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Cardiovascular Emergencies – Part II Acute Aortic Dissection Uncommon but lethal! Tear in the intimal layer of the aorta that results in a false lumen that is usually anterograde in nature. Usual locations: ascending aorta superior to aortic valve descending aorta at the ligamentum arteriosm Acute Aortic Dissection The most common and most lethal acute aortic dissection, which accounts for 2/3 of all dissections, occurs where? Acute Aortic Dissection Most common in men between the ages of 60 & 70 Factors: • hypertension • hereditary defects of connective tissue (Marfan’s) pregnancy blunt trauma iatrogenic factors (intra-arterial catheterization) Acute Aortic Dissection SUBJECTIVE DATA History Pain – sudden, sharp, tearing, excruciating, medications may not relieve, substernal (ascending), back/flank (descending) Syncope Altered LOC Paraplegia Acute Aortic Dissection OBJECTIVE DATA Physical Exam - variable BPs on right vs left - decreased peripheral pulses/ peripheral cyanosis - murmur - pallor, oliguria, altered LOC, - BP: hyper with distal dissection, hypo with proximal - extreme pain Acute Aortic Dissection OBJECTIVE DATA Diagnostics - CBC (Hct tends to fall, WBC 12,000-20,000) T&C,BUN/Creatinine - EKG: Normal in 1/3, LV hypertrophy if hx of HTN, signs of MI if proximal dissection - Acute Aortic Dissection CXR: -widened aortic silhouette -widened mediastinum, -left-sided pleural effusion Acute Aortic Dissection Diagnostics cont. - CT Scan Acute Aortic Dissection INTERVENTIONS ABC Pain relief Large bore IVs • – minimum of two sites Monitoring Medications: 1) to lower arterial BP: nitroprusside, labetalol Acute Aortic Dissection Medications cont: 2) To decrease contraction force: beta blockers preferred, may give calcium channel blockers if beta blockers contraindicated 3) To relieve pain: Morphine Position of comfort IVF in hypotensive setting Foley Acute Aortic Dissection Anticipate: ED thoracotomy, immediate need for OR, arterial & central venous cannulation Therapeutics: Explain all procedures to patient/family, maintain calm, allow family at bedside if possible Acute Pericarditis Result of inflammation of the pericardium that may extend to adjacent structures and may produce exudate. Factors: - infections: idiopathic, viral, bacterial, fungal - connective tissue disease (lupus, rheumatoid) - renal disease - neoplastic disorders - tissue injury Acute Pericarditis Acute pericarditis is more common in which gender and which age group? Acute Pericarditis SUBJECTIVE DATA Chest Pain – deep inspiration, recumbent, movement, severe, sharp or dull ache, retrosternal or epigastric radiating to back/neck/ side, sudden, persistent General malaise, fever, chills, weight loss Dyspnea, cough Acute Pericarditis SUBJECTIVE DATA cont. Medical History may include: • TB, congenital anomalies, immune disorders, MI, neoplastic disease, drug use, uremia, cardiac surgery, cardiac trauma, infections Acute Pericarditis OBJECTIVE DATA Physical Exam - pericardial friction rub (hallmark) – heard best at the left lower sternum during end expiration with patient leaning forward - tachycardia, fever, tachypnea Acute Pericarditis Diagnostics - EKG: FOUR STAGES (best seen in inferior leads) 1) ST elevation (early) with upright T waves, 2) T wave flattens and ST returns to baseline 3) T wave inversion 4) T wave returns to normal (weeks to months) - Lab: CBC, BUN/Cr, Electrolytes, cultures, UA - CXR: helpful to detect pericardial effusion or potential etiology - Echocardiogram: most accurate in detecting!! Acute Pericarditis INTERVENTIONS Supplemental O2, cardiac monitoring Position of comfort Anti-inflammatory medications Pericardiocentesis if necessary Labs as ordered Antibiotics as ordered Acute Pericarditis INTERVENTIONS cont Monitor/reassess Therapeutics: • maintain calm • explain all procedures • allow family at bedside if possible • reassurance Infective Endocarditis Infection