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 ◦ ◦ Chest X-ray Film ◦ Shows shape, size of heart ◦ Checks for exercise-induced problems 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  Dangerous component cells 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  1 st 20 minutes critical Time Line ◦ 1 st 20 min critical ◦ ◦ ◦ 48 hrs inflammation begins to subside 7 th 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 1 st ◦ 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 1 st

 ◦ ◦ ◦ ◦ 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 Hypovolemic Cardiogenic Anaphylactic Septic Neurogenic Mechanism

loss of blood or plasma Decreased pumping capability of heart Systemic vasodilation due to severe allergic reaction Vasodilation due to severe infection 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

   1 st ◦ ◦ ◦ ◦ ◦ ◦ 2 nd signs Shock, thirst, agitation, restlessness Often missed 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