on 20-Apr-2016 (Wed)

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#cardiology

Question

How do physiological mechanisms act to maintain arterial pressure and organ perfusion in CHF (failure of the cardiac pump)?

Answer

 Frank-Starling Mechanism: increase in end-diastolic ventricular volume increases tension in wall and enhances contractility

 Activation of the sympathetic nervous system
- Increase heart rate
- Increase myocardial contractility

 Activation of the renin-angiotensin system

 Myocardial adaptations, including hypertrophy and ventricular remodeling

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Question

The hypertrophied heart is vulnerable to [...]

Answer

decompensation

d/t:
 Increase in size of cardiac myocytes
 No proportional increase in capillary number!
 Oxygen consumption increased in hypertrophied heart but supply of oxygen and nutrients potentially more restricted

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Question

Differential Diagnosis of Cardiac Hypertrophy

Answer

Cardiomyopathic processes e.g. Hypertrophic cardiomyopathy
Volume overload processes e.g. Aortic insufficiency
Pressure overload processes e.g. Essential hypertension
Compensatory processes e.g. Atherosclerotic heart disease
Interstitial infiltrative processes e.g Amyloidosis
Storage disease processes e.g. Pompe Disease
Drugs e.g. Anabolic steroids

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Question

Physiological hypertrophy is:

Answer

increased size of cardiomyocytes without significant end organ damage (i.e. fibrosis)

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Question

Pathological hypertrophy is:

Answer

cardiomyocyte hypertrophy associated with both structural changes and molecular changes

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Question

Cardiac hypertrophy initially [...] but ultimately leads to [...]

Answer

decreases wall stress
decreased myocardial performance

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Question

What increases cardiac work? (4 things)

Answer

1) MI (regional dysfn w/ volume overload)
2) valvular ds (pressure and/or volume overload)
3) HTN (pressure overload)
4) cardiomyopathy (cellular contraction defect or myocarditis)

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Question

[...] → ↑ wall stress → cell stretch → hypertrophy and/or dilatation → systolic/diastolic dysfn

Answer

↑ cardiac work → ↑ wall stress → cell stretch → hypertrophy and/or dilatation → systolic/diastolic dysfn

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Question

↑ cardiac work → [...] → cell stretch → hypertrophy and/or dilatation → systolic/diastolic dysfn

Answer

↑ cardiac work → ↑ wall stress → cell stretch → hypertrophy and/or dilatation → systolic/diastolic dysfn

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Question

↑ cardiac work → ↑ wall stress → [...] → hypertrophy and/or dilatation → systolic/diastolic dysfn

Answer

↑ cardiac work → ↑ wall stress → cell stretch → hypertrophy and/or dilatation → systolic/diastolic dysfn

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Question

↑ cardiac work → ↑ wall stress → cell stretch → [...] → systolic/diastolic dysfn

Answer

↑ cardiac work → ↑ wall stress → cell stretch → hypertrophy and/or dilatation → systolic/diastolic dysfn

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Question

↑ cardiac work → ↑ wall stress → cell stretch → hypertrophy and/or dilatation → [...]

Answer

systolic/diastolic dysfn

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Question

Cardiomyopathy is:

Answer

a term used to describe heart disease resulting from an abnormality in the myocardium

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Question

Cardiac myopathy has multiple different etiologies:

Answer

 Primary cardiomyopathies represent diseases of the myocardium itself

 Secondary cardiomyopathies are other systemic disorders that also cause damage to the myocardium (e.g. Alcoholism, infectious myocarditis, thiamine deficiency, etc.)

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Question

What are the patterns of cardiomyopathy?

Answer

 Dilated cardiomyopathy (including arrhythmogenic right ventricular cardiomyopathy) - mix of genetic & acquired
 Hypertrophic cardiomyopathy - usually genetic (beta myosin chain)
 Restrictive cardiomyopathy - usually acquired (something causing stiffening of myocardium e.g. amyloid)

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Question

What are other causes of myocardial dysfunction or damage?

