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Clin Med > Clin Med Exam 5 > Flashcards

Clin Med Exam 5 Flashcards

1
Q

Pericarditis causes

A

Infectious/viral is the most common

Inflammation of pericardium, often occurs in the presence of MI

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2
Q

Acute pericarditis clinical findings

A

Chest pain- sharp, stabbing

Pain relieved by leaning forward

Intermitten fever, builds over a few days

Dyspnea

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3
Q

Acute pericarditis physicical exam

A

Possible pericardial effusion

Pericardial friction rub- expiration

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4
Q

Acute pericarditis EKG

A

Concave up ST elevation, PR segment depression

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5
Q

Constrictive pericarditis

A

Long term, chronic

Inflammation becomes thickened, fibrotic, adheres to pericardium

Restricts motion of ventricles, reduces diastolic filling

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6
Q

Constrictive pericarditis clinical findings

A 
Dyspnea
Fatigue
Orthopnea
Chronic edema
Weakness

Jugular venous distension, ascites, pleural effusion

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7
Q

Constrictive pericarditis clinical findings/diagnosis

A

Distant or muffled heart sounds
Elevated jugular venous pressure
Pericardial knock
Kussmaul sign (increased systemic venous pressure during inspiration)

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8
Q

Pericardial effusion clinical findings

A

Pain, dyspnea cough, N/V, fatigue, malaise

Dressler syndrome- fever, chest pain, pericardial friction rub

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9
Q

Pericardial effusion physical exam

A

Signs of shock or right heart failure (tachycardia, hypotension)

Pericardial friction rub
Low grade fever

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10
Q

EKG findings on pericardial effusion

A

Electrical alternans- pathognomonic

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11
Q

Cardiac tamponade

A

Decreased cardiac output from impaired ventricular filling due to the pericardial fluid

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12
Q

For cardiac tamponade, the prognosis depends…

A

Size and speed of effusion

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13
Q

Cardiac tamponade clinical findings

A

Becks triad- hypotension, JVD, muffled heart sounds

Pulsus paradoxus
Low voltage QRS

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14
Q

Biggest differentiation between musculoskeletal causes of chest pain and cardiac causes

A

Palpable tenderness

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15
Q

Most common cause of musculoskeletal chest pain

A

Costochondritis

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16
Q

Dilated cardiomyopathy clinical findings

A

Palpitations
Fatigues
Dyspnea
Arrhythmias

Holosystolic murmur, regurgitation

Lower SV

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17
Q

Dilated mardiomyopathy causes

A

Alcohol abuse is most common!!

Also peripartum cardiomyopathy, infection, genetics

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18
Q

Dilated cardiomyopathy treatment

A

LVAD

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19
Q

Restrictive cardiomyopathy causes

A

Amyloidosis, sarcoidosis, radiation of heart tissue, anything fibrosing the tissue

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20
Q

Restrictive cardiomyopathy clinical findings and diagnosis

A

Less blood filling the ventricle, causing diastolic herat failure

Dyspnea, distant heart sounds, exercise intolerance

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21
Q

Hypertrophic cardiomyopathy clinically

A

Interventricular septum grows larger, decreased stroke volume

Diastolic herat failure

Crescendo decrescendo murmur

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22
Q

Cause of HOCM

A

Autosomal dominant inherited

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23
Q

HOCM contraindication

A

Digoxin

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24
Q

What is the most common cause of death in young athletes?

A

HOCM

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25
Q

Takotsubo

A

Acute cardiac syndrome aka broken heart syndrome, presents like ACS

LV apical ballooning

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26
Q

Infective endocarditis general

A

Infection of heart valves or endothelium

Valvular disease is an important precursor- jet effects disrupt endothelium
Bacteremia prerequisite

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27
Q

Endocarditis microbiology

A

Staph and strep

HACEK

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28
Q

What is the most common cause of acute endocarditis?

