Sections View Full Chapter Figures Tables Videos Annotate Full Chapter Figures Tables Videos Supplementary Content + Download Section PDF Listen ++ For further information, see CMDT Part 12-19: Shock + Key Features Download Section PDF Listen +++ +++ Essentials of Diagnosis ++ Hypotension, tachycardia, oliguria, altered mental status Peripheral hypoperfusion and impaired oxygen delivery +++ General Considerations ++ Can be classified as Hypovolemic Cardiogenic Obstructive Distributive, including septic, neurogenic, and endocrine +++ Hypovolemic ++ Results from decreased intravascular volume secondary to loss of blood or fluids and electrolytes 15% loss of intravascular volume can result in hypotension and progressive tissue hypoxia +++ Cardiogenic ++ Results from cardiac failure with the resultant inability of the heart to maintain adequate tissue perfusion Clinical definition: evidence of tissue hypoxia due to decreased cardiac output (cardiac index < 2.2 L/min/m2) in the presence of adequate intravascular volume Most often caused by myocardial infarction but can also be due to cardiomyopathy, myocardial contusion, valvular incompetence or stenosis, or arrhythmias +++ Obstructive ++ Results from acute decrease in cardiac output due to cardiac tamponade, tension pneumothorax, or massive pulmonary embolism +++ Distributive ++ Causes include sepsis (most common), anaphylaxis, systemic inflammatory response syndrome produced by severe pancreatitis or burns, traumatic spinal cord injury, or acute adrenal insufficiency Reduction in systemic vascular resistance (SVR) results in inadequate cardiac output and tissue hypoperfusion despite normal circulatory volume Septic Clinically defined as Sepsis with fluid-unresponsive hypotension (systolic blood pressure < 100 mm Hg) Serum lactate level > 2 mmol/L Needing vasopressors to maintain mean arterial pressure > 65 mm Hg Gram-positive or gram-negative organisms most common cause Polymicrobial infections are almost as likely Incidence of sepsis caused by fungal organisms is increasing, but remains less than that for bacterial infections Risk factors Bacteremia Extremes of age Diabetes Cancer Immunosuppression History of a recent invasive procedure Sequential Organ Failure Assessment (SOFA) scoring system See https://en.wikipedia.org/wiki/SOFA_score An increase of 2 or more SOFA score points in a patient with infection is diagnostic of sepsis with a predicted 10% mortality Quick SOFA (qSOFA) scoring system See https://en.wikipedia.org/wiki/SOFA_score 1 point each is assigned for hypotension (systolic blood pressure < 100 mm Hg), altered mental status, or tachypnea (respiratory rate (RR) > 22 breaths per minute) A qSOFA score of 2 or more in a patient with suspected infection suggests worsened clinical outcomes and may influence triage decisions for ICU-level care Controversy remains over the utility of these scoring systems in the absence of strong evidence to advocate for universal adoption Systemic inflammatory response syndrome (SIRS) Defined as a systemic response to a nonspecific infectious or noninfectious insult—such as burns, pancreatitis, an autoimmune disorder, ischemia, or trauma The presence of two or more of the following clinical criteria help establish the diagnosis of SIRS Body temperature > 38oC (100.4oF) or < 36oC (96.8oF) Heart rate > 90 beats per minute Respiratory rate more than 20 breaths per minute or hyperventilation with an arterial carbon dioxide tension (PaCO2) < 32 mm Hg Abnormal white blood cell count (> 12,000/mcL or < 4000/mcL or > 10% immature [band] forms) When a source of infection is confirmed, SIRS is categorized as sepsis SIRS criteria have higher sensitivity than qSOFA for diagnosing sepsis SIRS may be better screening tool for sepsis while qSOFA may be better predicting tool of ICU mortality Neurogenic Caused by traumatic spinal cord injury or effects of an epidural or spinal anesthetic agent Reflex vagal parasympathetic stimulation evoked by pain, gastric dilation, or fright may simulate neurogenic shock, producing hypotension, bradycardia, and syncope Endocrine Can arise from hyperthyroidism, hypothyroidism or adrenal insufficiency Adrenal insufficiency Most often occurs with abrupt cessation of long-term corticosteroid use Can also be precipitated by infection, trauma, surgery, or pituitary injury (leading to secondary adrenal insufficiency) + Clinical Findings Download Section PDF Listen +++ +++ Symptoms and Signs ++ Hypotension Weak or thready peripheral pulses Cold or mottled extremities Splanchnic vasoconstriction may lead to oliguria, bowel ischemia, and hepatic dysfunction Mentation may be normal or altered (eg, restlessness, agitation, confusion, lethargy, or coma) +++ Hypovolemic ++ Jugular venous pressure is low Narrow pulse pressure indicative of reduced stroke volume +++ Cardiogenic ++ Jugular venous pressure is elevated Global hypoperfusion with oliguria Altered mental status Cool extremities May be evidence of pulmonary edema in the setting of left sided heart failure and evidence of ECG changes +++ Obstructive ++ Central venous pressure may be elevated +++ Distributive, including septic, neurogenic, and endocrine ++ Hyperdynamic heart sounds Warm extremities Wide pulse pressure indicative of large stroke volume Septic Evidence of infection in the setting of persistent hypotension Evidence of organ hypoperfusion, such as in lactic acidosis, decreased urinary output, or altered mental status despite adequate volume resuscitation Neurogenic Evidence of CNS injury and persistent hypotension despite adequate volume resuscitation Endocrine Weakness, nausea, abdominal pain, and confusion Hypothyroidism can lead to myxedema coma, presenting with vasodilation and depressed cardiac output Shock from hyperthyroidism most often produces high output heart failure + Diagnosis Download Section PDF Listen +++ +++ Laboratory Tests ++ Complete blood count Serum electrolytes, serum glucose Arterial blood gas determinations Coagulation parameters Lactate levels Typing and cross-matching Blood cultures +++ Imaging Studies ++ Chest radiograph Transesophageal echocardiography shows Reduced left ventricular filling in hypovolemic and obstructive shock Enlarged left ventricle in cardiogenic shock Point-of-care ultrasonography can rapidly assess Global cardiac function Presence of pericardial effusion Intravascular volume status via inferior vena cava inspection in cases of undifferentiated hypotension A transthoracic echocardiogram can more formally assess right- and left-sided filling pressures and cardiac output +++ Diagnostic Procedures ++ Electrocardiogram An arterial line should be placed for blood pressure and arterial oxygen monitoring Foley catheter should be inserted to monitor urinary output Pulmonary artery catheter Can distinguish cardiogenic from septic shock Can monitor effects of volume resuscitation or pressor medications Central venous pressure (CVP) < 5 mm Hg suggests hypovolemia > 18 mm Hg suggests volume overload, cardiac failure, tamponade, or pulmonary hypertension Cardiac index < 2 L/min/m2 indicates need for inotropic support > 4 L/min/m2 in a hypotensive patient is consistent with early septic shock SVR Low (< 800 dynes × s/cm–5) in septic and neurogenic shock High (> 1500 dynes × s/cm–5) in hypovolemic and cardiogenic shock + Treatment Download Section PDF Listen +++ +++ Medications ++ Norepinephrine First-line agent for cardiogenic shock Initial dosage: 1–2 mcg/min as an intravenous infusion, titrated to maintain the mean arterial blood pressure to at least 65 mm Hg Usual maintenance dosage: 2–4 mcg/min (maximum dose is 30 mcg/min) Patients with refractory shock may require dosages of 10–30 mcg/min Epinephrine May be used in severe shock and during acute resuscitation Vasopressor of choice for anaphylactic shock Initial dosage: 1 mcg/min as a continuous intravenous infusion Usual dosage: 1–10 mcg/min intravenously Dopamine Low doses (2–5 mcg/kg/min) stimulate dopaminergic and β-adrenergic receptors, producing increased glomerular filtration, heart rate, and contractility At doses of 5–10 mcg/kg/min, β1-adrenergic effects predominate, resulting in an increase in heart rate and cardiac contractility With higher doses (> 10 mcg/kg/min), α-adrenergic effects predominate, resulting in peripheral vasoconstriction Maximum dose is typically 50 mcg/kg/min Should only be used as an alternative to norepinephrine in select patients with septic shock, including those with significant bradycardia or low potential for tachyarrhythmias Phenylephrine can be used as a first-line agent for hyperdynamic septic shock when dysrhythmias or tachycardias prevent the use of agents with beta-adrenergic activity Vasopressin Used as an adjunctive therapy to catecholamine vasopressors in the treatment of distributive or vasodilatory shock Intravenous infusion of low-dose vasopressin (0.01–0.04 units/min) may be safe and beneficial in septic patients with hypotension that is refractory to fluid resuscitation and conventional catecholamine vasopressors Higher doses of vasopressin decrease cardiac output and may put patients at greater risk for splanchnic and coronary artery ischemia Studies do not favor the use of vasopressin as first-line therapy Angiotensin II (marketed as Giapreza) Can be considered as an additional agent in vasodilatory shock that is refractory to catecholamines and vasopressin Recommended starting dose: 20 ng/kg/min via continuous intravenous infusion through a central venous line Can be titrated every 5 minutes by increments of up to 15 ng/kg/min as needed to achieve MAP goals, but not to exceed 80 ng/kg/min during the first 3 hours of use Maintenance doses should not exceed 40 ng/kg/min Concurrent venous thromboembolism (VTE) prophylaxis is indicated because studies revealed a higher incidence of VTE with angiotensin II use Dobutamine Increases contractility and decreases afterload Used for patients with low cardiac output and high pulmonary capillary wedge pressure (PCWP) but who do not have hypotension Can be added to a vasopressor if There is reduced myocardial function is reduced (decreased cardiac output and elevated PCWP) Signs of hypoperfusion are present despite adequate volume resuscitation and an adequate mean arterial pressure Initial dose: 0.1–0.5 mcg/kg/min intravenous infusion, which can be titrated every few minutes as needed to achieve a hemodynamic effect; usual dosage range is 2–20 mcg/kg/min intravenously Tachyphylaxis can occur after 48 hours from the down-regulation of β-adrenergic receptors Amrinone or milrinone Can be substituted for dobutamine Increase cyclic AMP levels and increase cardiac contractility, bypassing the β-adrenergic receptor Vasodilation is a side effect of both Corticosteroids Treatment of choice for shock secondary to adrenal insufficiency Studies supporting use of corticosteroids in patients with shock from sepsis or other etiologies are limited Broad-spectrum antibiotics for septic shock +++ Volume Replacement ++ Critical in initial management of shock Hemorrhagic shock Rapid infusions of type-specific or type O negative packed red blood cells (PRBC) or whole blood, which also provides extra volume and clotting factors Each unit of PRBC or whole blood is expected to raise the hematocrit by 3% Hypovolemic shock secondary to dehydration: rapid boluses of isotonic crystalloid, usually in 1 L increments Cardiogenic shock in absence of fluid overload: requires smaller fluid challenges usually in increments of 250 mL Septic shock Usually requires large volumes of fluid for resuscitation Use of unwarmed fluids can produce hypothermia, which can lead to hypothermia-induced coagulopathy; warming fluids before administration can avoid this complication +++ Surgery ++ Transcutaneous or transvenous pacing or placement of an intra-arterial balloon pump or left ventricular assist device for cardiac failure Emergent revascularization by percutaneous angioplasty or coronary artery bypass surgery appears to improve long-term outcome +++ Therapeutic Procedures ++ Intravenous access and fluid resuscitation should be instituted along with cardiac monitoring and assessment of hemodynamic parameters such as blood pressure and heart rate Treatment is directed at maintaining a CVP of 8–12 mm Hg Mean arterial pressure of 65–90 mm Hg Cardiac index of 2–4 L/min/m2 Central venous oxygen saturation > 70% Pulmonary artery catheters (PACs) Allow measurement of Pulmonary artery pressure Left-sided filling pressure or the pulmonary capillary wedge pressure (PCWP) Mixed venous oxygen saturation (SvO2) Cardiac output However, routine use of PACs cannot be recommended because risk of infection, arrhythmias, vein thrombosis, and pulmonary artery rupture can be as high as 4–9% May be useful in distinguishing between cardiogenic and septic shock in complex situations Central venous catheter may be adequate in other types of shock In obstructive shock, pericardiocentesis or pericardial window, chest tube placement, or catheter-directed thrombolytic therapy can be lifesaving Urgent renal replacement therapy may be indicated for maintenance of fluid and electrolyte balance during acute kidney injury resulting in shock Lactate clearance of > 10% can be used as a potential substitute for central venous oxygen saturation (ScvO2) criteria if ScvO2 monitoring is not available + Outcome Download Section PDF Listen +++ +++ Prognosis ++ Septic shock mortality is 20–50% + References Download Section PDF Listen +++ + +Caironi P et al; ALBIOS Study Investigators. Albumin replacement in patients with severe sepsis or septic shock. N Engl J Med. 2014 Apr 10;370(15):1412–21. [PubMed: 24635772] + +Fernando SM et al. Prognostic accuracy of the quick sequential organ failure assessment for mortality in patients with suspected infection: a systematic review and meta-analysis. Ann Intern Med. 2018 Feb 20;168(4):266–75. [PubMed: 29404582] + +Gamper G et al. Vasopressors for hypotensive shock. Cochrane Database Syst Rev. 2016 Feb 15;2:CD003709. [PubMed: 26878401] + +Khanna A et al; ATHOS-3 Investigators. Angiotensin II for the treatment of vasodilatory shock. N Engl J Med. 2017 Aug 3;377(5):419–30. [PubMed: 28528561] + +Mouncey PR et al; ProMISe Trial Investigators. Trial of early, goal-directed resuscitation for septic shock. N Engl J Med. 2015 Apr 2;372(14):1301–11. [PubMed: 25776532] + +Rhodes A et al. Surviving Sepsis Campaign: international guidelines for management of sepsis and septic shock: 2016. Crit Care Med. 2017 Mar;45(3):486–552. [PubMed: 28098591] + +Semler MW et al. Balanced crystalloids versus saline in critically ill adults. N Engl J Med. 2018 May 17;378(20):1951. [PubMed: 29768150] + +Singer M et al. The third international consensus definitions for sepsis and septic shock (Sepsis-3). JAMA. 2016 Feb 23;315(8):801–10. [PubMed: 26903338] + +Thiele H et al. Management of cardiogenic shock complicating myocardial infarction: an update 2019. Eur Heart J. 2019 Aug 21;40(32):2671–83. [PubMed: 31274157]