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CVPR > Week 2b > Flashcards

Week 2b Flashcards

1
Q

Bipolar leads (3)

A

I, II, III

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2
Q

Unipolar leads (9)

A

avF, aVL, aVR (augmented) and V1-V6

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3
Q

Septal wall and ventricle leads

A

V1 and V2

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4
Q

Anterior surface of the heart leads

A

V3 and V4

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5
Q

Left ventricle (especially lateral) leads

A

V5 and V6

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6
Q

Inferior leads

A

II, III, aVF

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7
Q

Lateral Leads

A

I and aVL

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8
Q

Normal WRS axis: positive in? negative in?

A

positive I and II, negative III (-30 to +90 degrees)

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9
Q

L.A.D: positive in? negative in?

A

Predominantly negative in Lead II and positive I, negative III

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10
Q

R.A.D.: positive in? negative in?

A

Predominantly negative in Lead I and positive III, negative II

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11
Q

ECG findings in left bundle branch block

A

Late depolarization of LV

Away from V1 (R sided leads) and toward V6 (left sided leads), widened QRS

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12
Q

Hemiblocks

A

axis shift without widening of QRS

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13
Q

Anterior hemiblock: _AD

A

LAD

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14
Q

Posterior hemiblock: _AD

A

RAD

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15
Q

ECG of right bundle branch block

A

Late depolarization of RV

Towards V1 and Towards V6, widened QRS

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16
Q

What does hypertrophy cause in an ECG finding?

A

more conduction, thus more voltage on ECG

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17
Q

ECG left ventricular hypertrophy

A

V5,6 have greater voltage

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18
Q

ECG right ventricular hypertrophy

A

V1,2 greater voltage

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19
Q

ST depression=

A
  1. transient ischemia during times of high O2 demand

OR

  1. subendocardial infarct (if lasting 2-3 days)
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20
Q

Inverted T waves =

A

transient ischemia due to acute coronary blockage

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21
Q

ST elevation =

A
  1. transmural injury in acute coronary blockage (typically due to acute MI)

OR

  1. Acute pericarditis (if in all leads!)
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22
Q

Q waves (sizeable in at least two adjacent leads)

A

transmural necrosis

Location of Q wave indicates where infarct is

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23
Q

Anatomy and function of aortic valve (3)

A

i. Trileaflet
ii. Allows blood flow out of LV into aorta during systole
iii. Prevents blood backflow into LV during diastole

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24
Q

Anatomy and function of pulmonic valve

A

i. Trileaflet
ii. Allows blood flow from RV into pulmonary artery during systole
iii. Prevents blood backflow into RV during diastole

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25
Q

3 aortic diseases

A
  1. bicuspid aortic valve
  2. aortic stenosis
  3. aortic insufficiency
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26
Q

Bicuspid aortic valve disease (5)

A
  1. Congenital cardiac malformation
  2. Most common congenital cardiac defect
  3. Often familial (1st degree family members should be screened)
  4. Common cause of other valvular complications (aortic stenosis, aortic insufficiency, endocarditis)
  5. Causes vascular complications → aortic dilation, aneurysms, dissection
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27
Q

Treatment of bicuspid aortic valve disease

A

close monitoring of valve disease, and aortic size

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28
Q

Aortic stenosis

A

decreased aortic valve opening during systole, causing LV outflow obstruction → increased LV pressure, decreased CO

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29
Q

Causes of aortic stenosis (3)

A

a. Congenital (bicuspid)
b. Calcific (in elderly) → calcium build up
c. Rheumatic → fusion

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30
Q

Symptoms of aortic stenosis (3)

A

a. Dyspnea on exertion (due to elevated LV pressures and CHF)
b. Exertional lightheadedness or syncope (due to decreased CO)
c. Exertional angina

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31
Q

Diagnosis of aortic stenosis (3 techniques and findings of each)

A

a. ECHO: shows calcification of aortic valve
b. Cardiac catheterization: direct, invasive, hemodynamic measurements to determine aortic valve gradients
c. Physical Exam: Harsh, crescendo-decrescendo systolic murmur heard best over RUSB
i. Radiation to carotids
ii. Longer, late peaking murmur associated with more severe disease

