Shock, circulatory DESCRIPTION: Inadequate perfusion (oxygen supply) of tissues which results in organ dysfunction, cellular and organ

damage and, if not corrected quickly, death of the patient. Classification of shock: ypo!olemic shock " cardiac output is se!erely reduced due to loss of intra!ascular !olume which results in reduced return of !enous #lood to the heart. $ost often caused #y #lood loss. Cardiogenic shock " cardiac output is se!erely reduced due to a loss of myocardial muscle function, !al!ular dysfunction or arrhythmia. $ost often caused #y large myocardial infarctions. %#structi!e shock " cardiac output is se!erely reduced #y !ascular o#struction of !enous return to the heart (!ena ca!a syndrome), compression of the heart, (pericardial tamponade, tension pneumothorax) or outflow from the heart (aortic dissection, pulmonary em#olism) &istri#uti!e shock " maldistri#ution of #lood flow 'enous pooling (most often due to spinal shock or drug o!erdose) #eha!es much like hypo!olemic shock, cardiac output se!erely reduced #ecause #lood is pooled in peripheral !eins rather than #eing returned to the heart igh output or !asodilating shock (most often due to sepsis or septic like states such as toxic shock) is unique in that cardiac output is normal or ele!ated, #ut not distri#uted appropriately, resulting in o!er perfusion of some tissues and underperfusion (to the point of critical ischemia) of other tissues. Predominant age: (ll ages. &etermined #y underlying diseases causing shock. $ore frequent and less well tolerated in the elderly. Predominant sex: $ale ) *emale +I,-+ (-& +.$/0%$+: 1nderlying disease: 1pper gastrointestinal (1,I) #leeding (ulcer pain, hematemesis, melena) +epsis (fe!er, chills, dysuria and2or costo!erte#ral angle 3C'(4 tenderness with urinary tract infection) $yocardial infarction (chest pain, diaphoresis, nausea, !omiting, +5 or +6 gallop, new heart murmur, rales due to pulmonary edema) 1nderperfusion of organ systems: 7rain: confusion, anxiety, agitation, coma only if se!ere 8idney: oliguria +kin: peripheral cyanosis, sluggish capillary refill, mottling, coolness, may #e o!erly perfused

(flushed) in high output (septic) shock ,I: a#sence of #owel sounds Circulation: thready pulses, tachycardia, hypotension (mean arterial pressure 9 :; torr or systolic pressure 9 <; torr or #lood pressure = 5; torr less than usual #lood pressure in chronic hypertension), secondary cardiac ischemia (+0 depression) or heart failure may occur due to underperfusion of the heart during shock. >ugular" !enous distention (>'&), pulsus paradoxus in pericardial tamponade. CAUSES: ypo!olemic shock 7lood loss due to trauma or gastrointestinal #leeding 0hird space loss of plasma !olume (pancreatitis, #owel o#struction, infarction, anaphylaxis) &iarrhea (e.g., in cholera like states) 7urns Cardiogenic shock (cute myocardial infarction (= 5;? of @' mass) (rrhythmia (heart #lock, !entricular tachycardia, atrial fi#rillation with rapid !entricular response, etc.) (cute !al!ular dysfunction (mitral !al!e due to papillary muscle rupture following inferior $IAs or chordal rupture) aortic or mitral !al!e due to #acterial endocarditis 'entricular septal rupture following anterior2septal $IAs %#structi!e shock /ericardial tamponade Inferior2superior !ena ca!al o#struction usually due to neoplasms (ortic dissection $assi!e pulmonary em#olism &istri#uti!e shock 'enous pooling is due to a loss of !enous tone caused #y loss of sympathetic ner!ous system acti!ity due to acute spinal inBury, general or spinal anesthesia or o!erdose of sedati!e drugs igh output shock is due to sepsis, toxic shock or anaphylaxis (once plasma !olume normaliCed) RISK FACTORS: Included with Causes

DIAGNOSIS DIFFERENTIAL DIAGNOSIS:

-2( @(7%D(0%D.: +pecific to shock Ele!ated lactate (= F mmol2@) indicates anaero#ic meta#olism due to underperfusion of tissues Deduced mixed !enous /;F (9 FG mm g) (9 6.H k/a) o#tained from the pulmonary artery indicates !igorous extraction of oxygen from tissues due to underperfusion 1nderlying diseases responsi#le to shock EC,, C/8 (serial) Chest x"ray (rterial #lood gases ,ram stain and culture of infected sites 7lood cultures C7C (serial determination of g#2 ct in #leeding patients) Drugs that may alter lab results: -2( Disorders that may alter lab results: -2( PATHOLOGICAL FINDINGS: -2( SPECIAL TESTS: Certain tests are essential to making correct and prompt diagnosis in order to dictate specific therapy of disease states producing shock. *or example: Endoscopy2Dadioisotope #leeding scans ena#le localiCation of ongoing #leeding which may direct surgical inter!ention. 0he endoscopist may inter!ene directly !ia the endoscope. (e.g., inBection of sclerosants into !arices or ulcers). Echocardiograms may detect and2or quantify pericardial effusions in shock due to pericardial tamponade. /ericardiocentesis can then #e performed under echocardiographic guidance. (lso useful for detection of !al!ular failure. @ung scans and2or pulmonary arteriography for the detection of massi!e pulmonary em#olism /ulmonary artery (+wan",anC) catheteriCation for serial measurement of cardiac output, central !enous, pulmonary arterial and pulmonary arterial occlusion pressures (left atrial pressure) and !ascular resistance. $ixed !enous #lood gases can #e drawn from the catheter. Indicated when the etiology of shock is uncertain, in cardiogenic and septic shock, or when initial therapy of shock fails to pro!ide for rapid correction of perfusion failure. TREATMENT

