on resting ECG indicate

A

prior MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how does the diagnosis of angina change with presence of ST elevations or segmeental changes

A

unstable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

useful test for patients with an intermediate pretest probability of CAD based upon age gender and symptoms

A

stress test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

quick and dirty method for finding a persons maximum HR

A

220 - age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

patients with a positive stress test should undergo

A

cardiac cath

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the parameter by which a stress test is considered postive

A

ST segment depression
ventricular arrhythmia
hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

stress test is 75% sensitive if patients can complete what task during the test

A

increase HR to 85% maximum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

when is the echo performed in stress echo

A

after exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

patients with a positive stress echo should undergo

A

cardiac cath

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what cardiac pathology does not allow radioactive testing in cardiac workup

A

left bundle branch block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what should be done in cardiac workup if patient cannot exercise

A

pharmacologic testing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how do IV adenosine and dipyramidole work with pharmacologic testing

A

cause coronary vasodilation which means that the vessels supplying ischemic portions of the heart are already maximally dilated therefore the shunting of blood to the areas of the heart in which the vessels still have vasodilatory capacity will lead to ischemic changes in the vessels that supply ischemic portions of the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

how does dobutamine work in pharmacologic testing in cardiac workup

A

increases HR, strength of contraction, increases BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

can be useful for detecting silent ischemic, arrhythmias, heart rate variability and assess pacemaker/ ICD function

A

holter monitoring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

useful testing for unexplained dizziness and syncope if cardiovascular cause suspected

A

holter monitoring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

definitive test for CAD

A

cardiac catheterization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

most accurate test for detecting CAD

A

cardiac angiography

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

if CAD is severe typically with three vessel disease what should be done

A

surgical (CABG) repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what medication is commonly employed in lowering cholesterol and decrease risk for CAD

A

statins (HMG CoA reductase inhibitors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what types of fats should be avoided in patients with CAD

A

saturated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what medical therapy is indicated for all patients with CAD

A

aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

first line therapy that has been shown to decrease the number of coronary events in patients with CAD

A

beta blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

relieve angina by reducing preload myocardial O2 demand

VERY COMMON

A

nitrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

medical therapy that induces coronary vasodilation and afterload reduction

A

calcium channel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

If CHF is present in patients with CAD then what two medications can be added on to the typical therapeutic options of aspirin beta blockers and CCbs

A

diuretics and ACE inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Mild disease
normal EF
mild angina
single vessel

what should be done in terms of management on top of aspirin therapy

A

beta blockers and nitrates

consider CCBs if symptoms persist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

normal EF moderate angina and two vessel disease

A

coronary angiography to assess for revascularization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

decreased EF
severe angina
three vessel of left main or LAD disease

A

angiography to consider CABG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

T/F oxygen demand is increased in unstable agina

A

F (only the supply is diminished)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

significant because it indicates stenosis that has enlarged via throbosis hemorrhage or plaque rupture

A

unstable angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

chronic angina with increasing frequency duration or intensity of chest pain
new onset that is severe and worsening
angina at rest

A

unstable angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what is the only test that determines the difference between unstable angina and NSTEMI

A

cardiac enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

in what order should testing and management be carried out in patients with unstable angina

A

medically stabilize symptoms first before stress testing or angiography to assess for two/three vessel disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

patients with unstable angina should undergo what global management in terms of placement, nuts and bolts medical management

A

admission to hospital for continuous cardiac enzyme monitoring
establish IV access and give 2L fluids initially
give supplemental oxygen
control pain with nitrates and morphine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what is the aggressive medical management employed in a patient with unstable angina

A
supplemental oxygen
IV fluid resuscitation
beta blockers (if no contraindications)
aspirin/clopidogrel
LMWH
nitrates
K+ and Mg+ replacement (to avoid arrhythmia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

duration of aspirin and clopidogrel dual therapy in patients presenting with unstable angina

A

9 to 12 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

PERCENTAGE of patients that recover following initial aggressive medical management in the case of unstable angina

A

90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what should be done in the management of a patient with USA that responds to initial medical management

A

stress ECG to assess need for catheerization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what is the immediate management in an individual that fails initial medical management in the setting of USA

A

immediately proceed to the cath lab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what is continued following acute treatment of USA

A

aspirin beta blockers and nitrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what are the two beta blockers typically employed in the treatment of USA

A

metoprolol and atenolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

on top of continuing medical management what should be done in individuals with USA following acute treatment

A

reduce risk factors

smoking cessation
treat DM HTN HLD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

t/F following USA a patient should be started on statin regardless of LDL level

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

transient ST segment elevation classically occuring at night associated with ventricular dysrhythmia

A

prinzmetal (variant) angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what two medications are proven helpful with variant angina

A

CCBs and nitrates (those that vasodilate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

due to necrosis of myocardium as a result of an interruption of blood supply

A

MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

most cases of MI are due to

A

acute coronary thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

mortality rate associated with MI

A

30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what are the two medications that are utilized in the coronary angiography when looking for variant angina

A

ergonovine or acetylcholine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

intense substernal pressure sensation
radiation to neck jaw arms back
pain typically unresponsive to nitro
epigastric discomfort

A

MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

T/F MI can be asymptomatic in up to one third of patients

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

painless infarcts or atypical MI more likely in these 4 demographics

A

women
postoperative
elderly
diabetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

less common symptoms of MI

A
dyspnea
diaphoresis
weakness fatigues
nausea vomiting
snese of impending doom
syncope
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

very early sign of MI that is often missed

A

peaked T waves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

ECG sign indivating transmural injury and diagnostic of acute infarct

A

ST segment elevation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

evidence for necrosis usually seen late and typically absent acutely

A

Q waves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

T/F T wave inversion is specific for MI

A

F (sensitive not specific)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

ECG finding associated with subendocardial ischemia

A

ST segment depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

currently the diagnostic gold standard for MI versus USA

A

cardiac enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

time period over which troponins return to normal

A

5-14 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

when do troponins reach their peak

A

24-48 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

what is the utility of CKMB enzymes

A

reinfarction measurement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

PROVE IT TIMI 22 trial proved starting this agent should be part of maintenance therapy in MI management

A

statin (specifically atorvastatin 80mg)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

what are the 7 agents that should be initiated in the acute treatment of MI

A
morphine
oxygen
nitrates
aspirin
ace inhibitor 
statin
heparin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

this ultimate treatment should be incorporated to the treatment of all patients being managed for acute MI

A

revascularization ASAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

what is the time period in which revascularization should be attempted in any patient presenting with acute MI

A

within 90 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

this outcome occurs with rupture of papillary muscle infarction ischemia

A

mitral regurg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

length of time with which patients receiving a bare metal stent should be on dual platelet therapy

