Cardiovascular Disorders Study Guide

Ventricular tachycardia: This disorder is associated with chest pain, diaphoresis, hypotension, weak pulse and possible loss of consciousness. The ECG would show ventricular rate of 140-220 with wide and bizarre QRS complexes. There would be no visible P-waves. It appears on an EKG as: The treatment for ventricular tachycardia would include: ASLC protocol: for intubation if pulseless Drug therapy: o Amiodarone o Epinephrine o Lidocaine o Magnesium sulfate o Vasopressin CRP, if the patient has no pulse Synchronized cardioversion Implantable cardiac defibrillator Cardiac tamponade: This disorder is characterized by raise in the intrapericardial pressure that impairs the hearts ability to fill during the diastolic period. The rise in pressure is the usually the result of blood or fluid accumulation in the pericardial sac. If the fluid increase is a rapid process, it is commonly fatal and requires immediate intervention to preserve life. If the process is more gradual, symptoms will be less noticeable. This is because the pericardial sac can gradually stretch to accommodate 1-2 liters of fluid. Causes: Dressler’s syndrome: Pericarditis that results after a heart attack Effusion Hemorrhage from non-traumatic causes: o Rupture of the heart or great vessels o Anticoagulant therapy Hemorrhage form traumatic causes: o Gunshot or stab wound o Perforation of the heart by a catheter MI Uremia Clinical Manifestations: Anxiety Diaphoresis Dyspnea Hepatomegaly Increase in venous pressure Muffled heart sounds Narrowing pulse pressure Distention of the veins in the neck Pallor or cyanosis Pulsus paradoxus: this is an abnormal inspiratory drop in the systolic blood pressure greater than 15mm Hg Reduction of arterial blood pressure Tachycardia The patient assumes an upright and leans forward position Diagnostic tests: Chest x-ray that shows a slightly widened mediastinum and cardiomegaly Echocardiogram ECG may show changes. This test is more useful in ruling out other conditions Pulmonary artery catheterization will detect an increase in the pressures in the right atrium, right ventricular diastolic and central venous pressures. Treatments: Surgical intervention Drug therapy: o Adrenergic: o Heparin antagonist: in cases related to anticoagulation therapy with heparin o Inotropic agents, such as dopamine o Vitamin K in cases of Coumadin therapy Allow the patient to discuss fears and anxieties Monitor ECG closely for any signs of changes or hemodynamic instability The patient may require a thoracotomy Cardiogenic shock: This is the result of the heart failing. The heart’s ability to pump becomes inadequate, which results in a reduction in cardiac output and compromised tissue perfusion. The process by which Cardiogenic shock occurs is as follows: There is a decrease in stroke volume, which results in an increase in left ventricular volume. This increase in blood in the ventricle results in a back up of blood in the lungs. This causes pulmonary edema. The heart attempts to correct this condition, the heart increases heart rate and contractility. This increase in activity results in an increase in oxygen demand. The imbalance created between oxygen demand and supply increases the myocardial ischemia and further compromises the heart ability to pump. Risk Factors: MI Advanced heart block Cardiomyopathy Heart failure Papillary muscle rupture Myocarditis Clinical Manifestations: Cold and clammy skin Hypotension Narrowing pulse pressure Oliguria Tachycardia Anxiety Crackles in the lungs Jugular venous distention S3 and S4 heart sounds Tachypnea Hypoxia Weak and thready pulse Diagnostic tests: ECG will show signs of an MI: o Enlarged Q wave o Elevated ST segment ABG results that indicate respiratory alkalosis in early stages and metabolic acidosis in the late stages Blood chemistry results in an increase in BUN, creatine and cardiac troponin level Hemodynamic monitoring that shows: o decrease in stroke volume o o o o o decrease in cardiac volume increased in pulmonary artery pressure (PAP) increase in pulmonary wedge pressure (PAWP) increase in CVP increase in systemic