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ICM2 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Vector directions for standard EKG limb leads

A 
I = R arm to L arm
II = R arm to L foot
III = L arm to L foot
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2
Q

Where to place precordial leads?

A 
V1 = R 4th ICS adjacent to sternum
V2 = L 4th ICS adjacent to sternum
V4 = L 5th ICS in MCL
V6 = L 6h ICS in MAL
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3
Q

When current direction has a component vector in the SAME direction as a lead, ECG deflection is … ?
Other cases?

A

Positive
Negative if vice versa
Net deflection of 0 if perpendicular to current

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4
Q

Which EKG leads are usually most positive?

A

II, I
aVF
V4, V5, V6

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5
Q

Normal time intervals on EKG for QRS complex, PR interval, and QT interval?
Issues if abnormal?

A

QRS (begin Q to end S) less than 120ms (3 small boxes) = for determining heart blocks
PR (begin P to begin Q) less than 200ms (1 big box)
QT (begin Q to end T) less than 500ms (2.5 big boxes) = may be lengthened by some drugs

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6
Q

How do you estimate HR from an EKG?

A

300 / (number of big boxes per cycle)

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7
Q

Describe these common rhythms:
AFib
Atrial flutter
Junctional rhythm

A

AFib: No P-waves seen, gravely baseline, irregular rate
Atrial flutter: Sawtooth baseline from fast atrial cycling
Junctional: AV source causes (-) depolarization of atria

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8
Q

QRS axis:
Normally aVF and I are … ?
If L deviation, aVF and I are … ?
If R deviation, aVF and I are … ?

A

Normal: Both (+)
L deviation: aVF (-) and I (+)
R deviation: aVF (+) and I (-)

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9
Q

Left anterior fascicular block occurs when … ?

A

QRS axis deflection is larger than -30deg (90deg from II)

Anatomically impossible -> Electrical abnormality

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10
Q

Right bundle branch block

A

Right conductive branch from AV node is not conducting, so current flows from LV to RV more slowly via muscle to cause RV contraction.
Since R side is delayed, the QRS widens to over 120ms, and the terminal QRS will be (+) in V1 and (-) in V6
A repolarization T wave of opposite magnitude follows the QRS in each lead

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11
Q

Left bundle branch block

A

Left conductive branches from AV node not conducting, so current flows from RV to LV more slowly via muscle to cause LV contraction.
Since L side is delayed, the QRS widens to over 120ms, and the terminal QRS will be (-) in V1 and (+) in V6, although for LBBB the wide QRS may be the only obvious change
A repolarization T wave of opposite magnitude follows the QRS in each lead

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12
Q

How to determine QRS width?

A

Find the greatest width on any lead

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13
Q

1st degree AV block definition, severity

A

Fixed PR prolongation (over 200ms), but number of P-waves = number of QRS complexes
Benign

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14
Q

2nd degree AV block Type I definition, severity

A

Gradual PR prolongation due to AV nodal disease; PR increases until a QRS is dropped
Usually benign

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15
Q

2nd degree AV block Type II definition, severity

A

Unpredictable AV block with dropped QRS at unpredictable intervals, wide QRS complexes
Needs a pacemaker

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16
Q

3rd degree AV block definition

A

P-wave and QRS happen at independent rates

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17
Q

Trifascicular block

A

1st degree AV block + LAFB + RBBB

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18
Q

2:1 AV conduction block appearance

A

P-waves occur at twice the rate of QRS, every other P-wave may occur during and be hidden by the QRS

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19
Q

Most common cause for a pause in contraction

A

Nonconducted atrial contraction

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20
Q

Left posterior fascicular block appearance

A

May cause a right axis deviation, but is rare and often not detectable

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21
Q

ECG progression of a STEMI, treatment

A

Hyperacute giant T-waves -> ST elevation -> Q-wave development, diminished R-waves -> ST normalization and T-wave inversion -> T normalization
Persistent ST elevation = LV aneurysm
Take to cath lab immediately

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22
Q

NSTEMI treatment

A

Give nitrates, heparin, O2, aspirin immediately
Check troponin
This is transient damage, but unstable. Take to the cath lab within 24h or ASAP if it progresses

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23
Q

Determining dominance of heart

A

Does posterior descending artery come from L or RCA?