A

one month

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

how long should a patient be on dual platelet therapy following the placement of drug eluting stents

A

12 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

what is the most common cuase of inhospital mortality following MI

A

CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

what is the treatment for PVCs following acute MI

A

conservative management (no need for antiarrhythmic agent)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

what should be done in a stable patient that shows VTach that is sustained

A

IV amio

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

what should be done in an unstable patient that shows Vtach that is sustain

A

electrical cardioversion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

what is the treatment for vfib following MI

A

immediate desynchronized defibrillation and CPR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

sinus bradycardia management in the setting of acute MI

A

observation

if severe atropine may be helpful in increasing HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

asystole management in the setting of acute MI

A

elecrtrical defibrillation if thought to be 2/2 VFIB

transcutaneous pacing if asystole is clearly the cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

what is the typical cause for AV block in the setting of MI

A

infarction of the conduction tracts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

second or third degree block has a terrible prognosis in the setting of what type of MI

A

anterior

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

what should be done in second or third degree heart block in the setting of anterior MI

A

temporary pacing (transcutaneous or transvenous)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

initial management for heart block secondary to inferior MI

A

atropine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

treatment for heart block 2/2 inferior MI that is refractory to initial treatment with atropine

A

pacemaker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

T/F recurrent infarction is not as bad in prognosis as initial MIA

A

F (worse in both acute and long term prognosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

catastrophic mechanical complication of MI that occurs within the first TWO WEEKS after MI

A

free wall rupture

usually within the first 1-4 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

what are the usual immediate complications of free wall rupture

A

hemopericardium and cardiac tamponade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

what is the immediate treatment for free wall rupture

A

hemodynamic stabilization
pericardiocentesis
surgical repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

T/F interventricular septal rupture following MI is typically worse in prognosis than frree wall rupture

A

F (better prognostically)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

what is the indication for interventricular septal rupture following MI

A

emergent surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

time table for interventricular septal rupture following MI

A

within 10 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

new onset MR folloiwng MI cause

A

papillary muscle rupture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

what is the immediate indication for new onset MR following MI

A

echo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

what is the treatment for papillary muscle rupture

A

surgical (mitral valve replacement typically)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

why are ventricular pseudoaneurysms considered surgical emergencies

A

tend to become free wall ruptures if left alone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

acute pericarditis secondary to MI typically treated with

A

aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

what medications are contraindicated in the case of acute pericarditis following MI

A

NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Immunologically based syndrome consisting of fever malaise pericarditis leukocytosis and pleuritis occuring weeks to months after an MI

A

dressler syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

what is the most effective therapy for dressler syndrome

A

aspirin

Ibuprofen is a good secondary choice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

6 main causes/systems leading to chest pain

A
Cardiac
Pulmonary
GI
Chest wall
psychiatric
cocaine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Heart pericardium vascular causes for chest pain

A

stable angina
USA
variant angina

MI

Pericarditis

Aortic dissection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Pulmonary causes for chest pain (3)

A

pulmonary embolism

PNA

status asthmaticus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

GI causes for chest pain (4)

A

GERD
diffuse esophageal spasm
peptic ulcer disease
esophageal rupture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Chest wall causes for chest pain (5)

A
costochondritis
muscle strain
rib fracture
herpes zoster
thoracic outlet syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

3 main psych causes for chest pain

A

anxiety panic attacks somatization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

3 tests that are obtained for practically all patients presenting with chest pain

A

ECG
troponins
chest xray

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

clinical syndrome resulting from the hearts inability to meet the body’s circulatory demands under normal physiologic conditions

A

CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

what are the two most common causes for systolic CHF dysfunction

A

HTN and ischemia (MI)(

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

echocardiogram showing impaired relaxation of the left ventricle

A

diastolic dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

which form of CHF is most common

A

systolic (HTN AND ISCHEMIA MUCH MORE COMMON PATHOLOGIES)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

most common cause of diastolic CHF

A

HTN leading to hypertrophy of myocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

aoritc stenosis mitral stenosis and aortic regurg cause what form of CHF

A

diastolic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q
dyspnea
orthopnea
paroxysmal nocturnal dyspnea
nocturnal cough
confusion and memory impairment in advanced forms
diaphoresis and cool extremities at rest
A

CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

difficulty breathing in the recumbent position relieved by elecation of the head with pillows

A

orthopnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

rapid filling phase into a noncompliant left ventricular chamber leads to what pathologic heart sound

A

S3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

S3 heard best in what position

A

apex with the bell of the stethoscope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

S3 occurs at what phase in the cardiac cycle

A

following S2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

how to remember S3 S4 and their place in the cardiac cycle

A

4 is more than 3
tennessee has more letters than kentucky TEN-nes-see relates S4 prior to S1
ken-tuck-Y relates S3 following S2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

crackles and rales at the bases of the lungs in CHF indicates what pathologic process

A

pulmonary edema 2/2 fluid spilling into the alveoli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

dullness to percussion and decreased tactile fremitus of the lower lung fields is a sign of

A

pleural effusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q
peripheral pitting edema
nocturia
JVD
hepatomegaly
ascites
right ventricular heave

all signs of what sidded HF

A

rightr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

T/F given enough time left sided HF will always lead to right sided HF

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

short horizontal lines near periphery of the lung near the costophrenic angles and indicate pulmonary congestion secondary to dilation of pulmonary lymphatic vessels

A

kerley B lines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

prominent interstitial markings and pleural effusion a sign of what on CXR

A

CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

what is the initial test of choice in suspected CHF

A

transthoracic echo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

what is the importance of obtaining a TTE in the diagnosis of CHF

A

gives us the EF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

cutoff for preserved left ventricular function in patients treated for CHF

A

> 40%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

T/F ECG is often very helpful in CHF diagnosis

A

F (not particularly unless there is a component of MI or USA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

consider this test to rule out CAD as an underlying cause for CHF

A

coronary angiography

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

test used to assess dynamic response of HR heart rhythm and BP in the setting of CHF

A

stress testing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

conservative management of systolic dysfunction of CHF

A
sodium restriction
water restriction
smoking cessation
weight loss
etoh decrease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

most effective means of providing symptomatic relief to patients with moderate to severe CHF
recommended for patients with systolic failure and volume overload

A

diuretic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

T/F diuretics improve mortality in patients with CHF

A

F (not been shown)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

most potent diuretic that is usually used

A

lasix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

lasix is what type of diuretic

A

loop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

HCTZ is what type of diuretic

A

thiazide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

T/F spironolactone has been shown to have survival benefits in patients with CHRF

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

spironolactone used in what types of CHF

A

advanced forms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

which aldosterone antagonist does not cause gynecomastia

A

eplerenone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

usual initial treatment for symptomatic CHF patients

A

ACE inhibitor and diuretic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

T/F ACE inhibitors have reduced mortality benefit

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

CONSENSUS and SOLVD trials proved what point

A

ACE inhibitors reduce mortality in patients with CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

