lecture 3 Cardiac alteration
- 1. Lecture 3 : Cardiovascular Disorders
- 2. A. CORONARY ARTERY DISEASE
- 3. Pathophysiology of Coronary Artery Disease • Development of Atherosclerosis Atherosclerosis is a chronic inflammatory disorder that is characterized by an accumulation of macrophages and T lymphocytes in the arterial intimal wall. A high LDL cholesterol concentration is one of the triggers of vascular inflammation. The inflammation injures the wall, allowing the LDL cholesterol to move into the vessel wall below the endothelial surface. Blood monocytes adhere to endothelial cells and migrate into the vessel wall. Within the artery wall, some monocytes differentiate into macrophages that unite with and then internalize LDL cholesterol. The foam cells that result are the marker cells of atherosclerosis
- 5. B. Acute Coronary Syndrome • The term acute coronary syndrome (ACS) is used to describe the array of clinical presentations of CAD that range from unstable angina to acute MI • Angina • Angina pectoris, or chest pain, caused by myocardial ischemia is not a separate disease, but rather a symptom of CAD. • The lack of oxygen causes myocardial ischemia, which is felt as chest discomfort, pressure, or pain.
- 9. Types of Angina • Stable Angina. Stable angina is predictable and caused by similar precipitating factors each time; typically, it is exercise induced. Patients become used to the pattern of this type of angina and may describe it as “my usual chest pain.” Pain control should be achieved within 5 minutes of rest and by taking sublingual nitroglycerin. • Unstable Angina. Defined as a change in a previously established stable pattern of angina. It is part of the continuum of ACS. Unstable angina usually is more intense than stable angina, may awaken the person from sleep, or may necessitate more than nitrates for pain relief.
- 10. Types of Angina ..cont. • Variant Angina. Variant angina, or Prinzmetal angina, is caused by a dynamic obstruction from intense vasoconstriction of a coronary artery. Coronary artery spasm is treated with nitroglycerin or calcium channel blockers to vasodilate the coronary arteries • Silent Ischemia. Silent ischemia describes a situation in which objective evidence of ischemia is observed on an ECG monitor but the person does not complain of anginal symptoms.
- 11. Medical Management • Aspirin (if the patient cannot tolerate aspirin, then a thienopyridine such as clopidogrel can be given) • Patients with definite unstable angina or non–ST elevation myocardial infarction (UA or NSTEMI) should receive dual antiplatelet therapy on admission if an invasive strategy is imminent. • A glycoprotein (GP) IIb/IIIa inhibitor is administered unless bivalirudin is chosen; and a loading dose of clopidogrel is given at least 6 hours prior to the procedure.
- 13. Relieving Chest Pain • Oxygen: All patients with acute ischemic pain are administered supplemental oxygen to increase myocardial oxygenation. • Nitrates: A combination of intravenous and sublingual nitroglycerin is used to vasodilate the coronary arteries and decrease pain. After nitrate administration, the critical care nurse closely observes the patient for relief of chest pain, for return of the ST segment to baseline, and for the potential development of unwanted side effects such as hypotension and headache. Administration of a nitrate is avoided if the SBP is below 90 mm Hg.
- 14. Relieving Chest Pain …cont. • Analgesia: Morphine (2 to 4 mg given intravenously) is the analgesic opiate of choice for preinfarction angina. • Aspirin: Chewing an oral non–enteric-coated aspirin (162 to 325 mg) at the beginning of chest pain has been shown to reduce mortality.
- 15. Patient Education • After the anginal pain is controlled, longer-term education of th patient and the family can begin. Points to cover include: 1) Risk factor modification 2) Signs and symptoms of angina, 3) When to call the physician, 4) Medications, and 5) Dealing with emotions and stress.
