Mr. Tsigaridis

Diagnostic Tests for Cardiovascular Function

General Treatment Measures for Cardiac Disorders

Coronary Artery Disease (CAD)◦ Arteriosclerosis◦ Atherosclerosis◦ Myocardial Infarction

(MI)

Cardiac Arrhythmias◦ Sinus node abnormalities◦ Atrial conduction

abnormalities◦ Cardiac arrest

Congestive Heart Failure (CHF)

Arterial Diseases◦ Hypertension

Shock

ECG◦ Monitors arrhythmias, MI, infection, pericarditis◦ Studies conduction activation and systemic abnormalities

Auscultation◦ Studies heart sounds using stethoscope

Exercise stress test◦ Assess general cardiovascular function◦ Checks for exercise-induced problems

Chest X-ray Film◦ Shows shape, size of heart◦ Evidence of pulmonary congestion associated with heart

failure◦ Nuclear imaging

Cardiac Catheterization◦ Visualize inside of

heart, measure pressure, assess valve and heart function

◦ Determine blood flow to and from heart

Angiography◦ Visualization of

blood flow in coronary artery

◦ Obstruction assessed and treated Basic catheterization Balloon angioplasty

Dietary modification Regular exercise program Quit smoking Drug therapy

Vasodilators (Nitroglycerin)◦ Provide better balance of oxygen supply and

demand in heart muscle◦ May cause low bp

Beta-blockers (Metoprolol or Atenolol)◦ Treats angina, hypertension, arrhythmias◦ Blocks beta1-adrenergic receptors in heart

Prevent epine from increasing heart activity

Calcium ion channel blockers◦ Block movement of calcium◦ Decrease heart contraction

Antiarrhytmatic for excessive atrial activity Antihypertension and vasodilator

Digoxin◦ Treats heart failure◦ Increases efficiency of heart

Decreases conduction of impulses and HR Increases contraction of heart

◦ Patients must be checked for toxicity Antihypertensive drugs

◦ Decrease bp to normal levels◦ Include:

Adrenergic blocking agents Calcium ion blockers Diuretics Angiotensin-converting enzyme (ACE) inhibitors

◦ Used to treat hypertension, Congestive Heart Failure, after MI

Adrenergic Blocking drugs◦ Act on SNS, block arteriole alpha adrenergic

receptors, or act directly as vasodilator ACE Inhibitors

◦ Treat hypertension, Congestive Heart Failure Diuretics

◦ Remove excess water, sodium ions◦ Block resorption in kidneys◦ Treat high bp, Congestive Heart Failure

General term for all types of arterial changes

Best for degeneration in small arteries and arterioles

Loss of elasticity, walls thick and hard, lumen narrows

Presence of atheromas◦ Plaques

Consist of lipids, cells, fibrin, cell debris

◦ Lipids usually transported with lipoproteins

Analysis of serum lipids:◦ Total cholesterol, triglycerides, LDL, HDL

LDL◦ High cholesterol content◦ Transports cholesterol liver cells◦ Dangerous component

HDL◦ “good” ◦ Low cholesterol content◦ Transports cholesterol cells liver

Age Gender Genetic factors Obesity, diet high in cholesterol, animal

fats Cigarette smoking Sedentary life style Diabetes mellitus Poorly controlled hypertension

Decrease cholesterol and LDL Decrease sodium ion intake Control primary disorders Quit smoking Oral anticoagulant Surgical intervention

◦ Percutaneous transluminal coronary angioplasty (PTCA)

◦ Cardiac catheterization◦ Laser beam technology◦ Coronary artery bypass grafting

Coronary artery completely obstructed◦ Prolonged ischemia and cell death of

myocardium Most common cause is atherosclerosis

with thrombus 3 ways it may develop:

◦ Thrombus obstructs artery◦ Vasospasm due to partial occlusion◦ Embolus blocks small branch of coronary artery

Majority involve L ventricle◦ Size and location of infarction determine

severity of damage

Function of myocardium contraction and conduction quickly lost ◦ Oxygen supplies depleted

1st 20 minutes critical

Time Line◦ 1st 20 min critical◦ 48 hrs inflammation begins to subside◦ 7th day necrosis area replaced by fibrous tissue◦ 6-8 weeks scar forms

Pain◦ Sudden, substernal area◦ Radiates to L arm and neck◦ Less severe in females

Sweating, nausea, dizziness Anxiety and fear Hypotension, rapid and weak pulse (low

Cardiac Output)

Arrhythmias◦ 25% patients sudden death after Myocardial

Infarction Due to ventricular arrhythmias and fibrillation

◦ Heart block◦ Premature ventricular contraction (PVCs)

