m5 (1/4) - angina and acute coronary syndrome

ppt 5A

atherosclerosis

disease where fats and cholesterols such as LDLs build up into hard plaques inside arterial walls

blood vessel layer affected in atherosclerosis and what the disease results in

disease of the arteries’ tunica intima, forming fibrous fatty lesions. results in thicker artery walls with less elasticity, reduced blowflow and ischemia to related organs

etiology of atherosclerosis

endothelial (blood vessel) cell damage (smoking, diabetes, turbulent blood flow) causes increased endothelial permeability. leukocytes and monocytes migrate to the area

• monocytes differentiate to macrophages, ingest lipid to become lipid-filled foam cells

• macrophages also release growth factors proliferating smooth muscle

• tissues progressively become damaged and plaque lesion grows

LDLs

low density lipoproteins - a transport form of lipids in the blood

relationship between LDLs and foam cells

monocytes differentiate into macrophages → macrophages phagocytize LDLs and become lipid filled foam cells

progression of atherosclerotic plaque

1. lesion initiation

2. fatty streak

3. fibrous plaque

4. plaque rupture

there is a strong association between high levels of _____ and coronary artery disease

plasma LDLs

list some predisposing risk factors for atherosclerosis

• obesity

• diabetes

• elevated cholesterol

• smoking

• sedentary lifestyle

CAD

coronary artery disease (causes 1/3rd of all deaths in the west)

name of heart disease that CAD causes

ischemic heart disease (IDH)

IHD

(ischemic heart disease)

involves ischemia (reduced blood supply) of heart muscle

structure that coronary arteries originate from on the heart

aorta

structures that the right coronary artery supplies

right ventricle, posterior areas of heart

structures that the left coronary artery supplies

left ventricle, interventricular septum

myocardial bloodflow

• structures it mainly concerns

• mechanisms (2)

bloodflow of the heart muscle - mechanisms produce vasodilation or vasoconstriction of coronary blood vessels

• autonomic NS control (sympathetic, parasympathetic)

• local autoregulatory control

myocardial bloodflow: local autoregulation

• definition

• particles that are released, their effects

• what it meets the demands of

major control of myocardial bloodflow, producing either vasodilation or vasoconstriction of coronary blood vessels (vasodilation carried out with nitric oxide and adenosine)

• meets metabolic and oxygen demands of cardiac muscle

myocardial bloodflow is highest during [diastole / systole]

[diastole] - relaxing phase when heart chambers refill with blood

impact of coronary artery disease on myocardial bloodflow

• region of heart muscle most affected and why

• when does the impacted bloodflow become most apparent: diastole or systole?

subendocardial region of muscle gets damaged - cannot obtain adequate bloodflow

• reduced bloodflow is most apparent in systole (ventricles contracting) when muscle compresses muscle capillaries

anastomoses

collateral vessels where blood vessels unite to form intersections for bloodflow to a region - can protect the heart by providing alternative bloodflow path in acute ischemia

pathogenesis of atherosclerosis causing IHD

1. atherosclerotic plaque develops in the coronary arteries

2. plaque begins protruding into vessel lumens

3. begins to reduce bloodflow, causing ischemia

   1. plaque narrowing the vessel leads to stable angina

   2. plaque can rupture, forming thrombus and leading to ACS (acute coronary syndrome)

ACS

• duration of pain

• relieved by short-acting vasodilators?

• recovery vs no recovery

acute coronary syndrome - emergency (hence, acute) condition of severe blockage of bloodflow to the heart. is a spectrum of ischemic heart diseases

• pain lasting over 20 min, may increase in severity

• not relieved by short-acting vasodilators

• recovery means temporary effects

• no recovery means it can lead to MI/heart attack

2 main types of ACS

• unstable angina

• myocardial infarction

  1. STEMI

  2. nonSTEMI

stable angina

• plaque

• pain: predictable or unpredictable

• temporary or permanent

• long-lasting or short term

• myocardial ischemia: necrosis?

