Ischemic And Hypertensive HD

Question 1

Types of Ischemic Heart Disease

Answer 1

Angina pectoris
Myocardial infarction
Chronic IHD with heart failure
Sudden cardiac death

Question 2

Ischemic Hear disease pathogenesis

Answer 2

Demand> coronary perfusion due to:

Fixed coronary obstruction
Acute plaque change
Coronary thrombus
Vasospasm

Question 3

Fixed instructive lesion

Answer 3

> 75% cause symptomatic ischemia with exercise

> 90% cause symptomatic ischemia at rest

Question 4

Acute plaque change

Answer 4

Rupture or fissuring
Erosion or ulceration
Hemorrhage into the atheroma

Question 5

Coronary thrombus

Answer 5

Can cause partial occlusion to become total

Thromboangiitis are potent activators of smooth muscle growth-related signals (may contribute to atherosclerotic lesions)

Question 6

Vasoconstriction

Answer 6

Can cause a partial obstruction to become total

Stimulated by:
Adrenergic agonists
Impaired secretion of endothelial cell relaxing factors
Mediators released from perivascular inflammatory cells

Question 7

Angina Pectoris

Answer 7

Paroxysmal and usually recurrent attacks of substernal or precordial chest discomfort

Lasts 15 sec to 15 min

Due to myocardial ischemia

Question 8

Stable angina

Answer 8

Decreased coronary perfusion due to fixed obstruction

Makes heart vulnerable to ischemia caused by physical activity or emotional excitement

Usually relieved by rest or nitroglycerin

Question 9

Unstable angina

Answer 9

1 of ACUTE CORONARY SYNDROMES

Chest pain that occurs with increasing frequency and precipitated by progressively less effort

Due to disruption of atherosclerotic plaque with superimposed partially occluding thrombus

Question 10

Print metal angina

Answer 10

Due to coronary artery spasm

Episodic, may occur at rest

Not related to physical activity, heart rate or blood pressure

Ry: Nitroglycerin and Ca channel blockers

Question 11

Myocardial infarction

Answer 11

2 of the acute coronary syndromes

90% of transmittal infarcts due to acute plaque disruption

Other 10% due to vasospasm +/- atherosclerosis or emboli

Question 12

MI pathogenesis

Answer 12

First seconds: cessation of aerobic glycolysis and decreased creatine phosphate and ATP

> 2 min: loss of contractility begins, may precipitate acute heart failure- changes are still reversible at this point

20-40 min: irreversible injury to myocytes

> 1 hr: microvascular injury

Necrosis complete by 6 hrs

Question 13

Transmittal infarction

Answer 13

Most MIs are transmittal

Associated with atherosclerosis, acute plaque change, and completely obstructive thrombosis

CAUSE ST ELEVATION on EKG

Question 14

Subendocardial infarct

Answer 14

Infarct of inner 1/3-1/2 ventricular wall

area that is least well perfused

Due to atherosclerosis

NO PLAQUE DISRUPTION
NO SUPERIMPOSED THROMBUS

Non-ST elevation

Question 15

Left anterior descending artery

Answer 15

Supplies most of apex, ant wall of left ventricle and ant 2/3 of ventricular septum

Question 16

Left circumflex artery

Answer 16

Supplies lateral wall of left ventricle

If it gives rise to post descending artery (left dominant): supplies post 1/3 of ventricular septumand posterobasal wall of left ventricle

Question 17

Right coronary artery

Answer 17

Supplies entire right ventricular wall

If gives rise to post descending artery (right dominant) supplies posterior 1/3 of ventricular septum and posterobasal wall of left ventricle

Question 18

Location of transmittal infarcts

Answer 18

Almost always involve left ventricle

LAD 40-50% of infarcts

RCA 30-40% infarcts:
Inferior-posterior wall of left ventricle
Posterior portion of ventricular septum

Question 19

Coronary artery bypass graft

Answer 19

Treatment fo rmyocaridal infarction

Revascularization of RCA via a sap genius vein graft and internal mammary artery grafting to the LAD

Question 20

Thrombolytics therapy

Answer 20

Treatment for MI

Has no effect on underlying disrupted atherosclerotic plaque

Question 21

Angioplasty (PTCA)

Answer 21

Treatment for MI

Can improve stenosis and help stabilize the disrupted plaque

Question 22

Morphology of reperfused myocardium

Answer 22

Microscopic: contraction bands (intensely eosinophilic transverse bands of closely packed sarcomeres which contract when exposed to fresh Ca in plasma

Question 23

MI laboratory

Answer 23

easier serum levels of intracellular proteins that leak out of fatally injured myocytes:

CK (MM and MB isozymes)

Question 24

CK

Answer 24

Rises in first 2 to 4 hrs

Peaks at 24 hrs

CK-MB is sensitive but not specific since it is also found in skeletal muscle

Question 25

Troponins

Answer 25

Cardiac specific proteins Preferred bio markers for myocardial damage Remain elevated for 7 to 10 days

Question 26

MI consequences and complications

Answer 26

Contractile dysfunction causing hypotension, pulmonary vascular congestion ``` Arrhythmias Sinus bradycardia Asystole Tachycardia ventricular premature contractions Ventricular tachycardia Ventricular fibrillation ```

Question 27

Myocardial rupture

Answer 27

3-7 days after MI Of ventricular free wall-(most common) cardiac tamponade Of ventricular septum (less common)- left to right shunting Of papillary muscle (least common)- severe mitral regurgitation

Question 28

Pericarditis

Answer 28

Consequence for MI 2-3 days: fibrinoid or fibrinohemorrhagic, pericardium overlying inflamed myocardium

Question 29

Mural thrombus

Answer 29

Abnormal contractility or endocardium damage (may embolize) Consequence of MI

Question 30

Ventricular aneurysm

Answer 30

Consequence of MI Result of large transmittal anteroseptal infarct ``` Complications: Mural thrombus Arrhythmias Heart failure Rupture is rare because scar tissue is strong ```

Question 31

Anterior transmittal infarcts

Answer 31

Free-wall rupture, expansion, mural thrombus, and aneurysm, worse clinical course

Question 32

Inferior transmittal infarcts

Answer 32

Conduction blocks, right ventricular involvement

Question 33

Chronic ischemic heart disease

Answer 33

Coronary arteries: moderate to severe stenosis Most patients have previous Mi or a final attacks when develop heart failure

Question 34

Sudden Cardiac Death

Answer 34

Ultimate mechanism: lethal arrhythmia (asystole, V fib) #3 of the acute coronary syndromes

Question 35

Systemic left-sided hypertensive heart disease

Answer 35

History of htn Hypertrophy is adaptive response to pressure overload ``` Can lead to: Myocardial dysfunction Cardiac dilation CHF Sudden death ```

Question 36

Systemic left-sided hypertensive heart disease morphology

Answer 36

Eventually wall stiffens and impairs diastolic filling and LA enlarges

Question 37

Systemic left-sided hypertensive heart disease clinical

Answer 37

May present as atrial fibrillation (due to dilated LA) or CHF with atrial dilation or both May be asymptomatic and picked up on EKG

Question 38

Pulmonary right-sided hypertensive heart disease

Answer 38

RV hypertrophy Due to pulmonary htn from disorders of lungs or pulmonary vasculature

Question 39

Pulmonary hypertensive heart disease morphology

Answer 39

Acute: RV dilates NO increase in wall thickness Chronic: Ventricular wall thickens May compress LV chamber Tricuspid regurgitation may occur due to fibrous thickening of valve