ISCHEMIC HEART DISEASE; CONGESTIVE HEART FAILURE; SHOCK

1. ISCHEMIC HEART DISEASE; CONGESTIVE HEART FAILURE; SHOCK

2. 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

5. 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

6. 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

7. 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)

8. 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

9. 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

11. 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

12. 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

13. 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

15. 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

18. 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)

19. 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

21. Treatment • First 24 hours crucial • Hospitalization, bed rest • Pain relief • Morphine • Nitroglycerin • Thrombolytics to break down clots • Administer oxygen

22. 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

23. 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

24. 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)

25. 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)

26. 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?

27. 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

28. 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

29. 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

30. Treatment for shock: • Mechanical support of circulation • Augment contractility with drugs • Oxygenate • Treat edema