Answer

 Myocarditis - Infectious, Immune-mediated
 Cardiotoxic drugs - Cancer chemotherapy drugs, lithium, etc.
 Amyloidosis - Cardiac restricted (transthyretin), Systemic amyloidosis

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Question

fluid hemodynamics:
The capillary bed is the site of [...]

Answer

hemodynamic control

NB:
Arteriolar end – hydrostatic pressure predominates
Venular end – oncotic pressure predominates

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Question

fluid hemodynamics:
Exit of fluid at the [...] end is nearly balanced by influx of fluid at the venular end

Answer

arteriolar
venular

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Question

fluid hemodynamics:
Excess interstitial fluid is drained via [...]

Answer

lymphatics

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Question

CAUSES OF EDEMA

Answer

 Increased hydrostatic pressure: - Venous obstruction, congestive heart failure, arteriolar dilatation
 Reduced plasma oncotic pressure: - Cirrhosis, malnutrition, nephrotic syndrome
 Lymphatic obstruction
 Sodium Retention
 Inflammation

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Question

In Subcutaneous edema, Distribution is influenced by [...] and is most pronounced in the [...] parts of the body

Answer

gravity
dependant

NB: it may be the first clue to heart failure

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Question

pulmonary edema is Most commonly seen with [...]

Answer

left ventricular failure

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Question

Brain edema May be [...] or generalized (e.g. encephalitis, CSF outflow obstruction)

Answer

localized (e.g. with abscess or neoplasm)

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Question

Brain edema May be localized (e.g. with abscess or neoplasm) or [...]

Answer

generalized (e.g. encephalitis, CSF outflow obstruction)

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Question

CLINICAL CONSEQUENCES OF EDEMA

Answer

Effects range from merely annoying to fatal

 Subcutaneous edema most significant as a marker of an underlying problem with fluid hemodynamics
 Pulmonary edema can interfere with normal ventilatory function
 Severe brain edema can result in herniation and compression of critical structures

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Question

Obstruction to blood flow can take two forms:

Answer

 Obstruction to flow of blood through the heart (e.g. obstruction of a valve or great vessel)
 Obstruction to flow of blood to the heart (i.e. obstruction of a coronary vessel) - reducing blood supply to the heart when it needs it the most

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Question

Obstruction to blood flow through the heart is frequently due to problems with [...]

Answer

heart valves

E.g. Aortic valve stenosis, Congenital heart valve problems (e.g. Tricuspid atresia, bicuspid aortic valve), Endocarditis

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Question

A stenotic valve cannot open completely, thus hindering [...]

Answer

forward flow of blood

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Question

Valve stenosis can lead to [...] and can also lead to cardiac hypertrophy or potentially pump failure if untreated

Answer

increased work for the heart (pressure overload)

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Question

Valve stenosis can lead to increased work for the heart (pressure overload) and can also lead to [...] or potentially pump failure if untreated

Answer

cardiac hypertrophy

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Question

Valve stenosis can lead to increased work for the heart (pressure overload) and can also lead to cardiac hypertrophy or potentially [...] if untreated

Answer

pump failure

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Question

Obstruction to blood flow through coronary aa → MI
why?

Answer

Development of atherosclerotic plaque +/- thrombus (fixed or variable obstruction)

Occlusive thrombus on plaque (complete obstruction)

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Question

What is the triad of thrombosis?

Answer

hypercoagulability

abnormal blood flow

endothelial injury

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Question

What is the predominant cause of thrombosis?

Answer

Endothelial injury

-Particularly important for arterial or cardiac thrombus formation
-Frequently occurs over atherosclerotic plaques, or at sites of trauma or inflammatory vascular injury (vasculitis)
-May be due to physical disruption of endothelium with exposure of underlying collagen, or endothelial dysfunction

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Question

What types of abn blood flow can lead to thrombosis?