• treatment

stable

• plaque intact, w/ partial obstruction

• predictable pain from physical exertion, emotional stress

• myocardial ischemia is temporary, no necrosis

• short-term, less than 15 min (w/ rest)

• treatment of GTN (glycerol trinitrate) vasodilator

unstable angina

• plaque

• pain: predictable or unpredictable

• temporary or permanent

• long-lasting or short term

• myocardial ischemia: necrosis?

• treatment

• unstable plaque → small thromboses

• unpredictable, sudden chest pain

• temporary myoardial ischemia; no necrosis

• more severe, longer-lasting pain (>20 minutes)

• hospitalization, nitrates/vasodilator, aspirin (reduce clotting)

what unstable angina may predict/lead to

MI (myocardial infarction) aka heart attack

MI

myocardial infarction - heart attack from severe coronary occlusion

relationship btwn MI and ischemia, necrosis

MI causes severe blockage of the coronaries, leading to acute ischemia in myocardium which can lead to necrosis if not corrected

STEMI

• definition, change it produces in the heart

• affect on ECG

• intervention required

type of myocardial infarction where thrombus formed from ruptured plaque becomes lodged in the vessel, causing the entire myocardium thickness to become ischemic (complete blockage)

• ST segment on ECG is elevated

• requires emergency intervention

nonSTEMI

• definition, change it produces in the heart

• affect on ECG

type of myocardial infarction where thrombus formed from ruptured plaque partially blocks bloodflow

• only affects subendocardium - thrombus may disintegrate before tissue undergoes necrosis

• does not show persistent ST elevation; ST depression or T wave inversion may appear instead

diagnostic features of MI (2)

1. STEMI vs nonSTEMI ECG

2. serum cardiac biomarkers (troponin T)

list general manifestations of ACS

• tachycardia

• fatigue and weakness

• crushing pain: substernal, jaw, left arm, neck

• pale, cool, moist skin

or “silent MI” - no symptoms

3 causes of death in MI

1. decreased cardiac output

2. heart fibrillation

3. heart rupture

decreased cardiac output as a cause of MI death

• what other issues arise prior to shock

• type of shock occurring

pumping ability is reduced and cannot meet tissue needs. heart failure and peripheral ischemia occurs

shock = cardiogenic shock

ventricular fibrillation as a cause of MI death

• definition

• what cardiac output is during vfib

• ventricles quiver, erratic electrical impulses uncoordinatedly pump blood and myocardium is damaged

• cardiac output is ZERO

rupture of infarction as a cause of MI death

• when it occurs after infarction and why

• _____ ____ increases until the heart ruptures

• method of assessing severe MI

• occurs several days after infarction: muscle fibres necrose, degenerate

• [systolic stretch] increases until heart ruptures

• cardiac imaging to monitor

main cause of death in STEMI

VFIB

immediate care of ACS management

rANBop

• rest

• pain relief

• anticoagulant therapy (aspirin)

• nitroglycerin (GTN)

• beta blockers - slow HR, lengthen diastole

• oxygen therapy

explain using medical terminology why absolute body rest is important in ACS management

ACS places additional pressure and strain on the heart due to a thrombus or infarct; this can create ischemia that the body attempts to reverse by generating more force. decreasing the workload via resting can decrease injury from ischemia

explain why collateral circulation is important in ACS management, and why bedrest is important to maintain it

collateral circulation provides alternative pathways for bloodflow to assist damaged muscle during recovery. if the heart is highly active, coronary arteries can dilate and bypass this collateral circulation system to directly supply healthy muscle instead, which can slow recovery for injured tissues

explain the importance of pain relief in ACS management

an ischemic myocardium can produce severe crushing chest pain, and can increase the sympathetic response, increasing stress → cardiac output → workload on the heart

crushing chest pain in ACS may be related to the release of _____ ____ (because of…) and _______ mediators

[lactic acid - anaerobic respiration] [inflammatory mediators]

reperfusion strategies in ACS management

• stents and thrombectomies (percutaneous coronary intervention)