CARDIOVASCULAR SYSTEM

1. CARDIOVASCULAR SYSTEM MR OGUNDELE

2. Coronary artery disease • Coronary artery disease is a progressive disease leading to narrowing or occlusion of the coronary arteries. • As the vessel narrows, the patients may experience symptoms of ischemia such as chest tightness and angina.

3. PATHOPHYSIOLOGY • Accumulation of fatty deposits and minerals in the coronary arteries, called an atheroma or plaque, leads to stenosis and eventually occlusion of the artery. • In CAD, blood flow to the myocardium is reduced. The arteries are unable to dilate to meet increased metabolic needs.

4. PATHOPHYSIOLOGY • When myocardial oxygen demands are not met, ischemia results, which can cause chest pain. The pain associated with CAD occurs from a lack of oxygen to the myocardium from CAD and is called angina pectoris. • If coronary artery disease is not prevented or treated early, it can progress to more serious cardiac disorders. These include angina, myocardial infarction, heart failure, cardiac dysrhythmias, and even sudden death.

5. S/S • Asymptomatic. • Chest pain (angina) because of decreased blood flow to heart muscle and/or increase in myocardial oxygen demand resulting from stress. • Pain may radiate to the arms, back, and jaw.

6. MANAGEMENT • Most risk factors for heart disease are related to lifestyle and environmental factors. • Encourage and educate the patient on cessation of smoking, dietary changes, controlling hypertension, maintaining weight. • Diet change: lower sodium, lower cholesterol and fat, decreased calorie intake, increased dietary fiber

7. MANAGEMENT • Administer low doses of aspirin. • Administer beta-adrenergic blockers to reduce workload of heart: metroprolol, propranolol, nadolol. • Administer calcium channel blockers to reduce heart rate, blood pressure, and muscle contractility; helps with coronary vasodilation; slows AV node conduction. • Administer nitrate if patient has symptomatic chest pains to reduce discomfort and enhance blood flow to myocardium.

8. SURGICAL INTERVENTION Coronary Atherectomy • Coronary atherectomy is used to cut and remove plaque from atherosclerotic coronary arteries. The catheter has a central rotating blade that shaves off the plaque and contains it for removal and pathological analysis. Coronary Artery Stents • Coronary artery stents are used to prevent closure of a coronary artery from an atherosclerotic lesion. Stents are put in place during an angioplasty.

9. NURSING MGT • Monitor vital signs—signs of hypertension, irregular heart rate • Monitor electrocardiogram • Monitor labs—periodic lipid panel, liver function for patients on statins • Monitor for myalgias (muscle aches)

10. NURSING MGT • Educate and encourage patients to • Stop smoking • Reduce alcohol consumption • Change to a lower-fat, lower-cholesterol diet, as well as increased dietary fiber intake • Increase daily activity • Weight reduction

11. ANGINA PECTORIS • Angina pectoris is a clinical syndrome usually characterized by episodes or paroxysms of pain or pressure in the anterior chest. • The cause is usually insufficient coronary blood flow. The insufficient flow results in a decreased oxygen supply to meet an increased myocardial demand for oxygen in response to physical exertion or emotional stress.

12. PATHOPHYSIOLOGY • Angina pectoris (chest pain) is a symptom of ischemia and is the primary symptom of coronary artery disease and heart attack. • In the normal heart there is a balance between the oxygen supply and demand of the myocardium. • When an increased workload is placed on the heart, as in exercise or strenuous activity, there is an increased demand for oxygen.

13. PATHOPHYSIOLOGY • Normally, when the heart needs more oxygen, the coronary arteries dilate to carry more blood. • However, with CAD, the narrowed vessels are unable to dilate and supply the heart with this extra blood and oxygen. • This inability to supply more blood and oxygen causes myocardial ischemia and chest pain. Chest pain results from the ischemia but usually lasts only for a few minutes, especially if activity is stopped. • An episode of angina is typically precipitated by physical activity, excitement, or emotional stress.

14. ANGINA PECTORIS • There are three categories of angina. Stable angina— Chest pain occurring during periods of increased myocardial work because of reduced coronary perfusion. The pain is predictable and can usually be managed with nitroglycerin and rest.

15. ANGINA PECTORIS • Unstable angina— The episodes of chest pain with unstable angina increase in frequency and severity, placing the patient at risk for myocardial damage or sudden death. Rest does not decrease the chest pain of unstable angina. This pain may even occur when the patient is at rest. ; is of increasing intensity, force, or duration; isn't relieved by rest; and is slow to subside in response to nitroglycerin.

