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Cardiac Pathophysiology

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Title: Cardiac Pathophysiology


1
Cardiac Pathophysiology
2
Pericarditis
  • Often local manifestation of another disease
  • May present as
  • Acute pericarditis
  • Pericardial effusion
  • Constrictive pericarditis

3
Acute Pericarditis
  • Acute inflammation of the pericardium
  • Cause often unknown, but commonly caused by
    infection, uremia, neoplasm, myocardial
    infarction, surgery or trauma.
  • Membranes become inflamed and roughened, and
    exudate may develop

4
Symptoms
  • Sudden onset of severe chest pain that becomes
    worse with respiratory movements and with lying
    down.
  • Generally felt in the anterior chest, but pain
    may radiate to the back.
  • May be confused initially with acute myocardial
    infarction
  • Also report dysphagia, restlessness,
    irritability, anxiety, weakness and malaise

5
Signs
  • Often present with low grade fever and sinus
    tachycardia
  • Friction rub (sandpaper sound) may be heard at
    cardiac apex and left sternal border and is
    diagnostic for pericarditis (but may be
    intermittent)
  • ECG changes reflect inflammatory process through
    PR segment depression and ST segment elevation.

6
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7
Treatment
  • Treat symptoms
  • Look for underlying cause
  • If pericardial effusion develops, aspirate excess
    fluid
  • Acute pericarditis is usually self-limiting, but
    can progress to chronic constrictive pericarditis

8
Heart failure
  • Definition When heart as a pump is insufficient
    to meet the metabolic requirements of tissues.
  • Acute heart failure
  • 65 survival rate
  • Chronic heart failure
  • Most common cause is ischemic heart disease

9
Ischemic Heart Disease
  • Coronary Artery Disease (CAD), myocardial
    ischemia and myocardial infarction are
    progression of conditions that impair the pumping
    ability of the heart by depriving it of oxygen
    and nutrients.

10
Coronary Artery Disease
  • Any vascular disorder that narrows or occludes
    the coronary arteries.
  • Most common cause is atherosclerosis

11
  • The arteries that supply the heart are the first
    branches off the aorta
  • Coronary artery disease decreases the blood flow
    to the cardiac muscle.
  • Persistent ischemia or complete occlusion leads
    to hypoxia.
  • Hypoxia can cause tissue death or infarction,
    which is a heart attack, which accounts for
    about one third of all deaths in U.S.

12
Risk Factors
  • Hyperlipidemia
  • Hypertension
  • Diabetes mellitus
  • Genetic predisposition
  • Cigarette smoking
  • Obesity
  • Sedentary life-style
  • Heavy alcohol consumption
  • Higher risk for males than premenopausal women

13
Myocardial Ischemia
  • Myocardial cell metabolic demands not met
  • Time frame of coronary blockage
  • 10 seconds following coronary block
  • Decreased strength of contractions
  • Abnormal hemodynamics
  • See a shift in metabolism, so within minutes
  • Anaerobic metabolism takes over
  • Get build-up of lactic acid, which is toxic
    within the cell
  • Electrolyte imbalances
  • Loss of contractibility

14
  • 20 minutes after blockage
  • Myocytes are still viable, so
  • If blood flow is restored, and increased aerobic
    metabolism, and cell repair,
  • ?Increased contractility
  • About 30-45 minutes after blockage, if no relief
  • Cardiac infarct cell death

15
Clinical Manifestations
  • May hear extra, rapid heart sounds
  • ECG changes
  • T wave inversion
  • ST segment depression

16
Chest Pain
  • First symptom of those suffering myocardial
    ischemia.
  • Called angina pectoris (angina pain)
  • Feeling of heaviness, pressure
  • Moderate to severe
  • In substernal area
  • Often mistaken for indigestion
  • May radiate to neck, jaw, left arm/ shoulder

17
  • Due to
  • Accumulation of lactic acid in myocytes or
  • Stretching of myocytes
  • Three types of angina pectoris
  • Stable, unstable and Prinzmetal