T/F all patients with CHF should be on a ACE inhibitor regardless of symptomatology

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

ACE inhibitors should be started at a low dose to avoid

A

hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

patients that experience dry cough with ACE inhibitors can be switched to what type of medication

A

ARBs (-sartans)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

beta blockers are shown to decrease mortality in CHF for what specific patient demographic

A

post MI CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

stable patients with mild to moderate CHF should be given

A

beta blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

what are the three beta blockers known to be safe in CHF

A

metoprolol
bisoprolol
carvedilol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

useful agent in patients with EF <40%, severe CHF or severe Afib

A

digitalis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

typically employed for patients with refractory symptoms despite being on diuretic ACE inhibitor and aldosterone antagonist

A

digitalis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

two medications commonly employed in patients who cannot tolerate ACE inhibitors

A

hydralazine and isosorbide dinitrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

4 medication types that are contraindicated in CHF

A

metformin (can cause lethal lactic acidosis)
thiazolidinediones (fluid retention)
NSAIDs increase risk of CHF exacerbation
negative inotropic antiarrhythmics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

what are the medications that reduce mortality in diastolic heart failure

A

none

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

what are the two devices that shown to reduce mortality in select patients

A

ICD prevents SCD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

indicated for patients at least 40 days poist MI EF,35% and class II or III symptoms despite optimal medicla treatment

A

ICD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

biventricular pacemaker in patients with QRS >120 ms

A

CRT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

T/F most patients that meet criteria for CRT are also candidates for ICD and receive combined devices

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

last alternative if all else fails in CHF management

A

heart transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

acute dyspnea associated with elevated left sided filling pressures with or without pulmonary edema

A

acute decompensated HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

what are the two most common causes for acute decomp HF

A

LH systolic or diastolic dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

severe form of HF with rapid accumulation of fluid in the lungs

A

flash pulmonary edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

DIFFERENTIAL FOR RAPID RESPIRATORY DISTRESS

A

PULMONARY EMBOLISM ASTHMA pna AND FLASH PULMONARY EDEMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

diagnostic tests for an individual with flash pulmonary edema

A
chest xray
ecg
ABG BNP
echo
coronary angio (possibly)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

what is the management of a patient with acute pulmonary (flash) edema

A

oxygenation and ventilation assistance
diuretics
dietary sodium restriction
nitrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

present in 50% of adults who undergo holter monitoring and mean nothing in a healthy heart

A

PACs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

what is the treatment for asymptomatic PACs

A

usually just observation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

what is the treatment for symptomatic PACs (palpitations)

A

beta blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

causes for PVCs

A
hypoxia
electrolyte abnormalities
stimulants
caffeine
medications
structural heart disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

why is the QRS wider in PVCs than with regular electrical activity of the heart

A

through the ventricular muscle and not the conduction pathways, therefore takes a longer time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

patients with frequent repetitive PVCs and underlying heart disease are at increased risk for

A

sudden death (Vfib etc)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

what test should be ordered in patients with PVCs and underlying structural or physiologic heart disease

A

electrophysiology test (may benefit from ICD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

multiple foci in the atria firing continuously in a chaotic pattern causing a totally irregular rapid ventricular rate

A

atrial fib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

atrial rate in afib is usually over ______bpm but are blocked at the AV node so ventricular rate ranges between ___ and ____

A

400
75
175

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

T/F PVCs in patients with normal hearts is associated with increased mortality

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

what are the causes for afib (9) (double H triple S triple P E)

A
  1. Heart disease: CAD, MI, HTN, mitral valve disease
  2. Pericarditis and pericardial trauma (e.g., surgery)
  3. Pulmonary disease, including PE
  4. Hyperthyroidism or hypothyroidism
  5. Systemic illness (e.g., sepsis, malignancy
  6. Stress (e.g., postoperative)
  7. Excessive alcohol intake (“holiday heart syndrome”)
  8. Sick sinus syndrome
  9. Pheochromocytoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

acute hemodynamically unstable afib treatment

A

immediate cardioversion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

acute afib in a hemodynamically stable patient

A

rate control (60-100bpm)
beta blockers
CCBs (alternatively)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

delivery of a shock that is in synchrony with the QRS

A

cardioversion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

delivery of shock that is NOT in conjunction with the QRS complex

A

defibrillation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

if left ventricular dysfunction is present in the setting of afib
what two medications can be considered

A

amio or dig

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

three cases of cardioversion being appropriate in afib

A

hemodynamically unstable
those with worsening symptoms
those having their first ever case of AFib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

what is the use of ibutilide procainamide flecainide sotalol or amiodarone in afib

A

pharmacologic conversion if electrical cardioversion is unfeasible or doesnt work

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

when should anticoagulation be employed in the setting of atrial fibrillation

A

present greater than 48 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
Q

what are the timing parameters for anticoagulation surrounding cardioversion

A

3 weeks before and 4 weeks afterwards

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

what is the INR goal in anticoagulation in patients with afib prior to and following cardioversion

A

2-3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
193
Q

what can be done (in theory) to avoid 3 weeks of anticoagulation prior to cardioversion in the case of afib)

A

TEE to image the left atrium for thrombus, if none, start IV heparin and perform cardioversion within 24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
194
Q

T/F if the TEE route is carried out to expedite cardioversion, patients still need to be anticoagulated 4 weeks following cardioversion

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
195
Q

what are the two agents typically used in the setting of chronic afib for rate control

A

beta blockers

CCBs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
196
Q

patients with lone afib or afib in the absence of any underlying heart disease or cardiovascular risk can take what medication

A

aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
197
Q

patients with afib and underlying CVD or risk factors need what type of anticoagulation

A

warfarin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
198
Q

what is the most common cause for aflutter

A

heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
199
Q

ECG exhibiting a saw tooth baseling with a QRS complex appearing after every second or third tooth

A

aflutter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
200
Q

flutter waves seen best in which lead

A

II III AvF (inferior leads)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
201
Q

how many different P wave morphologies are required to make the diagnosis of MAT

A

3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
202
Q

MAT is identical to this separate diagnosis except that the heart rate in this other entity is between 60-100

A

wandering atrial pacemaker

203
Q

MAT is strongly associated with what type of disease

A

lung disease

204
Q

if LV function is not preserved in MAT what medication can be given

A

digoxin

205
Q

T/F electrical cardioversion is often effective in MAT

A

F (not effective do not use)

206
Q

what is the most common cause of PSVT

A

nodal re-entry tachycardia`

207
Q

ECG will show what characteristic in PSVT

A

narrow complexes with no discernible P waves (P waves buried in the QRS)

