Cardiac Pathophysiology

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Cardiac Pathophysiology
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Pericarditis

• Often local manifestation of another disease
• May present as
• Acute pericarditis
• Pericardial effusion
• Constrictive pericarditis

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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

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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

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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.

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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

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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

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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.

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Coronary Artery Disease

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

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• 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.

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Risk Factors

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

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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

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• 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

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Clinical Manifestations

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

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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

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

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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

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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

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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.

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Silent Ischemia

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

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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

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• ? 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.)

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Surgical treatment

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

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Myocardial infarction

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

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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

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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)

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

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ECG changes

• Pronounced, persisting Q waves
• ST elevation
• T wave inversion

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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

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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

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• 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

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• 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

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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

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Treatment

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

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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

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• 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

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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

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

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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

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Other risk factors

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

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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

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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)

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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).

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Clinical manifestations

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

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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

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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