A

Staph aureus

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29
Q

Bacteremia with strep bovis is strongly associated with…

A

Colon cancer

Colonoscopy is indicated for these patients

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30
Q

Endocarditis signs/symptoms

A

Fever
Murmur that is new/changing
Metastatic infection, emboli, immune phenomenon

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31
Q

Skin findings of endocarditis

A

Petechia/hemorrhage
(Palate, conjunctival, ungal)

Janeway lesions- painless red lesions on palms/soles

Osler nodes- painful, raised lesions on hands and feet

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32
Q

Roth spots

A

Endocarditis sign- exudative retinal lesions

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33
Q

Duke criteria endocarditis

A

2 major
1 major and 3 minor
0 major and 5 minor

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34
Q

Abscess and endocarditis

A

Perivalvular abscess is an important complication of IE

Reduced rate of cure

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35
Q

Prosthetic valve endocarditis

A

Rare but bad

TEE is diagnostic test of choice

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36
Q

Rheumatic fever

A

5-15 years age

Systemic immune process that is a sequela to GABHS

ASO titers to confirm

Mitral valve attacked in 75-80% of cases

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37
Q

Jones criteria rheumatic fever

A

Two major criteria

One major two minor

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38
Q

Major jones criteria for rheumatic fever

A

Carditis
Erythema marginatum and subq nodules
Sydenham chorea
Polyarthritis

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39
Q

Myocarditis general

A

Inflammation of heart muscle

Post viral

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40
Q

Hist. Changes of myocarditis

A

Inflammation and necrosis

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41
Q

Gold standard of myocarditis

A

Endomyocardial bx

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42
Q

Myocarditis presentation

A

SOB
DOE
Chest pain
VOLUME OVERLOAD

Aneurysms

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43
Q

EKG and CXR findings for myocarditis

A

EKG- ventricular ectopy

CXR- pulmonary venous congestion

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44
Q

Severe myocarditis

A

Left Ventricular assist devices

Impella (short term replacement of pump function)

Then total artificial heart and heart transplant

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45
Q

Frank starling effect

A

SV rises as end diastolic volume increases

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46
Q

Systolic dysfunction in heart failure

A

Decreased contractility, flattens frank starling curve

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47
Q

Diastolic dysfunction

A

Due to stiffened myocardium

Less compliant ventricle, requires more work from the atria to fill the ventricle

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48
Q

Pre/afterload dysfunction

A

Preload- end diastolic volume/pressure
Failing heart increases preload

Afterload- arterial pressure/systemic vasc resistance
Increased afterload in HF

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49
Q

Broad systolic HF description

A

HF with reduced left ventricle ejection fraction

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50
Q

Broad classification of diastolic heart failure

A

Heart failure with present ejection fraction

Abnormal diastolic dysfunction

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51
Q

Why does NE increase in heart failure and what does it say?

A

Compensating for the decreased pulse pressure and renal perfusion

Poor prognostic sign in HF

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52
Q

RAAS in HF

A

Increases to increase renal perfusion

ACEIs and ARBs are essential in HF

Increases vasoconstriction and retains fluid and acts like the patient is underperfused, but they are volume OVERLOADED

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53
Q

General heart failure symptoms

A 
Fatigue 
Dyspnea (most common sx)
Exercise intolerance 
Nocturnal
Cachexia
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54
Q

Right heart failure symptoms

A

Fluid retention- JVD
Dependent edema
HSM, ascites

Fluid backing up into the systemic system

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55
Q

Left heart failure symptoms

A

Dyspnea- pink frothy sputum/pulmonary edema

Orthopnea

Paroxysmal nocturnal dyspnea

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56
Q

Most common cause of RHF?

A

LHF

Failing LV, blood backs up into LV then pulmonary system then increases the afterload of RV

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57
Q

Exam findings for HF are…

A

90% specific but not very sensitive

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58
Q

HF exam findings

A

Mild
Dyspnea
Variable HR
BP normal to high early on, then low in late HF

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59
Q

Neck exam findings in HF

A

JVD

Hepatojugular reflux

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60
Q

Pulmonary exam findings HF

A

Rales/crackles

Pleural effusion

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61
Q

Cardiac exam findings HF

A

Displaced or prolonged or enlarged PMI

Parasternal lift

S3 (suggests systolic dysfunction)
S4

Murmurs

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62
Q

Abdomen exam HF

A

HSM

Jaundice (sublingual first)

