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A. Epidemiology

  1. Sudden cardiac death (SCD) causes 300,000-400,000 deaths per year
  2. About 250,000 out-of-hospital cardiac arrests per year [3]
    1. About 225,000 deaths per year from cardiac arrest prior to arrival at hospital
    2. Each minute delay in resuscitation associated with 7-10% reduction in survival
  3. Over 370,000 cases per year of cardiac arrest in hospital with attempted resuscitation
  4. About 70% of cardiac arrests with attempted resuscitation due to cardiac causes
  5. Witnessed arrests have considerably better outcomes than unwitnessed arrests
  6. Ventricular arrhythmias have with better outcomes than other causes of cardiac arrest
  7. Associated Diseases
    1. Coronary artery disease (CAD) in ~80% of cases
    2. Aortic stenosis also common in older persons with cardiac arrest
    3. Younger persons: congenital heart disease, WPW (see below), cardiomyopathies
    4. Early repolarization on ECG in ~30% with cardiac arrest versus 5% control subjects []
  8. Sudden Death in Young Athletes
    1. >80% of young deaths appear to be due to cardiac causes
    2. Hypertrophic cardiomyopathy was most common anomaly found at autopsy
    3. Coronary artery malformations were also found

B. Causes

  1. Tachyarrhythmias
    1. Ventricular Tachycardia (VT)
    2. Ventricular Fibrillation (VF)
    3. VT and VF represent ~25% of causes of SCD
    4. Wolff-Parkinson-White (WPW) syndrome
    5. Supraventricular tachycardias (SVT)
    6. Atrial Fibrillation (AFib) with rapid ventricular response
  2. Cardiac Dysfunction
    1. Asystole - associated with worst outcomes for all types of cardiac arrest
    2. Aortic stenosis
    3. Congenital heart disease
    4. Acute Cor Pulmonale - Pulmonary embolism [4]
    5. Cardiac tamponade
  3. Electromechanical Dissociation (EMD)
    1. Also called Pulseless Electrical Activity (PEA)
    2. Rapid determination of etiology required
    3. Increasing cause of SCD with very grim prognosis
  4. Electrolyte Disorders
    1. Hyperkalemia (most common)
    2. Hypokalemia
    3. Hypomagnesemia (particularly QTc prolongation)
  5. Acidosis
  6. Bradyarrhythmias
  7. Miscellaneous
    1. Electric shock
    2. Hypothermia
    3. Hypovolemia (severe)
    4. Tension pneumothorax
    5. Respiratory arrest - severe asthma, anaphylaxis, toxic fumes
    6. Temporal lobe epilepsy can also cause asystole [5]
  8. Risk Factors
    1. Risk factors for myocardial ischemia, mainly CAD, aortic stenosis
    2. Cocaine - risk factor for sudden death in young persons
    3. Early repolarization on ECG in ~30% with cardiac arrest versus 5% control subjects []
  9. Increased intake and blood levels of long chain n-3 polyunsaturated fatty acids (seafood) reduces risk of cardiac arrest [31]

C. Progression of Untreated Arrest Event

  1. Three Phases [1]
    1. Electrical (0-4 minutes): difibrillation is most important
    2. Circulatory (4-10 minutes): cardiopulmonary resuscitation (CPR) most important
    3. Metabolic (>10 minutes): worsening cardiac and other organ failure; limited therapies
  2. Permanent damage to cerebral cortex within 5 minutes
  3. Complete damage to cerebral cortex within 10 minutes (Brain Death)
  4. EMD (potentially fatal, non-arrest)
    1. Hypovolemia
    2. Cardiac Tamponade
    3. Tension Pneumothorax
    4. Hypoxemia
    5. Acidosis
    6. Pulmonary Embolism [6]
  5. Outcomes of In-Hospital Cardiac Arrest
    1. Survival to discharge for in-hospital cardiac arrest is improving to >10%
    2. The following were risk factors for DEATH for in-hospital cardiac arrest:
    3. Arrest was unwitnessed
    4. Resuscitation lasted >10 minutes
    5. Initial cardiac rhythm was not VTach or VF
    6. Age >75 years
    7. Use of automated external defibrillators (AED) to reduce response times beneficial
  6. Out-of-Hospital Cardiac Arrest [7]
    1. Vasopressin superior to epinephrine primarily for asystole
    2. Spontaneous circulation restored in ~30% in both groups
    3. About 33% of patients overall admitted to hospital
    4. About 10% of patients survived to hospital discharge overall
    5. About 33% of patients who survived to hospital discharge had good cerebral performance
    6. Thus, overall, ~3% of patients with out-of-hospital arrest survive with intact brain function