Answer

turbulence
-Contributes to arterial/cardiac thrombosis by promoting endothelial injury/dysfunction
-Also forms countercurrents and local pockets of static blood

stasis
-Major factor in the development of venous thrombi
-hyperviscosity

Turbulence and Stasis:
 Disrupt laminar blood flow
 Allow platelets to come into close contact with endothelium
 Prevent dilution of activated clotting factors
 Promote endothelial cell activation

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Question

Hypercoagulability is

Answer

Any alteration of the coagulation pathways that predisposes to thrombosis

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Question

What are causes of hypercoagulability?

Answer

Primary (genetic)
 Factor V Leiden
 Prothrombin mutation
 Homocysteinemia
 Protein C, S deficiency

Secondary (acquired)
 OCP, Pregnancy
 Smoking
 Prolonged immobilization
 Cancer

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Question

What is the fate of the thrombus?

Answer

Propagation
 Extension and growth of thrombus
 May eventually lead to vessel occlusion (bad with coronary aa)

Embolization
 Arterial vs. venous

Dissolution

Organization and recanalization (so thrombus may not cause much problem)

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Question

What is regurgitant blood flow?

Answer

Failure to maintain unidirectional flow of blood through the heart

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Question

[...] and [...] of blood flow through damaged valves may coexist

Answer

Obstruction
Regurgitation

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Question

Shunted blood flow is typically a ft of:

Answer

congenital cardiac anomalies, involving the heart and/or great vessels

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Question

Cardiac anomalies arise during gestational weeks [#] when major cardiovascular structures begin to form

Answer

3 - 8

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Question

Defects compatible with embryological development and maturation usually only affect [...] or [...]

Answer

one chamber
discrete region of the heart

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Question

What are different types of congenital cardiac anomalies?

Answer

 Malformations causing left-to-right shunt (more load on RV)
 Malformations causing right-to-left shunt (shunting de-O2 blood into systemic)
 Malformations causing an obstruction (e.g. coarctation of aorta w/ R to L shunt)

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Question

Type of arrhythmia depends on [...] to the conduction system and/or presence of [...]

Answer

location of disruption
ectopic foci of excitation

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Question

[...] is often a result of trauma, leading to massive loss of blood into body cavities, and shock

Answer

Rupture of the heart/great vessels

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Question

Rupture of the heart/great vessels is often a result of [...] , leading to massive loss of blood into body cavities, and shock

Answer

trauma

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Question

A smaller cardiac rupture may result in [...] into the [...]

Answer

leakage of blood
pericardial space

NB: can cause cardiac tamponade = mechanical restriction

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Question

Rupture of the great vessels may be seen with [2-3 things]

Answer

severe atherosclerotic or aneurysmal disease, diseases of collagen synthesis (i.e. Marfan syndrome, Ehlers-Danlos syndrome), etc.

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Question

What is shock?

Answer

Systemic hypoperfusion caused by reduction in effective circulating blood volume or cardiac output, resulting in impaired tissue perfusion and cellular hypoxia

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Question

What are causes of shock?

Answer

 Cardiogenic Shock (acute versions)
- Myocardial infarction, ventricular rupture, arrhythmia, cardiac tamponade, pulmonary embolism
 Hypovolemic Shock
- Hemorrhage, fluid loss, trauma, etc.
 (Septic Shock)
 (Neurogenic Shock)
 (Anaphylactic Shock)

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Question

What are the stages of shock?

Answer

1) initial non-progressive phase (compensatory mechanisms)
-Neurohumoral mechanisms act to maintain cardiac output and blood pressure
-Ex. Release of catecholamines, ADH, activation of reninangiotensin-aldosterone pathway, generalized sympathetic stimulation
-Net effect: tachycardia, peripheral vasoconstriction, renal conservation of fluid

2) progressive phase
-Widespread tissue hypoxia commences:

• ↓ pH due to lactic acid production (anaerobic glycolysis)
• ↓ vasomotor response with arteriolar dilatation and blood pooling in the peripheral circulation
• Vital organs begin to fail (AKI)

-clinically confused, urine output ↓

3) irreversible stage
-Widespread anoxic cellular injury occurs
 Leakage of lysosomal enzymes
 Marked electrolyte disturbances
 ↓ Myocardial contractility
 Complete renal shutdown due to acute tubular necrosis
 Multi-organ system failure ensues
 May develop disseminated intravascular coagulation

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Question

What are the 3 pathological distribution of atherosclerosis?