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32
Q

Treatment of aortic stenosis

A

a. Medical therapy:
i. Diuretics - reduce preload (problem is AS pts may be preload dependent)
ii. B-blockers - reduce contractility
iii. Vasodilators - HARMFUL, may cause hypotension
b. Aortic valve intervention (when symptoms develop and EF less than 50%)
i. Surgical aortic valve replacement, balloon valvuloplasty, transcatheter aortic valve replacement (TAVR)

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33
Q

Aortic insufficiency

A

insufficient valve closure so blood flows backwards into LV from aorta during diastole → increased LV volume load

→ LV dilation, systolic dysfunction, heart failure

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34
Q

Causes of aortic insufficiency

A

a. Valve disease: bicuspid AV, Calcific disease, Endocarditis, Rheumatic Disease
b. Aortic disease: dissection, Marfan, Aneurysm/dilation

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35
Q

Symptoms of aortic insufficiency (5)

A

a. Water hammer pulse (rapidly swelling and falling arterial pulse)
b. DeMusset’s sign: head bob with each heartbeat
c. Quincke’s pulses: capillary pulsations in fingertips
d. Mueller’s sign: systolic pulsations of uvula
e. Corrigan’s pulse: rapid forceful carotid upstroke followed by rapid decline

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36
Q

Diagnosis of aortic insufficiency

A

a. Physical Exam:
i. Early diastolic murmur (L sternal border)
ii. Austin-Flint Murmur: diastolic murmur at apex due to turbulent diastolic blood flow across mitral valve
iii. Systolic murmur may occur due to increased flow across aortic valve (mimics aortic stenosis)

ECHO: LV size and function, evaluate aortic pathology

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37
Q

Clinical presentation of aortic insufficiency

A

a. Long asymptomatic phase

b. Severe AI → LV dilation and dysfunction → CHF (dyspnea, pulmonary edema, orthopnea

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38
Q

Treatment of aortic insufficiency

A

a. Close monitoring
b. Medications: treat CHF (ACEI, ARB, BB, diuretics)
c. Surgical intervention: symptomatic severe AI with systolic EF less than 50%

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39
Q

Pulmonic valve disease is typically due to _____

A

congenital heart disease

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40
Q

Pulmonic stenosis is usually found in ______

A

children or early adolescents

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41
Q

Clinical presentation of pulmonic stenosis (4)

A

a. RVH and RV enlargement → RV failure
b. Long asymptomatic phase
c. Dyspnea on exertion, CP, syncope
d. Peripheral edema

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42
Q

Auscultation finding of pulmonic stenosis

A

a. Systolic ejection murmur (loudest at L upper sternal border)
i. Longer and late peaking → more severe disease
b. Split S2
c. Right sided S4 may be present

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43
Q

Primary causes of pulmonic insufficiency

A

a. Infectious, Rheumatic, Carcinoid
b. Congenital abnormality
c. Iatrogenic (surgical valvotomy or balloon valvuloplasty)

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44
Q

Clinical manifestations of pulmonic insufficiency (5)

A

a. Long asymptomatic phase
b. RV volume overload
c. RV volume dysfunction
d. Atrial and ventricular arrhythmias
e. Mild-moderate PI is a common finding on echo and does not warrant further testing or monitoring if asymptomatic with normal RV

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45
Q

Auscultation findings ion pulmonic insufficiency

A

Early diastolic murmur (best heard over L 2nd and 3rd IC spaces
- May increase in intensity with inspiration

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46
Q

Anatomy and function of mitral valve

A

i. Open in diastole to allow blood flow from LA to LV
ii. Closed in systole to prevent blood backflow from LV to LA
iii. Anatomy: Annulus, Leaflets, Chordae, Papillary muscles

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47
Q

Anatomy and fuction of tricuspid valve

A

i. Open in diastole to allow blood flow from RA to RV
ii. Closed in systole to prevent blood backflow into RA
iii. 3 leaflets + 3 papillary muscles

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48
Q

Mitral stenosis

A

decreased mitral valve opening → obstruction of flow from LA to LV during diastole → increased pressure in LA, pulmonary vasculature and right heart

