Lipp Vis Nursing ChaptLWBK1630_C02_p013-068

46  Chapter 2 • Cardiovascular Care

CARDIAC TAMPONADE Cardiac tamponade is a life-

threatening compression of the heart due to the pericardial accumulation of fluids as a result of inflammation, infection, trauma, and rupture of the heart or aortic dissection. Common causes of cardiac tamponade include: • Viral pericarditis and effusion • Ascending aortic dissection rupturing into the pericardium • LV free wall rupture after a large anterior MI • Trauma • Neoplasm/malignancy • Iatrogenic (invasive procedure- related, postcardiac surgery) • Collagen vascular diseases (systemic lupus erythematosus, rheumatoid arthritis, scleroderma) • Radiation induced • Uremia • Bacterial infection • Tuberculosis • Pneumopericardium Clinical Manifestations • Tachycardia • Hypotension • Pulsus paradoxus • Raised jugular venous pressure • Muffled heart sounds • Decreased electrocardiographic voltage with electrical alternans • Enlarged cardiac silhouette on chest x-ray • Pain in anterior chest, worsened by motion, may vary from mild to sharp and severe chest. Generally located in precordial area and may be relieved by leaning forward Treatment • Removal of the pericardial fluid (pericardiocentesis) Uncommon causes of cardiac tamponade:

Effects of Respiration and Cardiac Tamponade on Ventricular Filling and Cardiac Output

Pericardium

PICTURING PATHO

Left ventricle

Normal expiration

Normal inspiration

TIP: Abnormally large de- crease in systolic blood pressure ( > 10 mm Hg) on inspiration is a common finding in moderate to se- vere cardiac tamponade.

Tamponade (in inspiration)

Effects of respiration and cardiac tamponade on ventricular filling and cardiac output. During inspiration, venous flow into the right heart increases, causing the interventricular septum to bulge into the left ventricle. This produces a decrease in left ventricular volume, with a subsequent decrease in stroke volume output. In cardiac tamponade, the fluid in the pericardial sac produces further compression of the left ventricle, causing an exaggeration of the normal inspiratory decrease in stroke volume and systolic blood pressure. (Reprinted with permission from Porth C. Essentials of Pathophysiology . 4th ed. Philadelphia: Wolters Kluwer; 2015.)