vascular resistance (SVR) Treatments: Intra-aortic balloon pump (IAPB) Increase in oxygenation; intubation if necessary Decrease in activity; bedrest Continuous hemodialysis NPO Drug therapy Monitoring of hemodynamic stability Monitoring of respiratory status Monitor intake and output Monitor for early signs of fluid overload Monitoring level of consciousness Cardiomyopathy: Cardiomyopathy is the process by which the middle muscle layer, myocardium around the left ventricle becomes flabby. This causes alteration in cardiac function with a decrease in cardiac output. In the early stages, that heart compensates with an increase in muscle mass and heart failure in the later stages. There are three types of Cardiomyopathy. They are: Dilated or congestive: This is the most common form. The heart chamber dilates and contracts poorly by this process. This causes the blood to pool and reduces the cardiac output. Hypertrophic or obstructive: The hypertrophied muscle of the left ventricle is unable to relax and prevents proper filling. Restrictive or obliterative: This is a rare form of Cardiomyopathy. This is the result of stiffing of the ventricles that prevents proper filling. Risk Factors: Dilated: o Chronic alcoholism o Metabolic and immunological disorders o Infection o Pregnancy or postpartum disorders Hypertrophic o Hypertension o Congenital disorders Restrictive o Amyloidosis: the deposit of amyloid, a wax substance consisting of protein that is deposited on an organ o Cancer Clinical Manifestations: Murmur, S3 and S4 sounds Cough Crackles on lung auscultation Dependent pitting edema Dyspnea, paroxysmal nocturnal Dyspnea Fatigue Enlarge liver Jugular vein distention Diagnostic tests: ECG that shows left ventricle hypertrophy and nonspecific changes Echocardiogram shows decrease in myocardial function Cardiac catheterization to rule out coronary artery disease (CAD) Chest x-ray that shows cardiomegaly and pulmonary congestion Treatments: Dual chamber pacing in the case of hypertrophic Cardiomyopathy Drug therapy: o Beta-adrenergic blockers o Calcium channel blockers o Diuretics o Inotropic o Oral anticoagulant Surgical options: when drug therapy fails o Heart transplant: dilated Cardiomyopathy o Cardiomyoplasty: dilated Cardiomyopathy o Ventricular myotomy: hypertrophic Cardiomyopathy Monitoring of electrolytes Monitor hemodynamic stability Monitor respiratory status Decrease oxygen demand; bedrest Low salt fluid restrictive diet Keep patient in semi-fowler’s position Monitor ECG rhythms for arrhythmias Decrease oxygen demands Monitor intake and output Coronary Artery Disease: The condition known as coronary artery disease is a result of atherosclerosis. Atherosclerosis is the buildup of plaque in the arteries of the heart. This process results in a narrowing of the diameter in the arteries; leading to a reduction of blood flow in the myocardium. Risk Factors: Arteriosclerosis Atherosclerosis Aging Menopause Diabetes Genetics High fat diet Hyperlipidemia Hypertension Obesity Sedentary life Smoking Stress Clinical Manifestations: Chest pain lasting 3-5 minutes. Usually occurs under stress or emotional excitement. Diagnostic tests: Low high-density lipoproteins (HDL) and High low-density lipoproteins (LDL) Coronary Arteriography ECG – ST depression Stress test – ST changes Treatment: Lifestyle changes o Weight loss o Low-sodium, low-fat high fiber diet Coronary artery bypass surgery Coronary artery stent placement Drug therapy: o Anticoagulant: Heparin o Analgesic: Morphine o Antilipemic agents: Questran o Beta-adrenergic blocker: Lopressor o Calcium channel blocker: Procardia o Nitrates: Nitroglycerin o Aspirin Obtain ECG at time of chest pain Monitor cardiovascular status Monitor Intake and output Stress reduction Educate: o Diet o Exercise o Smoking cessation o Home Nitro for chest pain o Support groups Endocarditis: An infection of the Endocardium, either bacterial or fungal. This results in vegetative growth on the heart valves or endocardial lining. If untreated, is usually fatal, if the patient receives appropriate treatment, there is a 70% recovery rate. Bacterial Causes: Enterococci