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ISCHEMIC HEART DISEASE; CONGESTIVE HEART FAILURE; SHOCK. Coronary Artery Disease. Vascular disorder  narrowing/blockage of arteries to heart Arteries supplying heart branch directly from aorta Bring richly oxygenated blood Necessary to supply myocytes with oxygen, nutrients

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coronary artery disease
Coronary Artery Disease
  • Vascular disorder  narrowing/blockage of arteries to heart
    • Arteries supplying heart branch directly from aorta
      • Bring richly oxygenated blood
      • Necessary to supply myocytes with oxygen, nutrients
      • Heart needs constant supply of oxygen for muscle activities
slide5
Coronary artery disease  decr'd blood supply to cardiac muscle (Fig. 23-21)
    • So ischemia
    • Persistent ischemia  hypoxia
    • Infarction leads to “heart attack”
      • About 50% of all deaths in U.S.
  • Heart has high metabolic rate
    • Constantly contracting to pump oxygenated and nutrient-filled blood to rest of body
    • Urgent to life to maintain the health of heart, so
    • Urgent to life to maintain oxygen-rich blood flow to heart
slide6
Modifiable/nonmodifiable factors put some people more at risk than others
    • Same as for vascular disease:
      • Hyperlipidemia - incr'd plasma lipoproteins
      • Hypertension - may cause or exacerbate
      • Cigarette smoking - STOP!!
      • Diabetes
myocardial ischemia results
Myocardial ischemia results
  • Decr’d blood flow to heart (Fig.23-14)
  • Myocardial cell metabolic demands not met
  • Time frame of coronary blockage
    • 10 seconds following coronary block
      • Decr’d strength of contractions
      • Abnormal hemodynamics
    • Several minutes later
      • Decr’d glucose metab  decr’d aerobic metab, so
      • Anaerobic metab, so
      • Build-up of lactic acid (toxic within cell)
slide8
Time frame – cont’d
    • 20 minutes after blockage
      • Myocytes still viable, so
      • If blood flow restored, and incr’d aerobic metab, and cell repair,
      •  Incr’d contractility
    • About 30-45 minutes after blockage, if no relief
      • Cardiac infarct
slide9
Clinical
    • May hear extra, rapid heart sounds (S3)
    • ECG changes (Fig.23-18)
      • T wave inversion
      • ST segment depression
    • Chest pain
      • 20-30% of those suffering myocardial ischemia
      • Called angina pectoris
      • Feeling of heaviness, pressure
      • Moderate  severe
      • In substernal area
      • Often mistaken for indigestion
      • May radiate to neck, jaw, left arm/shoulder
slide11
Chest pain – cont’d
      • Due to
        • Accum’n lactic acid in myocytes, OR
        • Stretching of myocytes
      • Three types: stable, unstable, Prinzmetal
        • See p 645
  • Treatment
    • Pharmacologically manipulate bp, hr, contractility to decr oxygen demand of myocytes
      • Nitrates dilate peripheral blood vessels, and
        • Decrease oxygen demand
        • Increase oxygen supply
        • Relieve coronary spasm
slide12
Pharmacological treatment – cont’d
    • Beta blockers
      • Block sympathetic input, so
      • Decrease heart rate, so
      • Decrease oxygen demand
    • Digitalis
      • Increases force of contraction
  • Surgical
    • Angioplasty – mechanical opening of vessels
    • Revascularization (bypass)
      • Replace, shunt around occluded vessels
myocardial infarction endpoint
Myocardial infarction – endpoint
  • Necrosis of cardiac myocytes
    • Irreversible
    • Commonly affects left ventricle
    • Follows 30-45 mins unrelieved ischemia
    • Wound repair signalled
  • Structural, functional changes in heart tissue
    • Decr'd contractility
    • Decr'd LV compliance
    • Decr'd stroke volume
    • Dysrhythmias
slide15
Inflammatory response severe due to wound repair signals
    • Fibroblast proliferation to begin scar tissue formation
    • Leukocytes migrate to site of repair (myocytes)
    • Proteolytic enzymes released, degrade injured cells and dysfunctional biochemicals
    • Insulin secreted to increase glucose uptake, metabolism in myocytes
      • Aids repair
slide18
Scarring results
    • Tissue now strong but stiff
    • Can’t contract like healthy cells
  • Clinical
    • Sudden, severe chest pain
      • Similar to pain with ischemia but stronger
      • Not relieved by nitrates
      • Heavy, crushing
      • Radiates to neck, jaw, shoulder, left arm
    • Indigestion, nausea/vomiting
    • Abnormal heart sounds possible (S3,S4)
slide19
Clinical – cont’d
    • Blood tests show several markers:
      • Leukocytosis
      • Increased blood sugar
      • Increased plasma enzymes
        • Creatine kinase (CPK)
        • Lactate dehydrogenase (LDH)
        • Aspartate aminotransferase (AST or SGOT)
      • Cardiac specific troponin
    • ECG changes (Fig.23-22)
      • Pronounced, persisting Q waves
      • ST elevation
      • T wave inversion
slide21
Treatment
    • First 24 hours crucial
    • Hospitalization, bed rest
    • Pain relief
      • Morphine
      • Nitroglycerin
    • Thrombolytics to break down clots
    • Administer oxygen
manifestations of heart disease
Manifestations of Heart Disease
  • Congestive Heart Failure
    • Defined: heart progressively loses capacity, leading to back-up of blood flow through system
    • Leads to incr’d blood pressure, edema
    • Compensations to relieve effects at vasculature, heart
      • BUT compensations are limited
    • Affects about 3 million patients in the U.S.