208
Q

what is the underlying process in orthodromic AV reentrant tachycardia

A

accessory pathway between the atria and ventricles that conducts retrogradely

209
Q

what would be seen on ECG in orthodromic reentry AV tachy

A

narrow QRS complexes with P waves may or may not be discernible depending on the rate (could bne buried, re-entrant circuit takes longer the self contained AV reentry, therefore P waves have a higher chance to be revealed)

210
Q

Six (6) causes of SVT

A

a. Ischemic heart disease
b. Digoxin toxicity—paroxysmal atrial tachycardia with 2:1 block is the most
common arrhythmia associated with digoxin toxicity
c. AV node reentry
d. Atrial flutter with rapid ventricular response
e. AV reciprocating tachycardia (accessory pathway)
f. Excessive caffeine or alcohol consumption

211
Q

paroxysmal atrial tachycardia with 2:1 block is the most

common arrhythmia associated with ___________ toxicity

A

digoxin

212
Q

what is the agent of choice for correcting SVT

A

IV adenosine

213
Q

what is the reason that IV adenosine is the agent of choice in SVT

A

short duration of action and effectiveness in terminating SCTs
works by decreasing sinoatrial and AVE nodal activity

214
Q

what agents can be used in patients with SVT if left vent function is preserved as an alternative to IV adenosine

A

Iv verapamil and IV esmolol (less commonly digoxin)

215
Q

treatment preferred if episodes of SVT are recurrent and symptomatic

A

radiofrequency cardiac ablation

216
Q

narrow complex tachycardia and short PR interval with upward deflection seen before thje QRS complex

A

WPW syndrome

217
Q

what is the typical treatment used for WPW syndrome

A

radiofrequency cardiac ablation

218
Q

WHAT DRUGS should be avoided in WPW syndrome

A

drugs that act through blocking AV conduction (beta blockers CCBs digoxin) as they can facilitate conduction through the accessory pathway

219
Q

rapid repetitive firind of three or more PVCs in a row at a rate between 100 and 250

A

ventricular Tachy

220
Q

ventricular tachy typically originates where in the conduction structure

A

below the bundle of his

221
Q

what is the most common cause for ventricular tachy

A

prior MI with CAD

222
Q

causes for V tach

A

a. CAD with prior MI is the most common cause
b. Active ischemia, hypotension
c. Cardiomyopathies
d. Congenital defects
e. Prolonged QT syndrome
f. Drug toxicity

223
Q

Vtach progresses to what arrhythmia if left untreated

A

Vfib

224
Q

T/F Vtach lasts longer than 30 seconds and is almost always symptomatic

A

T

225
Q

brief limited runs of VT is an indipendent risk factor for SCD in what cases

A

with concurrent CAD and LV dysfunction

226
Q

connan A waves in the neck secondary toi AV dissociation and variable S1 intensity commonly associated with

A

Vtachy

227
Q

what are the more serious presentations of Vtachy

A

sudden death

cardiac shock

228
Q

ecg showing wide and bizarre QRS complexes with tachycardia

A

Vtachy

229
Q

all QRS complexes are identical in this form of Vtach

A

monomorphic

230
Q

QRS complexes are different in this form of Vtach

A

polymorphic

231
Q

T/F VT also responds to vagal maneuvers as with PSVT

A

F (does not)

232
Q

what should be given to patients with hemodynamically stable patients with mild symptoms and systolic BP >90

A

IV amio
IV procainamide
IV sotalol
(one of these)

233
Q

hemodynamically unstable patients with Vtachy or with severe symptoms treatment

A

immediate synchronous DC cardioversion

234
Q

what mnedication is given following DC cardioversion

A

amiodarone (sustains rhythm)

235
Q

nonsustained VT with no underlying heart disease a recent MI or evidence of left ventricular dysfunction or symptomatology

A

order electrophysiologic study

236
Q

electrophysiology study shows inducible rhythm in the case of nonsustained VT, what should be done

A

placement of ICD

237
Q

second line treatment for unsustained Vtach

A

amiodarone

238
Q

most episodes of Vfib happen following

A

Vtach

239
Q

T/F if Vfib is not associated with MI we shouldnt expect it to recur

A

F (Vfib not associated with MI has a higher rate of recurrence)

240
Q

what two treatments can be utilized in the treatment of patients with Vfib not associated with MI

A

prophylactic amiodarone or placement of ICD

241
Q

T/F if Vfib follows MI by <48hours then the outcome is bleak and recurrence rate is high

A

F (prognosis is good and recurrence is low)

242
Q

T/F chronic therapy is needed for patients with Vfib secondary to MI

A

F (not necessary)

243
Q

most common cause for vfib

A

ischemic heart disease

244
Q

cannot measure BP
unconscious patient
absent heart sounds and pulse

A

vfib

245
Q

ECG no strial P waves can be identified

no QRS complexes can be identified

A

VFIB

246
Q

what is the immediate treatment for vfib

A

(MEDICAL EMERGENCY)
IMMEDIATE cardiac defibrillation and CPR
immediate initiation of unsynchronized DC cardioversion immediately, if equipment not on hand, begin CPR immediately
up to three sequential shocks to establish another rhythm

247
Q

treatment for persistent vfib following sequential shocks

A

continue CPR
consider intubation
epi (1mg bolus initially and then every 3-5minutes)
attempt to defibrillate again 30s-1min following first epi dose

248
Q

if vfib persists past administration of epi, intubation and reshock

A

IV amiodarone followed by shock

lidocaine, magnesium procainamide alternatives

249
Q

If cardioversion is successful in vfib, what next

A

maintain continuous IV infusion of the effective antiarrhythmic agent
ICD mainstay of chronic therapy in these patients (those at risk for VF)

250
Q

bradycardia clinically significant when persistent below what threshold

A

45bpm

251
Q

pathologic causes for bradycardia (3)

A

cardiac ischemia
increased vagal tone
antiarrhythmic drugs

252
Q

what medication can be used to raise BP in the case of persistent bradycardia

A

atropine

253
Q

prolonged PR interval with a QRS following each P wave

A

1st degree heart block

254
Q

progressive prolongation of PR interval until a P wave fails to conduct

A

Mobitz type I

255
Q

T/F type I heart block is a benign condition that does not require treatment

A

T

256
Q

Pwaves fail to conduct sudndenly without a preceding PR interval prolongation
often progresses

A

Mobitz II

257
Q

where is the conduction defect in a Mobits II

A

His-Purkinje system of conduction

258
Q

what is the necessary treatment for MObitz II

A

placement of PCI

259
Q

absence of conduction of atrial impulses to the ventricles; no correspondence between P waves and QRS complexes