D. Treatment Overview [1,8]

  1. ABCD
    1. Airway - clear airway (oropharynx)
    2. Breathing - breath sounds; intubation preferred
    3. Circulation - pulse
    4. Defibrillation - for all arrhythmias; not recommended for EMD or asystole
    5. Epinephrine - in patients who fail defibrillation
    6. Vasopressin provides no benefit first line over epinephrine except in aystole [1,9]
  2. Cardiopulmonary Resuscitation (CPR)
    1. Delay in time to defibrillation of >10 minutes (into metabolic phase) makes CPR ineffective
    2. Standard methods with compression initiated as early as possible
    3. Use of CPR for ~90 seconds prior to defibrillation improved survival when response time to defibrillation was >4 minutes
    4. Chest compressions with or without mouth-to-mouth ventilation had similar outcomes in several studies [11,12]
    5. Current recommendations are 30:2 compressions to ventilations
    6. Delay in chest compression >20 seconds reduces likelihood of circulatory return
    7. Treatment of VF with defibrillator within 3 minutes by security officers or on airlines is associated with improved surival to hospital discharge [13,14]
    8. Treatment of out-of-hospital cardiac arrest with CPR + automated external defibrillators (AED) associated with ~25% survival to hospital discharge versus 14% for no AED [15]
    9. Advanced cardiac life support added no benefit to standard CPR in out-of-hospital cardiac arrest; rapid defibrillation out-of-hospital provided clear benefit [16]
    10. Goal time from arrest to defibrillation is now 3 minutes [8]
  3. Electrical Defibrillation
    1. For VF and decompensated VTach (or out-of-hospital cardiac arrest)
    2. Optimization of defibrillation use improved survival (<9 minute response times) [17]
    3. For witnessed cardiac arrest, CPR begun immediately but shock administered as soon as defibrillator is available
    4. If response interval >4 minutes, 90 seconds of CPR before defibrillation gave 27% survival versus 17% receiving defibrillation first
    5. Two types of defibrillations (monophasic, biphasic) with no clinical outcome differences
    6. For monophasic shocking, 360J energy is used for all defibrillations
    7. With biphasic pulses, 120-200J for first defibrillation; same or higher levels on subsequent
    8. Use of AED for in-hospital cardiac arrest increased surival 2.6X due to shorter times [18]
    9. Epinephrine or vasopressin are used next (may be used sequentially)
    10. Rapid defifrillation is required for good outcomes
  4. Automated External Defibrillators (AED) [3,32]
    1. AEDs are increasingly being used in public places (airplanes, casinos)
    2. Newer units deliver biphasic wave forms
    3. Provide equal success at lower energy levels (150J) than monophasic units
    4. Units typically allow electrocardiographic monitoring and analysis
    5. Modest training required for skilled use
    6. Associated with ~2X increase survival rates versus lack of use in public [32]
    7. AEDs also clearly beneficial for in-hospital cardiac arrest as well [17]
  5. Epinephrine [7]
    1. Increases aortic pressure, cerebral and myocardial blood flow
    2. Stimulates alpha- and beta-adrenergic receptors; alpha- activity most important
    3. Given by peripheral IV line followed by fluid bolus
    4. May be given by central line (subclavian or jugular) but not recommended via femoral line
    5. Epinephrine is not active in an acidic environment (always present after 10 minutes)
    6. Epinephrine initial dose: recommendations vary from 1-5mg IV