18
Stable angina pectoris
  • Caused by chronic coronary obstruction
  • Recurrent predictable chest pain
  • Gradual narrowing and hardening of vessels so
    that they cannot dilate in response to increased
    demand of physical exertion or emotional stress
  • Lasts approx. 3-5 minutes
  • Relieved by rest and nitrates

19
Prinzmetal angia pectoris (Variant angina)
  • Caused by abnormal vasospasm of normal vessels
    (15) or near atherosclerotic narrowing (85)
  • Occurs unpredictably and almost exclusively at
    rest.
  • Often occurs at night during REM sleep
  • May result from hyperactivity of sympathetic
    nervous system, increased calcium flux in muscle
    or impaired production of prostaglandin

20
Unstable Angina pectoris
  • Lasts more than 20 minutes at rest, or rapid
    worsening of a pre-existing angina
  • May indicate a progression to M.I.

21
Silent Ischemia
  • Totally asymptomatic
  • May be due abnormality in innervation
  • Or due to lower level of inflammatory cytokines

22
Treatment
  • Pharmacologically manipulate blood pressure,
    heart rate, and contractility to decrease oxygen
    demands
  • Nitrates dilate peripheral blood vessels and
  • Decrease oxygen demand
  • Increase oxygen supply
  • Relieve coronary spasm

23
  • ? blockers
  • Block sympathetic input, so
  • Decrease heart rate, so
  • Decrease oxygen demand
  • Digitalis
  • Increases the force of contraction
  • Calcium channel blockers
  • Antiplatelet agents (aspirin, etc.)

24
Surgical treatment
  • Angioplasty mechanical opening of vessels
  • Revascularization bypass
  • Replace or shut around occluded vessels

25
Myocardial infarction
  • Necrosis of cardiac myocytes
  • Irreversible
  • Commonly affects left ventricle
  • Follows after more than 20 minutes of ischemia

26
Structural, functional changes
  • Decreased contractility
  • Decreased LV compliance
  • Decreased stroke volume
  • Dysrhythmias
  • Inflammatory response is severe
  • Scarring results
  • Strong, but stiff cant contract like healthy
    cells

27
Clinical manifestations
  • Sudden, severe chest pain
  • Similar to pain with ischemia, but stronger
  • Not relieved by nitrates
  • Radiates to neck, jaw, shoulder, left arm
  • Indigestion, nausea, vomiting
  • Fatigue, weakness, anxiety, restlessness and
    feelings of impending doom.
  • Abnormal heart sounds possible (S3,S4)

28
  • Blood test show several markers
  • Leukocytosis
  • Increased blood sugar
  • Increased plasma enzymes
  • Creatine kinase
  • Lactic dehydrogenase
  • Aspartate aminotransferase (AST or SGOT)
  • Cardiac-specific troponin

29
ECG changes
  • Pronounced, persisting Q waves
  • ST elevation
  • T wave inversion

30
Treatment
  • First 24 hours crucial
  • Hospitalization, bed rest
  • ECG monitoring for arrhythmias
  • Pain relief (morphine, nitroglycerin)
  • Thrombolytics to break down clots
  • Administer oxygen
  • Revascularization interventions by-pass grafts,
    stents or balloon angioplasty

31
Atherosclerosis
  • A form of arteriosclerosis where soft deposits of
    intra-arterial fat and fibrin harden over time
    atheroma
  • May see build up in skin Xanthoma or arcus in
    cornea.
  • In general, patients suffer few symptoms unless gt
    60 of blood supply is blocked

32
  • Progressive over years
  • Starts with some injury to endothelium
  • Smoking, hypertension, hyperlipidemia, diabetes,
    autoimmune disease, and infection
  • Inflammation, release of enzymes by macrophages
    causes oxidation of LDL, which is then consumed
    by macrophages foam cells accumulate to form
    fatty streaks
  • Fatty streaks of lipid material appear first as
    yellow streaks and spots
  • Smooth muscle cells proliferate, and migrate
    over the streak forming a fibrous plaque