of the endocardium and heart valves SBE • subacute bacterial endocarditis usually occurs in patients with congenital or acquired valvular disease; patients are less toxic ABE • acute bacterial endocariditis usually affects normal heart valves and has a greatly accelerated pace of development; patients are extremely toxic with metastatic infections. Infective Endocarditis Infective agents (most common): - ABE: staphylococcus aureus - SBE: streptcoccus viridans Risk factors: - Valvular disease, congenital heart defects, rheumatic heart disease, prosthetic heart valves, IV drug abusers, LT vascular access catheters Infective Endocarditis General pathophysiology: • platelets and fibrin deposit on abnormal endothelium • organisms adhere and colonization begins • microorganisms or fragments shed into blood • infarction or infection can occur at any distal site • infection of cardiac tissue can lead to progressive heart failure, conduction disturbances, and dysrhythmias. Infective Endocarditis Which age population is infective endocariditis rarely seen in? Infective Endocarditis SUBJECTIVE DATA Fever: SBE – low grade, ABE – 102 degrees F Anorexia, weight loss, night sweats Arthralgia, myalgia, fatigue, malaise Dyspnea, cough, pleuritic chest pain, hemoptysis HA, signs of stroke, confusion Abdominal and back pain Infective Endocarditis Subjective Data Suspect if history of: Cardiac surgery Congenital or aquired heart valve disease IV drug use Rheumatic heart disease Cardiac pacemaker Recent GI or GU disorder with valve disease Prosthetic valves with recent dental procedures without prophylactic ATX Infective Endocarditis OBJECTIVE DATA Fever – may be absent in elderly, chronic renal Murmur “Janeway lesions” - petechial lesions on hands, feet; “Roth’s Spots” on ophthalmic exam; splinter hemorrhages on nails; “Osler’s nodes” – painful lesions of fingertips; petechiae Splenomegaly, hematuria, proteinuria, clubbing with LT SBE, neurological changes Infective Endocarditis DIAGNOSTICS Blood cultures – most important in decision making process! CBC (anemia common with SBE), BUN/Cr, Electrolytes, Glucose, Sed rate (elevated in both types), UA EKG – conduction abnormalities may be present with septal abscess Echocardiogram – can view vegetation and amount of dysfunction Head CT Infective Endocarditis INTERVENTIONS ABC/monitoring/reassessments IV and NS at TKO Labs as ordered – especially MULTIPLE blood cultures! Medications: Anti-pyretics, antibiotics Therapeutics – family at bedside, calm, etc. Acute Arterial Occlusion Caused by acute disruption of blood flow from an embolism (most common), thrombosis, or trauma. Majority of emboli lodge in femoral artery. Leads to ischemia in areas/tissues supplies by the affected artery Immediate recognition and treatment required to maintain limb or organ viability. Acute Arterial Occlusion Approximately 80% of emboli originate in the __________. Acute Arterial Occlusion SUBJECTIVE DATA Pain • with movement or rest, burning, throbbing, radiates distal to occlusion, excruciating, relentless Coldness, numbness Paralysis Past Medical HX: • MI, Rheumatic heart disease, a-fib, cardiac surgery, LV aneurysm, chronic CHF, extremity trauma, recent placement of intra-atrial catheters. Acute Arterial Occlusion OBJECTIVE DATA Pallor, cyanosis, mottled, coldness Pulseless (distally), paresthesia, paralysis Tenderness on palpation, muscle rigor with prolonged ischemia Petechiae Acute Arterial Occlusion DIAGNOSTICS PT, PTT, CBC EKG Acute Arterial Occlusion INTERVENTIONS Elevate HOB (allow for increased flow to ischemic extremity Anticoagulants as ordered Acute Arterial Occlusion INTERVENTIONS cont Monitor and reassess (especially the 5 Ps) Position of comfort Warm environment (DO NOT apply heat to area!) Maintain extremity at level position (DO NOT elevate) Explain procedures and allow family as able Venous Thrombosis An occlusion of a vein by a blood clot, commonly of the lower extremities, often