    7. Subsequent epinephrine doses: 5-10mg iv usually q 5 min to 20mg
    8. High dose (7mg) epinephrine not superior to standard dose (1mg) in CPR cases [19]
    9. High dose (0.05-0.2mg/kg) epinephrine after standard dose (0.01mg/kg) is not superior and may be harmful in children with in hospital cardiac arrest [20]
    10. Combination of epinephrine + vasopressin recommended in asystolic arrest [1]
  6. Vasospressin (ADH, Pitressin®) [7]
    1. Causes vasoconstriction without affecting adrenergic receptors
    2. Unlike epinephrine, vasopressin is active in an acidic environment
    3. Overall, vasopressin of no benefit over epinephrine for first line arrest treatment [7,9]
    4. Vasopressin + epinephrine was numerically (but not statistically) inferior to epinephrine alone for first line arrest; therefore epinephrine alone recommended [10]
    5. For asystole, vasopressin was superior to epinephrine in all outcomes [7]
    6. For asystole, combination of vasopressin + epinephrine recommended [1]
    7. Vasospressin may have some efficacy where epinephrine has failed
    8. Vasopressin 40 Units IV once may be used initially after failed defibrillation [8]
  7. Atropine
    1. Anticholinergic agent (inhibits parasympathetic outflow)
    2. Indicated especially in bradycardia and asystole when epinephrine has failed
    3. May be combined with epinephrine and vasopressin
    4. Dose: 1mg iv usually after second dose of epinephrine
  8. Aminophylline can increase heart rate but has shown no clinical benefit in bradysystolic cardiac arrest (see below) [16]
  9. Antiarrhythmics [1,8]
    1. Amiodarone (Type III) - first line, all shock-refractory arrhythmias
    2. Lidocaine (Type Ib) - second line after amiodarone
    3. Magnesium sulfate 1-2gm loading dose is used to treat Torsades de pointes
    4. Implantable cardioverter-defibrillator (ICD) may be useful in refractory patients
    5. Bretyllium (Type III) is no longer available
  10. Amiodarone
    1. Indicated for all patients with shock-refractory VT or VF
    2. Dose is 300mg IV with cardioversion; aqueous amiodarone can be given as a push
    3. For emergency arrest resistant to other agents, may show efficacy
    4. May be used in patients with very low ejection fraction (EF)
    5. Recommended (300mg IV push and load) for out-of-hospital cardiac arrest [21]
    6. Amiodarone 5mg/kg showed 22.8% survival to hospital admission versus 12.0% for lidocaine in patients with out-of-hospital VF resistant to epinephrine and shocks [22]
  11. Lidocaine
    1. Recurrent or refractory VTach or VF, or after countershock for VTach or VF
    2. Dose 1mg/kg initial, 0.5mg/kg subsequent to max dose of 3mg/kg
    3. Amiodarone 5mg/kg may be superior to lidocaine in many settings
  12. Calcium Guconate / Chloride
    1. Indicated only for HYPERKALEMIC Arrest and Calcium channel blocker overdoses
    2. No longer generally recommended because of lack of benefit
  13. Sodium Bicarbonate
    1. No longergenerally recommended for correction of acidemia (no benefit)
    2. May be useful in some situations with acidosis exacerbating decline (see below)
  14. Aminophylline [21]
    1. Efficacy 250mg iv push in small trials for bradyasystolic arrests ± MI setting
    2. No clinical benefit in patients with bradysystolic out-of-hospital cardiac arrest [16]
  15. Coronary Angiography
    1. Most cases of cardiac arrest in adults (~80%) associated with CAD
    2. Many cases of cardiac arrest are caused by acute coronary occlusion
    3. In survival of cardiac arrest, immediate coronary angiography appears beneficial

