Ischemic And Hypertensive HD Flashcards
Types of Ischemic Heart Disease
Angina pectoris
Myocardial infarction
Chronic IHD with heart failure
Sudden cardiac death
Ischemic Hear disease pathogenesis
Demand> coronary perfusion due to:
Fixed coronary obstruction
Acute plaque change
Coronary thrombus
Vasospasm
Fixed instructive lesion
> 75% cause symptomatic ischemia with exercise
> 90% cause symptomatic ischemia at rest
Acute plaque change
Rupture or fissuring
Erosion or ulceration
Hemorrhage into the atheroma
Coronary thrombus
Can cause partial occlusion to become total
Thromboangiitis are potent activators of smooth muscle growth-related signals (may contribute to atherosclerotic lesions)
Vasoconstriction
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
Angina Pectoris
Paroxysmal and usually recurrent attacks of substernal or precordial chest discomfort
Lasts 15 sec to 15 min
Due to myocardial ischemia
Stable angina
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
Unstable angina
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
Print metal angina
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
Myocardial infarction
2 of the acute coronary syndromes
90% of transmittal infarcts due to acute plaque disruption
Other 10% due to vasospasm +/- atherosclerosis or emboli
MI pathogenesis
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
Transmittal infarction
Most MIs are transmittal
Associated with atherosclerosis, acute plaque change, and completely obstructive thrombosis
CAUSE ST ELEVATION on EKG
Subendocardial infarct
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
Left anterior descending artery
Supplies most of apex, ant wall of left ventricle and ant 2/3 of ventricular septum
Left circumflex artery
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
Right coronary artery
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
Location of transmittal infarcts
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
Coronary artery bypass graft
Treatment fo rmyocaridal infarction
Revascularization of RCA via a sap genius vein graft and internal mammary artery grafting to the LAD
Thrombolytics therapy
Treatment for MI
Has no effect on underlying disrupted atherosclerotic plaque
Angioplasty (PTCA)
Treatment for MI
Can improve stenosis and help stabilize the disrupted plaque
Morphology of reperfused myocardium
Microscopic: contraction bands (intensely eosinophilic transverse bands of closely packed sarcomeres which contract when exposed to fresh Ca in plasma
MI laboratory
easier serum levels of intracellular proteins that leak out of fatally injured myocytes:
CK (MM and MB isozymes)
CK
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
Troponins
Cardiac specific proteins
Preferred bio markers for myocardial damage
Remain elevated for 7 to 10 days
MI consequences and complications
Contractile dysfunction causing hypotension, pulmonary vascular congestion
Arrhythmias Sinus bradycardia Asystole Tachycardia ventricular premature contractions Ventricular tachycardia Ventricular fibrillation
Myocardial rupture
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
Pericarditis
Consequence for MI
2-3 days: fibrinoid or fibrinohemorrhagic, pericardium overlying inflamed myocardium
Mural thrombus
Abnormal contractility or endocardium damage (may embolize)
Consequence of MI
Ventricular aneurysm
Consequence of MI
Result of large transmittal anteroseptal infarct
Complications: Mural thrombus Arrhythmias Heart failure Rupture is rare because scar tissue is strong
Anterior transmittal infarcts
Free-wall rupture, expansion, mural thrombus, and aneurysm, worse clinical course
Inferior transmittal infarcts
Conduction blocks, right ventricular involvement
Chronic ischemic heart disease
Coronary arteries: moderate to severe stenosis
Most patients have previous Mi or a final attacks when develop heart failure
Sudden Cardiac Death
3 of the acute coronary syndromes
Ultimate mechanism: lethal arrhythmia (asystole, V fib)
Systemic left-sided hypertensive heart disease
History of htn
Hypertrophy is adaptive response to pressure overload
Can lead to: Myocardial dysfunction Cardiac dilation CHF Sudden death
Systemic left-sided hypertensive heart disease morphology
Eventually wall stiffens and impairs diastolic filling and LA enlarges
Systemic left-sided hypertensive heart disease clinical
May present as atrial fibrillation (due to dilated LA) or CHF with atrial dilation or both
May be asymptomatic and picked up on EKG
Pulmonary right-sided hypertensive heart disease
RV hypertrophy
Due to pulmonary htn from disorders of lungs or pulmonary vasculature
Pulmonary hypertensive heart disease morphology
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
