Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Board Exam > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Causes of Takotsubo Cardiomyopathy

A

disordered response of the myocardium d/t enormous amount of catecholamine being produced (i.e. stress, grief)

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

Takotsubo cardiomypoathy

A

Stress-induced cardiomyopathy
Mimics a STEMI
Typically follows severe emotional or physiologic stress
May be due to an anatomic predisposition to ischemia in states of extreme catecholaminergic tone

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

Takotsubo cardiomyopathy: Labs/Dx

A

ST-elevations or pronounced T-wave inversions

Cardiac Cath is required to make the diagnosis through an absence of significant coronary disease on angiography
- kinesis of the LV apex (apical ballooning)

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

Wolff-Parkinson-White syndrome: EKG changes

A

delta waves
wide QRS
shortened PR
ST-T wave repolarization abnormalities
pseudo-inferior MI pattern suggesting accessory AV conduction

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

Wolff-Parkinson-White syndrome: complications

A

tachyarrhythmias that can lead to VF and death

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

Wolff-Parkinson-White syndrome: what meds are contraindicated?

A

nodal blocking agents: digoxin, beta blockers, CCBs

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

Wolff-Parkinson-White syndrome: treatment

A

ablation

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

Grade I murmur

A

barely audible

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

Grade II murmur

A

audible but faint

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

Grade III murmur

A

moderately loud; easily heard

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

Grade IV murmur

A

loud; associated with a thrill

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

Grade V murmur

A

very loud; heard w/one corner of stethoscope lifted off the chest

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

Grade VI murmur

A

loudest

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

A murmur heard at the 5th ICS is associated with…

A

the apex of the heart
mitral valve

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

A murmur heard at the 2nd or 3rd ICS is associated with…

A

base of the heart
aortic valve

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

A murmur heard during systole is associated with…

A

mitral regurgitation
aortic stenosis

Ms. ArD & Mr. AsS

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

A murmur heard during diastole is associated with…

A

mitral stenosis
aortic regurgitation

Ms. ArD & Mr. AsS

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

arterial ulcers: presentation

A

Punched out or stellate appearance
Painful
Surrounding red, tight skin
May be pale or have eschar
Often associated with trauma and occur over pressure points

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

most common cause of lower extremity ulcers

A

chronic venous stasis disease

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

venous stasis ulcers: presentation

A

Typically appear on the lower legs above the ankle
Tender, shallow
Exudative with granulation tissue at the base
Irregular borders

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

AHA recommendation for daily sodium intake for hypertension

A

<1.5g/day

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

S1

A

mitral/tricuspid (AV) valves close
aortic/pulmonic (semilunar) valves open

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

S2

A

mitral/tricuspid (AV) valves open
aortic/pulmonic (semilunar) valves close

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

period between S1 and S2

A

systole

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

period between S2 and S1

A

diastole

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

S3

A

increased fluid states (e.g. heart failure, pregnancy)

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

S4

A

stiff ventricular wall (e.g. MI, LVH, chronic hypertension)

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

HFrEF

A

systolic failure
inability to contract
results in decreased cardiac output

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

HFpEF

A

diastolic failure
inability to relax and fill
results in decreased cardiac ouptut

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

acute heart failure

A

L sided failure
abrupt onset
usually follows MI or valve rupture
can result in LVH d/t L ventricular failure 2/2 chronic hypertension

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

chronic heart failure

A

R sided failure
develops as a result of inadequate compensatory mechanisms that have been employed over time to improve cardiac output
result of L sided failure

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

L heart failure: S/Sx

A

dyspnea at rest
coarse rales all over lung fields
wheezy frothy cough
appears generally healthy except for the acute event
S3 gallop
murmur of mitral regurgitation (systolic murmur loudest at apex)

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

R heart failure: S/Sx

A

Appears chronically ill
JVD
Diffuse chest wall heaves
Displaced PMI
S3 and/or S4
hepatomegaly
splenomegaly
Abdominal fullness
dependent edema d/t increased capillary hydrostatic pressure
paroxysmal nocturnal dyspnea
fatigue on exertion

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

NYHA Functional Classification of Heart Failure: Class I

A

no limitations on physical activity

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

NYHA Functional Classification of Heart Failure: Class II

A

slight limitations of physical activity but comfortable at rest (physical activity results in fatigue, palpitations, dyspnea, angina)

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

NYHA Functional Classification of Heart Failure: Class III

A

marked limitations of physical activity but comfortable at rest
3 pillows to sleep but able to sleep
- ACEI indicated