Cardiogenic shock Congestive Heart Failure

Rest, oxygen therapy, morphine Anticoagulant Drugs Cardiac rehabilitation Prognosis depends on site/size of infarct,

presence of collateral circulation, time elapsed before treatment

Mortality rate in 1st year◦ 30-40% due to complications, recurrences

Alteration in HR or rhythm ECG monitors

◦ Holter monitors decreases efficiency of heart’s pumping

cycle◦ Slight increase in HR increases CO◦ Very rapid HR prevents adequate filling in

diastole◦ Very slow HR reduces output to tissues

Irregular contraction inefficient◦ Interferes with normal filling/emptying cycle

Cardiac Arrhythmias

Brachycardia◦ Regular but slow HR

Less than 60 beats/min◦ Results from vagus nerve stimulation or PNS

stimulation Tachycardia

◦ Regular rapid HR 100-160 beats/min

◦ SNS stimulation, exercise, fever, compensation for low blood volume

Premature Atrial Contractions (PAC)◦ Extra contraction or ectopic beats of atria◦ Irritable atrial muscle cells outside conduction

pathway Interfere with timing of next beat

Atrial flutter◦ HR 160-350 beats/min◦ AV node delays conduction

Slower ventricular rate

Cause should be determined and treated Easiest to treat are those due to meds SA node problems may require a

pacemaker Some may require defibrillators

Cessation of all activity in the heart No conduction of impulses (flat line) May occur b/c:

◦ Excessive vagal nerve stimulation (decreases heart rate)

◦ Drug toxicity◦ Insufficient oxygen to maintain heart tissue

Blood flow to heart and brain must be maintained to resuscitate

Heart unable to pump sufficient blood to meet metabolic needs of body

Acute or chronic Results from

◦ Problem in heart itself◦ Increased demands placed on heart◦ Combo

One side usually fails 1st

Causes of failure on affected side:◦ Infarction that impairs pumping ability or

efficiency of conduction system◦ Valve defects◦ Congenital heart defects◦ Coronary artery disease

Increased demands on heart cause failure◦ Depends on ventricle most adversely affected◦ Ex: Hypertension increases diastolic bp

Requires Left ventricle to contract more forcibly to open aortic valve

◦ Ex: Pulmonary disease Damages lung caps, increases pulmonary resistance Increase work load to Right ventricle

Forward effects◦ Similar with failure on either side◦ Decrease blood supply to tissue and general

hypoxia◦ Fatigue, weakness, dyspnea (breathlessness),

cold intolerance, dizziness Compensation mechanism

◦ Indicated by tachycardia

Systemic backup effects of Right-sided failure◦ Edema in feet, legs◦ Hepatomegaly, splenomegaly

Underlying problem should be treated Decrease work load on heart Prophylactic measures Other methods

◦ Diet ◦ Drugs

Increased bp Insidious onset, mild symptoms and signs 3 major categories

◦ Essential (primary)◦ Secondary ◦ Malignant

Can be classified as diastolic or systolic Develops when bp consistently over

140/90 Diastolic more important

Over long time, high bp damages arterial walls ◦ Sclerosis, decreased lumen◦ Wall may dilate, tear

Aneurysm Areas most frequently damaged:

◦ Kidneys, brain, retina End result of poorly controlled

hypertension:◦ Chronic renal failure◦ Stroke◦ Loss of vision◦ CHF

Increases with age Males more freq and severe Genetic factors High sodium ion intake Excessive alcohol Obesity Prolonged, recurrent stress

Asymptomatic in early stages Initial signs vague, nonspecific

◦ Fatigue, malaise, morning headache

Treated in sequence of steps◦ Life style changes◦ Mild diuretics, ACE inhibitors◦ One or more drugs added

Patient compliance is an issue Prognosis depends on treating underlying

problems and maintaining constant control of bp

Results from decreased circulating blood volume◦ General hypoxia◦ Low Cardiac Output

Type Mechanism

Hypovolemic loss of blood or plasma

Cardiogenic Decreased pumping capability of heart

Anaphylactic Systemic vasodilation due to severe allergic

reaction

Septic Vasodilation due to severe infection

Neurogenic Vasodilation due to loss of SNS and vaso-motor

tone

Bp decreases when blood volume, heart contraction, or peripheral resistance fails

Low CO, microcirculation◦ = decreased oxygen, nutrients for cells

Compensation mechanism◦ Sympathetic Nervous System, adrenal medulla

stimulated◦ Renin secreted◦ Increased secretion of ADH◦ Secretion of glucocorticoids◦ Acidosis stimulates respiration

Complications of shock◦ Acute renal failure◦ Adult respiratory distress syndrome (ARDS)◦ Hepatic failures◦ Hemorrhagic ulcers◦ Infection of septicemia◦ Decreased cardiac function

Hypovolemic shock◦ Loss of blood, plasma

Burn pts, dehydration Cardiogenic shock

◦ Assoc w/ cardiac impairment Distributive shock

◦ Blood relocated b/c vasodilation Anaphylactic shock Neurogenic shock

Septic shock◦ Severe infection

1st signs◦ Shock, thirst, agitation,

restlessness◦ Often missed

2nd signs◦ Cool, moist, pale skin;

tachycardia; oliguria◦ Compensation◦ Vasoconstriction

Direct effects◦ Decrease bp and blood

flow◦ Acidosis

Prolonged◦ Decreased

responsiveness in body◦ Compensated metabolic

acidosis progresses to decompensated

◦ Acute renal failure◦ Monitoring

Primary problem must be treated Hypovolemic shock

◦ Whole blood, plasma, electrolytes, bicarbonate required Anaphylactic shock

◦ Antihistamines, corticosteroids Septic

◦ Antimicrobials, glucocorticoids Maximize oxygen supply Epine reinforces heart action and

vasoconstriction Dopamine, dubutamine increase heart function Good prognosis in early stages Mortality increases as irreversible shock develops