    • Slow developing
slide23
Pathophysiology may include
    • Altered contractility
      • Cardiac sarcomeres stretched too far
        • May occur with altered preload
        • So contractile force limited
        •  inadequate ejection
    • Altered afterload (Fig.23-37)
      • Alteration in force against which heart must pump
      • May be due to
        • Vascular stenosis
        • Increased vascular resistance
      • To maintain cardiac output
        • Heart incr’s stroke volume
        • Heart incr’s rate
        • Results in incr’d need for oxygen by heart muscle
slide24
Pathophysiology – cont’d
    • Restrictions to pumping
      • Due to
        • Valve dysfunctions
        • Dysrhythmias
        • Pericardial disease
    • Altered demand for oxygen by the heart
  • Compensations – body needs to:
    • Increase blood return to the heart, by
      • Increasing blood volume through renin/angiotensin system (kidney)
      •  incr’d LV volume, which
      •  incr’d fiber stretch, which
      •  incr’d contractility
        • BUT may  cardiac sarcomeres stretched too far (one cause of cardiac problem to begin with)
slide25
Compensations – cont’d
    • Increase heart rate and increase C.O.
      • Through nervous system
        • Need to incr sympathetic input
    • Hypertrophy of cardiac muscle
      • Results in incr’d LV wall thickness
      • Should incr force of contractions
  • Heart will ultimately fail because compensations limited, sometimes cause other problems, may result in further cardiovascular damage or complications (Fig.23-28)
slide26
Clinical
    • Breathlessness/difficulty breathing
      • Especially lying down
      • Due to pulmonary edema
    • Chest pain
      • Due to hypoxia at heart, resulting myocyte damage
    • Fatigue/confusion
      • Due to decr’d blood flow to skeletal muscles and brain
    • Skin pale, cold, sweaty
    • Pulse, lung sounds abnormal
  • Treatment
    • Decrease cardiac work
    • Drugs to augment contractility
    • Reduce afterload
      • How might you do this?
manifestations of heart disease cont d
Manifestations of Heart Disease – cont’d
  • Shock
    • Defined: clinical syndrome of underperfusion of organs (KNOW THIS!!)
    • May be due to:
    • Cardiac dysfunction (cardiogenic shock) (Fig.23-43)
      • Electrical dysfunction
        • Tachycardia (incr’d heart rate), or
        • Bradycardia (decr’d heart rate)
      • Mechanical dysfunction
        • Valve dysfunction
        • Trauma, pericarditis, etc.
          • When >40% of LV function lost, LV fails to pump sufficient blood to systemic circulation
slide28
Clinical (w/ respect to cardiogenic shock)
      • Decr’d contractility
        •  decreased stroke volume
        •  decreased C.O.
        •  decreased blood to organs
      • Pulmonary edema
        • Why should this occur?
      • Reflex vasoconstriction
        • Why should this occur?
  • Volume disorders- heart appears normal, but organs underperfused for other reasons (Fig.23-44):
    • Volume loss (causing hypovolemic shock), due to
      • Hemorrhage
      • Edema
      • Burns
      • Dehydration
slide29
Shock due to volume disorders – cont’d
    • Volume maldistribution (causing vascular shock).
      • Vasculature dilates  altered hemodynamics (or greatly reduced blood pressure)
      • May happen in:
        • Septic shock -- bacteria release toxins that cause extensive vasodilation (example: toxic shock syndrome)
        • Anaphylactic shock (Fig.23-46) -- histamines cause extensive vasodilation
    • In both cases (cardiogenic or volume disorders  shock)
      • Overall cardiac work increases  heart failure over time
      • Organs underperfused  organ failure over time
        • Most susceptible organs: lungs, kidneys, liver, g.i. tract
    • Compensation through heart, vasculature, kidneys to try to increase blood pressure and blood delivered to tissues
slide30
Treatment for shock:
    • Mechanical support of circulation
    • Augment contractility with drugs
    • Oxygenate
    • Treat edema