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

NYHA Functional Classification of Heart Failure: Class IV

A

severe; inability to carry out any physical activity without discomfort (symptomatic at rest
-continuous IV inotropic support indicated

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

Heart failure: labs/Dx

A

ABG: hypoxemia, hypocapnia
BMP normal unless chronic heart failure is present
Obtain baseline BNP or NT-proBNP

UA

CXR: pulmonary edema, Kerley B lines, effusions
TTE to assess L ventricular function

EKG may show deviation or underlying problem: acute MI, dysrhythmia

PFTs for wheezing

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

Heart failure: non pharmacologic management

A

sodium restriction
rest/activity balance
weight reduction

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

Heart failure: pharmacologic management

A

1st line: diuretics
ACEI or ARB
beta blocker
Sacubitril/valsartan (Entresto) - useful for HFrEF
Digoxin
ACs for AFib

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

dilated cardiomyopathy

A

dilation of the heart muscle
most common type of cardiomyopathy

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

hypertrophic cardiomyopathy

A

hypertrophy of the left, and occasionally the right, ventricle

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

restrictive cardiomyopathy

A

scarring/stiffening of the heart muscle
the least common type of cardiomyopathy

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

arrhythmogenic right ventricular dysplasia

A

irregular heart rhythms caused by the dying of muscle tissue in the right ventricle that is replaced by scar or fat tissue

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

transthyretin amyloid cardiomyopathy (ATTR-CM)

A

abnormal protein buildup (deposits of amyloid protein fibrils) in the walls of the left ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

cardiomyopathy: routine management

A

Three drug combination for most patients with HF: diuretic, ACEI/ARB, beta blocker
- Beta blockers once euvolemia is achieved

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

cardiomyopathy: long-term management

A

Lifestyle changes: diet, exercise, sleep patterns, stress reduction, avoidance of alcohol and other drugs
Maintaining treatment of comorbidities

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

cardiomyopathy: acute management

A

Symptomatic relief: vasodilators to reduce preload and afterload (nitrates, hydralazine, nitride, nesiritide, ACEIs/ARBs, diuretics)

Inhibition of neurohormonal activation: ACEIs/ARBs, beta blockers, aldosterone antagonists

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

inpatient management of acute pulmonary edema

A

supplemental O2 while awaiting ABGs
sitting or semi-fowler position

Morphine 2-4mg IVP, repeat 20-30 min PRN, stop if hypercapnia occurs
Furosemide 40mg IVP; repeat in 10 min if no response

Severe bronchospasm: inhaled sympathomimetics

Severe pulmonary edema: nitroprusside, hydralazine for afterload and preload reduction

If cardiac index remains low: dobutamine

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

hypertension: S/Sx

A

elevated BP
epistaxis in the late afternoon
dizziness/lightheadedness
S4 r/t LVH
AV nicking (chronic sign)

severe: suboccipital pulsating headache, occurring early in the morning and resolving throughout the day

tearing chest pain may indicate aortic dissection

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

hypertension: labs/Dx

A

rule out secondary causes
- renovascular disease studies
- CXR if cardiomegaly suspected
- plasma aldosterone level to rule out aldosteronism
- AM/PM cortisol levels to rule out Cushing’s syndrome

CBC, BMP, ca, phos
cholesterol, triglycerides
UA, uric acid
EKG

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

JNC Normal BP

A

SBP <120 and DBP <80

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

JNC elevated BP

A

SBP 120-129 and DBP >80

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

JNC stage 1 hypertension

A

SBP 130-139 or DBP 80-89

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

JNC stage 2 hypertension

A

SBP >140 or DBP >90

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

hypertension: pharmacologic management for non-African American

A

thiazide diuretic
ACEI
ARB
CCB

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

hypertension: pharmacologic management for African American

A

thiazide diuretics
CCB?