IV drug abuse Mitral valve prolapse Prosthetic heart valve Rheumatic heart disease Streptococci Staphylococci Risk factors: Coarctation of the aorta Dengenerative heart disease Marfan syndrome Pulmonary stenosis Subaortic and valvular disease Tetralogy of Fallot Ventricular septal defects Clinical Manifestations: Chills Intermittent, recurring fever Anorexia Arthralgia Fatigue Loud murmur Malaise Night sweats Valvular insufficiency Weakness Weight loss Diagnostic tests: Elevated WBC Echocardiography – valvular damage ECG – Arterial fibrillation Blood culture – three or more positive blood cultures in a 24hr period identify the causative agent Treatments: Bed rest Maintaining sufficient fluid intake Surgery – if necessary to replace valve Drug therapy: o Antibiotics o Aspirin Assess for sign of embolization Assess renal status Assess for heart failure Patient education Heart failure: Heart failure is the result of the heart’s inability to pump enough blood to meet the body’s oxygen demand. It can be left-sided (associated with respiratory problems) or right-sided (associated with systemic failure). Risk Factors: Atherosclerosis Cardiac conduction defects (left-sided) Chronic obstructive pulmonary disease (right-sided) Fluid overload Hypertension MI Pulmonary hypertension Valvular insufficiency Valvular stenosis Clinical Manifestations: Left-sided failure: Anxiety Arrhythmias Cough Crackles Dyspnea Fatigue Gallop rhythm; S3 and S4 Orthopnea Paroxysmal nocturnal dyspnea Tachycardia Tachypnea Right-sided: Anorexia Ascites Dependent edema Fatigue Gallop rhythm; S3 and S4 Hepatomegaly Jugular vein distention Nausea Tachycardia Weight gain Diagnostic tests: Left-sided: Arterial blood gas – hypoxemia and hypercapnia Decrease serum potassium and sodium Chest X-ray – pulmonary congestion ECG – left ventricular hypertrophy Echo – increase size of cardiac chambers Hemodynamic monitoring – increase pulmonary artery pressure and decreased cardiac output Right-sided: Arterial blood gas – hypoxemia Decrease serum potassium and sodium Chest X-ray – pulmonary congestion and cardiomegaly ECG – right ventricular hypertrophy Echo – increase size of cardiac chambers Hemodynamic monitoring – increase central venous pressure and decreased cardiac output Treatment: IABP Dietary changes o Low sodium o Limited fluid intake Oxygen therapy Left-ventricular assist device(left-sided) Paracentesis(right-sided) Thoracentesis(right-sided) Drug therapy o Analgesic: morphine o Angiotensin-converting enzymes (ACE) inhibitors: Capoten o Inotropic agents: Dopamine o Cardiac glycoside: Digoxin o Diuretics: Lasix o Nitrates: Isordil o Vasodilators: Nitropress Hemodynamic stability Respiratory status Semi-fowler’s position Oxygen therapy I&O Assess for electrolyte imbalances Suction if necessary Daily weights Measure abdominal girth Allow patient to express feelings Myocardial Infarction (MI): This is a condition of decreased blood flow through a coronary artery that results in myocardial ischemia, injury or necrosis. Risk Factors: Aging Diabetes mellitus Hypertension Low HDL Family history Obesity Menopause Sedentary lifestyle Smoking Stress Usage of illegal drugs Clinical Manifestations: Arrhythmias Anxiety Chest pain: o Substernal o Jaw o Back o Arms o Not relieved by rest Diaphoresis Elevated temperature Nausea and vomiting Pallor Diagnostic tests: ECG: o ST segment – elevated or depression o T-wave – inversion o Q-wave – enlarged CK-MB – positive LD1 – flipped Troponin – elevated Treatments: Monitor: o Vital signs o ECG o Arrhythmias o Heart failure o Cardiogenic shock o Pericarditis I&O Oxygen Pulmonary artery catheterization Drug therapy: o ACE inhibitors: Capoten o Analgesics: Morphine o Antiarrhythmics: Lidocaine o Anticoagulants: Aspirin or Heparin o Beta-adrenergic blockers: Inderal o Calcium channel blockers: Procardia o Nitrates: Nitroglycerin o Possible Thrombolytic therapy: Streptase Lifestyle changes: o Increase activity o Decrease stress o Calm environment o Smoking cessation o Reducing alcohol intake Dietary changes: o Low sodium o Low cholesterol Bed rest Myocarditis: This is a focal or diffuse