Week 2b Flashcards

(123 cards)

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
3 aortic diseases
1. bicuspid aortic valve 2. aortic stenosis 3. aortic insufficiency
26
Bicuspid aortic valve disease (5)
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
27
Treatment of bicuspid aortic valve disease
close monitoring of valve disease, and aortic size
28
Aortic stenosis
decreased aortic valve opening during systole, causing LV outflow obstruction → increased LV pressure, decreased CO
29
Causes of aortic stenosis (3)
a. Congenital (bicuspid) b. Calcific (in elderly) → calcium build up c. Rheumatic → fusion
30
Symptoms of aortic stenosis (3)
a. Dyspnea on exertion (due to elevated LV pressures and CHF) b. Exertional lightheadedness or syncope (due to decreased CO) c. Exertional angina
31
Diagnosis of aortic stenosis (3 techniques and findings of each)
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
32
Treatment of aortic stenosis
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)
33
Aortic insufficiency
insufficient valve closure so blood flows backwards into LV from aorta during diastole → increased LV volume load → LV dilation, systolic dysfunction, heart failure
34
Causes of aortic insufficiency
a. Valve disease: bicuspid AV, Calcific disease, Endocarditis, Rheumatic Disease b. Aortic disease: dissection, Marfan, Aneurysm/dilation
35
Symptoms of aortic insufficiency (5)
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
36
Diagnosis of aortic insufficiency
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
37
Clinical presentation of aortic insufficiency
a. Long asymptomatic phase | b. Severe AI → LV dilation and dysfunction → CHF (dyspnea, pulmonary edema, orthopnea
38
Treatment of aortic insufficiency
a. Close monitoring b. Medications: treat CHF (ACEI, ARB, BB, diuretics) c. Surgical intervention: symptomatic severe AI with systolic EF less than 50%
39
Pulmonic valve disease is typically due to _____
congenital heart disease
40
Pulmonic stenosis is usually found in ______
children or early adolescents
41
Clinical presentation of pulmonic stenosis (4)
a. RVH and RV enlargement → RV failure b. Long asymptomatic phase c. Dyspnea on exertion, CP, syncope d. Peripheral edema
42
Auscultation finding of pulmonic stenosis
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
43
Primary causes of pulmonic insufficiency
a. Infectious, Rheumatic, Carcinoid b. Congenital abnormality c. Iatrogenic (surgical valvotomy or balloon valvuloplasty)
44
Clinical manifestations of pulmonic insufficiency (5)
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
45
Auscultation findings ion pulmonic insufficiency
Early diastolic murmur (best heard over L 2nd and 3rd IC spaces - May increase in intensity with inspiration
46
Anatomy and function of mitral valve
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
47
Anatomy and fuction of tricuspid valve
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
48
Mitral stenosis
decreased mitral valve opening → obstruction of flow from LA to LV during diastole → increased pressure in LA, pulmonary vasculature and right heart
49
Causes of mitral stenosis
a. Rheumatic (80-99% of MS cases) - occurs years after acute rheumatic fever b. Calcific (advanced age, renal disease)
50
Clinical presentation of mitral stenosis (6)
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
Auscultation findings in mitral stenosis
a. Loud S1 b. Opening snap following S2 c. Diastolic rumble
52
Diagnosis of mitral stenosis
a. EKG: LA enlargement, RVH if pulmonary HTN present, AFIB | b. ECHO: LA enlargement, thickened mitral valve leaflets, elevated pressure in LA
53
Treatment of mitral stenosis
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
Mitral regurgitation
inadequate mitral valve closure → blood backflow into LV from LA during systole
55
Primary mitral valve disease
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
Secondary mitral valve disease
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
Clinical presentation of mitral regurgitation
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
Ausculation findings in mitral regurgitation
a. Holosystolic murmur at apex, radiating to axilla | b. Midsystolic click followed by systolic murmur = Specific to MVP
59
Things that prolong a murmur caused by mitral regurgitation
hand grip (increase afterload)
60
Things that decrease a murmur caused by mitral regurgitation
Valsalva = exhalation (decrease preload)
61
Signs of LV dysfunction (3)
i. S3, S4 ii. Lateral displacement of apical impulse iii. Edema, crackles, JVD
62
Treatment of mitral regurgitation
a. Meds: i. Diuretics for CHF ii. Afterload reduction (ACE inhibitors, ARBs) b. Surgery: MV repair preferred over replacement
63
Tricuspid regurgitation
backflow into RA during systole
64
Causes of tricuspid regurgitation
80% of cases secondary to annular dilation and leaflet tethering due to RV dilation from volume and/or pressure overload
65
Clinical presentation of tricuspid regurgitation (4)
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
Auscultation findings in tricuspid regurgitation
Holosystolic murmur heard best along sternal border (louder with inspiration (increases venous return to R side of heart)
67
Treatment of tricuspid regurgitation
a. Medications: diuretics | b. Surgery: Tricuspid repair or replacement (usually only if in OR for some other heart repair already)
68
Causes of tricuspid stenosis
Rare Rheumatic heart disease
69
Clinical presentation of tricuspid stenosis
a. Dyspnea b. Edema c. Often occurs simultaneously with mitral stenosis
70
Auscultation findings in tricuspid stenosis
Same as mitral murmur but heard closer to sternum, intensifies with inspiration
71
Treatment of tricuspid stenosis
Meds: diuretics surgery
72
S1 = S2 = S1-S2 interval = S2-S1 interval =
``` S1 = mitral/tricuspid close S2 = aortic/pulmonic close ``` S1-S2 interval = systole S2-S1 interval = diastole
73
Name the systolic murmurs (5) and where you hear them
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
Name the problem: Systolic ejection click followed crescendo-decrescendo murmur
Aortic Stenosis | or pulmonic stenosis depending on location
75
Name the problem: Holosystolic murmur
Mitral regurgitation or tricuspid regurgitation depending on location/radiation
76
Name the problem: midsystolic click followed by crescendo murmor
Mitral valve prolapse
77
Aortic Stenosis what kind of murmur? what makes it?
