Chapter 18: Alterations in Cardiac Function

Characterization of Coronary Heart Disease

Insufficient delivery of oxygenated blood to myocardium (ischemia) because of atherosclerotic coronary arteries (CAD)

Coronary Heart Disease Can Lead To:

Angina pectoris (chest pain)
Myocardial infarction (tissue death)
Dysrhythmias
Heart failure
Sudden cardiac death

Etiology of Coronary Heart Disease

Atherosclerosis causes narrowing of arterial lumen and can lead to cardiac ischemia
Plaque accumulates causes vessels to spasm
Lack of open space

Cause of Coronary Artery Disease

Atherosclerosis

Apoproteins

transport lipids through blood

Lipoproteins

Greater risk of atherosclerosis

Atherosclerotic plaque formation is initiated by

Injury to coronary artery endothelium

Lipoproteins contain:

Triglycerides
Phospholipids
Cholesterol
Protein

Types Of Lipoproteins

High density lipoprotein (HDL)
Intermediate density lipoprotein (IDL)
Low density lipoprotein (LDL)
Very low density lipoprotein (VLDL)

Chylomicrons

Produced by intestine
Packaged with dietary lipids
Transport dietary lipids to hepatic and peripheral cells

Hyperlipidemia

Elevated concentration of lipids in blood

Major plasma lipids

Total cholesterol
Triglycerides

Risk factors of hyperlipidemia (primary)

Genetic predisposition for CHD
Cigarette smoking
Elevated total cholesterol
Decreased HDL cholesterol
Elevated triglycerides
Increasing age
Male gender

Risk factors of hyperlipidemia (secondary)

Lack of exercise
Obesity
Stress
Elevated lipoprotein, homocysteine, intermediate density lipoproteins
Renal failure

Mechanism of Coronary Atherosclerosis

Vulnerable plaques may rupture
Clot formation is stimulated on plaque

Vulnerable plaque have

Large lipid core
Thin cap
High shear stress

If there is not fibrous cap...

Atherosclerosis is not stable

Pathophysiology of Ischemia

Local, temporary deprivation of the coronary blood supply
Oxygen supply is insufficient to meet metabolic demands

Factors for meeting cellular demands for oxygen

Rate of coronary perfusion
Myocardial workload

Coronary perfusion can be impaired by

Large, stable atherosclerosis plaque
Acute platelet aggregation and thrombosis
Vasospasm
Failure of autoregualtion by microcirculation
Poor perfusion pressure

Myocardial work load depends on

Heart rate
Preload
Afterload
Contractility

Chronic coronary syndrome

slow progression due to chronic obstruction from stable atherosclerotic plaques

Acute coronary syndrome

acute changes in plaque morphology and thrombosis (plaque is unstable)

Angina pectoris (chronic coronary syndrome)

intermittent myocardial ischemia
chest pain
inefficient cardiac pumping causing pulmonary congestion and shortness of breath

Unstable angina (chronic coronary syndrome)

No exertion
Disruption of plaque
Ischemia
Thrombosis
Pre warning for infarction

Treatment of Angina (chronic coronary syndrome)

Dietary/lifestyle modifications
Cholesterol lowering drugs
Aspirin/platelet inhibitors
Decrease in demand for oxygen (beta and calcium channel blockers)
Increase vasodilation
Angioplasty, stenting, bypass surgery

Acute Coronary Syndrome

Plaque rupture with acute thrombus development

Unstable Angina (Acute Coronary Syndrome)

Occlusion is partial

Myocardial Infarction (Acute Coronary Syndrome)

Occlusion is complete
Extended obstruction of myocardial blood supply
Drop in CO2, triggering compensatory response

SNS causes increased workload which increases (Acute Coronary Syndrome)

Heart rate
Contractility
Blood pressure

Treatment of MI (Acute Coronary Syndrome)

Repercussion the heart (does not restore necrotic or dead fiber, only reversibly injured ones)
Anticoagulants
ACE inhibitors (helps to reduce workload)

Biomarkers

Cardiac troponin T and I
Myoglobin
CK-isoforms

Troponin C (Bind and Location)

Binds to calcium
Found in heart and skeletal muscle

Troponin T (Bind and Location)

Binds tropomyosin
Cardiac specific

Troponin I (Bind and Location)

Inhibit binding of myosin to actin
Cardiac specific

What regulates muscle contraction?

Troponin complex
Calcium
Tropomyosin

What helps diagnose MI?

Troponin

Myoglobin Location

Cardiac and Skeletal Muscle

Change in myoglobin concentration is seen in

MI
Renal failure injury
Trauma
Skeletal muscle disease

Creatine Kinase (CK)

Cytosolic enzyme involved in the transfer of energy in muscle metabolism

Subunits of CK

Brain form (B)
Muscle form (M)

CK Isoenzyme

CK-BB (blood - brain barrier)
CK-MM (activity in skeletal system)
CK-MB (activity in the heart)

Sudden Cardiac Death

Unexpected death from cardiac causes within 1 hour of symptom onset

Non-Atherosclerotic Sudden Cardiac Death (Diseases)

Congenital coronary artery disease
Aortic stenosis
MVP
Myocarditis
Cardiomyopathy

Chronic Ischemic Cardiomyopathy

Heart failure develops insidiously due to progressive ischemic myocardial damage
Supply does not meet demand overtime