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49
Q

Causes of mitral stenosis

A

a. Rheumatic (80-99% of MS cases) - occurs years after acute rheumatic fever
b. Calcific (advanced age, renal disease)

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50
Q

Clinical presentation of mitral stenosis (6)

A

1) Dyspnea (increased LA pressure = increased pulmonary venous and capillary pressure → pulmonary edema)
2) Hemoptysis (increased pulmonary vascular pressure → rupture of bronchial vein into lung parenchyma)
3) Pulmonary HTN
4) Right sided heart failure (edema, ascites)
i. Due to chronic overwork due to increased resistance of pulmonary HTN
5) Atrial fibrillation (elevated LA pressures = LA dilation)
6) Thromboembolic event (stagnant blood flow in LA → clot formation)

51
Q

Auscultation findings in mitral stenosis

A

a. Loud S1
b. Opening snap following S2
c. Diastolic rumble

52
Q

Diagnosis of mitral stenosis

A

a. EKG: LA enlargement, RVH if pulmonary HTN present, AFIB

b. ECHO: LA enlargement, thickened mitral valve leaflets, elevated pressure in LA

53
Q

Treatment of mitral stenosis

A

Meds:

i. B-blockers (slow HR = more time for blood to cross mitral valve in diastole)
ii. Diuretics (treat CHF symptoms)
iii. Warfarin (prevent stroke)
b. Valve Replacement (Bioprosthetic valves or mechanical valves) vs. balloon valvuloplasty

54
Q

Mitral regurgitation

A

inadequate mitral valve closure → blood backflow into LV from LA during systole

55
Q

Primary mitral valve disease

A

problems with valve itself

a. Myxomatous → mitral valve prolapse
- Excess mitral leaflet tissue
- Most often sporadic, sometime hereditary
- MR common in pts with severe LV dysfunction/dilation

b. Endocarditis
c. Chordal rupture

56
Q

Secondary mitral valve disease

A

problems with heart that cause issue with otherwise well-functioning valve (aka Functional MR)

a.Caused by problems with LV (dilation, dysfunction) → dilation of annulus, tethering of chordae, restriction of leaflets

57
Q

Clinical presentation of mitral regurgitation

A

a. CHF symptoms (dyspnea, orthopnea, edema)
- Increased LA volume and pressure → pulmonary edema and pulmonary HTN

b.LA dilation, Atrial arrhythmias (AFIB)

c. LV dilation, dysfunction
- Decreased forward CO

58
Q

Ausculation findings in mitral regurgitation

A

a. Holosystolic murmur at apex, radiating to axilla

b. Midsystolic click followed by systolic murmur = Specific to MVP

59
Q

Things that prolong a murmur caused by mitral regurgitation

A

hand grip (increase afterload)

60
Q

Things that decrease a murmur caused by mitral regurgitation

A

Valsalva = exhalation (decrease preload)

61
Q

Signs of LV dysfunction (3)

A

i. S3, S4
ii. Lateral displacement of apical impulse
iii. Edema, crackles, JVD

62
Q

Treatment of mitral regurgitation

A

a. Meds:
i. Diuretics for CHF
ii. Afterload reduction (ACE inhibitors, ARBs)

b. Surgery: MV repair preferred over replacement

63
Q

Tricuspid regurgitation

A

backflow into RA during systole

64
Q

Causes of tricuspid regurgitation

A

80% of cases secondary to annular dilation and leaflet tethering due to RV dilation from volume and/or pressure overload

65
Q

Clinical presentation of tricuspid regurgitation (4)

A

a. Elevated RA pressure → LE edema, ascites, hepatic congestion (hepatomegaly)
b. RV enlargement and dysfunction over time
c. JVD with visible v wave
d. Fatigue due to low CO

66
Q

Auscultation findings in tricuspid regurgitation

A

Holosystolic murmur heard best along sternal border (louder with inspiration (increases venous return to R side of heart)

67
Q

Treatment of tricuspid regurgitation

A

a. Medications: diuretics

b. Surgery: Tricuspid repair or replacement (usually only if in OR for some other heart repair already)