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63
Q

Extremities exam HF

A

Cool to touch
Cyanosis
Edema (pitting, dependent)
Untied shoes

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64
Q

High output heart failure

A

Symptoms of heart failure but increased cardiac output

Eventually will progress to low output HF

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65
Q

Chronic HF

A

Gradual onset and progressive signs

Generally remains stable

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66
Q

Flash pulmonary edema description

A

Dramatic presentation of acute, decompensated HF

Increased LV pressure, rapid fluid accumulation in alveoli

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67
Q

Flash pulmonary edema presentation

A

Severe cough
Dyspnea- pink frothy sputum
Tachypnea

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68
Q

Pulmonary venous HTN CXR findings

A

Increased pulmonary veins

Cephalization

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69
Q

CXR interstitial edema findings

A

Interstitial infiltrates

Kerley B lines (short, parallel lines at periphery)

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70
Q

Brain natriuretic peptide

A

Released in response to ventricular stretch

Helpful in volume overload

Need to know baseline BNP

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71
Q

NYHA classes

A

1- asymptomatic
2- asymptomatic at rest, symptoms with walking up a couple of blocks or flights of stairs
3- asymptomatic at rest, symptoms with walking up 1 flight of stairs
4- symptomatic at rest

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72
Q

NYHA classes major points

A

Widely used, class can change and even quickly

Somewhat subjective

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73
Q

ACCF/AHA guidelines

A

A- at high risk for HF but no structural disease or sx

B- structural heart disease without signs/sx of heart failure

C- structural heart disease with prior or current sx of HF

D- refractory HF requiring specialized interventions

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74
Q

Right to left shunt

A

Bypasses pulmonary circulation

Cyanosis

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75
Q

Left to right shunt

A

Increased pulmonary circulation

No cyanosis

Can cause right heart failure from the volume overload

76
Q

Eisenmenger syndrome

A

Prolonged left to right shunt causing pulmonary hypertension, then the right ventricle pressure exceeds the left

The shunt reverses, and the left ventricle ejects more deoxygenated blood

Very bad

77
Q

Ventricular septal defect

A

Failure of any component of ventricular septum to develop fully

Symptoms depend on size and pulmonary vascular resistance

78
Q

VSD exam

A

Loud, pansystolic murmur

Increased flow through the lungs

Left to right shunt

79
Q

Atrial septal defect (types_

A

Primum- inferior
Secundum- superior
Sinus venosus defect- around inlet of vena cava, develops into SA node

Left to right shunt

80
Q

ASD findings

A

Rarely symptomatic due to low pressure system

Soft systolic ejection murmur, fixed s2 splitting

81
Q

Patent ductus arteriosus general

A

Allows blood to flow from the pulmonary artery into the aorta

Left to right shunt with pulmonary hypertension

82
Q

PDA and NSAIDs

A

Prostaglandins keep the ductus open during pregnancy- which is why pregnant women cannot take NSAIDs while they are pregnant

Closure can be induced by NSAIDs

83
Q

Endocardial cushion defect

A

ASD, VSD, and A-V valve malformations

Left to right shunting

AV valvular insufficiency

CHF, pulmonary hypertension

Needs surgical repair

84
Q

Pulmonary stenosis

A

DOE, fatigue, right herat failure if severe

85
Q

Aortic stenosis

A

Post stenotic dilation of aorta, LVH as well

Severe stenosis is fatigue, syncope

Systolic ejection murmur

86
Q

Coarctation of the aorta

A

Narrowing of aortic lumen, generally near the ductus

PDA reduces symptoms in these patients!

87
Q

Coarctation of the aorta findings

A

Baby- poor feeding, resp. Distress, shock

Older- exertional leg discomfort, epistaxis, upper extremity HTN

Systolic ejection murmur

**BP/oximetry screening of multiple extremities

88
Q

Tetralogy of Fallot

A

VSD
Pulmonary stenosis
Overriding aorta
RVH

89
Q

Tetralogy of Fallot findings

A

Hypoxic “tet” spells

Squat to increase venous return, cyanotic

90
Q

Transposition of great arteries

A

Reversal of pulmonary artery and aorta

Desaturated blood returns to right heart and is sent through the aorta to the systemic system

Death occurs rapidly

91
Q

Transposition of great arteries findings

A

CXR- egg on a string

Hyperdynamic herat

Quiet tachypnea

92
Q

Tricuspid atresia

A

Absent tricuspid valve
Hypoplastic RV
Requires PDA or VSD to perfuse pulmonary artery and ASD needed to allow blood flow to left heart