A

complete HB

260
Q

what is the treatment of choice for complete heart block

A

cardiac pacemaker

261
Q

Most common type of cardiomyopathy

A

dilated cardiomyopathy

262
Q

ischemia infection alcohol casuing dysfunction of left ventricular contractility leads to what type of cardiomyopathy

A

dilated

263
Q

what is the prognosis for dilated cardiomyopathy

A

poor

most die within 5 years of diagnosis

264
Q

what is the most common cause for dilated cardiomyopathy

A

idiopathic

265
Q

toxins that lead to dilated cardiomyopathy

A

alcohol
doxorubicin
adriamycin

266
Q

ALL CAUSES FOR dilated cardiomyopathy (>;))

A

a. CAD (with prior MI) is a common cause
b. Toxic: Alcohol, doxorubicin, Adriamycin
c. Metabolic: Thiamine or selenium deficiency, hypophosphatemia, uremia
d. Infectious: Viral, Chagas disease, Lyme disease, HIV
e. Thyroid disease: Hyperthyroidism or hypothyroidism
f. Peripartum cardiomyopathy
g. Collagen vascular disease: SLE, scleroderma
h. Prolonged, uncontrolled tachycardia
i. Catecholamine induced: Pheochromocytoma, cocaine
j. Familial/genetic

267
Q

what heart sounds are typically associated with dilated cardiomyopathy

A

S3 S4 and mitral regurg or tricuspid insufficiency

268
Q

what is the common pathology associated with the enlarged ventricles of dilated cardiomyopathyt

A

cardiac arrhythmia

269
Q

this type of testing might be warranted in a patient with DCM with no cause and fam hx of disease

A

genetic testing

270
Q

what is the treatment for DCM

A

(similar to treatment for CHF)
beta blockers
diuretics
dig

271
Q

should be considered because DCM patients have risk of embolization

A

anticoagulation

272
Q

Hypertrophic cardiomyopathy mode of inheritance

A

autosomal dominance

273
Q

diastolic dysfunction due to a stiff hypertrophied ventriclewith elevated diastolic filling pressures

A

HTCM

274
Q

what kind of obstruction can occur in patients with assymmetric hypertrophy of the ventricular septum

A

dynamic outflow obstruction

275
Q
dyspnea on exertion
chest pain
syncope after exertion or the valsalva
palpitations
arrhythmias
cardiac failure
sudden death
years without symptomatology
A

HTCM

276
Q

sustained PMI
loud S4
systolic ejection murmur
decreases with squatting lying down or straight leg raise
intensity increased with valsalve and standing (decreases LV size and increases obstruction)

A

HTCM

277
Q

effect of the murmur with HTCM with sustained handgrip

A

decrease due to increased systemic resistance leading to decreased gradient across aortic valve

278
Q

rapidly increasing carotic pulse with two upstrokes indicative of

A

HTCM

279
Q

what is the test that establishes the diagnosis of HTCM

A

cardiac echo

280
Q

T/F asymptomatic patients with HTCM do not need treatment

A

T

281
Q

what is the initial drug used in symptomatic patients with HTCM

A

beta blockers

282
Q

used in HTCM if patient nonresponsive to beta blockers

A

CCBs

283
Q

surgery for HTCM

A

myomectomy

284
Q

opening snap followed by a low pitched diastolic rumble and presystolic accentuation

A

mitral stenosis

285
Q

S2 followed by opening snap

A

mitral stensosi

286
Q

the distance between S2 and the opening snap of mitral stenosis tells us

A

severity of the valvular disease

287
Q

long standing disease of mitral stenosis can lead to what clinical findings

A
(right heart failure)
right ventricular heave
JVD
pulmonary congestion
hepatomegaly
ascites
288
Q

most important test in confirming mitral stenosis

A

echocardiogram

289
Q

what are the two medications commonly used in mitral stenosis

A
diuretics (if signs of RHF)
beta blockers (decrease HR and CO)
290
Q

what are t he two options surgically for mitral stenosis

A

perc balloon valvuloplasty

open commissurotomy and mitral valve replacement

291
Q

when the aortic valve falls below what threshold is the cardiac output not able to increase with exertion, resulting in angina

A

0.7

292
Q

what is the cause for mitral regurg with long standing aortic stenosis

A

LV dilation pulls the leaflets of the mitral valve apart resulting in MR

293
Q

what are the three main causes for aortic stenosis

A

calcification of a bicuspid valve
calcification in the elderly
rheumatic fever

294
Q

development of what symptoms would be a sign that aortic stenosis is worsening

A

syncope
angina
CHF

295
Q

which of angina syncope and CHF in the setting of aortic stenosis carries the worse prognosis

A

CHF

296
Q
harsh crescendo-decreascendo systolic murmur
heard in second right intercostal space
radiating to carotid arteries
soft S2
S4
parvus et tardus
sustained PMI
precordial thrill
A

aortic stenosis

297
Q

what is parvus et tardus

A

delayed and diminished carotid upstrokes

298
Q

which test is diagnostic in aortic stenosis

A

echocardiography

299
Q

what is the definitive diagnostic test in aortic stenosis

A

cardiac angiography

300
Q

what test can measure valve gradient and calculate valve area in aortic stenosis

A

cardiac catheterization

301
Q

what is the treatment for aortic stenosis

A

valvular replacement in all symptomatic patients

302
Q

treatment for asymptomatic aortic stenosis

A

none

303
Q

inadequate closure of aortic valve leaflets causing blood to flow into left ventricle during diastole

A

aortic regurg

304
Q

what occurs in the left ventricle in response to aortic regurgitation

A

LV dilation and hypertrophy to maintain stroke volume

305
Q

5 year survival for chronic regurgitation

A

75%

306
Q

how long do patients typically survive following onset of angina with aortic regurg

A

4 years

307
Q

how long do patients typically survive following onset of CHF with aortic regurg

A

2 years

308
Q

4 main causes for acute aortic regurgitation

A

infective endocarditis
trauma
aortic dissection
iatrogenic

309
Q

causes for primary valvular aortic regurgitation (6)

A
rheumatic
biscupid aortic valve
marfans
ehlers danlos
ankylosing spondylitis
SLE
310
Q

causes for aortic root disease leading to aortic regurg (6)

A
syphilitic aortitis
osteogenesis imperfecta
aortic dissection
behcet
reiter syndrome
systemic HTN
311
Q

widened pulse pressure concerning for what valvular disease

A

aortic regurgitation

312
Q

low pitched diastolic rumble due to competing flow anterograde from the LA and retrograde from the aorta

A

austin flint murmur

aortic regurgitation

313
Q

rapidly increasing pulse that collapses suddenly as arterial pressure decreases rapidly in late systole and diastole