68
Q

Causes of tricuspid stenosis

A

Rare

Rheumatic heart disease

69
Q

Clinical presentation of tricuspid stenosis

A

a. Dyspnea
b. Edema
c. Often occurs simultaneously with mitral stenosis

70
Q

Auscultation findings in tricuspid stenosis

A

Same as mitral murmur but heard closer to sternum, intensifies with inspiration

71
Q

Treatment of tricuspid stenosis

A

Meds: diuretics

surgery

72
Q

S1 =
S2 =

S1-S2 interval =

S2-S1 interval =

A 
S1 = mitral/tricuspid close
S2 = aortic/pulmonic close

S1-S2 interval = systole

S2-S1 interval = diastole

73
Q

Name the systolic murmurs (5) and where you hear them

A

1) Aortic stenosis (2nd R intercostal space, radiates to neck and carotids)
2) Pulmonic stenosis (2nd-3rd L intercostal space, no radiation)
3) Mitral regurgitation (apex, radiation to axilla)
4) Tricuspid regurgitation (L lower sternal border)
5) Mitral valve prolapse (apex, radiation to axilla)

74
Q

Name the problem:

Systolic ejection click followed crescendo-decrescendo murmur

A

Aortic Stenosis

or pulmonic stenosis depending on location

75
Q

Name the problem:

Holosystolic murmur

A

Mitral regurgitation

or tricuspid regurgitation depending on location/radiation

76
Q

Name the problem:

midsystolic click followed by crescendo murmor

A

Mitral valve prolapse

77
Q

Aortic Stenosis

what kind of murmur?

what makes it?

A

Systolic ejection click followed crescendo-decrescendo murmur

-due to turbulent blood flow through aortic valve during systole

(increases and decreases as blood flow through aorta increases and decreases)

78
Q

Mitral regurgitation

What kind of murmur?

A

Holosystolic murmur

-valve can’t fully close, so back flow from LV into LA creates murmur throughout all of systole as LV contracts

79
Q

Mitral valve prolapse

What kind of murmur?

A

midsystolic click followed by crescendo murmor

  • valve closes (S1) but then accelerates into LA when its pushed by LV contraction –> stops abruptly causing the mid-systolic click
  • followed by crescendo murmur because blood flows back into LA
80
Q

You listen with your bell for what?

A

Low frequency - small pressure gradient

e.g. mitral stenosis

81
Q

You listen with your diaphragm for what?

A

High frequency - large pressure gradient

e.g. aortic stenosis

82
Q

S3 heart sound

A

due to LV volume overload

occurs right after S2 during early diastole during the rapid LV filling phase

“Ken-tuc-ky”

83
Q

S4 heart sound

A

sign of stiff ventricle (pressure overload)

-occurs at end of diastole, right before S1

“Ten-ne-see”

84
Q

Diastolic murmurs (4) and where you hear them

A

1) Aortic regurgitation (L sternal border)
2) Pulmonic regurgitation (upper L sternum)
3) Mitral stenosis (apex)
4) Tricuspid stenosis (L lower sternal border)

85
Q

Name the problem:

early diastolic decrescendo

A

aortic regurgitation

or pulmonic regurgitation

86
Q

Name the problem:

opening snap followed by mid diastolic rumble

A

Mitral stenosis

or tricuspid stenosis

87
Q

Aortic regurgitation

what kind of murmur

A

early diastolic decrescendo

-back flow into LV form aorta during diastole

88
Q

Mitral stenosis

what kind of murmur

A

opening snap followed by mid diastolic rumble

-mitral valve opens at S2 , then sound of turbulent blood going through stenotic mitral valve that increases at the end of diastole as atria contract for final kick

89
Q

Rhabdomyoma

A

(benign) - skeletal muscle cells - most common primary cardiac tumor of heart in infancy/childhood

90
Q

Cardiac Myxoma

in who?
where?
complications (3)?