Damage to endocardium and valves caused by:

Inflammation and scarring
Calcification
Congenital malformations

Stenosis

Failure for a valve to open completely
Backflow
Extra pressure work
for heart due to high resistance of narrow valve opening

Regurgitation

Inability of a valve to close completely results in
extra volume work
for the heart
Does not prevent back flow

Mitral Valve Prolapse (MVP)

Degeneration of mitral valve (regurgitation)
Valve bulges into left atrium during ventricular systole
Connective tissue disorder

Clinical Features of Mitral Valve Prolapse

Asymptomatic
Mid-systolic "click"
Holosystolic murmur if regurgitating (between S1 and S2 noises)
Chest pain, dyspnea

Manifestations of MVP

Dizziness
Light headed
Shortness of breath
Fatigue

Mechanical valve

Carbon material
Attract clots/thrombosis

Xenograft Valve

Animal
Not at risk for clotting

Rheumatic fever

inflammatory disease caused by a delayed immune response to infection
type 2 hypersensitivity

Febrile illness

Inflammation of the joints, skin, nervous system, and heart

Jones Criteria

C: carditis
A: migratory polyarthritis
N: nodules
C: Sydenham chorea
ER: erythema marginatum

Rheumatic heart disease

acute inflammatory disease that follows infection

Infective endocarditis

Invasion and colonization of endocardial structures by microorganisms with resulting inflammation
Colonize on valves

Acute Infective Endocarditis

Usually have something abnormal with heart to begin with

Bacteria of Infective Endocarditis

Strep
Staph

Who does acute infective endocarditis effect?

IV drug users

Endocarditis

Inflammation of endocardium

Causes Of Endocarditis

bacteria
viruses
fungi
rickettsia
parasites

Pathogenesis of endocarditis

Colonization occurs on valves (become calcified)
Blood-borne microorganism adherence
Proliferation of the microorganisms

Myocarditis

inflammatory disorder
Dilation of all four chambers
Left ventricle dysfunction

Characterizations of myocarditis

necrosis and degeneration of myocytes

Cardiomyopathy

Noninflammatory disorder

Characterization of cardiomyopathy

Genetic or acquired

Causes of myocarditis

Microbial agents
Immune-mediated diseases
Physical agents

Etiology of myocarditis

Virus (Coxsackie B), bacteria, parasites
Inflammatory disease (SLE)
Toxins (drugs and radiation)

Causes of cardiomyopathy

Hypertension
Inflammatory
Autoimmune
Muscular dystrophy
Genetic disorder
Drugs
Viral myocarditis
Aortic regurgitation
Mitral regurgitation

Primary cardiomyopathy

no known cause

Secondary cardiomyopathy

known cause

Dilated cardiomyopathy

cardiac failure associated with dilation of one or both ventricular chambers
heart is big and flabby

Causes Of Dilated Cardiomyopathy

Alchohol toxicity
Pregnancy
Postviral myocarditis
Genetic abnormality

Precursor of dilated cardiomyopathy

Myocarditis
ETOH

Dilated cardiomyopathy found in

Pregnant women
Drug users
Alcoholics

Hypertrophic cardiomyopathy

thickened walls
ventricles can't relax

Causes of hypertrophic cardiomyopathy

Genetic abnormality
Increased pulmonary resistance
Pulmonary hypertension
Left heart failure and lung disease
Pulmonic valve stenosis

Sarcomere proteins related to genetic abnormality of hypertrophic cardiomyopathy

Beta-myosin heavy chain
Troponin T
Alpha-tropomyosin
Myosin binding protein C

Pathology of hypertrophic cardiomyopathy

Massive hypertrophy
Asymmetric septum
Disarray of myocytes
Interstitial fibrosis

Clinical aspects of hypertrophic cardiomyopathy

Decrease in chamber volume
Decrease in stroke volume
Decrease in diastolic filling

Restrictive cardiomyopathy (rare)

Idiopathic disease where walls become restricted but chamber size and wall thickness are normal
Decrease in ventricular compliance
Affects diastole
Decreased cardiac output and left-sided heart failure

Tamponade

Severe restriction of heart
Venous congestion, JVP, distant heart sounds
Accumulate fluid in pericardial sac
Squeezes heart causing pressure
Back flow into systemic veins (swelling)

Treatment of Tamponade

Relieving the pericardial pressure by aspirating the offending fluid

Acute Pericarditis

Idiopathic
Pleuritic chest pain
Pericardial rub

Causes of acute pericarditis

Infection: virus, TB, bacteria
Connective tissue disease: lupus, rheumatoid arthritis
Drugs
Cancer
Renal failure
Radiation
Trauma
MI

Congenital Heart Diseases

Abnormality of heart that is present from birth

Etiology of congenital heart disease

Oxygenated blood shoot across right atrium to left atrium and bypass lungs
Septum doesn't always develop all the way

Causes of congenital heart disease

Maternal rubella
Exposure to cardiac teratogens
Genetic influences

Shunt

Abnormal path of blood flow through the heart or great vessels

Obstruction

Interference with blood flow leading to increased workload of affected chamber

Atrial Septal Defect

Abnormal opening between the atria
Shunts go right to left because blood bypasses lungs

Ventricular Septal Defect

Abnormal communication between ventricles
Shunts left to right or right to left