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24
Q

Inferior ECG leads

A

II, III, aVF

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25
Q

Anteroseptal ECG leads

A

V1, V2

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26
Q

Anterior ECG leads

A

V3-V5

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27
Q

Lateral ECG leads

A

I, aVL, V6

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28
Q

Anterior MI due to occlusion of what vessel?

A

LAD

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29
Q

Lateral MI due to occlusion of what vessel?

A

Proximal L circumflex artery

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30
Q

Inferior MI due to occlusion of what vessel?

A

R circumflex OR distal L circumflex artery including posterior descending artery (determine dominance)

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31
Q

Inferior AND lateral MI due to occlusion of what vessel?

A

L circumflex artery MI in L dominant heart occluding distal posterior descending artery

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32
Q

Infective endocarditis definition, causes

A

Microbial infection of endocardium, which may include valves and chordae tendinae
Caused by Staph aureus, Staph epidermidis from prosthetics, and various Strep species, including S. bovis in elderly (perform colonoscopy)
Also caused by ‘HACEK’ - Haemophillus, Actinobacillus, Cardiobacterium hominis, Eikenella, Kingella
Bartonella from flea bite

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33
Q

Infective endocarditis risk factors

A 
Poor dental hygiene
IV drug use
Dialysis
Indwelling catheters
Diabetes mellitus
Prosthetic valves
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34
Q

Infective endocarditis signs and symptoms

A

Systemic: Fever, weight loss, fatigue, night sweats, septic shock
Skin: Petechiae, conjunctival and splinter hemorrhages, Osler nodes (pain, subcu on fingers and toes, SUBACUTE), Janeway lesions (no pain, palms and soles, ACUTE)
Heart failure, heart murmur
Splenomegaly
Roth spots (hemorrhage w/pale center) on fundoscopy

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35
Q

Perivalvular abscesses cause … ?

A

Valve dysfunction (murmurs), heart block, stroke

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36
Q

Infective endocarditis diagnosis

A

2 Major / 1 M + 3 m / 5 minor

Major:
Lab evidence from 2 + blood cultures (1 + for Coxiella burnetti)
Endocardial involvment on transthoracic or -esophageal echo (TTE/TEE)
New valvular regurgitation, esp. mitral

Minor:
Predisposing heart condition
Fever
Vascular phenomenon (Emboli, mycotic aneurysm, hemorrhages)
Immunologic phenomenon (Glomerulonephritis, Osler node, +RF)
Positive blood culture

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37
Q

Infective endocarditis treatment

A

2-6w IV abx
If G+ and penicillin-sensitive, use PCN/Ampicillin + Aminoglycoside (usually gentamicin)
If G+ and not PCN-sensitive, use Vancomycin + Aminoglycoside
Do not use anticoagulation treatment: Doesn’t prevent embolism and ups bleeding risk

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38
Q

Libman-Sacks endocarditis associated with what?

A

SLE

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39
Q

Carcinoid syndrome associated with what finding?

A

Flushed skin

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40
Q

What murmurs increase with inspiration?

Which with expiration?

A 
Inspiration = RS murmurs increased
Expiration = LS murmurs increased
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41
Q

Likely CXR findings with tricuspid regurgitation

A

Cavitary lesions and pulmonary edema from congestion

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42
Q

Uses of TTE and TEE

A

For detecting endocarditis of native (TTE) and prosthetic (TEE) valves

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43
Q

Indications for endocarditis prophylaxis

A

Patient has: Prosthetic valve, heart transplant recipient, previous endocarditis history, or uncorrected cyanotic heart disease
Patient is undergoing: Dental work w/ bleeding or tonsillectomy/adenoidectomy

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44
Q

Right-sided heart failure causes what?

A

Systemic veinous congestion -> Anasarca

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45
Q

Left-sided heart failure causes what?