A

(benign) - most common primary tumor of heart in teens and adults but is RARE

Locations: LA&raquo_space; RA

Complications:

  • Fragments can embolize into systemic circulation and lodge in brain, kidneys, or other organs
  • Syncope or sudden death
  • Obstruction or damage to mitral valve
91
Q

Common infectious organisms of myocardium that cause infectious myocarditis

A

Viral = Coxsackievirus A or B or enteroviruses

Parasitic = Trichinosis, Chagas Disease

Fungal = candida

92
Q

Autoimmune causes of myocarditis are typically _________ autoimmune diseases processes

A

systemic

collagen vascular disease, connective tissue diseases - SLE

93
Q

Common non-medication causes of toxic cardiomyopathy (3)

A

1) Ethanol (with associated nutritional deficiencies)
2) Cobalt (from artificial joint prostheses)
3) Hemochromatosis (iron deposition)

94
Q

Amyloidosis

common associated disease?

A

too much protein circulating in the blood → protein deposition as B-pleated sheets around blood vessels and in the parenchyma of various organs (NOT specific for identity of protein)

  • stiffens heart
  • Plasma Cell Neoplasm associated with AL amyloid made of immunoglobulin light chain proteins
95
Q

Myocarditis

A

infectious or inflammatory process

96
Q

Cardiomyopathy

A

heart disease resulting from a primary abnormality in myocardium (electrical and/or mechanical dysfunction) with innappropriate ventricular hypertrophy or dilation

Secondary cardiomyopathies EXCLUDED (e.g. ischemic disease, hypertensive disease, valve-associated abnormality)

97
Q

Hypertrophic cardiomyopathy is a ________ dysfunction due to impairment of ________.

A

Diastolic

compliance (cannot relax in diastole)

98
Q

HCM

A

Thickened interventricular septum bulges into LV outflow tract during early systole → outflow obstruction through aortic valve → ejection murmur

  • CONCENTRIC HYPERTROPHY
  • Myocyte disarray and hypertrophy

Complications: sudden death, arrhythmias, blockage of LV outflow

99
Q

3 common mutations associated with HCM

A

Myosin-binding protein C
B-myosin heavy chain
Cardiac Troponin T

HCM almost 100% genetic causes

100
Q

Dilated cardiomyopathy is due to _______ dysfunction and impaired __________

A

systolic

systolic contraction

heart BIG and dilated

101
Q

DCM causes

A

Causes: genetic and non-genetic

alcohol, peripartum, genetic, myocarditis, hemochromatosis, chronic anemia, doxorubicin, sarcoidosis

Genetic mutations (30-40% of cases): desmin, dystrophin, sarcoglycans, Lamin A/C

102
Q

Complications of DCM

A

mural thrombus formation → systemic embolization, arrhythmia

103
Q

Restrictive cardiomyopathy is _________ dysfunction with impaired _________

A

diastolic dysfunction

impaired compliance (Cannot relax during diastole, but systolic function is normal)

fibrotic or infiltrated myocardium

104
Q

Causes of RCM

A
  • idiopathic
  • amyloidosis
  • sarcoidosis
  • hemochromatosis
  • scleroderma
  • radiation-induced fibrosis

Typically acquired (not genetic)

105
Q

Effects of chronic systemic HTN

A

affects L heart

sustained pressure overload on LV → CONCENTRIC HYPERTROPHY of myofibers

Additional sarcomeres / myofibrils added to existing cardiomyocytes

Same # of myocytes, increased # of sarcomeres

106
Q

Clinical manifestations of HTN

A

headache, dizziness, or NONE (silent killer)

107
Q

Complications of HTN

A

1) Atherosclerosis/aneurysm
2) Cerebrovascular disease (ischemic/arteriosclerosis or hemorrhage)

3) Kidney disease: HTN is a KEY cause
Arteriosclerosis, glomerulosclerosis, CHF (pulmonary edema)

  • kidney disease can cause HTN and can be caused by HTN
    4) CHF - Left HF which can then cause R HF
108
Q

Causes of pulmonary HTN (4)

A

1) Things that cause hypoxia and lung vessels to contract
- Emphysema
- Interstitial lung disease
- Morbid obesity, muscular dystrophy (can’t take a deep breath)

2) Left heart failure
3) Congenital heart disease
4) Primary pulmonary vessel disease