inflammation of cardiac muscle. It may be an acute or chronic condition. Risk Factors: Bacterial infections Chemical poisons Helminthic infections Hypersensitive immune reactions Parasitic infections Radiation therapy Viral infections Clinical Manifestations: Cardiomyopathy Arrhythmias Murmurs: S3 and S4 gallops Chronic valvulitis Dyspnea Fatigue Fever Mild, continuous pressure or soreness in chest Palpitations Thromboembolism Diagnostic test: ECG – diffuse ST segment and T-wave abnormalities CK-MB – positive WBC – elevated ESR – elevated Throat culture – causative bacteria Treatments: Bed rest Dietary changes: low sodium Drug therapy: o Antibiotics o Antiarrhythmics: Amiodarone o Anticoagulants: Coumadin o Cardiac glycosides: Digoxin o Diuretics: Lasix Assess: o Vital signs o S/S of heart failure o Arrhythmias Monitor for digitalis toxicity Acute Pericarditis: Pericarditis is an inflammation of the pericardium, the fibroserous sac that surrounds the heart. Risk Factors: Bacterial, fungal or viral infection Hypersensitivity or autoimmune disease High-dose radiation to the chest Neoplasm Post cardiac injury Uremia Clinical Manifestations: Pericardial friction rub Chest pain: o Sudden sharp chest pain o Increases with inspiration o Decreases when sitting up Symptoms of heart failure Symptoms of cardiac tamponade Diagnostic test: WBC – elevated Echo – shows free space between the ventricle and pericardium ECG – ST elevation Culture of pericardial fluid Treatments: Bedrest Surgery: o Pericardiocentesis o Partial pericardectomy o Total pericardectomy Drug therapy: o Antibiotics o Corticosteroids o Nonsteroidal anti-inflammatory drugs High fowler’s position Oxygen therapy Pain relief Assess for: Allow patient to verbalize feelings Vascular Disorders Abdominal Aortic Aneurysm: This disorder is a result of damage to the medial layer of the abdominal aorta. The damage weakens the wall of the aorta. The disorder is compounded by the high force of blood flow in this section of the aorta. This pressure and damage causes the weakened portion of the wall to extend out. The aneurysm that results can lead to hemorrhage, hypovolemic shock and possible death. There are four types of abdominal aneurysms: Dissecting: this is the process by which the vessel wall ruptures and a blood clot retained in the out pouching of tissue False: this is a pulsating hematoma that is the result of trauma Fusiform: this is the bilateral out pouching of the vessel wall Saccular: this is a unilateral out pouching of the vessel wall Risk Factors: Atherosclerosis Congenital defect Infection Hypertension Marfan syndrome Trauma Syphilis Clinical Manifestations: Abdominal pulsation Abdominal mass, to the left of mid-line Diminished femoral pulses Lower abdominal pain Lower back pain Lower systolic blood pressure in the legs when compared to the arms Commonly asymptomatic Diagnostic tests: Abdominal CT scan Abdominal ultrasound Arteriography Chest x-ray An ECG can differentiates aneurysm from an MI Treatments: Drug therapy: o Analgesic o Antihypertensive o Beta-blockers Assessment of cardiovascular status Monitor intake and output Observe patient for signs and symptoms of hypovolemic shock Avoid palpation of the abdomen Check peripheral circulation o Temperature o Color o Pulses Assess for pain Encourage patients to discuss feels of anxiety Thoracic aortic aneurysm: As mentioned before an aneurysm is an out pouching of artery. In this case, it is weakening of the wall of the aorta. This weakening can be in either in the ascending, transverse or descending aorta. Risk Factors: Atherosclerosis Congenital defect Infection Hypertension Marfan syndrome Trauma Syphilis Clinical Manifestations: Ascending Bradycardia Pain: severe, boring or ripping Pericardial friction rub Weakened right carotid and radial pluses Descending Pain sharp and tearing Transverse Dry cough Dyspnea Dysphagia Hoarseness Pain: sharp and tearing Diagnostic tests: Aortography Hemoglobin – low Chest X-ray – widening of aorta CT scan Echo ECG Transesophageal echo Treatments: Surgery Drug therapy: o Analgesic: Morphine o Antihypertensives: nitroprusside o Negative