E. VF and Pulseless VTach [1,8]

  1. Similar for VF and Pulseless VTach
  2. Precordial Thump (if witnessed arrest)
  3. CPR until defibrillator available or at least 90 seconds if >4 minutes since arrest
  4. Verify Rhythm
  5. Defibrillate: Single shock: 360J monophasic or 120-200J biphasic
  6. Establish IV Access / Intubate if possible
  7. Epinephrine or Vasopressin [1,7]
    1. Epinephrine 1:10,000 1mg IV push (or 10cc via endotracheal tube) OR
    2. Vasopressin 40U IV x 1 dose only (do not repeat)
    3. Epinephrine repeat q3-5 minutes prn
  8. Defibrillate again as above single shock if shockable rhythm after 5 cycles (30:2) CPR
  9. Consider amiodarone IV 300mg (or 5mg/kg) push
  10. Defibrillate with up to as above after 5 cycles (30:2) CPR
  11. Repeat Cycles of Shocks and consider additional Anti-arrhythmics
    1. Lidocaine, 0.5mg/kg IV push or
    2. Magnesium sulfate 1-2gm in 100mL in 5% dextrose over 2 minutes
    3. Aminophylline may show some efficacy, particularly with underlying bradycardias
  12. Consider Bicarbonate 1mEq/kg but not generally recommended
  13. If rhythm degenerates to asystole or EMD (no pulse), treat as asystole
  14. If pulse is present, begin post-resuscitation care

F. Asystole and Electromechanical Dissociation (EMD)

  1. In pulseless arrest, confirm rhythm in at least 2 leads on ECG
  2. Continue CPR; Supplemental O2 100%
  3. IV Access / Intubate if possible
  4. Institute transcutaneous pacing if available
  5. Vasopressin 40U IV x1 is preferred initial therapy [7]
  6. Then give epinephrine, 1mg IV push, repeat q 3-5 minutes after vasopressin
  7. Consider atropine, 1mg IV push; repeat q 3-5 minutes to total of 3mg
  8. Consider aminophylline 250mg iv rapid bolus or bicarbonate
  9. If shockable rhythm occurs, treat as above for VF/VTach
  10. Attempt to identify treatable causes
    1. Hypovolemia: treat with IV Fluids
    2. Cardiac Tamponade: Pericardiocentesis
    3. Tension Pneumothorax: Release intrathoracic pressure
    4. Pulmonary Embolism (possible DVT, R Axis Deviation ECG): Vasodilators, Clot Lysis
  11. For asystole lasting at >10 minutes with CPR, consider cessation of resuscitation if [8]:
    1. VF eliminated
    2. Successful endotracheal intubation accomplished
    3. Adequate ventilation provided
    4. Appropriate medications given
  12. Tissue plasminogen activator showed no benefit in EMD [23]

G. Ventricular Tachycardia (VT) [25]

  1. VTach without Pulse: Treat as VF (above)
  2. Sustained Stable (No Symptoms) VTach with Pulse
    1. Oxygen, IV Access
    2. Amiodarone bolus 150mg (aqueous) may be repeated and is clearly more effective than lidocaine for VTach [24]
    3. Lidocaine 0.5mg/kg q8 to 3mg/kg total (48 minutes)
    4. Cardioversion (as in Unstable Patient)
  3. Sustained VTach, unstable (with Pulse)
    1. Unstable Symptoms: chest pain, dyspnea, hypotension, CHF, ischemia, MI
    2. Oxygen, IV Access
    3. Consider Sedation
    4. Cardioversion (Monophasic): 50 J; if fails, 100 J; if fails, 200 J; if fails up to 360 J
    5. If recurrent, add lidocaine and cardioversion as above (begin 50 J)
    6. IV water soluble amiodarone 150mg as above may be effective [12]

H. Bradycardia

  1. Sinus, Junctional Bradycardia and Second Degree Heart Block Type I
    1. Asymptomatic: Observe
    2. Symptomatic: Treat as Below
  2. Heart Block 2° Type II and 3°
    1. Asymptomatic: Transvenous Pacemaker
    2. Symptomatic: Treat as emergency
  3. Treatment (Emergent)
    1. Atropine 0.5-1.0mg; repeat as needed
    2. Transvenous (through cordice) or transcutaneous (Zoll) pacing
    3. Dopamine 5-15µg/kg/min
    4. Epinephrine, 0.5-1.0 mg
    5. Isoproterenol (2-10µg/min; out of favor)
    6. Consider aminophylline, 250mg iv bolus, though this has shown no mortality reduction [16]