Answer

1) branch points
2) curvatures
3) regions of complex blood flow

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Question

Pathological Consequences of Atherosclerosis

Answer

1.Coronary artery disease
2.Abdominal aortic aneurysms
3.Cerebrovascular disease – stroke syndromes
4.Peripheral vascular disease
5.Mesenteric disease
6.Renovascular disease

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Question

the [...] is the master vascular regulator

Answer

endothelial cell

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Question

Pathophysiology of atherosclerosis:

[...] → endothelial dysfn → inflm cell recruitment → foam cell formation & fatty streaks (cycles w/ inflm cell recruitment) → intermediate lesion → fibrous plaque → thrombus formation

Answer

Pathophysiology of atherosclerosis:

toxic insult → endothelial dysfn → inflm cell recruitment → foam cell formation & fatty streaks (cycles w/ inflm cell recruitment) → intermediate lesion → fibrous plaque → thrombus formation

Tags

#cardiology #pathology

Question

Pathophysiology of atherosclerosis:

toxic insult → [...] → inflm cell recruitment → foam cell formation & fatty streaks (cycles w/ inflm cell recruitment) → intermediate lesion → fibrous plaque → thrombus formation

Answer

Pathophysiology of atherosclerosis:

toxic insult → endothelial dysfn → inflm cell recruitment → foam cell formation & fatty streaks (cycles w/ inflm cell recruitment) → intermediate lesion → fibrous plaque → thrombus formation

Tags

#cardiology #pathology

Question

Pathophysiology of atherosclerosis:

toxic insult → endothelial dysfn → [...] → foam cell formation & fatty streaks (cycles w/ inflm cell recruitment) → intermediate lesion → fibrous plaque → thrombus formation

Answer

Pathophysiology of atherosclerosis:

toxic insult → endothelial dysfn → inflm cell recruitment → foam cell formation & fatty streaks (cycles w/ inflm cell recruitment) → intermediate lesion → fibrous plaque → thrombus formation

Tags

#cardiology #pathology

Question

Pathophysiology of atherosclerosis:

toxic insult → endothelial dysfn → inflm cell recruitment → [...] → intermediate lesion → fibrous plaque → thrombus formation

Answer

Pathophysiology of atherosclerosis:

toxic insult → endothelial dysfn → inflm cell recruitment → foam cell formation & fatty streaks (cycles w/ inflm cell recruitment) → intermediate lesion → fibrous plaque → thrombus formation

Tags

#cardiology #pathology

Question

Pathophysiology of atherosclerosis:

toxic insult → endothelial dysfn → inflm cell recruitment → foam cell formation & fatty streaks (cycles w/ inflm cell recruitment) → [...] → fibrous plaque → thrombus formation

Answer

Pathophysiology of atherosclerosis:

toxic insult → endothelial dysfn → inflm cell recruitment → foam cell formation & fatty streaks (cycles w/ inflm cell recruitment) → intermediate lesion → fibrous plaque → thrombus formation

Tags

#cardiology #pathology

Question

Pathophysiology of atherosclerosis:

toxic insult → endothelial dysfn → inflm cell recruitment → foam cell formation & fatty streaks (cycles w/ inflm cell recruitment) → intermediate lesion → fibrous plaque → [...]

Answer

thrombus formation

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Question

What is the spectrum of lesions in atherosclerosis?

Answer

1.Stable eccentric atheroma, with:
a. Thin fibrous cap overlying necrotic lipid core (vulnerable plaque)
b. Stable fibromuscular plaque
c. Stable fibrocalcific plaque
2.Acute plaque hemorrhage with rapid expansion of plaque
3.Atherosclerosis with non‐occlusive luminal thrombus
4.Atherosclerosis with occlusive luminal thrombus
5.Atherosclerosis with recanalized, organized thrombus
6.Atherosclerosis with obliterated lumen

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Question

What are the typical ft's of atheresclerosis?