93
Q

Tricuspid atresia findings

A

Surgery is essential, prostaglandins given to maintain ductus until surgery

94
Q

Truncus arteriosus

A

Truncus does not separate into aorta and pulmonary arteries

Variable cyanosis

Needs surgical repair

95
Q

Total anomalous pulmonary venous return

A

Pulmonary veins drain into right atrium, no oxygenated blood goes to the right heart

Obstruction- severe cyanosis

Surgery essential

96
Q

Hypoplastic left heart syndrome

A

Cyanotic disease

Failure of development of mitral or aortic valve/aortic arch

Small left ventricle

Urgent surgery needed

97
Q

Patent foramen ovale

A

Foramen ovale does not close, allows for right to left shunting

Increased left heart pressure should close it usually

Often clinically silent

98
Q

Patent foramen ovale findings

A 
Maybe:
Stroke
Migraine
Hypoxia 
Risk of atrial fib
Decompression illness with air embolism 
Dyspnea and decreased o2 saturation when upright
99
Q

Ruling out valvular heart disease- diagnostic approach to a murmur

A

Careful H&P

EKG to verify rhythm

CXR to rule out pulmonary issues

Echo with doppler flow to visualize blood flow

100
Q

Best diagnostic for valvular disorders?

A

Echo

101
Q

What are the majority of mitral stenosis cases caused by?

A

Rheumatic fever

More common with multiple infections and multiple bouts of rheumatic fever

102
Q

Mitral stenosis auscultation findings

A

Opening snap following s2

Localized diastolic murmur (if disease is farther along)

Best heart at apex

103
Q

Systemic effects of mitral stenosis

A

Long asymptomatic phase

Right heart failure and low cardiac output

Sudden increase in HR causing pulmonary HTN/edema

104
Q

Mechanical prosthetic valves

A

Last 30-50 years

Can cause endocarditis, paravalvular leaks

**most importantly, thrombosis. Need to be anticoagulated for life

105
Q

Bioprosthetic valves

A

Last 5-10 years

Anticoagulation not needed

106
Q

When do you use a bioprosthetic valve?

A

Anticoag CI or not desired

Desire to be pregnant

> 70 year old patients

107
Q

When do you use a mechanical valve?

A

Patients less than 60 years old that can be anticoagulated

Re operation is dangerous

108
Q

Mitral regurgitation auscultation

A

Pansystolic murmur best heard at apex, radiating to the axilla

109
Q

Mitral regurgitation systemic findings

A

LV enlargement (reflects severity/chronicity)

Chronic dz can be asymptomatic

Afterload reduction is helpful

110
Q

What is going on in the heart because of mitral regurgitation?

A

Increased preload, but decreased afterload

Enlarged left ventricle

Increased ejection fraction

Acute- pulmonary edema
Chronic- LA/V enlargement

111
Q

What can chronic mitral regurg cause?

A

Valvular atrial fibrillation

112
Q

Mitral valve prolapse general

A

Usually females

Can see arrhythmias

Asymptomatic or SOB, fatigued, palpitations

113
Q

Auscultation mitral valve prolapse

A

Mid systolic click

Murmur (could be absent or late/pansystolic, which is severe)

114
Q

How does valsalve effect mitral valve prolapse?

A

Increased murmur (if there is one) because of the decreased venous return

115
Q

What are skeletal/collagen disorders seen with mitral valve prolapse?

A

Pectus excavatum, scoliosis/straight back

Marfan, ehlers-danlos

116
Q

Symptoms for tricuspid stenosis

A

Right heart failure

JVD with a giant “a wave” (aka resistance to R atrial emptying)

117
Q

Auscultating tricuspid stenosis

A

Diastolic rumble at LLSB

118
Q

Tricuspid stenosis EKG/CXR findings

A

EKG- RA enlargement

CXR- cardiomegaly with normal PA size

119
Q

What valve is preferred to replace tricuspid stenotic valve?

A

Bioprosthetic, less risk of thrombosis

120
Q

Tricuspid regurgitation causes

A

Valve defects

RV dilation from any cause

121
Q

Tricuspid regurg signs/symptoms

A

Asymptomatic

R heart failure

Systolic murmur at LLSB

Obliteration of x descent in jugular pulse wave

122
Q

Pulmonic stenosis general

A

Most commonly sen as congenital heart disease, can be valvular, supravalvular or subvalvular

123
Q

Pulmonic stenosis symptoms

A

Often asymptomatic

Fatigue, DOE, right heart failure (if severe)

124
Q

Pulmonic regurgitation causes

A

High pressure (pulmonary HTN)

Low pressure (valve disorders)

125
Q

Which ventricle tolerates volume load better than pressure load?