109
Q

Effects of pulmonary HTN

A

affects R heart

  • Ascites, splenomegaly, LE edema
  • Passive congestion of liver (“nutmeg liver”)
110
Q

Rheumatic heart disease

A
  • post-infection autoimmune response
  • Takes years or decades to develop after acute rheumatic fever
  • Ab vs. M protein of Group A strep (strep pyogenes) crossreacts with own glycoproteins
  • Results in “Pancarditis”
  • Anschoff bodies present in mycardium
  • Fish mouth stenosis
  • manifests as mitral valve disease +/- aortic valve disease
  • Jones criteria for diagnosis
111
Q

Valve abnormalities increase risk for…(4)

A

nodular calcifications, vegetation formation, fibrosis, and infection

112
Q

Myxomatous degeneration (mitral valve prolapse) can be caused by…

Mitral valve prolapse can result in…

A

mostly unknown

1) Defect in metabolism of ECM → accumulation of myxomatous extracellular material → softening/ enlargement of leaflets and elongation/fibrosis of chordae tendinea
2) Marfan syndrome (fibrillin defect, elastic fiber problem)

Can cause enlargement of LA → arrhythmias, stroke emboli formation, and increases risk for endocarditis

113
Q

Calcific aortic stenosis is mostly due to __________

A

wear and tear (elderly patients), but can occur in younger patients with underlying valve abnormality

114
Q

Non-infectious endocarditis

A

“Sterile Vegetations”

Thrombus (clot) formation on valve with NO organisms or inflammation

Complications: embolism, valve function deficits, potential for infection

115
Q

Infectious endocarditis

A
  • Primary infection of normal or damaged valve (higher risk)
  • Blood culture to determine causative organism (bacteria usually - staph aureus, strep viridans)
  • Fungal organisms can occur, but much less common
  • Highly virulent organisms (s. aureus) can quickly destroy valves → acute onset CHF
116
Q

Pathophysiology of DCM

A

decreased CO sensed –> RAAS, neurohormonal activation, sympathetic activation –> volume increase and ventricular remodeling

117
Q

Symptoms of DCM

A

Volume overload → dyspnea, orthopnea, PND, S3 gallop (filling of dilated ventricle in beginning of systole), rales, edema

  • Ventricular thrombus formation
  • Mitral/tricuspid regurgitant murmurs
  • Arrhythmias due to injury, fibrosis and dilation
118
Q

ECG findings associated with DCM (4)

A

LVH
LA enlargement
wide QRS
arrhythmias (AFIB, PVCs)

119
Q

Symptoms of HCM

How do you make the murmur louder and softer?

A

DOE

-Anginal chest pain (thick walls, increased LV systolic pressure decreases blood flow to myocardium)

  • Systolic murmur louder with standing/valsalva and softer with squatting
  • ONLY murmur louder with valsalva → decrease preload –> smaller LV = more obstruction of aortic outflow path by mitral valve (SAM)

-Most frequent cause of SCD in young athletes

120
Q

Pathophysology of HCM (4)

A

1) Cardiac myocyte hypertrophy and disarray
2) EF usually normal or hyperdynamic with abnormal compliance (diastolic dysfunction)

3) Possible dynamic LV outflow tract obstruction
- Systolic arterial motion of mitral valve when ventricle contracts → pushes mitral valve into outflow tract causing dynamic obstruction

4) Elevated LV filling pressure

121
Q

Treatment of HCM

A
  • Avoid extreme exertion
  • Decrease contractility - B-blockers, verapamil
  • Implantable cardiac defibrillator
  • Transplantation, surgical myomectomy, alcohol ablation
122
Q

Treatment of RCM

A

Pericardial stripping
Transplantation

TREAT UNDERLYING CAUSE:
Steroids for sarcoidosis
Chelation therapy for hemochromatosis
BMT for amyloid

123
Q

Acute myocarditis

A

acute inflammation of cardiac muscle, usually viral cause

  • Usually occurs in young adults and children
  • 50% have preceding respiratory or GI symptoms
  • Fever, chest pain (with ECG changes), arrhythmia
  • can lead to chronic heart failure

CVPR (12 decks)

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