NUR 301 Spring 2018 Alterations of Cardiovascular Function -24 - MI, ACS, Pericarditis, Endocarditi

Glycogen depletion mitochondrial swelling and may be

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Glycogen depletion, mitochondrial swelling and may be reversed if circulation is restored to ischemic area Irreversible cell injury and death of cells occurs within 40 minutes if circulation not restored Reperfusion –fibrinolytics, revascularization Stunned myocardium following reperfusion Diagnosis and Treatment Prognosis related to arrhythmias and pump failure Sudden death from ventricular fibrillation To treat identify is patient is candidate for reperfusion Oxygen, ASA, Nitrates, Analgesics, Beta blocking agents Vasodilate (nitroglycerine) decreases venous return/preload and arterial BP/afterload reducing oxygen consumption/need Morphine manages pain (decreases stress response) and slightly vasodilates coronary arteries Beta blockers decrease oxygen need by decreasing HR, contractility, and BP Reperfusion Percutaneous coronary intervention PTCA percutaneous transluminal coronary angioplasty - balloon Stent placement
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5 Coronary artery bypass grafting Emergent – 4 to 6 hrs Saphenous vein graft Internal mammary artery graft Radial artery graft Fibrinolytic drugs break up clots MI Recovery Necrotic myocardial cells replaced with scar tissue following inflammation, macrophage arrival, vascularized granulation tissue, fibrous (scar) tissue Scar tissue is not as elastic which may alter cardiac output Damaged cells may not conduct resulting in arrhythmias Pericarditis, stroke, emboli, valvular change, septal and/or ventricular wall rupture, aneurysms, heart failure may occur Dressler Syndrome – early to several weeks post MI – autoimmune response to damaged tissue resulting in pericarditis Sharp, stabbing pain increased by inhalation and position changes Disorders of the Heart Wall 622 Disorders of the Pericardium 622 Pericardium - Pericardial Sac Visceral pericardium – thin layer that adheres to the epicardium Parietal pericardium – fibrous outer layer attached to the great vessels Layers separated by thin layer of serous fluid – decrease friction, can stretch Pericardia cavity – 50 ml of serous fluid Pathological processes – congenital, infections, trauma, immune Disorders often associated with other heart or surrounding structure pathologies Acute Pericarditis 622 Inflammation of pericardium of less than 2 weeks Coxsackievirus and echovirus most common, idiopathic (unknown), bacteria, connective tissue disorders (systemic lupus erythematosus - SLE, rheumatoid arthritis- RA ), uremia, post cardiac surgery, neoplasia, radiation, trauma, drug toxicity, inflammations from lungs Inflammation -increased capillary permeability – plasma proteins enter pericardial space – this exudate varies with agent involved – heals by resolution, scar tissue, adhesions Manifestations 1. Pain – sharp, abrupt onset, precordial, may radiate , increase with deep breath , cough, swallow, relieved by leaning forward 2. Pericardial friction rub –leathery 3. ECG changes – Diagnosis Clinical S/S, ECG, x-ray, echocardiogram Treatment Antibiotics (specific to causative agent), ASA, NSAIDS Recurrent pericarditis
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