A

water hammer pulse, indicates aortic regurg

314
Q

what happens to aortic regurg with handgrip sustained

A

increases

315
Q

what is the utility of echo in aortic regurg

A

assess chronic patients for surgery over time

316
Q

what is the treatment for chronic asymptomatic aortic regurg

A
conservative
restrict salt
diuretics vasodilators
afterload reduction
restriction of strenuous activity
317
Q

what is the definitive treatment for aortic regurgitation

A

surgical replacement

318
Q

abrupt elevation of left atrial pressure in the setting of normal LA size and compliance with pulmonary edema
possible hypotension and shock due to decreased CO

A

acute MR

319
Q

gradual elevation of left atrial pressure in setting of dilated LA and LV
pulmonary HTN can result from chronic backflow

A

chronic MR

320
Q

3 main acute causes for MR

A

endocarditis
papillary muscle ruption (infarction)
chordae tendinae rupture

321
Q

4 main chronic causes for MR

A

rheumatic fever
mitral valve prolapse
marfans
cardiomyopathy

322
Q

T/F chronic MR has a worse prognosis than acute MR

A

F (acute is worse prognostically)

323
Q

holosystolic murmur at the apex radiating to the back or clavicle

A

MR

324
Q

what arrhythmia is common seen with MR

A

afib

325
Q

what diagnostic tests can show signs of MR

A

CXR

echo

326
Q

device used as a bridge to surgery for MR

A

IABP

327
Q

what medication outcome should be sought in patients with symptomatic MR

A

afterload reduction

328
Q

what is the definitive treatment for MR

A

valvular replacement

329
Q

results from a failure of the tricuspoid valve to close completely during systol causing regurgitation of blood into the RA

A

tricuspid regurg

330
Q

TR regurg usually 2/2

A

RV enlargement

331
Q

what is the most common cause for tricuspid regurg with LV dilation

A

left ventricular failure

332
Q

when is tricuspid endocarditis typically seen

A

IV drug users

333
Q

congenital malformation of the tricuspid valve in which there is a downward displacement of the valve into the RV

A

epstein anomaly

334
Q

TR regurg usually asymptomatic unless what occurs

A

development of RGF or Pulmonary HTN

335
Q

what would be expected to be some of the symptoms of tricuspid regurg

A
ascites
hepatomegaly
edema
JVD
pulsatile liver
prominent V waves in jugular venous pulse with rapid y descent
inspiratory S3 along LLSB
blowing holosystolic murmur at LLSB increased with inspiration reduced during expiration or valsalva
336
Q

how is the diagnosis of tricuspid regurg made

A

echo

337
Q

treatment for volume overload and venous congestion/edema of TR regurg

A

diuretics

338
Q

what needs to be absent in order for tricuspid valve resplacement surgery to be an available option

A

pulmonary hypertension

339
Q

typical mid systolic click and murmuer

A

mitral valve prolapse

340
Q

common valvular disease in patients with connective tissue disorders

A

MVP

341
Q

most common cause of MR in developed countried

A

MVP

342
Q

what do standing and valsalva do in regard to the murmur involved with MVP

A

increase

343
Q

what does squatting down have in terms of effect on MVP

A

decrease

344
Q

what is the most useful diagnostic tool for MVP

A

echo

345
Q

what should be used for the atypical chest pain that can accompany MVP

A

beta blockers shown to be helpful

346
Q

T/F MVP often requires surgery

A

F (often benign, asymptomatic for peoples entire lives)

347
Q

most common valvular abnormality 2/2 rheumatic heart disease

A

mitral stenosis

348
Q

what are the major signs of acute rheumatic fever

A
migratory arthritis
acute myocarditis
subcutaneous Nodules
erythema marginatum
syndenham chorea
349
Q

what medication should be given to patients with streptococcal pharyngitis to avoid rheumatic fever

A

penecillin or rythromycin

350
Q

how is acute rheumatic fever treated

A

NSAID

351
Q

what marker is used to track treatment progress

A

C-RP

352
Q

infection of the endocardial surface of the heart

A

endocarditis

353
Q

acute endocarditis most commonly caused by

A

staph aureus

354
Q

acute endocarditis happens on what type of heart valve

A

normal

355
Q

if acute endocarditis is left untreated what is the outcome

A

fatal in 6 weeks

356
Q

subacute endocarditis caused by

A

strep viridans and enterococcus

357
Q

subacute endocarditis occurs on what type of valves

A

previously injured

358
Q

what are the more rare forms of native valve endocarditis

A

HACEK organisms (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kindella)

359
Q

most common organism for prosthetic valve endocarditis

A

staph epi (and then staph aureus)

360
Q

Endocarditis in IV drug users

A

Right sided endocarditis

361
Q

what valve is typically involved in right sided endocarditis

A

tricuspid

362
Q

which bug is most common in right sided endocarditis

A

staph aureus

363
Q

what are the four main complications from endocarditis

A

cardiac failure
myocardial abscess
various solid organ damage from showered emboli
glomerulonephritis

364
Q

what combination of Duke criteria is necessary for the diagnosis of endocarditis

A

2 major
1 major 3 minor
5 minor

365
Q

what are the major DUKE criteria

A

sustained bacteremia

endocardial involvement diagnosed by echo or by new valvular murmur on clinical exam

366
Q

what are the minor DUKE criteria for endocarditis

A

predisposing condition (abnormal valve or abnormal risk)
fever
vascular phenomena (septic arterial or pulmonary emboli mycotic aneurysms intracranial hemorrhage janeway lesions)
Immune phenomena (Glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor)
Positive blood cultures not meeting major crit
Positive echo not meeting major crit

367
Q

what is the treatment for endocarditis

A

extended parenteral antibiotics (4-6 weeks)

368
Q

what are the two factors necessary to warrant endocarditis antibiotic prophylaxis

A
qualifying cardiac indication:
prosthetic heart valve
history of infective endocarditis
congenital heart disease
cardiac transplant with vulvulopathy

Qualifying procedure
Dental procedures
procedures involving biopsy or incision of respiratory mucosa
procedures involving infected skin or musculoskeletal tissue

369
Q

associated with debilitating illnesses susch as metastatic cancer
sterile deposits of fibrin and platelets forming along the closure line of cardiac valve leaflets
vegetations can embolize to the brain or periphery

A

marantic endocarditis (nonbacterial thrombotic endocarditis)

370
Q

typically involving the aortic valves in individuals with SLE
characterized by the formation of small warty vegetations on both sides of valve leaflets and may present with regurgitant murmurs
can be a source of systemic embolization

A

libmann sacks endocarditis

371
Q

what is the most common type of atrial septal defect

A

ostium secundum

372
Q

what are the three types of ASDs

A
ostium secundum (central portion opening)
ostium primum (low in septum)
Sinus venosus (high in the septum)
373
Q

what is the rare but serious complication that can occur with ASD

A

pulm HTN

374
Q

what is the tell tale sign on clinical exam for ASD

A

fixed split S2

375
Q

what is the diagnostic test for ASD

A

TEE with bubble study (bubbles can be seen crossing through the defect often used and can aid in the Dx)