A

Pulmonary veinous congestion -> Pulmonary edema

AND decreased ejection and systemic perfusion

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46
Q

Mainstay diagnostic tool for valvular disease?

A

Echos - TTE or TEE

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47
Q

Causes of tricuspid stenosis

A

Rheumatic fever = w/regurgitation and MV stenosis, no calcification)
Carcinoid scarring = endocardial fibrosis causes decreases movement, causes combined stenosis and regurgitation
Congenital = Ebstein’s anomaly (TV pulled down into RV), atresia

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48
Q

Tricuspid stenosis symptoms

A

Fatigue, dyspnea
Forward failure = low CO, up RAA
Backward failure = anasarca

49
Q

TV stenosis findings

A

Mid-diastolic murmur over L lower sternal border
Increases w/ inspiration (RS)
Hepatomegaly w/o pulsations
Anasarca

50
Q

TV stenosis labs

A

CXR shows large RA, no pulmonary artery enlargement, and clear lungs (Pathognomonic triad)
EKG shows large p-waves unless AFib present

51
Q

TV regurgitation causes

A

Rheumatic fever, endocarditis, trauma, carcinoid, myxoma
Functional causes from MV regurgitation (majority)
Congenital = Ebstein’s anomaly

52
Q

TV regurgitation findings

A 
Dyspnea, AFib
Pansystolic murmur, increases w/ inspiration (RS)
Hepatomegaly w/ pulsations
JVD
Anasarca
53
Q

TV treatment

A

Observe mild-mod cases
Medical treatment for functional disease caused by left-sided lesion
Ring valvuloplasty/repair for severe disease
Commissurotomy to treat congenital/rheumatic stenosis
Replacement in infective, carcinoid, calcified stenosis

54
Q

Ross procedure

A

Remove pulmonary valve as an autograft to replace an aortic valve in children to avoid future heart surgery

55
Q

Mitral stenosis symptoms

A

Down CO, LA hypertrophy, Pulmonary hypertension and edema

Cough, hemoptysis, dyspnea on exertion

56
Q

MV stenosis findings

A

LV normal or small
Auscultatory triad = apical diastolic rumble, loud S1, opening snap
CXR shows large LA, normal heart size, and straight L heart border
MV calcified on imaging
Engorged pulmonary lymphatics (Kerley’s lines)

57
Q

MV stenosis cause

A

Rheumatic disease -> Fibrosis, calcification

58
Q

MV stenosis treatment

A

Observation/medical - keep up w/ echos, use anticoagulation if thrombus or AFib if asymptomatic
Percutaneous balloon commissurotomy if minimal calcification, mild disease, and no LA thrombus
Open commissurotomy or replacement with severe stenosis
Repair is rare due to fibrosis
Pulmonary HTN reverses post-op

59
Q

MV regurgitation causes

A 
Rheumatic
Infective endocarditis
Secondary to MI, cardiomyopathies, LV aneurysm
CT diseases
Myxoma
Prolapse
Trauma
Papillary muscle rupture/dysfunction
60
Q

MV regurgitation findings

A

Loud pansystolic murmur transmitting to axilla
Up LA and pulm vein pressure
Fatigue, dyspnea, AFib, palpitations
LA hypertrophy
If acute due to ruptured muscle post MI, pulm edema due to inability of LA to compensate

61
Q

MV treatment

A

Observe mild disease w/ echos for thrombi
Medical - diuresis to reduce afterload, anticoagulation, maybe b-blockers
Surgery - repair/annuloplasty for symptomatic severe cases, replacement if repair impossible
Acute cases require urgent surgery

62
Q

Aortic stenosis causes

A

Degeneration/Calcification - most common, may block conduction with lots of Ca
Congenitally bicuspid valve
Rheumatic w/ MV disease

63
Q

Aortic stenosis pathology

A

Up afterload, concentric LV hypertrophy (wall only) that depends on atrial contraction to fill; AFib with this is bad
LV hypertrophy can lead to LV failure as increased muscle increases O2 demands -> ischemia, microinfarcts -> failure
Most common fatal valve lesion