I. Ventricular Ectopy Suppression

  1. Treatable Causes: potassium, digitalis, bradycardia, other drugs
  2. Amiodarone 300mg IV as above, followed by maintenance dosing
  3. ß-Blockade is probably safest medication for suppression of ectopy
  4. Consider Overdrive Pacing
  5. Lidocaine has also been used

J. Supraventricular Tachycardia

  1. Treat only if symptomatic (CP, dyspnea, ischemia, hypotension, CHF) or dangerous (such as post-Myocardial infarction)
  2. Supplemental Oxygen, IV Access
  3. Stable Paroxysmal SVT
    1. Consider Vagal Maneuvers (while monitored)
    2. Verapamil, 5mg IV; 10mg IV in 15-20 minutes
    3. Diltiazem: 15-25mg iv
    4. Consider Adenosine 6-12µg iv fast
    5. Cardioversion, Digoxin, ß-Blockade, Pacing as needed
  4. Synchronized Cardioversion
    1. Atrial Flutter: 25 J
    2. Paroxysmal Supraventricular Tachycardia: 75-100 J
    3. Atrial Fibrillation: 100 J

K. Post-Arrest

  1. ECG Monitoring with review of 12 Lead [25]
  2. Supplemental Oxygen
    1. Nasal Canula
    2. Facemask
    3. Intubation
  3. Check Heart and Lung Fields
  4. Urine Output, Electrolytes including Ca and Mg, Arterial Blood Gas (ABG)
  5. Chest Radiograph (XRay)
    1. Cardiac Size: Failure, Pericardial Tamponade
    2. Lung Fields: wet versus dry
    3. Consider Aspiration
  6. Consider invasive monitoring
    1. Arterial Pressure
    2. Swan-Ganz Pulmonary Artery Catheter
  7. Hypothermia [28,29]
    1. Hypothermia to 32-34°C for 12-24 hours provided to post-arrest resuscitated patients
    2. Reduced mortality by ~40% and improved neurologic recovery
  8. Long term survivors of out-of-hospital cardiac arrest have similar similar quality of life and mortality to patients without cardiac arrest [26]
  9. Poor Neurological Outcome or Death Predictors [27]
    1. Absent corneal reflexes at 24 hours after arrest: 12.9X risk for poor outcome
    2. Absent pupillary response at 24 hours: 10.2X
    3. No motor response at 24 hours: 4.9X
    4. Absence withdrawal response to pain at 24 hours: 4.7X
    5. No motor response at 72 hours at 24 hours: 9.2X
    6. No clinical findings predict good neurological outcome

L. Respiratory System

  1. Chest radiograph including decubitus positions if pleural fluid suspected
  2. Mechanical Ventilation
    1. IMV: intermittent mandatory ventilation (preset # of breaths per minute)
    2. A/C: assist control. Patient initiates breath, machine delivers breath
    3. Tidal Volume: 8-10ml/kg of ideal body weight
    4. I:E Ratio (inspiratory / expiratory) - 1.5 to 2.0
    5. Rate: 10-12 per minute (adjust as necessary to maintain pCO2 and pO2)
    6. Pressure Limit (PAP): 10cm higher than delivered pressure
    7. PEEP (positive end-expiratory pressure): set initially at 5cm; higher for ARDS
    8. FiO2 - initially 100%. Aim for pO2 70-90mm: (reported pO2 - 100)÷ 7 = new %FiO2
  3. Tracheal Secretions should be aspirated and sent for culture
  4. ABGs: 20 minutes post-resuscitation; Should be followed to monitor ventilatory status
  5. Intrapulmonary Shunt - Causes
    1. Cardiogenic Pulmonary Edema
    2. Aspiration and Non-Aspiration (eg. Inhalation) Pneumonitis
    3. Fat Emboli (Bone Marrow origin) to Pulmonary System following Trauma
    4. ARDS - see below
    5. Atelectasis
    6. Thermal Injury / Toxic Chemicals, others
    7. Shunt may often be treated with increased PEEP