involves inflammation. Etiology – “Virchow’s Triad” - integrity of veins, stasis of blood flow, & hypercoagulability states Factors: age > 40, cardiac disease, malignancy, hx of hypercoag., and use of estrogens and BCPs Venous Thrombosis The major complication associated with venous thrombosis is emboli. ? Venous Thrombosis SUBJECTIVE DATA Pain – aching, localized at point of occlusion, constant, worse with walking Swelling, deep muscle tenderness, fever Medical Hx Recent surgery or anesthesia, recent traumatic event, postpartum, prolonged bedrest, heart failure, malignancy, obesity, BCPs, recent MI, thrombotic disease, hematological disorders Venous Thrombosis OBJECTIVE DATA Erythema, swelling, indurations, warmth Deep muscle tenderness Asymmetry between extremities Fever Positive Homan’s sign Venous Thrombosis DIAGNOSTICS CBC, Sed rate, PT/PTT Doppler US flow study Venous Thrombosis INTERVENTIONS Position of comfort, elevate effected extremity, bed rest Analgesia, anticoagulants, and thrombolytics as ordered Warm, moist compresses to area Elastic stockings or ACE wraps as ordered I&O, reassessments PVD Major cause is arteriosclerosis, or hardening of the large and medium-sized arteries. Symptoms related to the decrease in blood flow to the specific areas; Worsen as disease worsens. Factors: Heredity, male sex, increasing age, cigarette smoking, HTN, & hyperlipidemia. Other types: Raynaud’s Disease & Buerger’s Disease PVD RAYNAUD’S Episodic intense vasospasms of the digits in response to cold or stress. Affects women more than men. Vasospasm produces ischemia, which produces pallor followed by cyanosis, coldness, and numbness of the affected digit. As spasm resolves, there is an intense rubor and throbbing pain prior to digit returning to normal. PVD BUERGER’S DISEASE Inflammatory disorder characterized by thrombous formation in usually medium sized arteries of the lower leg and foot. Men affected more than women. Results in ischemia, pain, intermittent claudication, decreased or absent pulses, and changes in skin color. Skin becomes thin and shiny, hair growth retarded, nails thicken, and gangrene/ulcerations may develop. PVD SUBJECTIVE DATA Pain – cold environment, stress, exercise, relieved by removal of agonist, severe, throbbing Numbness, tingling OBJECTIVE DATA Cold to touch, decreased/absent pulses, pallor, cyanosis, rubor Thin, shiny skin; thickened nails; ulcerations/ necrosis PVD DIAGNOSTICS CBC Doppler studies PVD INTERVENTIONS Stop precipitating factors Vasodilators (calcium channel blockers or adrenergic blockers) and analgesics as ordered Reassess 5 P’s Position of comfort, DO NOT elevate affected extremity Warm environment General therapeutics Myocardial Contusion Usually a result of blunt trauma Injuries may range from petechiae to fullthickness contusions to rupture of the heart Lesions caused are similar to that of acute MI from occlusions; major difference is amount of hemorrhage! RARELY FATAL! At risk for sudden dysrhythmias Myocardial Contusion SUBJECTIVE DATA Recent blunt trauma to chest, chest pain similar to MI but does not respond to vasodilatory drugs Pain with inspiration usually secondary to fractured sternum Medical HX – angina, previous MI, HTN, CHF, ETOH or drug use, previous CV surgery Myocardial Contusion OBJECTIVE DATA Exam may be normal without signs of trauma or may be associated with severe trauma Contusion to chest wall, tachycardia, tachypnea, hypo- or hypertension Signs of LV failure • crackles Myocardial Contusion DIAGNOSTICS EKG: Premature atrial or ventricular contractions, A-Fib, SA block, nodal rhythm, AV block, nonspecific ST & T wave abnormalities, BBB (usually right), and infarct pattern. Cardiac serum markers Echocardiography CXR Myocardial Contusion INTERVENTIONS ABC Supplemental O2, monitoring Large bore IV (minimum of 2) & IVF as needed Medicate with antidysrhymics and analgesics as ordered/needed Position of comfort General therapeutics Cardiac Tamponade