Answer

• Typical eccentric plaque
• Necrotic core (outgrow blood supply)
• May have thin fibrous cap
• Chronic inflammation common
• Remodelling of vessel wall common
• Luminal stenosis (here severe)
• Calcification common

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Question

What is an acute myocardial infarction?

Answer

• kills by causing heart failure or arrhythmia (via ischemia)
• acute coagulative necrosis
• Usually localizes to vascular territory perfused by occluded artery
• Left ventricle most often effected
• Starts in subendocardial zone and may become transmural

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Question

Early myocardial ischemia / infarction shows [...] on histology

Answer

contraction bands
-takes 6h to develop

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Question

When do you start to see acute inflm in early MI?

Answer

>12-16 hours

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Question

Early healing myocardial infarction shows [...] and [...] on histology

Answer

macrophages
loss of cardiomyocytes

-takes place after >1 day
-moving in of chr inflm cells
-fibroplasia to stabilize wall (can cause arrhythmia)

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Question

Complications of an Acute Myocardial Infarction

Answer

Arrhythmia / sudden death (~20%)
Free wall or septal rupture / hemopericardium (tamponade)
Mitral insufficiency / acute heart failure
Papillary muscle rupture (→ acute valvular insufficiency - can kill you quickly)
Aneurysm / mural thrombus / embolism
Congestive heart failure (long term)

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Question

With chr ischemia, there is [...] and [...] without history of myocardial infarction

Answer

Myocardial fibrosis
degeneration

-myocardium in survival mode; no fn

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Question

Any coronary artery luminal stenosis of [...] % significantly increases the risk of sudden and unexpected death at any time

Answer

> 70‐75

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Question

Any coronary artery luminal stenosis of > 70‐75% significantly increases the risk of [...]

Answer

sudden and unexpected death at any time

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Question

Any coronary artery luminal stenosis of > 70‐75% significantly increases the risk of sudden and unexpected death at any time – especially when..

Answer

there exists a supply vs. demand mismatch such as with exercise, emotional stress, etc

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Question

What are 3 atherosclerotic aortic ds's?

Answer

aortic dissection (most d/t HTN)
intramural hematoma
penetrating aortic ulcer

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Question

What is atheroembolic ds?

Answer

bits of plaque get released and occlude little vessels down stream (can → acute renal failure)

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Question

What is "trash foot"?

Answer

Ulcerations & gangrene on the feet d/t atheroemboli occluding small vessels after catherization

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Question

What is a coronary atheroma?

Answer

Buildup of cholesterol, calcium, and inflammatory cells

Results in coronary artery narrowing

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Question

The largest risk factor of coronary artery ds is [...]

Answer

Age

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Question

What are the big 5 risk factors for CAD ?

Answer

1. cigarette smoking
2. hyperlipidemia
3. diabetes
4. hypertension
5. family history of premature CAD

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Question

Smoking is associated w/ [2 things]

Answer

acute plaque rupture (d/t accelerated plaque progression) and heart attack
-very important risk factor @ young age

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Question

What is angina?

Answer

symptom due to myocardial ischemia from myocardial oxygen demand exceeding supply

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Question

What are ft's not characteristic of angina?

Answer

• Location: solely middle/lower abdomen, radiates into lower extremities, localized to one finger tip
• Character: reproduced by movement or palpation, pleuritic (sharp brought on by respiration)
• Duration: very brief (few seconds or less), constant for many hours

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Question

Aggravating and alleviating factors of angina?

Answer

precipitants:
• Exercise
• Emotion
• Eating
• Cold
• Sexual activity

relievers:
• Rest
• Nitroglycerin (vasodilator)

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Question

How is severity of angina classified?