16. ANGINA PECTORIS • VARIANT ANGINA (PRINZMETAL’S ANGINA). The pain of variant angina is similar to the pain in stable angina except it has a longer duration and may occur at rest. The pattern of occurrence is often cyclical, with the pain presenting about the same time each day. This type of angina is often caused by coronary artery spasms and usually does not cause damage to the myocardium

17. S/S • Chest pain lasting 3 to 5 minutes—not all patients get substernal pain (NB: Some pt. describe the pain as heaviness, tightness, squeezing, or crushing pain in the center of the chest) • Pain can occur at rest or after exertion, excitement, or exposure to cold—due to increased oxygen demands or vasospasm. • Pain may radiate to other parts of the body such as the jaw, back, or arms—

18. S/S • Sweating (diaphoresis) • Tachycardia—heart pumping faster trying to meet oxygen needs as anxiety increases. • Difficulty breathing, shortness of breath (dyspnea)—increased heart rate increases respiratory rate and increases oxygenation.

19. DIAGNOSIS • Electrocardiogram during episode: T-wave inverted with initial ischemia, which is reduced blood flow due to myocardium. • Troponins, CK-MB, which is an enzyme released by damaged cardiac tissue 2 to 6 hours following an infraction. • Chest x-ray to determine signs of heart failure.

20. DIAGNOSIS • Coronary arteriography to determine plaque build-up in coronary arteries. • Echocardiogram or stress-echo to determine any abnormality of wall motion due to ischemia.

21. MANAGEMENT • The treatment is directed at relieving and preventing anginal episodes that could lead to a myocardial infarction. When suspecting chest pain, always give oxygen as the first line of defense. • The risk factors identified for the patient determine the course of treatment. Weight reduction; a low-fat, low cholesterol diet; and stress reduction may help slow disease progression. • The three major groups of medication used for angina are vasodilators, calcium channel blockers, and beta blockers.

22. MANAGEMENT • Administer nitrates— Nitrates dilate coronary arteries to increase oxygen to the myocardium, and dilate peripheral vessels so the heart does not have to work so hard to pump blood into them. Nitroglycerin—sublingual tablets or spray; timed-release tablets. • Administer Calcium channel blockers: It relaxes vascular smooth muscle, which leads to decreased peripheral vascular resistance (afterload) and decreased myocardial oxygen demand. These drugs dilate main coronary arteries, increasing the myocardial oxygen supply. Nifedipine

23. MANAGEMENT • Administer beta-adrenergic blocker—this class has a cardioprotective effect, Beta blockers decrease heart rate, lower blood pressure, and prevent release of rennin. This results in decreased workload on the heart to help prevent anginal attacks • Statins: Cholesterol and inflammation in artery walls are involved in atherosclerosis development. Statins lower cholesterol levels by reducing cholesterol production in the liver.

24. MANAGEMENT • Aspirin for antiplatelet effect. • Analgesic—typically morphine intravenously during acute pain. The medicine is very fast-acting when given this way and will decrease myocardial oxygen demand as well as decrease pain.

25. NURSING MANAGEMENT • Monitor vital signs—look for change in BP, P, R; irregular pulse; pulse deficit; • Monitor cardiac status using a 12-lead electrocardiogram (EKG) • Record fluid intake and output. Assess for renal function. • Assess chest pain each time the patient reports it.

26. NURSING MANAGEMENT Remember PQRST (an acronym for a method of pain assessment)   Determine the • Place, • Quality (describe the pain—stabbing, squeezing, etc.), • Radiation (does the pain travel anywhere else?), • Severity (on a scale of 1 to 10), • Timing (when it started and how long it lasts and what preceded the pain).

27. NURSING MANAGEMENT Educate and encourage the patient to • Rest when pain begins to decrease oxygen demands. • Avoid stress and activities that bring on an angina attack. • Stop smoking. Smoking is associated with heart disease. • Adhere to the prescribed diet and exercise plan.

28. Myocardial infarction (MI) • A myocardial infarction (MI), commonly known as a heart attack, results in the death of heart muscle. The affected myocardial cells in the heart are permanently destroyed.

29. PATHO • Myocardial infarction does not happen immediately. Ischemic injury evolves over several hours before complete necrosis and infarction take place. • Blood supply to the myocardium is interrupted for a prolonged time due to the blockage of coronary arteries. • The ability of the heart to contract, relax, and propel blood throughout the body requires healthy cardiac muscle

30. PATHO • This results in insufficient oxygen reaching cardiac muscle, causing cardiac muscles to die (necrosis). • The body’s attempt to compensate for decreased cardiac function triggers the sympathetic nervous system to increase heart rate. The change in heart rate increases myocardial oxygen demand, further depressing the myocardium.

31. PATHO • The extent of the cardiac damage varies depending on the location and amount of blockage in the coronary artery. • Patients are typically (not always) symptomatic, but some patients will not be aware of the event; they are said to have silent MI.

32. S/S • Chest pain that is unrelieved by rest or nitroglycerin, unlike angina • Pain that radiates to arms, jaw, back and/or neck • Shortness of breath, especially in the elderly or women • Nausea or vomiting • Anxiety

33. S/S • Restlessness • Feeling of impending doom • Pale, cool, clammy skin; sweating (diaphoresis) • Sudden death due to arrhythmia usually occurs within first hour

34. DIAGNOSIS • ECG: T-wave inversion—sign of ischemia. ST-segment elevation • Decreased pulse pressure because of diminished cardiac output. • Elevated creatine kinase MB (CK-MB)— • Elevated troponin I- and troponin T-proteins elevated within one hour of myocardial damage. • Less than 25 ml/hr of urine output due to lack of renal blood flow

35. MANAGEMENT • The goal of medical management is to minimize myocardial damage,preserve myocardial function, and prevent complications. • Medications are used to enhance blood flow to the heart musclewhile reducing the workload of the heart. • OXYGEN: Supplemental oxygen is used to help meet myocardial oxygen demand. Oxygen is administered immediately, usually at 2 L per minute via nasal cannula.