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

hypertension: pharmacologic management for diabetics

A

ACEI (or ARB)

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

hypertension: pharmacologic management for adults with CKD

A

ACEI - slow the progression of CDK and decrease proteinuria

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

hypertension: treatment algorithm for initial treatment

A

1 month
then increase the dose
then add a second drug

continue to assess monthly until goal is reached

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

Using an ACEI and ARB together is a risk for

A

hyperkalemia

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

first line treatment for hypertension

A

thiazide diuretics

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

hypertensive urgency

A

> 180/110
May or may not be associated with severe headache, SOB, epistaxis, severe anxiety

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

hypertensive urgency: treatment

A

oral therapies such as clonidine

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

hypertensive emergency

A

> 180/120
Requires immediate (within 1 hour) BP reduction to prevent or limit target organ damage

or

<180/120 with any of the following:
-malignant hypertension
-hypertensive encephalopathy
-ICH
-unstable angina
-acute MI
-acute heart failure
-dissecting aortic aneurysm
-eclampsia

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

hypertensive emergency: management

A

ICU
nicardipine, sodium nitroprusside (Nitride)

For compelling conditions (e.g. aortic dissection, severe preeclampsia, eclampsia, pheochromocytoma crisis): SBP should be reduced to <140 in the first hour
- <120 in aortic dissection

For adults without a compelling condition: SBP should be reduced by no more than 25% within the first hour
- if stable, to 160/100 within the next 2-6 hours
- cautiously to normal during the next 24-48 hours

Lowering BP too quickly can damage blood flow to organs accustomed to functioning at high levels and cause ischemia or infarction

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

stable angina

A

exertional
most common

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

Prinzmetal’s angina

A

occurs at various times, including rest
d/t sudden influx of intracellular calcium
- treat w/CCBs

ST elevations on EKGs rather than depressions
Dx of exclusion often in Cath lab

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

unstable angina

A

pre-infarction, rest or crescendo, coronary syndromes

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

microvascular angina

A

metabolic syndrome

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

angina: labs/Dx

A

EKG: normal with ST depressions
Exercise EKG
Serum lipid levels

definitive diagnostic procedure: coronary angiography

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

Normal lipid panel

A

total cholesterol <200
triglycerides <150
VLDL <150
LDL <100
HDL 40-60

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

angina: management

A

Diet
Low dose aspirin
Nitrates
Beta blockers
CCBs
Optimize lipid panel values

Identify patients who would benefit from statin therapy
-ASCVD
-elevated LDL
-DM

74
Q

Bile acid sequestrates

A

lower LDL
may increase triglycerides

Examples:
-cholestyramine (Questran)
-Colesevelam
-colestipol

75
Q

Fibrates

A

lower triglycerides
slightly lower LDL
possibly elevate HDL

Examples:
-gemfibrozil
-fenofibrate
-fenofibric acid

76
Q

Cholesterol absorption inhibitor

A

used w/statin to lower LDL

Example:
-ezetimibe (Zetia)

77
Q

Niacin

A

lowers LDL and triglycerides
elevates HDL
high doses may cause “flushing” sensation which will pass

78
Q

How are ACEIs helpful after MI

A

prevent ventricular remodeling

79
Q

MI/ACS management

A

ASA 325 to chew
NTG SL Q5 min x3
O2
12 lead EKG
Morphine
Furosemide if pulmonary edema present
Metoprolol IV x3 if not contraindicated
ACEIs
Heparin vs Lovenox
Monitor therapeutic coagulation values

80
Q

Normal INR

A

0.8-1.2 s

81
Q

Normal aPTT

A

28-38 sec

82
Q

normal PT

A

11-16 sec

83
Q

normal PTT

A

60-90 sec

84
Q

MI/ACS: indications for pharmacologic revascularization

A

Unrelieved chest pain (>30 min and <6 hrs) with ST elevations >0.1 mV in two or more contiguous leads

85
Q

MI/ACS: contraindications for pharmacologic revascularization (tPA)

A

Prior ICH
Ischemic stroke within 3 months
Intracranial or intraspinal surgery within 2 months
Significant closed head trauma or facial trauma within 3 months
Structural cerebral vascular lesion or malignant intracranial neoplasm
Suspected aortic dissection
Severe uncontrolled hypertension (>185/110)
Active bleeding or risk thereof, including abnormal coagulation values

86
Q

PVD: pathology

A

arteriosclerotic narrowing of the lumen of arteries resulting in decreased blood supply to the extremities

87
Q

PVD: Causes/Risk factors

A

atherosclerosis
HLD
smoking
DM

88
Q

PVD: S/Sx

A

Common first symptom: intermittent claudication, calf pain
increased pain with elevation of lower extremities
progresses to pain at rest
cold/numbness to extremities
shiny/hairless skin
dependent rubor
pallor
cyanosis
ulcerations
reduced pulses