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
Mitral regurgitation What kind of murmur?
Holosystolic murmur -valve can't fully close, so back flow from LV into LA creates murmur throughout all of systole as LV contracts
79
Mitral valve prolapse What kind of murmur?
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
You listen with your bell for what?
Low frequency - small pressure gradient e.g. mitral stenosis
81
You listen with your diaphragm for what?
High frequency - large pressure gradient e.g. aortic stenosis
82
S3 heart sound
due to LV volume overload occurs right after S2 during early diastole during the rapid LV filling phase "Ken-tuc-ky"
83
S4 heart sound
sign of stiff ventricle (pressure overload) -occurs at end of diastole, right before S1 "Ten-ne-see"
84
Diastolic murmurs (4) and where you hear them
1) Aortic regurgitation (L sternal border) 2) Pulmonic regurgitation (upper L sternum) 3) Mitral stenosis (apex) 4) Tricuspid stenosis (L lower sternal border)
85
Name the problem: early diastolic decrescendo
aortic regurgitation | or pulmonic regurgitation
86
Name the problem: opening snap followed by mid diastolic rumble
Mitral stenosis | or tricuspid stenosis
87
Aortic regurgitation what kind of murmur
early diastolic decrescendo -back flow into LV form aorta during diastole
88
Mitral stenosis what kind of murmur
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
Rhabdomyoma
(benign) - skeletal muscle cells - most common primary cardiac tumor of heart in infancy/childhood
90
Cardiac Myxoma in who? where? complications (3)?
(benign) - most common primary tumor of heart in teens and adults but is RARE Locations: LA >> 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
Common infectious organisms of myocardium that cause infectious myocarditis
Viral = Coxsackievirus A or B or enteroviruses Parasitic = Trichinosis, Chagas Disease Fungal = candida
92
Autoimmune causes of myocarditis are typically _________ autoimmune diseases processes
systemic | collagen vascular disease, connective tissue diseases - SLE
93
Common non-medication causes of toxic cardiomyopathy (3)
1) Ethanol (with associated nutritional deficiencies) 2) Cobalt (from artificial joint prostheses) 3) Hemochromatosis (iron deposition)
94
Amyloidosis common associated disease?
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
Myocarditis
infectious or inflammatory process
96
Cardiomyopathy
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
Hypertrophic cardiomyopathy is a ________ dysfunction due to impairment of ________.
Diastolic compliance (cannot relax in diastole)
98
HCM
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
3 common mutations associated with HCM
Myosin-binding protein C B-myosin heavy chain Cardiac Troponin T HCM almost 100% genetic causes
100
Dilated cardiomyopathy is due to _______ dysfunction and impaired __________
systolic systolic contraction heart BIG and dilated
101
DCM causes
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
Complications of DCM
mural thrombus formation → systemic embolization, arrhythmia
103
Restrictive cardiomyopathy is _________ dysfunction with impaired _________
diastolic dysfunction impaired compliance (Cannot relax during diastole, but systolic function is normal) fibrotic or infiltrated myocardium
104
Causes of RCM
- idiopathic - amyloidosis - sarcoidosis - hemochromatosis - scleroderma - radiation-induced fibrosis Typically acquired (not genetic)
105
Effects of chronic systemic HTN
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
Clinical manifestations of HTN
headache, dizziness, or NONE (silent killer)
107
Complications of HTN
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
Causes of pulmonary HTN (4)
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
Effects of pulmonary HTN
affects R heart - Ascites, splenomegaly, LE edema - Passive congestion of liver (“nutmeg liver”)
110
Rheumatic heart disease
- 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
Valve abnormalities increase risk for...(4)
nodular calcifications, vegetation formation, fibrosis, and infection
112
Myxomatous degeneration (mitral valve prolapse) can be caused by... Mitral valve prolapse can result in...
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
Calcific aortic stenosis is mostly due to __________
wear and tear (elderly patients), but can occur in younger patients with underlying valve abnormality
114
Non-infectious endocarditis
"Sterile Vegetations" Thrombus (clot) formation on valve with NO organisms or inflammation Complications: embolism, valve function deficits, potential for infection
115
Infectious endocarditis
- 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
Pathophysiology of DCM
decreased CO sensed --> RAAS, neurohormonal activation, sympathetic activation --> volume increase and ventricular remodeling
117
Symptoms of DCM
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
ECG findings associated with DCM (4)
LVH LA enlargement wide QRS arrhythmias (AFIB, PVCs)
119
Symptoms of HCM How do you make the murmur louder and softer?
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
Pathophysology of HCM (4)
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
Treatment of HCM
- Avoid extreme exertion - Decrease contractility - B-blockers, verapamil - Implantable cardiac defibrillator - Transplantation, surgical myomectomy, alcohol ablation
122
Treatment of RCM
Pericardial stripping Transplantation TREAT UNDERLYING CAUSE: Steroids for sarcoidosis Chelation therapy for hemochromatosis BMT for amyloid
123
Acute myocarditis
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