- 16. Cardiac Care : Acute • See appendix 1
- 17. MYOCARDIAL INFARCTION • Myocardial infarction (MI) is the term used to describe irreversible myocardial necrosis (cell death) that results from an abrupt decrease or total cessation of coronary blood flow to a specific area of the myocardium. • Three mechanisms can block the coronary artery and are responsible for the acute reduction in oxygen delivery to the myocardium: 1. Plaque rupture 2. New coronary artery thrombosis 3. Coronary artery spasm close to the ruptured plaque
- 18. Pathophysiology A. Ischemia The outer region of the infarcted myocardial area is the zone of ischemia, or penumbra. B. Injury The infarcted zone is surrounded by injured but still potentially viable tissue in an area known as the zone of injury C. Infarction The area of dead muscle (necrosis) in the myocardium is known as the zone of infarction
- 20. 12-Lead Electrocardiographic Changes • The changes in repolarization are seen by the presence of new Q waves. These new, pathologic Q waves are deeper and wider than tiny Q waves found on the normal 12-lead ECG B- inversion T wave indicated to Ischemia C- T wave inversion and ST- segment elevation Indicated to Ischemia and current injury D- Q wave indicated to necrosis A- normal ECG
- 21. Non–ST-Segment Elevation Myocardial Infarction • One reason for the lack of ST-segment elevation may be that the infarction and subsequent necrosis are not full thickness lesions. Because some of the muscle in the area can still be depolarized, ST- segment elevation may not occur. • This type of MI is also less likely to develop Q waves on a subsequent 12-lead ECG after the acute phase has passed. This situation is diagnostically known as an NSTEMI.
- 23. Cardiac Biomarkers During Myocardial Infarction
- 24. Complications of Acute Myocardial Infarction Sinus Bradycardia heart rate less than 60 beats per minute [beats/min Sinus Tachycardia. Sinus tachycardia (heart rate more than 100 beats/min) Atrial Dysrhythmias. Premature atrial contractions (PACs) occur frequently in patients who sustain an acute MI. Ventricular Dysrhythmias. Premature ventricular contractions (PVCs) are seen in almost all patients within the first few hours after an MI. Atrioventricular Heart Block During Myocardial Infarction. Heart block can occur in 6% to 14% of patients with STEMI, and those patients have increased mortality rates.
- 25. Complications of Acute Myocardial Infarction … cont. Ventricular Aneurysm After Myocardial Infarction. Ventricular Septal Rupture After Myocardial Infarction Heart Failure and Acute Myocardial Infarction
- 26. Medical Management • Recanalization of the Coronary Artery fibrinolytic therapy or PCI to open the occluded artery for the patient with an acute STEMI • Anticoagulation For patients who will receive fibrinolytic therapy, an initial heparin bolus of 60 units/kg (maximum 5000 units) is given intravenously, followed by a continuous heparin drip at 12 units/kg/hr (maximum 1000 units/hr) to maintain an activated partial thromboplastin time (aPTT) between 50 and 70 seconds (1.5 to 2.0 times) control for 48 hours or until revascularization.
- 27. Medical Management … cont. • Dysrhythmia Prevention The antidysrhythmic with the best safety record after STEMI is amiodarone. Beta-blockers are another class of antidysrhythmics that are recommended for all patients after STEMI. Beta-blockers prevent ventricular dysrhythmias, lower blood pressure, and prevent reinfarction, especially in patients with left ventricular dysfunction. Prevention of Ventricular Remodelling Many patients are at risk for development of heart failure after STEMI. Vasodilating medications (ACEIs or ARBs) can stop or limit the ventricular remodeling that leads to heart failure.
- 30. HEART FAILURE • Pathophysiology I. a condition in which the heart cannot pump blood at a volume required to meet the body’s needs. II. CAD with resultant necrotic damage to the left ventricle is the underlying cause of heart failure in most patients. III. Other major conditions that lead to heart failure include valvular dysfunction
- 32. Type of heart failure. 1. Left Ventricular Failure defined as a disturbance of the contractile function of the left ventricle, resulting in a low cardiac output state. This leads to vasoconstriction of the arterial bed that raises systemic vascular resistance (SVR), a condition also described as “high afterload,” and creates congestion and edema in the pulmonary circulation and alveoli. Ptients presenting with left ventricular failure have one of the following: 1) decreased exercise tolerance 2) fluid retention 3) discovery during examination of noncardiac problems.