APPROPRIATE HEALTH CARE: Emergency room or intensi!e or coronary care unit Continuous electrocardiographic monitoring with frequent assessment of #lood pressure, respiratory status, and urine output GENERAL MEASURES: 0herapy must proceed quickly #efore extensi!e damage to !ital organs occur. 0herapy is directed simultaneously to correct #oth the deficit in tissue perfusion and the underlying disease causing shock (see (ssociated conditions). $aintain +a%F = <I? with supplemental oxygen. Intu#ate and mechanically !entilate patient if patient cannot #e oxygenated with J;;? oxygen or has markedly increased #reathing effort (excessi!e oxygen cost of #reathing). $aintain p a#o!e H.6 (#ut less than H.I) to preser!e !ascular responsi!eness to endogenous or exogenous catecholamines. Correct plasma !olume deficits rapidly #y !olume expanders consisting of isotonic saline (.<-s or DingerAs lactate) with or without colloid (al#umin I? or hydroxyethyl starch :?) /acked red #lood cell transfusion to correct or pre!ent anemia. 7 maintained at or a#o!e J; grams2dl. (dminister coagulation factors (fresh froCen plasma, cryoprecipitate) and platelets if coagulopathy (prolonged /0, /00 or platelet count 9 I;,;;;) is present in a patient who is #leeding 0achyarrhythmias (other than sinus tachycardia) should #e promptly corrected #y electrocardio!ersion. 0rans!enous pacemakers should #e placed to correct #radyrhythmias. 'asopressors (see $edications) to correct hypotension or low cardiac output due to myocardial failure or hypotension due to low !ascular resistance End points of resuscitation: adequate #lood pressure (= :; mm g 3G.; k/a4 mean or = <; mm g 3JF.; k/a4 systolic or within 5; mm g 3I.6F k/a4 of patientAs normal #lood pressure). /atient is awake2alert, urine output adequate, heart rate 9 J;;, warm skin with #risk capillary refill, #owel sounds present. @actate 9 F mmol2@, mixed !enous /%F = 6; mm g.

MEDICATIONS DRUG(S) OF CHOICE: &opamine, low dose, J"5 Kg2kg2min augments contractility and cardiac output (#eta"J) and

increases heart rate. 0his pro!ides increased #lood flow to kidneys and gut. (lso acts directly on dopaminergic receptors in the renal !asculature to enhance renal #lood flow. &opamine = 5 Kg2kg2min: augments contractility, and cardiac output (#eta"J) and increased heart rate. Increases #lood pressure #y a com#ination of increased cardiac output and !asoconstriction (alpha). -orepinephrine F"JF Kg2min: augments #lood pressure #y increased !ascular resistance (alpha). Deduced #lood flow to splanchnic #ed can #e re!ersed #y low dose dopamine. /henylephrine F;"F;; Kg2min: see norepinephrine &o#utamine I"J; Kg2kg2min augments contractility and cardiac output (#eta"J). as #oth !asoconstricti!e (alpha) and !asodilator (#eta"F) properties. 0hese effects ha!e a minimal effect on systemic !asculature. Contraindications: Defer to manufacturerAs profile of each drug Precautions: $yocardial oxygen consumption is increased #y increased heart rate, afterload, and contractility /ressors can increase myocardial ischemia if present $ay precipitate or worsen tachyarrhythmias +hould #e used in lowest possi#le dose for as limited period of time as possi#le Significant possible interactions: Defer to manufacturerAs profile of each drug

Encephalopathy and2or cere#ro!ascular accident EXPECTED COURSE AND PROGNOSIS: $ortality is determined #y a complex interaction of primary disease causing shock, age, coexisting chronic disease and shock se!erity as marked #y the num#er of acute organ system failures that follow shock 7est outcome (= <;? sur!i!al) in young patient with transient shock due to trauma or gastrointestinal #lood loss without chronic irre!ersi#le illnesses /oor outcome (= <;? mortality) in elderly patient with septic shock, underlying chronic li!er disease, who de!elops acute renal failure, (D&+, and coagulopathy

MISCELLANEOUS ASSOCIATED CONDITIONS: ,astrointestinal #lood loss: may require endoscopic or surgical inter!ention if #leeding doesnAt spontaneously cease, e.g., electrocoagulation or inBecting sclerosant for #leeding peptic ulcers, sclerotherapy in esophageal !arices +epsis: empiric anti#iotic therapy, anti#odies against gram negati!e antigens Cardiogenic shock: therapy should help reduce cardiac ischemia (oxygen, nitrates) and accomplish rapid reperfusion of inBured, #ut potentially !ia#le, myocardium (throm#olysis with fi#rinolytic agents, #alloon angioplasty of stenotic !essels or surgical #ypass grafting) ( #alloon pump may temporiCe #y pro!iding impro!ed coronary #lood flow during and following diagnostic testing and re!asculariCation therapy. If shock is due to acute failure of the mitral or aortic !al!e, surgical !al!e replacement may #e lifesa!ing. /ulmonary em#olism Cardiac tamponade

FOLLOW UP PATIENT MONITORING: Careful monitoring of all life functions in intensi!e care PREVENTION/AVOIDANCE: +hock is #est a!oided #y prompt recognition and treatment of underlying diseases which cause shock (e.g., early anti#iotic therapy for infections) POSSIBLE COMPLICATIONS: $ultiple organs may #e damaged #y underperfusion during shock (cute tu#ular necrosis Ischemic hepatitis Ischemic #owel &isseminated intra!ascular coagulopathy (dult respiratory distress syndrome ((D&+)