376
Q

what are the CXR findings c/w ASD

A

Large pulm arteries

increased pulm markings

377
Q

pulmonary HTN for ASD typically occurs after what age if at all

A

40

378
Q

late complication of ASD in which irreversible pulm HTN leads to reversal of shunt, HF and cyanosis

A

eisenmenger syndrome

379
Q

most common of the congenital cardiac malformations

A

VSD

380
Q

what happens to the shunt in VSD if PVR becomes larger than SVR

A

reversal of shunt and potential eisenmenger syndrome

381
Q

sign symptoms of eisenmenger syndrome

A
high PVR
SOB
dyspnea on exertion
chest pain
syncope
cyanosis
382
Q

harsh blowing holosystolic murmur with thrill at fourth left intercostal space that decreases with valsalva and handgrip

A

VSD

383
Q

is a louder or softer VSD more concerning

A

softer (smaller VSD causes louder murmur)

384
Q

what is the structure that is responsible for the enlarged cardiac silhouette seen on CXR in VSD

A

enlargement of the pulmonary artery

385
Q

what are the complications associated with VSD

A

endocarditis
progressive aortic regurg
heart failure
pulmonary HTN and shunt reversl (eisenmengers)

386
Q

when is endocarditis PPX not recommended in VSD

A

uncomplicated and no prior history of endocarditis

387
Q

narrowing/constriction of aorta usually at the origin of left subclavian artery near ligamentum arteriosum

A

coarctation of the aorta

388
Q

hypertension in the upper extremities and hypotension in the lower extremitis

A

coarctation of the aorta

389
Q

well developed upper body with underdeveloped lower bodyu

A

coarctation of the aorta

390
Q

CXR showing notching of the ribs

A

coarctation of the aorta

391
Q

prevalence of this cardiac malformation is increased in patients with Turner syndrome

A

coarctation of the aorta

392
Q

what are the 4 main complications associated with coarctations of the aorta

A

severe HTN
rupture of cerebral aneurysms
infective endocarditis
aortic dissections

393
Q

communication between the aorta and pulmonary artery that persists after birth

A

patent ductus arteriosus

394
Q

what are the two factors that maintain patent ductus arteriosus during fetal development

A

low O2 tension

prostaglandins

395
Q

when does cyanosis occur in PDA

A

late

396
Q

cardiac malformation associated with rubella syndrome
high altitude
premature births

A

PDA

397
Q

continuous machine like murmur at the left second intercostal space
RVH
wide pulse pressure and bounding peripheral pulses

A

PDA

398
Q

CXR showing increased pulmonary vascular markings
dilated pulmonary artery
enlarged cardiac silhouette
calcifications in tract coming off of the aorta

A

PDA

399
Q

If pulmonary vascular disease is absent what is the treatment for PDA

A

surgical ligation

400
Q

when is surgery contraindicated in PDA

A

when there is significant right to left shunting

401
Q

what is the medication that can be used for closure of PDA

A

indomethacin

402
Q

medication used to keep PDA open in cases of transposition

A

PGE1

403
Q

Ventricular septal defect
right ventricular hypertrophy
pulmonary artery stenosis
overriding aorta

A

tetrology of fallot

404
Q

tetrology of fallot arise secondary to defects in the development of what structure

A

infundibular septum

405
Q

most common symptom of tetrology of fallot

A

cyanosis

406
Q

degree of symptoms in tetrology of fallot depends on

A

degree of pulmonary outflow obstruction

407
Q

three substances that can be used in patient with frequent tet spells that are refractory to mechanical position to correct

A

oxygen
morphine
beta blockers

408
Q

what is the diagnostic modality of choice in tet of fallot patient

A

echo

409
Q

CXR showing boot shape to the heart

A

TOF

410
Q

what is the treatment for TOF

A

surgery

411
Q

two most common causes of death following surgery for TOF

A

sudden cardiac death and CHF

412
Q

hypertensive emergency defined as

A

systolic above 220
diastolic above 120

in addition to end organ damage

413
Q

elevated BP levels of hypertensive emergency without end organ damage

A

urgency

414
Q

5 systems that need to be assessed in a patient with blood pressures in the emergency range

A

eyes : papilledema
CNS: AMS or hemorrhage, confusion
kidneys: failure, hematuria
heart: USA, MI, CHF, aortic dissection

415
Q

radiographic condition postulated to be caused by autoregulatory failure of cerebral vessels as well as endothelial dysfunction

A

PRES

416
Q

insidious onset of headache altered level of consciousness visual changes and seizures with posterior cerebral white matter edema
hypertensive or normotensive

A

PRES

417
Q

how should BP be brought down in hypertensive emergencies

A

reduce MAP by 25% in 1 to 2 hours (get the patient out of danger and then decrease gradually)

418
Q

rate typically sought for BP decrease in hypertensive urgency

A

normotensive in 24 hours

419
Q
long standing HTN
cocaine use
trauma
connective tissue diseases
bicuspid aortic valve
coarctation
third trimester pregnancy
A

aortic dissection

420
Q

what are the two classifications of aortic dissection

A

type A
Ascending
Type B (distal to subclavian)
descending

421
Q

servere tearing rippin stabbing pain
typically abrupt in onset
anterior or back opf chest interscapular

A

aortic dissection

422
Q

anterior chest pain is more common with what type of aortic dissection

A

A

423
Q

posterior chest pain more common with what type of aortic dissection

A

B

424
Q

CXR finding typical for aortic dissection

A

widened mediastinum

425
Q

which is more accurate for aortic dissection MRI or CT

A

MRI

426
Q

best test for determining the extent of dissection in aorta for surgery

A

angiography

427
Q

what medication should be initiated immediately in aortic dissection

A
beta blockers
IV nitroprusside (BP below 120)
428
Q

most type A dissections are treated as surgical emergencies to avoid

A

MI aortic regurg or cardiac tamponade

429
Q

what is the typical management of type B dissections

A

lower blood pressure, IV beta blockers

morphine for pain

430
Q

abnormal localized dilation of aorta typically between the renal arteries and iliac bifurcation

A

AAA

431
Q

average ages for diagnosis of AAA

A

65=70

432
Q

most cases of AAA what process is occuring in vessel

A

atherosclerosis

433
Q

5 things other than atherosclerosis that predispose to AAA

A

HTN smoking vasculitis truama pos famHx

434
Q

pulsatile mass on abdominal exam

A

AAA

435
Q

sudden onset of severe pain in the back or lower abdomen with ecchymoses on back and flanks and ecchymoses aroiund umbilicus