Answer

I
No limitation to ordinary activity.
Angina with strenuous, rapid or prolonged exertion

II
Slight limitation to ordinary activity
Angina walking > 2 level blocks or > 1 flight of stairs

III
Marked limitation to ordinary activity
Angina walking < 2 level blocks or < 1 flight

IV
Inability to carry out any activity.
Angina may be present at rest

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Question

What are the classifications of angina?

Answer

Typical angina (definite) - needs to meet all 3 criteria
1) substernal chest discomfort - burning, tightness, squeezing
2) provoked by exertion or emotional stress and
3) relieved by rest or nitroglycerin

Atypical angina (probable)
-meets 2 of the of characteristics

Noncardiac chest pain
-meets ≤ 1 of the typical angina characteristics

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Question

The pre-test probability is based on [3 things]

Answer

age
sex
classification of angina (typical, etc)

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Question

What types of diagnostic testing do we do for angina?

Answer

functional
-exercise stress test
-nuclear test
-stress ECHO

structural
-coronary angiogram
-CT coronary angiogram

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Question

What 2 components do all functional tests (for angina) have?

Answer

Stress – some method of increasing myocardial demand (by dropping resistance)
Test – some measure of adequacy of blood supply (ECG, Nuclear, ECHO - imaging the resulting flow)

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Question

How can we induce stress for functional tests?

Answer

Exercise (most common)

Pharmacologic stresses (if can't exercise)
– Dobutamine (beta agonist) - causes HR to go up, and causes heart to contract more vigorously -> higher demand (checks can epicardial aa supply enough)

Vasodilators
– Persantine
– Adenosine

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Question

Coronary flow is autoregulated by [...]

Answer

arteriolar smooth muscle tone

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Question

How much stenosis is required to bring on exercise & rest chest pain?

Answer

exercise pain @ 70%
rest pain @ 90%

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Question

What is the ischemic cascade?

Answer

Different things you can measure as ischemia progresses over time:
1) blood flow changes (Nuclear)
2) wall motion abnormalities (ECHO)
3) ECG changes (ECG)
4) pain (symptomatic) - very last

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Question

Describe the 3 functional tests for angina

Answer

Exercise treadmill stress test
-Treadmill protocol (most common: Bruce) - speed & incline gradually increases every few min
- 65% accurate for severely narrowed arteries (so not very good)
-Assess for symptoms, and changes in blood pressure and ECG

Nuclear testing
-IV radioactive tracers (don't want to do too many in esp young women)
-Taken up by myocardium proportional to blood flow
-Emits radiation which can be measured
-85% accuracy (more accurate, more expensive)
-if change at rest vs stress, reversible defect = ischemia
-if no change at rest/stress, fixed defect = prior infarct

ECHO (u/s) testing
-Normal heart muscle thickens 50% when it contracts
-Abnormal heart thickening referred to as “wall motion abnormality”
-Wall motion abnormalities during stress but not at rest suggest ischemia
-90% accuracy, also expensive

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Question

What are the 2 structural tests for angina?

Answer

Coronary angiography
-Gold standard (100% accuracy)
-Invasive
-1:1000 risk of serious complications

CT coronary angiogram
-CT scan with contrast opacification of coronary arteries
-95-98% accurate

Tags

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Question

Bayes theorem:
A tests predictive value is dependent on [...]

Answer

pretest probability

NB:
pre-test probability - 10% -> 50% (w/ +ve test) or 1% (w/ -ve test)
- 50% -> 90% (+ve) or 10% (-ve)
- 90% -> 99% (+ve) or 50% (-ve)

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Question

Non‐pharmacologic treatment of Stable CAD

Answer

• Exercise
• Weight loss
• Mediterranean diet (fruits, vegetables, olive oil, nuts, fish)
• Smoking cessation

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Question

Pharmacologic treatment of Stable CAD

Answer

• Risk factor modification: Treat diabetes, hypertension, dyslipidemia (statins) - rx these aggressively
• Antiplatelet: aspirin - to prevent acute events from plaques
• Anti‐anginals
– Beta‐blockers (e.g. bisoprolol) - first line
– Nitrates (sublingual spray, patch, pills) - vasodilators
– Calcium channel blockers (e.g. amlodipine) - also vasodilates

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Question

What are 2 ways of revascularization in CAD?