36. MANAGEMENT • Administer antiarrhythmicsbecause arrhythmias are common as are conduction disturbances. Amiodarone. • Administer thrombolytic therapy within 3 to 12 hours of onset because it can re-establish blood flow in an occluded artery, reduce mortality, and halt the size of the infarction. Alteplase. Streptokinase. • Administer beta-adrenergic blockers because they reduce the duration of ischemic pain and the incidence of ventricular fibrillation; decreases mortality. Propranolol, Nadolol.

37. MANAGEMENT • Administer analgesics to relieve pain, reduce pulmonary congestion, and decrease myocardial oxygen consumption. Morphine sulfate is the most commonly used narcotic for several reasons • Administer nitrates to reduce ischemic pain by dilation of blood vessels; helps to lower BP. Nitroglycerin. • Post-MI all patients should be commenced on a statin lipid lowering drug.

38. NURSING MANAGEMENT • Monitor Vital signs, look out for changes in pulse, heart sounds, murmur. • Continuous monitoring of ECG to detect arrhythmias • Educate and encourage the patient on low-fat, low-cholesterol, low-sodium diet. Medication. Smoking cessation.

39. NURSING MANAGEMENT Patient should be encouraged to • Limit activities. • Reduce stress • Adhere to lifestyle changes such as increase in exercise, diet changes.

40. HEART FAILURE • Is a complication of other cardiovascular condition rather than a disease in itself. • HF occurs when the muscular layer of the heart weakens causing it to fail as a pump and a circulator of blood.

41. Causes • Infection of the muscle • Myocardial infraction • Ageing • Long standing HTN

42. PATHO • Heart failure is a complex syndrome that can result from any cardiac disorder (structural or functional) resulting in a failure to maintain sufficient cardiac output to meet the demands of the body. • The clinical syndrome of heart failure is characterised by breathlessness, fatigue and fluid retention.

43. PATHO • The mechanism by which the heart fails to deliver a sufficient cardiac output is dependent on the underlying cause. The circulatory system is exactly that: a system failure of one component affects the entire system. • HF may be classified as right sided HF or left sided HF.

44. Left Sided HF • It can be caused by Aortic Stenosis, Cardiomyopathy, Hypertension, Heart Muscle Infections, Myocardial Infarction etc • Normally, the ventricles of the heart contracts while the atria relax allowing for filling and emptying. • If the muscle of the left ventricle cannot contract effectively, some blood is left in the left ventricle.

45. Left Sided HF • This prevent part of the blood in the left atrium from progressing into the ventricle and in turn blood backs up into the pulmonary vessel, pressure within those vessels increases and fluid leaks into lung tissue producing congestion • Alveolar edema is more serious because it reduces gas exchange across the alveolar capillary membrane. Shortness of breath and cyanosis may result from the decreased oxygenation of the blood leaving the lungs and eventually pulmonary oedema. • If not corrected, left sided heart failure will lead to failure of the right side of the heart.

46. S/S Left-Sided Heart Failure • Dyspnea on exertion • Dry hacky cough, especially supine • Crackles, wheezing • Orthopnea • Paroxysmal nocturnal dyspnea • Cyanosis • Tachypnea, tachycardia • Nocturia.

47. Right Sided HF • It can be caused by chronic lung disease (corpulmonale), pulmonary embolism, pulmonary hypertension, Left-Sided HeartFailure etc • The major cause of right-sided heart failure is leftsided heart failure. When the left side fails, fluid backs up into the lungs and pulmonary pressure is increased. The right ventricle must continually pump blood against this RESISTANCE. • Right sided HF leads to backward build-up of blood in the systemic blood vessels. As the blood backs up jugular neck veins become distended

48. Right Sided HF • Edema may occur in the peripheral tissues, and the abdominal organs can become engorged. • Congestion in the gastrointestinal tract causes anorexia, nausea, and abdominal pain. The liver can becomes congested, known as hepatomegaly. • Congestion of the blood to and from the kidney may lead to impaired renal function, preventing normal excretion of urine and causing fluid accumulation. • Inadequate circulation to and from the brain may cause mental confusion and irritability which sometimes progresses to delirium and coma.

49. S/S RIGHT-Sided Heart Failure • Jugular vein distention • Dependent peripheral edema • Ascites • Weight gain • GI pain, anorexia, nausea • Fatigue, weakness • Tachycardia • Nocturia

50. DIAGNOSTIC EVALUATION • Physical examination • Electrocardiogram • Chest x-ray examination • Coronary angiography