89
Q

PVD: labs/Dx

A

1st line: ankle-brachial index (ABI) <0.9 (least invasive)

doppler US to evaluate flow
X-rays may show calcification

Arteriography: most definitive test, but invasive

90
Q

PVD: management

A

Lifestyle changes:
-Stop smoking/tobacco
-Exercise, stop during pain and resume when pain subsides to develop collateral circulation
-weight reduction as needed

Cilostazol (Pletal)
manage DM, HLD
angioplasty
bypass surgery
amputation

91
Q

chronic venous insufficiency: pathology

A

impaired venous return d/t either destruction of valves, changes d/t DVT, leg trauma, or sustained elevation of venous pressure

92
Q

chronic venous insufficiency: causes/risk factors

A

more common in women
may have genetic predisposition
Hx of leg trauma
may be associated with varicose veins

93
Q

chronic venous insufficiency: S/Sx

A

BLE heaviness and pain relieved with elevation of the legs or with walking
edema after prolonged standing
skin discoloration
numbness
tingling
pruritis
telangiectasis and varicosities are frequently seen
stasis leg ulcers
dermatitis
cool to touch

94
Q

chronic venous insufficiency: labs/Dx

A

r/o edema d/t HF and other causes

95
Q

chronic venous insufficiency: management

A

bed rest with legs elevated to diminish edema
compression stockings
weight reduction, exercise
aspirin may accelerate healing

treat dermatitis/ulcers
acute weeping dermatitis
- tap water compresses
- hydrocolloid dressings
- hydrocortisone cream

96
Q

pericarditis

A

inflammation of the pericardium

97
Q

pericarditis: causes

A

viruses: most common cause
post MI
renal failure
neoplastic, TB, septicemia
endocarditis
collagen diseases (e.g. scleroderma, RA, SLE, etc)
drug/trauma induced

98
Q

pericarditis: S/Sx

A

very localized retrosternal/precordial chest pain, pleuritic in nature
pain increased by deep inspiration, coughing, swallowing, or recumbent
pain relieved by sitting forward
SOB 2/2 pain w/inspiration
malaise
headache

99
Q

pericarditis: physical findings

A

pericardial friction rub - best heard w/patient leaning forward; high pitched
pleural friction rub may also be present (creaking/scratching sound/sandpaper)
fever may be present depending on underlying cause

100
Q

endocarditis

A

infection of the endothelial surface of the heart
usually affects the valves

Dx of infective endocarditis must be considered and excluded in all patients with a heart murmur and FUO

101
Q

endocarditis: causes

A

usually caused by bacteria
known valvular heart disease; esp in rheumatic, bicuspid aortic valve/mitral valve prolapse with significant regurgitation
recent dental/oropharyngeal surgery
GU instrumentation
surgery of the respiratory tract
congenital heart disease
prolonged use of IV catheters or TPN
patients with burns
hemodialysis

102
Q

endocarditis: S/Sx

A

fever and malaise
night sweats
weight loss
general “sick” feeling

103
Q

endocarditis: physical findings

A

murmur often present
fever
Osler’s nodes
petechiae
purpura
pallor
splinter hemorrhages
splenomegaly
Janeway lesions
Roth spots

104
Q

Osler’s nodes

A

painful red nodules in the distal phalanges

seen in endocarditis

105
Q

Splinter hemorrhages

A

linear, subungal splinter-appearing

seen in endocarditis

106
Q

Janeway lesions

A

small painless macules on the palms and soles

Seen in endocarditis

107
Q

Roth spots

A

small retinal infarcts, white in color, encircled by areas of hemorrhage

seen in endocarditis

108
Q

endocarditis: labs/Dx

A

WBC normal or elevated, but always a left shift
TEE for valvular damage
BC for causative organism
- three separate cultures at three separate sites in 1 hour
ESR always elevated

109
Q

endocarditis: management

A

Subacute endocarditis (delayed): empiric therapy is generally not started until BC results

Acute endocarditis (rapidly progressive): usually due to staphylococcus aureus (both MRSA and MSSA), streptococci, and enterococci
-empiric therapy: vancomycin until BC results

110
Q

pericarditis: labs/Dx

A

ST elevations in all leads
-return of ST segment to normal in a few days followed by temporary T wave inversion
Depression of PR segment

ESR elevated
BC if bacterial cause suspected
CBC to r/o infx
baseline BMP

echo to confirm presence of pericardial fluid or other abnormalities

111
Q

pericarditis: Management

A

1st line: colchicine

NSAIDs
-indomethacin
-ketorolac
-ibuprofen

Corticosteroids only for refractory pericarditis or very severe symptoms
-can increase viral replication