64
Q

Aortic stenosis findings

A

Angina, syncope, CHF, sudden death
May be asymptomatic for years, but then malignant once sx develop
Systolic ejection murmur at R 2nd ICS radiating to carotids
EKG shows LVH, maybe blocks like R/LBBB, AVB, AFib
CXR shows valve calcification, aortic enlargement

65
Q

Aortic stenosis treatment

A

Observe mild-mod disease
Medical - control HTN, arrhythmias
Surgery if severe for valve replacement

66
Q

Aortic regurgitation causes

A 
Degenerative calcified AV, mixed AS/AR
Rheumatic
Bacterial endocarditis
Congenital
RA, AnkSp
Marfan's
Aortic dissection
Trauma
VSD involving valve leaflets
Myxoma
67
Q

Aortic regurgitation pathology

A

AR causes LV volume overload -> massive LV dilatation, eccentric hypertrophy (up chamber size and wall thickness) -> LV failure
Decreased diastolic coronary flow from regurg -> May get angina with normal coronaries

68
Q

Aortic regurgitation symptoms

A

Dyspnea, angina
May be asymptomatic until LV dysfunction and impending CHF
Widened pulse pressure
Blowing diastolic murmur
Austin-Flint murmur from turbulent flow against MV heard at apex
Water hammer pulse = bounding, forceful peripherally
Quincke’s pulse = pulsating nail beds
De Musset’s sign = head bobbing w/ cardiac cycle
Duroziez’s = sys/diastolic murmur of femoral aa
Traube’s = pistol shot sound over large aa

69
Q

Aortic regurgitation labs

A

LVH, pulmonary edema, regurgitant jet on echo, enlarged ascending aorta

70
Q

Aortic regurgitation treatment

Surgical comparison to AS?

A

Observe mild-mod w/ serial echos
Medical - reduce afterload by diuresis, treat HTN
Surgery to replace valve if severe, repair occasionally; May need to replace ascending aorta
AR patients do worse than AS patients post-op in general

71
Q

When to place a pacemaker in CHF?

A

When EF below 30% with MI OR 35% w/o improvement of chronic condition despite Rx

72
Q

CHF treatments (general, daily Rx, refractory Rx)

A

Diuretics, vasodilators, inotropes

General treatments:
Limit Na+, monitor weight for rapid gain, vaccinations to stop infxn
ACE inhibitors
b-blockers
Spironolactone
Hydralazine
Diuretics
Digoxin
Pacemaker / resynchronization

Refractory treatments:
Dobutamine, milrinone for inotropic support
LV assist device - assists pumping
Cardiac transplant

73
Q

Heart failure definition

A

Syndrome from structural or functional cardiac disorders impairing heart’s ability to fill with or eject blood

74
Q

Reasons for acute CHF decompensation

A

Dietary or medication noncompliance
Inappropriate medications
Don’t seek care
Acute ischemia, HTN, arrhythmias

75
Q

Backward failure causes ?

Forward failure causes ?

A 
Backward = congestion, needs vasodilators and diuresis
Forward = poor perfusion, needs inotropes
76
Q

Signs of L-sided CHF

A

Low CO -> RAA and SNS activation -> fluid retention (up preload) and vasoconstriction (up afterload) -> Up LV end-diastolic P ->
Pulmonary edema and high PV pressure
Patient uses accessory muscles for breathing (like COPD)
Rales
Hemoptysis
Paroxysmal nocturnal dyspnea, orthopnea

77
Q

Signs of R-sided CHF

A

Dilated liver veins
JVD
Pitting edema, weight gain, fatigue

78
Q

Causes of HF

A 
Coronary atherosclerosis (about 1/2)
HTN
DM
Valvular disease
Alcohol
Infection
79
Q

HF diagnosis

A

Clinical exam
Echo
BNP levels up when RV/RA pressures up
CXR: cardiomegaly, vascular engorgement, Kerley B lines, pleural effusion

