Cardiovascular Disorders

1. Cardiovascular Disorders Mr. Tsigaridis

2. Overview • Cardiac Arrhythmias • Sinus node abnormalities • Atrial conduction abnormalities • Cardiac arrest • Congestive Heart Failure (CHF) • Arterial Diseases • Hypertension • Shock • Diagnostic Tests for Cardiovascular Function • General Treatment Measures for Cardiac Disorders • Coronary Artery Disease (CAD) • Arteriosclerosis • Atherosclerosis • Myocardial Infarction (MI)

3. 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 Diagnostic Tests for Cardiovascular Function

4. Diagnostic Tests • Cardiac Catheterization • Visualize inside of heart, measure pressure, assess valve and heart function • Determine blood flow to and from heart

5. Diagnostic Tests • Angiography • Visualization of blood flow in coronary artery • Obstruction assessed and treated • Basic catheterization • Balloon angioplasty

6. Dietary modification Regular exercise program Quit smoking Drug therapy General Treatment Measures for Cardiac Disorders

7. 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

8. Drug Therapy • 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

9. Drug Therapy • 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

10. CAD—Arteriosclerosis: Pathophysiology • 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

11. CAD—Atherosclerosis: Pathophysiology • Presence of atheromas • Plaques • Consist of lipids, cells, fibrin, cell debris • Lipids usually transported with lipoproteins

12. Atherosclerosis--Pathophysiology • 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

13. Development of Atheroma

14. Atherosclerosis—Etiology • Age • Gender • Genetic factors • Obesity, diet high in cholesterol, animal fats • Cigarette smoking • Sedentary life style • Diabetes mellitus • Poorly controlled hypertension

15. Atherosclerosis—Treatment • 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

16. CABG

17. Coronary Artery Disease: Myocardial Infarction Pathophysiology • 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

18. Myocardial Infarction Pathophysiology • 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

20. Myocardial Infarction - Signs and Symptoms • 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)

21. Myocardial Infarction - Complications • 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

22. Myocardial Infarction—Treatment • 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

23. Cardiac Arrhythmias • 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

24. Cardiac Arrhythmias

25. Cardiac Arrhythmias: Sinus Node Abnormalities • 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

27. Cardiac Arrhythmias: Atrial Conduction Abnormalities • 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

28. Treatment of Cardiac Arrhythmias • 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

30. Cardiac Arrest • 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

31. Congestive Heart Failure - Pathophysiology • 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

32. Congestive Heart Failure - Etiology • Causes of failure on affected side: • Infarction that impairs pumping ability or efficiency of conduction system • Valve defects • Congenital heart defects • Coronary artery disease

33. Congestive Heart Failure - Etiology • 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

35. Congestive Heart Failure - Signs and Symptoms • 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

36. Congestive Heart Failure - Signs and Symptoms • Systemic backup effects of Right-sided failure • Edema in feet, legs • Hepatomegaly, splenomegaly

37. Congestive Heart Failure - Treatment • Underlying problem should be treated • Decrease work load on heart • Prophylactic measures • Other methods • Diet • Drugs

38. Arterial Diseases: Hypertension—Pathophysiology • 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

39. Hypertension—Pathophysiology • 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

40. Hypertension—Etiology • Increases with age • Males more freq and severe • Genetic factors • High sodium ion intake • Excessive alcohol • Obesity • Prolonged, recurrent stress

41. Hypertension—Signs and Symptoms • Asymptomatic in early stages • Initial signs vague, nonspecific • Fatigue, malaise, morning headache

42. Hypertension—Treatment • 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

43. Shock (Hypotension) • Results from decreased circulating blood volume • General hypoxia • Low Cardiac Output

44. Classification and Mechanisms of Shock

46. Shock—Pathophysiology • 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

47. Shock—Pathophysiology • Complications of shock • Acute renal failure • Adult respiratory distress syndrome (ARDS) • Hepatic failures • Hemorrhagic ulcers • Infection of septicemia • Decreased cardiac function

48. Shock—Etiology • 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

49. Shock—Signs and Symptoms • Prolonged • Decreased responsiveness in body • Compensated metabolic acidosis progresses to decompensated • Acute renal failure • Monitoring • 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

50. Shock—Treatment • 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