ABX if bacterial infx

Monitor for tamponade (hypotension, JVD, muffled/distant heart sounds, pulsus paradoxus)

112
Q

Adverse effects of amiodarone

A

hypo/hyperthyroidism
interstitial lung disease
elevated LFTs
skin photosensitivity
corneal deposits
optic neuropathy

113
Q

Before starting amiodarone, what should you check

A

thyroid levels
LFTs
baseline PFTs
referral to ophthalmology for monitoring may be needed

114
Q

metabolic syndrome

A

large waistline: men >40 in, women >35 in
hypertension
hyperglycemia
high triglycerides, low HDL

115
Q

Indications for urgent referral to a vascular surgeon or vascular laboratory in patients with ischemic arterial ulcers

A

Cellulitis
Gangrene
Visible tendon or bone at the ulcer base
Severe infection
ABI <0.5

116
Q

Wolff-Parkinson-White Syndrome: S/Sx

A

during episodes of tachyarrhythmia:
-diaphoresis
-cool skin
-hypotension
-crackles d/t pulmonary vascular congestion

117
Q

aortic stenosis: symptoms

A

dyspnea
heart failure
angina
syncope on exertion
systolic murmur over the 2nd R ICS radiates to carotid arteries
S4 gallop

118
Q

1st line therapy for hyperlipidemia

A

statin

2nd line: niacin

119
Q

digoxin toxicity

A

GI upset
visual disturbances with yellow-green halos
palpitations, dyspnea, syncope
bradycardia, PVCs, LBBB

diltiazem potentiates the effects of digoxin

120
Q

Indications for statin therapy

A

Clinical evidence of ASCVD
Elevated LDL >190
Age 40-75 with diabetes and LDL 70-189 but no ASCVD
LDL 70-189 with no diabetes or ASCVD, but estimated 10-year risk of ASCVD >7.5

121
Q

Statins potentiate the effects of what medications?

A

anticoagulants

122
Q

TEE or TTE for endocarditis?

A

TEE is more specific

123
Q

Patients with a history of ventriculostomies such as tetralogy of Fallot have an increased risk of…

A

ventricular tachycardia

124
Q

Diagnostic test for POTS

A

tilt table test

125
Q

S4 gallop is most commonly associated with…

A

aortic stenosis

126
Q

Holosystolic murmurs are most often associated with…

A

mitral valve regurgitation

127
Q

An opening snap can be heard in patients with…

A

mitral valve prolapse
mitral valve regurgitation

128
Q

cardiac tamponade: S/Sx

A

Beck’s Triad:
-hypotension
-JVD
-muffled/distant heart sounds

pulsus paradoxus
decreased cardiac output
tachycardia
increased RR
weak peripheral pulses
cool skin
dark yellow urine

EKG: low voltage, no ST or T wave changes

129
Q

cardiac tamponade: labs/Dx

A

echo

130
Q

cardiac tamponade: management

A

pericardiocentesis

diuretics are contraindicated - may cause intravascular volume depletion and worsen hypotension

131
Q

1st medication to give for suspected or confirmed cardiac ischemia

A

aspirin due to anti platelet effect

132
Q

1st choice for management of ischemic cardiac pain due to vasodilatory effects

A

nitroglycerin

133
Q

1st medication to give for acute heart failure

A

IV diuretic

134
Q

pericardial effusion: S/Sx

A

dyspnea
fatigue
weight loss
occasional fever
dry cough
constant chest pain
pericardial friction rub

135
Q

pericardial effusion: management

A

Assess cardiac function with TTE
Pericardiocentesis

136
Q

PE: management

A

anticoagulant therapy for 3 months after initial therapy

137
Q

Goal BP for patients with CKD

A

<130/80 if proteinuria is also present

138
Q

ACE Inhibitors: mechanism

A

reduce afterload, preload, systolic wall stress
increase cardiac output without increasing heart rate

139
Q

Cushing’s triad

A

increased SBP, decreased DBP (widening pulse pressure)
decreased RR
decreased HR

140
Q

When do you see Cushing’s triad?

A

acute elevations of ICP

141
Q

STEMI: management

A

Priority: PCI
fibrinolytic therapy within 30 mins of admission to the hospital

142
Q

HFpEF or HFrEF: which has better outcomes?