80
Q

Ejection fraction and heart failure

A

Normal over 50%
Mild less than 50%
Moderate less than 40%
Severe less than 30%

81
Q

Pericardium description

A

Double-layered fibroelastic sac w/ 15-50mL plasma ultrafiltrate filling it

82
Q

Causes of pericarditis

A

Idiopathic - most common
Infection - bacterial (TB/from HIV, pneumococcus, strep, staph, legionella), viral (coxsackie A/B, echo, mumps, adeno, HIV), fungal (histo, coccidio, candida, blasto)
Radiation
Neoplasm
Trauma
Autoimmune - SLE (drug associated w/ procainamide, isoniazid, hydralazine)
Metabolic - hypothyroidism or uremia
Cardiac - early infarction pericarditis, post-cardiac injury (Dressler’s), myocarditis, dissecting aortic aneurysm

83
Q

Pericarditis pathology

A

Usually serous fluid accumulation or exudate due to infection, may cause adhesions

84
Q

Pericarditis signs

A

Sharp, stabbing chest pain unrelated to exertion that’s worst laying flat
Pericardial friction rub, ECG changes, pericardial effusion, fatigue, dyspnea, may have fever

85
Q

Pericarditis evaluation - ECG and CXR

A

ECG shows inflammation of epicardium, not epicardium (electrically inert) = DIFFUSE ST-elevation and PR-depression, later duffuse T-inversions w/ normal STs and PRs; Also sinus tachycardia
Normal CXR

86
Q

Acute pericarditis complications

A

Pericardial effusion and tamponade
Constrictive pericarditis (late stage)
Relapse

87
Q

Acute pericarditis DDx

A

ACS, myocarditis, aortic dissection
Pleurisy, pneumonia, PE, pneumothorax
MSK or esophageal pain

88
Q

Pericarditis treatments

A

Idiopathic and viral: NSAIDs, colchicine
Post-acute MI: Aspirin, colchicine (avoid NSAIDs to allow scar formation)
Glucocorticoids, esp. for autoimmune

89
Q

Causes of pericardial effusion

A

Acute pericarditis
Radiation, malignancy
Cardiac perforation

Hypothyroidism
CT disease
Post-MI/heart surgery
Chronic renal failure
Aortic dissection
90
Q

Signs of pericardial effusion

A

Electrical alternans on ECG w/ sinus tach, low voltage
CXR shows new grossly enlarged heart
CHF symptoms w/ clear lungs = Edema, JVD

91
Q

Pericardial tamponade pathology

A

Pericardial fluid increases pressure, impedes diastolic filling of LV/RV -> SV, CO, BP down; HR up

92
Q

Pulsus paradoxus and its mechanism

A

Fall of systolic BP of at least 10mm w/ inspiration

Inspiration normally ups RV inflow, but w/ fluid compression, septum shifts and LV volume downed

93
Q

Pericardial tamponade findings

A

Sinus tach
Tachypnea
Hypotension, narrow pulse pressure, pulsus paradoxus
JVD w/ loss of Y-descent
Edema
ECG w/electrical alternanas and low voltage
EMERGENCY - perform pericardiocentesis

94
Q

Constrictive pericarditis pathophys, causes, signs, findings

A

Pericardial scarring -> Encasement, impaired diastolic filling of ventricles
Idiopathic, viral, cardiac surgery, radiation
‘Dip and Plateau’/’Square root’ sign on ECG
Unexplained R heart failure - may be misdiagnosed as cirrhosis
JVD, prominent x and y descents, pericardial knock, Kussmaul’s, anasarca
CXR shows pericardial calcification or thickening
Low voltage ECG w/ ST and T changes

95
Q

Kussmaul’s sign?