Fluid accumulation in the pericardial sac, which elevates intracardiac pressure, progressive decrease in diastolic pressure, and ultimately decrease in stroke volume and cardiac output. Prognosis dependent on etiology & timelines of intervention. Cardiac Tamponade Causes: - malignancies, pericarditis, uremia, & trauma Types: - acute: patient is in extremis; may be less than 100c - chronic: patient not in extremis; may be 1-2L Cardiac Tamponade Cardiac Tamponade SUBJECTIVE DATA Penetrating or blunt injury, recent repair of cardiac lesions Dyspnea, anxious, chest pain, fatigue, malaise Medical Hx: Cardiac disease, infectious or neoplastic disease, renal failure Cardiac Tamponade SUBJECTIVE DATA cont. Cold, moist skin; cyanotic lips and digits Decreased UO Decreased LOC, coma Hepatomegaly Pericardial Tamponade OBJECTIVE DATA Visual wound Tachypnea, rales, Kussmal’s sign (rise in venous pressure with inspiration) JVD,tachycardia Pericardial Tamponade OBJECTIVE DATA Beck’s Triad: •Venous pressure elevation •Arterial pressure decline •Muffled heart tones Cardiac Tamponade DIAGNOSTICS CXR Pericardiocentesis (Hct will be lower in pericardial blood than venous sample & generally pericardial blood will not clot) Echocardiogram T&C, CBC EKG Cardiac Tamponade ANALYSIS Cardiac output decreased related to impaired cardiac filling and contractility and decreased venous return secondary to increased intrathoracic pressure Cardiac Tamponade INTERVENTIONS ABC Large bore IVs (minimum of 2), IVF as needed Monitoring, reassessment Prepare: pericardiocentesis, thoracotomy, internal cardiac massage Foley & NG Prepare for immediate surgical intervention Traumatic Aortic Injury Result from blunt or penetrating trauma - MVCs are the most common cause 90% result in complete rupture and sudden death at “the scene” Tearing may occur at points of attachment or may be pinched between the spinal column and manubrium. Tears not involving the adventital layer (outer) may result in patient survival. Traumatic Aortic Injury Traumatic Aortic Injury SUBJECTIVE DATA Deceleration mechansim, blunt force to chest or abdomen Pain: severe, unrelenting pain in chest, midscapular, or back region Medical Hx: atherosclerotic heart disease, prior thoracic injuries or surgeries Traumatic Aortic Injury OBJECTIVE DATA Dyspnea, tachypnea Tachycardia, discrepancy between BPs in right and left arms, harsh systolic murmur, varying degrees of shock, decreased quality of femoral vs radial pulses Chest wall ecchymosis, paraplegia Traumatic Aortic Injury DIAGNOSTICS CXR: widened mediastinum, obliteration of aortic knob, tracheal deviation to the right, presence of pleural cap, fx of 1st & 2nd ribs, depression of left main stem bronchus, deviation of esophagus to right, shift of right main stem bronchus up and to right Traumatic Aortic Injury DIAGNOSTICS cont CT scan EKG T&C CBC Traumatic Aortic Injury INTERVENTIONS ABC, monitoring, reassessment Large bore IVs (minimum of 2), IVF as needed Prepare for blood transfusion & autotransfusion as needed Foley & NG Monitor arterial pH Prepare for immediate surgical intervention Administer antihypertensives & beta blockers as ordered if surgical repair delayed Arterial Trauma Result from blunt (MVC & crush injuries) or penetrating (GSW & stab wounds) trauma Vessels injuries include lacerations, hematomas, and pseudoaneurysms Neurological signs usual present due to close proximity of nerves Major consequence is ischemia distal to injury; immediate surgery required is damage is severe Arterial Trauma SUBJECTIVE DATA Numbness, tingling, pain, paralysis Mechanism Medical Hx: diabetes, PVD Arterial Trauma OBJECTIVE DATA Hemorrhage from wound, varying stages of shock related to volume of blood loss, pulsatile or expanding hematoma Difference in BPs in different extremities, prolonged cap refill, diminished or absent distal pulses Pallor, paresthesia, coolness, paralysis Arterial Trauma DIAGNOSTIC Doppler study Questions?????