A

AAA rupture

436
Q

Grey turner sign

A

ecchymoses on flank/back

437
Q

cullen sign

A

ecchymoses around umbilicus

438
Q

triad of abdominal pain
hypotension
palpable pulsatile abdominal mass

A

AAA rupture

439
Q

AAA rupture treatment

A

immediate laparotomy and repair

440
Q

test of choice to evaluate location and size of AAA

A

US

441
Q

test that can be used in hemodynamically stable patients with AAA for preop planning

A

CT

442
Q

size at which surgical repair of AAA should be recommended

A

> 5cm diameter

443
Q

most common site for peripheral vascular disease

A

superficial femoral artery

444
Q

what is the most important risk factor for PVD

A

smoking

445
Q

patient with PVD and intermittent claudication prognosis

A

best

446
Q

patient with PVD and rest pain / non healing ulcers prognosis

A

bad

447
Q

ABI above what value indicates severe PVD

A

1.3

448
Q

claudication ABI

A

<0.7

449
Q

rest pain ABI in PVD

A

<0.4

450
Q

gold standard for diagnosing and locating PVD

A

arteriography

451
Q

conservative management for PVD

A
stop smoking!
graduated exercise program
foot care
atherosclerosis reduction
avoid extreme temp
aspiring +/- ticlopidine/clopidogral
cilostazol
452
Q

three indications for PVD surgery

A

rest pain
ischemic ulcerations
severe symptoms refractory to conservative therapy

453
Q

two main options for surgery in PVD

A

angioplasty

bypass

454
Q

most common site of acute arterial occlusion

A

common femoral artery

455
Q

most common site and cause for embolus of acute arterial occlusion

A

heart afib

456
Q

6 Ps of acute arterial occlusion

A
pain
pallor
poikilothermia (cold blooded)
paralysis
paresthesias
pulseless
457
Q

three tests usually obtained in acute arterial occlusion

A

arteriogram
ecg (MI, afib)
echo (valves thrombus shunts)

458
Q

amount of time that skeletal muscle can tolerate ischemia

A

6 hours

459
Q

what is the immediate therapy for embolus causing acute arterial occlusion

A

immediate IV heparin

surgical embolectomy with cutdown and fogarty balloonm)

460
Q

when is bypass employed for acute arterial occlusion

A

failure of embolectomy

461
Q

small discrete areas of tissue ischemia
blue black toes
renal insufficiency
abdominal pain or bleeding

treatment

A

cholesterol embolization syndrome\

Do not anticoagulate
control BP
surgical only in very extreme circumstances

462
Q

aneurysm resulting from damage to aortic wall 2/2 infection

A

mycotic aneurysm

463
Q

what is a luetic heart

A

complication of spyphilitic aortitis in which the dilation of the proximal aorta blocks the aortic branches most commonly the coronaries

needs surgical repair

464
Q

virchows triad

A

venous stasis
endothelial injury
hypercoaguable

465
Q

lower extremity swelling/pain
calf pain on ankle dorsiflexion
palpable cord
fever

A

DVT

466
Q

initial test for DVT

A

doppler and duplex US

467
Q

duplex is good for what location of DVT

A

proximal

468
Q

most accurate test for DVT of calf

A

venography

469
Q

intermediate to high pretest probability of DVT plus Doppler +

A

begin anticoagulation

470
Q

intermediate to high pretest prob of DVT with neg doppler

A

repeat doppler 2-3days for 2 weeks

471
Q

low-intermediate pretest prob of DVT and soppler neg

A

no need for anticoagulation

472
Q

painful blue swollen leg following DVT

A

phlegmasia cerulea dolens

473
Q

indicated treatment for phlegmasia cerulea dolens

A

venous thrombectomy

474
Q

how long should warfarin be kept following DVT

A

3-6 months

475
Q

indicated for DVT/PE massive with hemodynamic instability

A

systemic thrombolytics

476
Q

treatment for patient with DVT and absolute contraindication to anticoagulation

A

inferior vena cava filter

477
Q

what is the typical preceding illness that leads to venous stasis

A

DVT (destroys valvs in the system)

478
Q

what is the reason for the brawny induration and bron black color of sjkin in chronic venous insufficency

A

extrav of proteins and RBCs

479
Q

what is the complication common with chronic venous stasis

A

venous ulceration

480
Q

how does elevation of legs differ in chronic venous insufficiency versus acute arterial insufficency

A

provides relief in venous disease

481
Q

mildly painful ulcears rapidly recurring

above the medial malleolus

A

chronic venous stasis

482
Q

three main treatment s to combat complications of chronic venous insufficiency

A

leg elevation
avoiding long periods of sitting and standing
compression stockings

483
Q

superficial thrombophlebitis in lower extremities usually associated with

A

Varicose veins

484
Q

superficial thrombophlebitis in upper extremity usually associated with

A

IV placement

485
Q

neoplasms of the heart are commonly of what origin

A

metastatis

486
Q

benign helatinous growth usually pedunculated and arising from the interatrial septum of the heart in the region of the fossa ovalis

A

atrial myxoma

487
Q

fatigue fever syncope palpitations malaise and a low pitched diastolic murmur that changes character with changing body position

A

atrial myxoma

488
Q

tachycardia decrease in BP and malfunction of underperfused organ systems

A

shock

489
Q

fever and possible site of infection in shock patient

A

septic

490
Q

trauma gi bleed vomiting or diarrhea in shock patient

A

hypovolemic

491
Q

MI angina or heart disease in shock patient

A

cardiogenic

492
Q

JVD present in a shock patient

A

cardiogenic

493
Q

spinal cord injury or neurologic deficits are present

A

neurogenic shock

494
Q

initial steps in ALL shock patients

A

establish two large bore venous catheters +/- central line and art line
fluid bolus of 2L
draw CBC lytes renal funcrtion PT/pTT
ECG CXR
pulse ox
vasopressors if still hypotensive following fluids

495
Q

Changes in the following for cardiogenic shock
CO
SVR
PCWP

A

-
+
+

496
Q

Changes in the following for hypovolemic shock
CO
SVR
PCWP

A

-
+
-

497
Q

Changes in the following for neurogenic shock
CO
SVR
PCWP

A

-

498
Q

Changes in the following for septic shock
CO
SVR
PCWP

A

-

499
Q

treatment

A

start with ABCs!

fluid resuscitation

500
Q

most common cause for cardiogenic shock

A

MI

501
Q

vassopressor usually used in cardiogenic shock

A

dopamine

502
Q

what is more important in hypovolemic shock, the rate or amount of loss

A

rate

503
Q
% of blood loss in following classes of hypovolemic shock
I
II
III
IV
A

10-15%
20-30
30-40
40>