A

Right ventricle

126
Q

Signs for pulmonic regurgitation

A

Split s2, systolic click, right sided gallop, RV lift

Diastolic murmur, graham steel murmur

127
Q

Aortic sclerosis general

A

Common in elderly

Atherosclerotic calcification of valve leaflets, **does not effect valve function

Gradual evolution to aortic stenosis

128
Q

Aortic sclerosis signs

A

Maybe systolic murmur

Incidental echo finding

Irregular leaflet thickening

129
Q

Aortic stenosis causes

A

Uni/bicuspid valve

Degenerative/calcification

130
Q

Which is the most common surgical valve lesion?

A

Aortic stenosis

131
Q

Symptoms of aortic stenosis

A

Heart failure, angina, syncope (50% 3 year mortality)

LVH

Arrhythmia

132
Q

Aortic stenosis exam findings

A

Systolic ejection murmur

Best heart at aortic area, transmitted to neck and apex with patient leaning forward

Maybe preceded by AV click

If severe, s2 split

133
Q

Gallavardin phenomenon

A

Aortic stenosis

Musical murmur best heard at apex, maybe vibrations from the stenotic valve.

Handgrip increases arterial resistance and thus decreases the AS murmur

134
Q

Aortic regurgitation common cause

A

Aortic root dz (marfan, aortic dissection)

135
Q

Aortic regurg compensatory mechanisms

A

Left ventricular dilation increasing the stroke volume

If EF drops, time to replace the aortic valve

136
Q

Aortic regurgitation symptoms

A

Usually chronic with no side effects aside from diastolic murmur

LV failure can arise and be sudden

LVH if chronic

137
Q

Aortic regurgitation exam

A

High SV with rapid runoff, causing:

Wide pulse pressure

Water-hammer/corrigan pulse

Musset sign

Quincke pulse

138
Q

Aortic regurgitation murmur

A

Systolic ejection murmur with increased SV

Diastolic murmur from the regurg

Austin flint murmur- rumbling apical diastolic murmur

139
Q

When do you treat aortic regurg?

A

If symptoms, need surgery

140
Q

What medications help aortic regurg?

A

Beta blockers to reduce afterload

ACEI to reduce aortic stiffness

141
Q

What are the 4 major factors that determine myocardial work and therefore oxygen demand?

A

Heart rate
Systolic blood pressure
Myocardial wall tension/stress
Myocardial contractility

142
Q

Right coronary artery perfuses mostly…

A

Lateral and inferior parts of the heart

143
Q

Left coronary artery perfuses mostly…

A

The posterior aspect of the heart

144
Q

Left anterior descending artery perfuses mostly…

A

The anterior aspect of the heart

145
Q

Causes of angina:

A
  1. Obstruction of coronary arteries
  2. Structural cardiac abnormalities
  3. Increased metabolic demands
  4. Cardiac syndrome X
146
Q

What is cardiac syndrome x?

A

Cause of angina

Angina like chest pain with exertion
ST depression on stress test
Normal coronary arteries without vasospasm

147
Q

What are some hypermetabolic states?

A 
Hyperthyroid
Anemia
Sepsis/infection
Trauma
Pregnancy
148
Q

What is prinzmetal’s angina?

A

Coronary vasoconstriction occuring as a result of spasm of the large coronary arteries

Spontaneously or from cold, stress, or drugs

Usually women <50, early morning chest pain waking them up, often associated with arrhythmias or conduction defects

149
Q

What is the time frame for angina versus MI or unstable angina?

A

<30 minutes is angina

> 30 minutes, consider unstable or MI

150
Q

Low risk

A

<10%, watch and follow

151
Q

Intermediate risk

A

10-90%, stress test

152
Q

High risk

A

> 90%, stress test or heart cath or something!

153
Q

Silent ischemia

A

Most common manifestation of CHD

Common in diabetics, elderly, prior MI or revascularization procedures

154
Q

After stress test, what dictates a worse prognosis?