33
  • Fibrous plaque results in necrosis of underlying
    tissue and narrowing of lumen
  • Inflammation can result in ulceration and
    rupture of the plaque, resulting in platelet
    adherence to the lesion complicated lesion
  • Can result in rapid thrombus formation with
    complete vessel occlusion ? tissue ischemia and
    infarction

34
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35
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36
Clinical manifestations
  • Signs and symptoms of inadequate perfusion
    TIAs, often associated with exercise or stress
  • When lesion becomes complicated, can result in
    tissue infarction
  • Coronary artery disease myocardial ischemia
  • In brain major cause of stroke

37
Treatment
  • Exercise
  • Smoking cessation
  • Control of hypertension and/ or diabetes
  • Reduce LDL cholesterol by diet or medication or
    both

38
Other arterial problems
  • Aneurism dilation in the arterial wall
  • Most arise in aorta or major branches as a result
    of atherosclerotic wall damage
  • Males over 50 at greatest risk for aortic
    aneurysms
  • Disturbs blood flow, predisposing to thrombus
    formation - can release thromoemboli

39
  • Asymptomatic until rupture
  • Embolism
  • Death
  • Treatment by surgical repair
  • Aortic Dissection bleeding into vessel wall,
    separating vessel layers
  • Men in 40-60 y.o. age group with hypertension
  • Younger persons with connective tissue disease or
    congenital defects
  • Presents with pain life threatening

40
Systemic Hypertension
  • A consistent increase in arterial blood pressure
    caused by increased Cardiac output or increased
    peripheral resistance or both
  • Leads to damage of vessel walls
  • If arteries constrict over a long time with
    increased pressure in vessel, the wall becomes
    thicker to withstand the stress.
  • Results in narrowing of arterial lumen
  • Leads to inflammatory response

41
  • Causes one in eight deaths worldwide
  • Third leading cause of death in the world
  • Affects 50 million Americans

42
Primary hypertension
  • Also called essential or idiopathic hypertension
  • 92- 95 of all cases
  • No specific cause identified
  • Can happen with retention of sodium and water ?
    increased blood volume.
  • Also low dietary potassium, calcium and magnesium
    intakes

43
Other risk factors
  • Smoking
  • Nicotine is a vasoconstrictor
  • Greater than 3 alcoholic drinks/ day
  • 2-4 drinks / week lowers blood pressure

44
Suspected causes
  • Interaction of genetics and environment
  • Overactivity of sympathetic nervous system
  • Overactivity of renin / angiotensin/ aldosterone
    system
  • Salt and water retention by kidneys
  • And others

45
Secondary hypertension
  • Caused by a systemic disease process that raises
    peripheral resistance or cardiac output 5 - 10
    of cases.
  • Renal vascular disease
  • Adrenocortical tumors
  • Adrenomedullary tumors
  • Drugs ( oral contraceptives, corticosteroids,
    antihistamines)

46
Complicated hypertension
  • Sustained primary hypertension that damages the
    structure and function of the vessels themselves.
  • Commonly affects heart, aorta, kidneys, eyes,
    brain, and lower extremities (target-organ
    damage).

47
Clinical manifestations
  • None in early stages other than elevated BP
  • Some individuals never have symptoms others
    become very ill and die

48
Treatment
  • Modification of life style
  • Drugs
  • Diuretics, beta-blockers, angiotensin converting
    enzyme inhibitor
  • Compliance is often difficult patients stop
    taking medication when they feel better can get
    rebound effects

49
Venous Disorders
  • Varicose veins dilations, can lead to valvular
    insufficiency
  • Can occur in superficial veins (saphenous) or
    deep veins
  • Causes of secondary varicose veins
  • Deep vein thrombosis
  • Congenital defects and pressure on abdominal veins
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