A

Lack of inspiratory decline in JVP = opposite of normal

96
Q

Constrictive pericarditis treatment

A

Diuretics, pericardial stripping

97
Q

Chronic ischemic heart disease risk factors

A

(Same as atherosclerosis)

Age, FH, DM, HTN, smoking, cholesterol, obesity, lack of exercise

98
Q

Metabolic syndrome

A

Any 3 of:

HTN, abdominal obesity, low HDL, high triglycerides, high fasting glucose

99
Q

Manifestations of coronary artery disease

A 
Chronic stable angina
Unstable angina
MI
CHF
Sudden cardiac death
Silent ischemia
100
Q

Typical angina features vs atypical angina

A

Substernal pain, brought on by exertion/stress, relieved by rest/NTG
Atypical missing one or more of these

101
Q

Chest pain DDx

A

Coronary artery disease, myocardial ischemia
Aortic dissection (sudden, bad pain, unequal pulse), hematoma
Pericarditis (Sharp, worse with inspiration)
PE (sudden dyspnea), pneumonia, pneumothorax, pleurisy
Esophageal spasm, inflam, or stricture; GERD (burning w/ meals)
Anxiety
Musculoskeletal (fleeting, reproduced w/ palpation)

102
Q

Non-atherosclerotic coronary artery diseases

A 
Coronary vasospasm - Prinzmetal angina
Anomalous coronary arteries
Coronary arteritis
Coronary dissection
Myocardial bridge (myocardium crosses one of coronary arteries)
Coronary embolization
103
Q

When to perform a stress test (or any test)?

A

When a positive or negative test result will determine the therapy the patient will receive

104
Q

Evaluation of ischemic heart disease

A

Confirm the diagnosis of CAD
Assess functional limitations due to symptoms
Assess modifiable risk factors
Assess the ischemic burden - how much muscle, how many vessels, how severe - can you revascularize?
Assess LV function

105
Q

Bad prognostic ST changes in stress tests

A

Worse signs: Greater magnitude, earlier timing, longer duration, more leads involved

106
Q

When to do stress imaging w/o exercise

A 
Patient can't exercise, has an abnormal ECG, or known CAD
Use dobutamine (ino-/chronotropic) or adenosine (coronary vasodilatation -> relative hypoperfusion of stenosed artery)
107
Q

Stress imaging findings indicative of high risk

A

Wall motion abnormalities in multiple coronary territories
Large wall motion abnormalities in single territory
LV dysfunction (low EF)

108
Q

When to do cardiac catheterization?

A

In patients with stenosis AND ischemia

W/o ischemia, don’t catheterize = medical therapy

109
Q

Ischemic heart disease management

A 
Aspirin
Sublingual NTG as needed
Lipid lowering therapy
Healthy lifestyle
Activity as dictated by symptoms
Report symptom changes immediately
110
Q

Risks for STEMI

A 
Age over 65y
At least 3 CAD risks
ST-deviation on ECG at admission
Prior coronary stenosis over 50%
At least 2 angina episodes in last 24h
Elevated cardiac markers
Aspirin use in last 7d
111
Q
  1. If ECG shows ST-elevation or new LBBB or true posterior MI, then … ?
  2. If ECG shows ST-depression or T-inversion?
A
  1. This is a STEMI

2. Are troponins raised? YES = NSTEMI, NO = Unstable angina

112
Q

T-inversion globally in leads may be a sign of what?

A

Intracranial hemorrhage

113
Q

STEMIs vs NSTEMIs and risk of death

A

STEMI patients are more likely to die in hospital

NSTEMI patients are more likely to die after being sent home inappropriately

114
Q

Nitrates mechanism, use, CIs

A

Up NO formation -> Up guanylate cyclase activity -> Up cGMP -> Vascular smooth muscle relaxation
For angina control
CI if on phosphodiesterase inhibitors (Viagra) or RV infarction (Hypotension, JVD, but clear lungs; ST-elev in R leads)

115
Q

Beta-blockers mechanism, use, CIs, ones to avoid

A

Decrease O2 demand (Down HR, Afterload, contractility) -> Down O2 deficit
Use in all patients w/ ACS unless CI (hypotension, bronchospasm, bradycardia, coronary spasm)
Avoid b-blockers w/ ISA (partial agonists)

116
Q

Aspirin substitutes?

A

Clopidogrel (Plavix)
Prasugrel - not as often used b/c of bleeding risk
Ticagrelor

117
Q

Heparin

A

Low MW heparin is better than unfractionated heparin for reducing risk in ACS

118
Q

GP IIb/IIIa inhibitors

A

Abciximab, intelligrin

ICM2 (5 decks)

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