A

> 2mm depression at lower workload

Low HR

Hypotension during the test

155
Q

Positive stress test?

A

> 1 mm horizontal or downsloping ST segment depression 80 ms after J point

156
Q

When do you use vasodilators for pharmacologic stress testing? What are the drugs?

A

Dipyridamole, adenosine

Avoid with bronchospastic dz, HOTN, high degree AV block

157
Q

Synthetic catecholamine? When do you use it with pharm. stress testing?

A

Dobutamine

Preferred in stress echo

Avoid in ventricular arrhythmias, recent MI, aortic dissection, LV outflow tract obstruction

158
Q

Scintigraphy

A

Myocardial nuclear perfusion imaging

Radionuclide uptake goes to areas of adequate** myocardial blood flow

Good for determining reversible damage or nonreversible infarct

159
Q

Echo

A

Higher specificity, lower cost

Assesses cardiac anatomy and function

Wall motion abnormalities with increasing myocardial demand

160
Q

CTA

A

Useful for low likelihood of significant CAD, non invasive

161
Q

EBCT

A

Quantifies coronary artery calcification

Best for intermediate risk patients

162
Q

Cardiac MRI

A

Used more for tissue diseases, like pericardium or neoplasm

163
Q

Coronary angiography

A

Gold standard test to diagnose CAD

Used when noninvasive testing is inconclusive or severe CAD

164
Q

Narrowing of >50%

A

Hemodynamically and clinically significant

165
Q

Narrowing of >70%

A

Ischemia!

166
Q

Coronary vasospasm diagnostics

A

IV ergonovine and ST segment elevation on an EKG

167
Q

USPSTF ASA guidelines

A

low dose ASA for adults 50-59 with

> 10% 10 year CVD risk
No risk for bleeding
Life expectancy of 10 years
Willing to take for 10 years

168
Q

Treatment of stable, chronic angina

A

1st line- beta blockers!

Long acting nitrates

Ranolazine

CCBs (3rd line)

169
Q

Acute coronary syndromes 3 presentations

A
  1. Unstable angina
  2. ST elevation MI
  3. NSTEMI
170
Q

ACS presentation vs. chronic stable angina

A

Similar symptoms as stable chronic angina, but occur at rest or with minimal exertion

More severe

NTG has little effect

171
Q

Respiratory distress and edema indicating HF killip classification:

A

Class 1: absence of rales & S3
Class II: rales don’t clear with coughing less than 1/3 of lung field or presence of S3
Class III: rales do not clear with coughing over >1/3 lung fields
Class IV: cardiogenic shock

172
Q

NSTEMI diagnostics

A

Biomarkers of myocardial necrosis positive in addition to at least one of the following:

Ischemic symptoms
Q waves
Ischemic ST segment changes on EKG or imaging or coronary intervention

173
Q

Cardiac enzymes and biomarkers timing

A

3 sets, measured at 6-8 hour intervals after the patients presentation

174
Q

Which biomarkers is quickest to rise and when does it normalize?

A

CK-MB, normalizes in 24 hours

175
Q

Which biomarker is latest to peak and how long will it stay elevated?

A

Troponin I & T, stay elevated for 5-7 days

176
Q

Acute magement of STEMI

A

PCI or fibrinolytics

Dual antiplatelet therapy

Anticoagulation therapy

177
Q

CABG

A

Patients with stable angina

Rarely performed in STEMI patients, unless failure of previous intervention, shock, or life threatening arrhythmia

178
Q

After CABG prognosis

A

Mortality beneficit is most evident in first decade after surgery, then falls off

179
Q

MI deaths

A

About half occur before arrival to ED

180
Q

Neurally mediated syncope

A

Vasovagal

Situational

181
Q

Orthostatic hypotension syncope

A

Hypovolemia

Medication

Underlying disease

182
Q

Primary cardiac syncope

A

Structural

Arrhythmia

Decreased CO

183
Q

What is the most important part in the evaluation of a syncopal patient?

A

History

184
Q

Reassuring features of syncope

A

Prodrome of weakness, lightheadedness, diaphoresis, nausea

185
Q

Non-reassuring features of syncope

A

Sudden onset

Prodrome of chest pain and/or palpitations

186
Q

Physical exam of syncope

A

Assess for trauma, then look for causes

Clin Med (7 decks)

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