A

HFrEF
HFpEF is managed with diuresis and BP control, but there is no medical treatment proven to reduce mortality and morbidity

143
Q

HFpEF or HFrEF: L ventricle is normal in size

A

HFpEF

144
Q

HFpEF or HFrEF: associated with exercise intolerance

A

both

145
Q

HFpEF or HFrEF: associated with pulmonary hypertension

A

both

146
Q

HFpEF or HFrEF: dilated left ventricle

A

HFrEF

147
Q

aortic dissection: presentation

A

severe, sudden onset back pain between shoulder blades
tearing, ripping, stabbing chest pain
BP unequal in both arms
CXR: widened mediastinum

148
Q

aortic dissection: management

A

emergent CT angiogram
cardiac surgery consult

149
Q

Intervention that decreases the final size of the infarcted myocardium in the acute phase of an anterior STEMI

A

PCI

150
Q

Intervention for patients who do not stabilize after PCI or fibrinolytic therapy

A

IABP counterpulsation therapy

151
Q

Who is IABP counterpulsation therapy indicated for?

A

patients with mechanical defects such as VSD or mitral regurgitation

152
Q

In decompensated heart failure, what medications may support cardiac function and cardiac output?

A

IV inotropic agents (e.g. dobutamine)
-especially useful for patients who can’t tolerate vasodilator therapy
-useful for afterload reduction

153
Q

acute onset AFib: management

A

cardiac glycosides (e.g. digoxin) to increase contractility and decrease HR
CCBs to control ventricular response

154
Q

statins: side effect

A

elevated CK d/t skeletal muscle breakdown

155
Q

heart failure r/t dilated cardiomyopathy: management

A
  1. Afterload reducing agent (ACEI)
  2. IV inotropic agent
  3. LVAD after medical management has been maximized
156
Q

VTach is most frequently associated with

A

heart failure

157
Q

2nd degree AV block Type II is most frequently associated with

A

anterior wall MI

158
Q

junctional tachycardia is most frequently associated with

A

digoxin toxicity

159
Q

hypertrophic cardiomyopathy: presentation, EKG

A

syncope
non-radiating systolic murmur
biphasic P wave in leads V1 and V2
Deep narrow Q waves in lateral leads I, aVL, V5, V6

160
Q

hypertrophic cardiomyopathy: confirmed by?

A

echo

161
Q

What medications are contraindicated in systolic heart failure but can be used to treat tachycardia in diastolic heart failure?

A

CCBs

162
Q

most likely etiology of aortic valve disease in elderly

A

calcification

163
Q

most likely etiology of aortic valve disease in adults (not elderly)

A

congenital bicuspid aortic valve

164
Q

Rheumatic fever as a child can cause…

A

mitral stenosis

165
Q

hypertension: management

A
  1. diuretics
  2. ACE, ARB, CCB
166
Q

common complication of CEA

A

hypoglossal nerve damage
-tongue deviates to ipsilateral side of surgery
-order swallow study

167
Q

sudden cardiac death following MI is usually caused by..

A

VF 2/2 myocardial scarring
–ICD

168
Q

Right coronary artery: EKG leads

A

Inferior leads: II, III, aVF

169
Q

Left circumflex artery: EKG leads

A

Lateral leads: I, aVL, V5, V6
Inferior leads: II, III, aVF

170
Q

Left anterior descending (or interventricular artery): EKG leads

A

Septal: V1, V2
Anterior: V3, V4

171
Q

Diagonal branch: EKG leads

A

Lateral leads: I, aVL, V5, V6

172
Q

Lateral leads

A

I
aVL
V5
V6

173
Q

Anterior leads

A

V3
V4

173
Q

Septal leads

A

V1
V2

174
Q

Inferior leads

A

II
III
aVF

175
Q

nitroglycerin

A

ventilator used to increase myocardial blood flow

176
Q

acute ventriclar septal defect

A

complication of MI
acute onset SOB and CP
associated with cardiogenic shock

177
Q

Which valvular disorder is most commonly associated with an aortic aneurysm?

A

aortic regurgitation

178
Q

Patients with Marfan syndrome commonly have which valvular disorders?

A

mitral valve prolapse
mitral regurgitaiton

179
Q

complications after anterior MI

A

Post-infarct angina
Ventricular rupture
Septal aneurysms
Arrhythmias
L heart failure
Cardiogenic shock
Acute mitral regurgitation

180
Q

Valve most often affected by endocarditis

A

tricuspid

181
Q

IVDU is associated with what valvular disorder?

A

mitral valve regurgitation

Board Exam (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions