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Cardiogenic shock Resident Survival Guide
Overview
Causes
FIRE
Diagnosis
Treatment
Do's
Don'ts

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ahmed Zaghw, MBChB. [2]

Overview

The clinical definition of cardiogenic shock includes decreased cardiac output with evidence of tissue hypoxia in the presence of adequate intravascular volume.

Diagnositic Criteria

Criteria for bedside diagnosis

• Sustained hypotension (systolic blood pressure <90 mm Hg or mean arterial pressure 30 mm Hg below baseline in preexisting hypertension for at least 30 minutes)
• Evidence of tissue hypoperfusion (such as oliguria, cyanosis, cool extremities, and altered mental status)
• Presence of myocardial dysfunction after exclusion or correction of non-myocardial factors contributing to tissue hypoperfusion (such as hypovolemia, hypoxia, and acidosis)

Criteria based on hemodynamic parameters

• Sustained hypotension (systolic blood pressure <90 mm Hg or mean arterial pressure 30 mm Hg below baseline in preexisting hypertension for at least 30 minutes)
• Depressed cardiac index (<1.8 L/min/m² of body surface area without support or <2.0–2.2 L/min/m² of body surface area with support) in the presence of an elevated pulmonary capillary wedge pressure (>15 mm Hg).

Causes

Life Threatening Causes

Cardiogenic shock is a life-threatening condition and must be treated as such irrespective of the underlying cause.

Common Causes

• Arrhythmic

• Atrioventricular block
• Sinoatrial block
• Supraventricular tachycardia
• Ventricular tachycardia

• Mechanical

• Acute mitral regurgitation (papillary muscle rupture, chordae tendinae rupture)
• Free wall rupture
• Hypertrophic cardiomyopathy
• Obstruction to left ventricular filling (mitral stenosis, left atrial myxoma)
• Obstruction to left ventricular outflow tract (aortic stenosis, hypertrophic obstructive cardiomyopathy)
• Ventricular septal defect

• Myopathic

• Cardiomyopathy
• Myocardial contusion
• Myocardial infarction
• Myocarditis
• Myxedema coma
• Postischemic myocardial stunning
• Septic myocardial depression

• Pharmacologic

• Anthracyclines
• Calcium channel blockers

Click here for the complete list of causes.

FIRE: Focused Initial Rapid Evaluation

A Focused Initial Rapid Evaluation (FIRE) should be performed to identify patients in need of immediate intervention.

Boxes in the salmon color signify that an urgent management is needed.

Abbreviations: CBC, complete blood count; CI, cardiac index; CK-MB, creatine kinase MB isoform; CVP, central venous pressure; DC, differential count; ICU, intensive care unit; INR, international normalized ratio; LFT, liver function test; MAP, mean arterial pressure; MVO2, mixed venous oxygen saturation; PCWP, pulmonary capillary wedge pressure; PT, prothrombin time; PTT, partial prothrombin time; SaO2, arterial oxygen saturation; SBP, systolic blood pressure; SCVO2, central venous oxygen saturation; SMA-7, sequential multiple analysis-7.

Does the patient have cardinal findings that increase the pretest probability of cardiogenic shock? ❑  Arterial hypotension ❑  SBP <90 mm Hg or ❑  MAP ↓ >30 mm Hg below baseline ❑  Evidence of tissue hypoperfusion ❑  Altered mental status ❑  Cool extremities ❑  Cyanosis ❑  Oliguria ❑  Presence of myocardial dysfunction after exclusion or correction of non-myocardial factors contributing to tissue hypoperfusion

YES

NO

Ventilate—Infuse—Pump (VIP) ❑  Oxygen ± mechanical ventilation ❑  Normal saline 300–500 mL over 20–30 min ❑  ± Norepinephrine 0.1–2.0 μg/kg/min

Consider other causes (eg, chronic hypotension, syncope)

Workup ❑  ECG monitor ❑  Pulse oximeter ❑  Arterial blood gas ❑  Central venous catheter ❑  CBC/DC/SMA-7/LFT/PT/PTT/INR ❑  Troponin, CK-MB ❑  Lactate ❑  Chest radiograph ❑  Echocardiography ❑  Foley catheter ❑  ICU admission ❑  ± Transfusion (Indications) ❑  ± Cultures of blood, urine, etc. ❑  ± Pulmonary artery catheter (Indications)

Immediate Goals ❑  SaO2 >90%–92% ❑  CVP 8–12 mmHg ❑  MAP >65–70 mmHg ❑  PCWP 12–15 mmHg ❑  CI >2.1 L/min/m2 ❑  MVO2 >60% ❑  SCVO2 >70% ❑  Hemoglobin >7–9 g/dL ❑  Lactate <2.2 mM/L ❑  Urine output >0.5 mL/kg/h

Identify the cause

NO, then proceed to complete diagnostic approach below

Complete Diagnostic Approach

History

Review all medications Antihypertensives can cause significant hypotension, especially in the setting of volume depletion or over-diuresis. Anaphylaxis should be considered if the patient recently started on a new drug and presented with respiratory distress. Findings suggestive of hypovolemic shock Abdominal pain Diarrhea Dry skin, mucosa, axillae Hematemesis Hematochezia Melena Postoperative Trauma Vomiting Findings suggestive of cardiogenic shock Chest pain Dyspnea Palpitations Findings suggestive of distributive shock Altered mental status Chills Dyspnea Dysuria Fatigue Fever Flushing Headache Hematuria Malaise Myalgias Photophobia Productive cough Rash Tachycardia Tachypnea

Physical Examination

Vital signs Temperature Fever may suggest sepsis or anaphylactic reaction related to transfusion. Hypothermia may be associated with sepsis, adrenal crisis, or myxedema. Pulse Bradycardia or tachycardia can either be a primary or secondary process. Pulsus paradoxus may be seen in cardiac tamponade, pulmonary embolism, hemorrhagic shock, or tension pneumothorax. Pulsus alternans may be seen in heart failure, severe aortic insufficiency, or hypovolemic shock. Respiration Tachypnea commonly occurs in pneumothorax, sepsis, and cardiogenic shock. Hypopnea may be seen in narcotic or sedative overdose. Blood pressure Confirm arterial hypotension by checking blood pressure in both arms manually. Arterial line may be considered. Postural hypotension suggests volume depletion or autonomic dysfunction. Do not test orthostatic hypotension in hypotensive patients. Mental status Altered mental status may indicate inadequate perfusion to vital organs or use of sedatives or narcotics. Cutaneous Decreased skin turgor and dry mucous membrane signify dehydration. Cool extremities, clammy and mottled skin, peripheral cyanosis, and delayed capillary refill are commonly noted in cardiogenic shock and hypovolemic shock, whereas warm and moist skin may represent hyperdynamic phase of septic shock. Extensive burns and severe trauma may be evident on inspection and are associated with significant fluid loss. Hyperpigmentation may be an indicator of adrenal crisis. Neck Elevated jugular venous pressure (JVP) correlates with increased left ventricular end diastolic pressure (LVEDP) and decreased left ventricular ejection fraction (LVEF). Jugular venous distention or elevated JVP typically occurs in: Heart failure Tricuspid stenosis Pulmonary hypertension Superior vena cava obstruction Constrictive pericarditis Cardiac tamponade Kussmaul's sign Constrictive pericarditis Restrictive cardiomyopathy Tricuspid stenosis Superior vena cava obstruction Right ventricular infarction Abdominojugular reflux (a positive abdominojugular reflux correlates with a PCWP of 15 mmHg or greater) Cardiac tamponade Constrictive pericarditis Tricuspid insufficiency Inferior vena cava obstruction Heart failure (except for pure backward left-sided heart failure) Jugular venous pressure waveform Blunted y descent suggests cardiac tamponade or tricuspid stenosis. Steep y descent suggests constrictive pericarditis or severe tricuspid insufficiency. Cardiovascular Decrescendo early systolic murmur Acute severe mitral regurgitation Third heart sound (S3) Heart failure Pansystolic murmur along lower left sternal border with palpable thrill Ventricular septal defect Pericardial friction rubs Pericarditis Distant, muffled heart sounds Cardiac tamponade Pulmonary Tracheal deviation Tension pneumothorax Stridor and wheezing Anaphylaxis Acute exacerbation of chronic obstructive pulmonary disease Rales Anaphylaxis Pneumonia Heart failure Chest percussion may aid in the diagnosis of tension pneumothorax, pleural effusions, and pneumonia Abdominal Grey Turner's sign Acute pancreatitis Blunt abdominal trauma Retroperitoneal hemorrhage Ruptured abdominal aortic aneurysm Ruptured ectopic pregnancy Cullen's sign Acute pancreatitis Blunt abdominal trauma Ruptured abdominal aortic aneurysm Ruptured ectopic pregnancy Hepatomegaly Inferior vena cava obstruction Heart failure Rebound tenderness with absent bowel sounds Sepsis due to Intraabdominal infection Ischemic colitis Gastrointestinal hemorrhage Pulsatile mass Abdominal aortic aneurysm Rectal Bright red blood or melena Gastrointestinal hemorrhage Diminished sphincter tone Spinal cord injury Extremities Digital clubbing Heart failure Edema Heart failure Erythema at the site of venous access Catheter-associated infection Pelvic girdle pain or instability Pelvic fracture Genitals Perform a pelvic examination in women of childbearing age to rule out ectopic pregnancy or pelvic inflammatory disease. Neurologic Agitation or delirium Poor cerebral perfusion Meningeal signs (nuchal rigidity, Brudzinski's sign, and Kernig's sign Meningitis

Laboratory Findings

Complete blood count In acute blood loss, hemoglobin and hematocrit levels may remain normal until volume repletion. Leukocytosis with or without a left shift of neutrophils suggests sepsis. Thrombocytopenia with alterations in coagulation panel indicates disseminated intravascular coagulation (DIC), which may be a complication of sepsis. Electrolytes Decreased bicarbonate levels may be the primary deficit in metabolic acidosis or the compensatory change in respiratory alkalosis. Hyperkalemia due to transcellular shift is commonly associated with metabolic acidosis. Coagulation panel (PT, PTT, INR, etc.) Abnormalities in coagulation panel may be caused by disseminated intravascular coagulation (DIC), over-anticoagulation, or hepatic failure. Cardiac markers Check troponin and CK-MB levels when suspecting myocardial infarction. Elevation in cardiac markers may be associated with both cardiac and extracardiac etiologies. Liver function Increased levels of conjugated bilirubin, alkaline phosphatase, and hepatic aminotransferases are typically seen in ischemic hepatitis ("shock liver") due to cardiogenic shock. Renal function Prerenal azotemia and/or acute tubular necrosis may be associated with conditions of hypovolemia or reduced cardiac output. Oliguria (urine output <0.5 mL/kg/h) is usually evident. Lactate Hyperlactatemia generally reflects the development of anaerobic metabolism in hypoperfused tissue and/or imparied hepatic clearance. Lactate level could decrease within hours with effective therapy. Arterial blood gas Lactic acidosis may be an indicator of tissue hypoperfusion typically seen in septic shock. Combined acid-base disorders are fequently encountered in different stages of shock. Severe acidosis could blunt the effectiveness of vasopressors and potentiate the development of arrhythmias. Cultures Samples of blood, urine, and/or sputum should be sent for culture before administering antibiotics if sepsis is concerned. Nasogastric aspirate A negative nasogastric aspirate does not rule out upper gastrointestinal bleeding. Pregnancy test A pregnancy test should be performed on hypotensive women of childbearing age presenting with lower abdominal pain.

Radiographic Findings

Chest radiograph may aid in establishing diagnosis in the following conditions: Aortic dissection Cardiac tamponade Pneumonia complicating septic shock Pulmonary edema complicating cardiogenic shock Tension pneumothorax CT scan may aid in directing management in the following conditions: Occult internal hemorrhage Pulmonary embolism

Hemodynamic Profiles and Echocardiography Findings

Type of Shock Etiology CO SVR PCWP CVP SVO2 Echocardiographic Findings Cardiogenic Acute Ventricular Septal Defect ↓↓ ↑ N — ↑ ↑↑ ↑ — ↑↑ Large ventricles with poor contractility Acute Mitral Regurgitation ↓↓ ↑ ↑↑ ↑ — ↑↑ ↓ Myocardial Dysfunction ↓↓ ↑ ↑↑ ↑↑ ↓ RV Infarction ↓↓ ↑ N — ↓ ↑↑ ↓ Dilated RV, small LV, abnormal wall motions Obstructive Pulmonary Embolism ↓↓ ↑ N — ↓ ↑↑ ↓ Dilated RV, small LV Cardiac Tamponade ↓ — ↓↓ ↑ ↑↑ ↑↑ ↓ Pericardial effusion, small ventricles, dilated inferior vena cava Distributive Septic Shock N — ↑↑ ↓ — ↓↓ N — ↓ N — ↓ ↑ — ↑↑ Normal cardiac chambers with preserved contractility Anaphylactic Shock N — ↑↑ ↓ — ↓↓ N — ↓ N — ↓ ↑ — ↑↑ Hypovolemic Volume Depletion ↓↓ ↑ ↓↓ ↓↓ ↓ Small cardiac chambers with normal or high contractility

Treatment

Do's

• Initial Management

• Resuscitation should be initiated while investigation is ongoing. Correct the cause of shock immediately once it is identified.
• The VIP (Ventilate-Infuse-Pump) approach is useful for ensuring an orderly sequence of therapeutic-diagnostic maneuvers.

• Ventilate

• Endotracheal intubation should be performed in patients with severe dyspnea, hypoxemia, or persistent or worsening acidemia (pH <7.30).

• Infuse

• A central venous catheter should be placed for the infusion of fluids and vasoactive agents and to guide fluid therapy.
• A pulmonary artery catheter should be inserted for monitoring of blood pressure and blood sampling unless shock is rapidly reversed. (Indications)
• An infusion of 300–500 ml of crystalloid fluid is usually administered during a period of 20–30 minutes.
• End point of fluid therapy can be defined as a central venous pressure (CVP) of a few millimeters of mercury (mmHg) above the baseline to prevent fluid overload.

• Pump

• Vasopressors are indicated in hypotension that is severe or refractory to fluid challenge.
• Norepinephrine (0.1–2.0 μg/kg/min IV) is the first choice of vasopressor, while epinephrine (0.1–0.5 μg/kg/min IV) is reserved for severe hypotension as the second-line agent.
• Isoproterenol (0.5–5.0 μg/min IV) should be limited to the treatment of hypotensive patients with severe bradycardia.
• Adjunctive vasopressin (0.01–0.04 U/min IV) to norepinephrine should be considered only in hyperdynamic phase of distributive shock.

Don'ts

• Do not test orthostatic hypotension in hypotensive patients.
• Do not rely solely on SpO2 readings from pulse oximeter. SaO2 from blood gas analysis provides more precise status of oxygenation.
• Do not administer low-dose dopamine (<5 μg/kg/min) to preserve renal function in patients with shock.

References