Inotropic: Inderal Assess: o Vital signs o Level of consciousness o Respiratory status Systolic blood pressure less 120 Arterial occlusive disease: This disorder ranges from a narrowing to the complete obstruction in the lumen of arterial vessel. This decrease in blood flow results in tissue hypoxia to the affected areas. It is most common in the lower extremities. Risk Factors: Atherosclerosis Emboli formation Thrombosis Trauma or fracture Risk facture: o Age increase incidence with age o Sex more common in males o Diabetes o Family history of vascular disorders o Hyperlipidemia o Smoking o Hypertension The area that is affected will determine the symptoms found: Internal and external carotid arteries: Absence or decreased pulsation in the affected vessel Stroke Transient ischemic attacks (TIA) Femoral, popliteal or innominate arteries: Mottled extremity Pallor Paresthesia Pulselessness distal to occlusion Sudden and localized pain in affected extremity Temperature change that occurs distal to the occlusion Subclavian artery: This results in Subclavian Steel Syndrome. This is a process by which the back-flow of blood from the brain through the vertebral artery on the same side as the occlusion, into the Subclavian artery distal to the occlusion. The sign and symptoms of this disorder include a vertebrobasilar occlusion and exercise induced arm claudication. Diagnostic tests: Arteriography will indicate the type (thrombus or embolus), location and degree of obstruction as well as collateral circulation. EEG and CT scan may be used to rule out a brain lesion. Ophthalmodynamometry can help to determine the degree of an occlusion in the internal carotid artery. The treatment for the different areas includes: Possible surgery: Drug therapy: o Anticoagulants:  Heparin  Fragmin  Lovenox  Coumadin o Antiplatelets  Aspirin  Trental o Thrombolytic agents:  Activase  Streptase No smoking Pain relief as necessary Venous Occlusion This disorder is a result of platelet aggregation to the venous walls. The resulting occlusion decreases the venous return from the affected area. Risk Factors: History of varicose veins. Hypercoagulation Neoplastic disease Cardiovascular disease Recent surgery Recent injury Elderly Those who take oral contraceptives People who travel for long distances without ambulating Clinical Manifestations: Edema Warmth Tenderness Positive Homan’s sign Treatments: Anticoagulation therapy: o Heparin IV  Duration 5-7 days  PTT is therapeutic range (1 ½ - 2 times the control)  PTT monitored every 6 hours o Coumadin therapy begins when the PTT is at therapeutic range  Coumadin therapy may last 3- 6 months Prevention is the key and early identification of those at risk Hypertension: This is a condition of persistent elevation of systolic or diastolic blood pressure. There are two types: essential hypertension- most common, of unknown cause and secondary- caused by renal disease or other systemic disease. Stages of hypertension: Pre-hypertension: 120-139/80-89mm/Hg Stage 1: 140-159/90-99 mm/Hg Stage 2: greater than 160/greater than 100 mm/Hg Risk Factors: Coarctation of aorta Cushing’s disease Neurological disorders Oral contraceptives Pheochromocytoma Pregnancy Primary Hyperaldosteronism Renovascular disease Endocrine disorder Illegal drug use Risk factors: o Aging o Diet o Family history o Obesity o Race(African-American) o Sex(Male) o Smoking o Stress Clinical Manifestations: Asymptomatic Cerebral ischemia Elevated blood pressure Dizziness Headache Left ventricular hypertrophy Papilledema Renal failure Visual disturbances Diagnostic tests: Elevated blood pressure ECG – left ventricular hypertrophy Ophthalmoscopic exam – Papilledema Urinalysis – proteinuria Treatments: Lifestyle changes: o Increase activity o Decrease stress o Calm environment o Smoking cessation o Reducing alcohol intake Dietary changes o Low sodium o Low cholesterol Drug therapy o ACE inhibitors: Capoten o Beta-adrenergic blockers: Inderal o Calcium channel blockers: Procardia o Diuretics: Lasix o Vasodilators: Nitropress Cardiovascular assessment Take an average of two or more blood pressures Neurologic assessment