M. Cardiovascular System

  1. Assessment
    1. Peripheral Pulses (hands and feet), Vital Signs
    2. Neck Veins
    3. ECG, 12 Lead
    4. Chest radiograph, serum electrolytes, others as above
  2. Pulmonary Artery (Capillary) Wedge Pressure (PCWP)
    1. Usually with Swan-Ganz Catheter (Quadruple Lumen)
    2. For determination of cardiac output (CO), peripheral resistance, cardiac pressures
    3. Proximal Port measures RA pressure (normal up to 8 mm)
    4. Distal Port: pulmonary artery pressure (25/10 mm), PCWP (<12), mixed venous blood
    5. Thermistor: thermal dilution measurements for CO determinations
    6. Used for assessing cardiac function, usually poor output versus reduced peripheral resistance (eg. sepsis)
    7. Note that mechanical ventilation (especially PEEP) increases PCWP
  3. Echocardiography
    1. Post-MI for prognosis
    2. Assessment of LV (and RV) Function - ejection fraction (EF), valve abnormalities, clots
    3. Assess for pericardial fluid
    4. LV function is currently the best single prognostic marker for long term outcomes
  4. Recurrent Malignant Ventricular Arrhythmias [25]
    1. Implantable cardioverter defibrillator (ICD) is the treatment of choice
    2. Amiodarone, 400mg/day is also effective (though less so than ICD)
    3. Sotalol is effective but has negative inotropic acitivty (use only with EF >40%)
    4. Amiodarone and ICD may be combined
    5. Older agents (mexilitine, quinidine) do not prolong life and may increase mortality
  5. Indications for ICD [25]
    1. Cardiac arrest due to VF or VTach, not due to transient or reversible causes
    2. Spontaenous sustained VTach
    3. Syncope of undetermined origin with clinically relevant VTach or VF on EPS
    4. Nonsustained VTach with coronary artery disease, LV dysfunction
    5. Nonsustained VTach with EPS inducible VF or sustained VTach not suppressed by drug

N. Kidneys

  1. Kidneys are highly sensitive to hypoperfusion
  2. Acute Renal Failure (ARF)
    1. Common complication after cardiac arrest or any hypotensive episode
    2. Assess urine output (UO), monitor BUN and Creatinine
    3. Oliguria is UO < 400cc/day or <25cc/hr
    4. May have nonoliguric renal failure (normal UO with increased BUN and Creatinine
  3. Must distinguish between Prerenal, Intrinsic and Post-renal causes
    1. Prerenal: hypoperfusion results in increased Na and BUN resorption (BUN/Cr>20; FENA<1)
    2. Intrinsic: glomerulosclerosis with ischemic failure
    3. Post: obstruction not uncommon; renal Stone, Prostatic hyperplasia must be ruled out
  4. FENa is Fractional Excretion of Sodium (Na)
    1. Definition: FENA = (U/P Sodium ÷ U/P Creatinine) x 100
    2. Measures resorption activity of tubules
    3. In prerenal failure, Na is actively resorbed and FENA >1
    4. With intrinsic renal disease, kidney cannot resorb Na well so that Na is lost, FENA <0.5
  5. Treatment
    1. Foley Catheter closed system insertion
    2. Monitor fluid status: BUN, Creatinine, Urine electrolytes and Creatinine
    3. Diuretics may be used to convert oliguric to non-oliguric renal failure
    4. Non-oliguric failure is easier to handle because volume status can be controlled

O. Cerebral Function

  1. Cerebral damage occurs with circulation delay of 5-11 seconds (total oxygen depletion)
    1. Anaerobic metabolism begins as soon as cerebral oxygen is depleted
    2. Leads to rapid fall in intracellular pH (acidosis)
    3. ATPase pump function impaired leads to intracellular K+ depletion
    4. Ca2+ floods cells and Calpain (protease) is activated and can mediate tissue destruction
  2. Cerebral glucose stores depleted within 5 minutes in normal patients
  3. Currently, no pharmacologic agents known to prevent or slow cerebral damage
  4. Experimental Pharmacologics
    1. Phenytoin
    2. Prostaglandin Inhibitors
    3. Benzodiazapines
    4. Desferroxamine
    5. Calcium blocking agents
    6. NMDA antagonists
    7. Anti-oxidants

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