- 33. 2. Right Ventricular Failure • defined as ineffective right ventricular contractile function. Pure failure of the right ventricle may result from an acute condition such as a pulmonary embolus or a right ventricular infarction • The common manifestations of right ventricular failure are: jugular venous distention, elevated central venous pressure (CVP), weakness, peripheral or sacral edema, hepatomegaly (enlarged liver), jaundice, and liver tenderness. Gastrointestinal symptoms include poor appetite, anorexia, nausea, and an uncomfortable feeling of fullness
- 35. 3. Systolic Heart Failure The term systolic dysfunction describes an abnormality of the heart muscle that markedly decreases contractility during systole (ejection) and lessens the quantity of blood that can be pumped out of the heart. 4. Diastolic Heart Failure abnormality of the heart muscle that makes it unable to relax, stretch, or fill during diastole. Diastolic heart failure (DHF) is caused by left ventricular dysfunction.
- 37. Pulmonary Complications of Heart Failure • Breathlessness in heart failure is described by the following terms: Dyspnea: the patient’s sensation of shortness of breath, which from pulmonary vascular congestion and decreased lung compliance Orthopnea: difficulty breathing when lying flat because of an increase in venous return that occurs in the supine position Paroxysmal nocturnal dyspnea: a severe form of orthopnea in which the patient awakens from sleep gasping for air Cardiac asthma: dyspnea with wheezing, a non-productive cough, and pulmonary crackles that progress to the gurgling sounds of pulmonary edema Pulmonary Edema in Heart Failure Pulmonary edema, or protein-laden fluid in the alveoli, inhibits gas exchange by impairing the diffusion pathway between the alveolus and the capillary. It is caused by increased left atrial and ventricular pressures and results in an excessive accumulation of serous or serosanguineous fluid in the interstitial spaces and alveoli of the lungs.
- 38. Medical Management A. Relief of Symptoms and Enhancement of Cardiac Performance. Acute phase of advanced heart failure, the patient may have a pulmonary artery catheter in place so that left ventricular function can be monitored closely. • Control of symptoms involves management of fluid overload and improvement of cardiac output by decreasing SVR and increasing contractility. • Diuretics are administered to decrease preload and to eliminate excess fluid from the body. • Morphine is given to facilitate peripheral dilation and decrease anxiety. • Afterload is decreased by vasodilators such as sodium nitroprusside (Nipride) and nitroglycerin. • Sodium nitroprusside is a balanced vasodilator medication that relaxes arterial resistance and venous capacitance vessels. • Nitrates are used to decrease preload and vasodilate the coronary arteries if CAD is an underlying cause of the acute heart failure.
- 39. Medical Management … cont. A. Chronic phase • After the acute exacerbation is resolved, the patient is transitioned to oral agents • patient with heart failure will receive ACEIs to inhibit left ventricular chamber remodelling and slow left ventricular dilation. • Digoxin may be added to the regimen, especially if the person has concomitant AF.
- 41. Patients education related to Heart Failure
- 42. VALVULAR HEART DISEASE appendix 3 • Mitral Valve Stenosis The term mitral valve stenosis describes a progressive narrowing of the mitral valve orifice. Symptoms occur when the normal valve size is reduced to 2 cm2 or less. Symptoms occur at rest when the valve area is reduced below 1 cm. • Mitral Valve Regurgitation Mitral valve regurgitation results in retrograde flow of blood into the left atrium with each ventricular contraction.
- 43. VALVULAR HEART DISEASE … cont. • Aortic Valve Stenosis describes a narrowing of the aortic valve area. • Aortic Valve Regurgitation Aortic valve incompetence results in a reflux of blood back into the left ventricle during ventricular diastole. • Tricuspid Valve Stenosis It often occurs in conjunction with mitral or aortic disease. Tricuspid valve stenosis increases the pressure work of the usually low- pressure right atrium, resulting in right atrial hypertrophy
- 44. Medical Management • Management of valvular disorders includes pharmacologic therapy to control symptoms of heart failure and then cardiac surgical repair or replacement of the affected valve.