Answer

Percutaneous Coronary Intervention - stents
• Bare metal stents
– Stainless steel
• Drug eluting stents
– Stainless steel/Platinum chromium
– Drugs (anticancer drugs to prevent cell growth into stents)
• Everolimus
• Zotarolimus

Coronary Artery Bypass Grafting
• Internal mammary and saphenous vein grafts used to bypass blockages

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Question

What are the 2 classes of acute coronary syndromes (ACS)?

Answer

Unstable angina

MI
-STEMI
-non-STEMI

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Question

What is unstable angina?

Answer

Clinical syndrome characterized by new or worsened coronary ischemia

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Question

What is an MI?

Answer

Myocardial necrosis due to coronary artery occlusion

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Question

What shows ST-elevation?

Answer

STEMI

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Question

What shows no ST-elevation?

Answer

non-STEMI
unstable angina

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Question

In general, [...] imply more loss of myocardium

Answer

Q waves

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Question

In general, Q waves imply [...]

Answer

more loss of myocardium

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Question

Central mechanism of ACS is [...]

Answer

Plaque Rupture

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Question

[...] is pathognomonic of infarction

Answer

Acute ST elevation is pathognomonic of infarction

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Question

Acute ST elevation is pathognomonic of [...]

Answer

Acute ST elevation is pathognomonic of infarction

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Question

Chest pain [how long] suggests infarction

Answer

> 20 min to hours

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Question

What falls under unstable angina?

Answer

• New onset angina
• Accelerated angina (classic)
– Decreasing exercise capacity
– Increased duration, frequency
– Crescendo angina
• Rest angina
• Post-MI

NB: these pt's likely have ruptured plaque

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Question

What ECG findings would you see with unstable angina/non-STEMI?

Answer

• Normal
• T inversion
• ST depression

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Question

What ECG findings would you see with STEMI?

Answer

• ST elevation
• New LBBB

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Question

Which ECG leads measure what wall of the heart and function of which vessel?

Answer

V1 – V4	Anterior Wall	LAD
II, III, aVF	Inferior Wall	RCA
V5 – V6	Lateral Wall	Circumflex

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Question

What cardiac enzymes are Reasonably specific for myocardial damage?

Answer

• Creatine Kinase; CK-MB (myocardial)
• Troponin: T and I

Elevated within 4 – 6 hours if necrosis

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Question

What are symptomatic therapies for ACS?

Answer

• Rest
• O2
• Pain control
– Nitroglycerine
– morphine

Tags

#cardiology #exam

Question

What therapies improve survival in ACS?

Answer

Thrombus: Heparin

Platelets (dual-antiplt therapy):
1) ASA
2) clopidogrel/Prasugel/Ticagrelor (some 2nd agent)
3) IIb/IIIa inhibitors (not used much)

Beta-blockers

CAD (long term improvement): statins, ACE-inhibitors

Education

Regular exercise

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#cardiology #exam

Question

What are important mimics of MI?

Answer

pulmonary embolus (most common)
pericarditis (assc w/ ST elevation)
aortic dissection (get chest pain)
NB: heparin is contraindicated in the above 2

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Question

What are complications of MI?

Answer

tachyarrhythmia
bradyarrhythmia
LV failure
myocardial rupture (3-7days)
pericarditis
RV failure
stroke

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#cardiology

Question

What is the STEMI therapy?

Answer

• Principles of non-ST elevation ACS apply

• Reperfusion is the goal

• Anti-platelet therapy
• Heparin
• Beta-blockers

• Treat underlying CAD

Tags

#cardiology

Question

How can you provide reperfusion in STEMI?

Answer

thrombolytic therapy (being replaced by primary angioplasty)
– TNK (tenectaplase)
– t-PA (tissue plasminogen activator)
– Streptokinase

Coronary Angioplasty
• Provides prompt anatomic information
• Establish patency mechanically
• Most reliable vessel patency if prompt