PEA and Asystole (Non-Shockable Rhythms)

Quick Answer

Critical: PEA (Pulseless Electrical Activity) and asystole are non-shockable cardiac arrest rhythms with poorer prognosis than VF/pVT. Management focuses on high-quality CPR, immediate adrenaline administration, and aggressive identification and treatment of reversible causes (4Hs and 4Ts). Survival depends on finding and treating a reversible cause.

PEA is defined as an organised electrical rhythm on the monitor in the absence of a palpable central pulse, while asystole represents the complete absence of ventricular electrical activity [1]. Together, these non-shockable rhythms account for 65-70% of all cardiac arrests and are increasing in proportion as VF/pVT rates decline [2]. Unlike shockable rhythms, defibrillation is not indicated - instead, the focus is on continuous high-quality CPR, immediate adrenaline (as soon as IV/IO access is obtained), and systematic identification of reversible causes [3]. Prognosis is worse than for shockable rhythms: asystole survival to discharge is typically 1-2%, while PEA survival ranges from 5-10%, with better outcomes when a reversible cause is identified and treated [4]. Per ARC/ANZCOR Guideline 11, the key intervention is treatment of the underlying cause [5].

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ACEM Exam Focus

Primary Exam Relevance

• Physiology: Difference between electrical and mechanical cardiac activity; why PEA produces organised ECG without effective cardiac output; coronary perfusion pressure (CPP) in non-shockable rhythms; cellular hypoxia cascade
• Pharmacology: Adrenaline pharmacokinetics and timing (alpha-1 vasoconstriction for CPP augmentation); why amiodarone is NOT indicated for non-shockable rhythms; antidotes for specific toxins causing PEA (calcium for hyperkalaemia, bicarbonate for TCA)
• Pathology: Mechanisms of the 4Hs and 4Ts leading to non-shockable arrest; electromechanical dissociation pathophysiology; myocardial ATP depletion and rhythm degradation

Fellowship Exam Relevance

• Written SAQ Topics: Non-shockable algorithm application, distinguishing PEA from asystole, pseudo-PEA concept and POCUS use, specific management of 4Hs/4Ts, when to consider termination of resuscitation
• OSCE: Resuscitation leadership with non-shockable rhythm - expect a scenario starting with PEA/asystole requiring identification of reversible cause. Communication station may involve discussing futility with family when asystole persists.
• Key domains tested: Medical Expert (algorithm knowledge, cause identification), Leader (team coordination, decision on termination), Communicator (discussing prognosis with family)

High-Yield Exam Points

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Key Points

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Epidemiology

Australian and New Zealand Data

Aus-ROC Epistry Data for Non-Shockable Rhythms

The Australian Resuscitation Outcomes Consortium (Aus-ROC) Epistry captures comprehensive data on cardiac arrest outcomes [10]:

• Increasing proportion: Non-shockable rhythms (PEA + asystole) now represent 65-70% of all OHCA, up from 50% two decades ago [2]
• Reason for shift: Better primary prevention of VF (ICDs, beta-blockers, revascularisation) means fewer patients present in VF [14]
• PEA is increasing fastest: PEA has doubled in proportion over 20 years as medical care improves (patients survive longer to have non-cardiac causes of arrest) [15]
• Geographic variation: Rural/remote areas have higher rates of asystole (delayed EMS = rhythm degradation from VF) [10]
• Witnessed vs unwitnessed: Unwitnessed arrests more likely to be non-shockable (VF degenerates over time) [16]

Aetiology Distribution

Age and Sex Distribution

• Median age: 68 years for non-shockable rhythms (older than VF/pVT median ~62 years) [10]
• Male:Female ratio: 1.5:1 (less male predominant than shockable rhythms at 2:1) [2]
• Elderly preponderance: greater than 80 years have over 80% non-shockable initial rhythm [17]
• Paediatric: 90% of paediatric arrests are non-shockable (respiratory aetiology) [18]

Risk Factors for Non-Shockable Presenting Rhythm

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Pathophysiology

PEA - Pulseless Electrical Activity

Definition

PEA is defined as the presence of organised electrical activity on the cardiac monitor in the absence of a palpable central pulse [1]. It represents a heterogeneous group of conditions where there is electromechanical dissociation.

Mechanism

Organised electrical activity (depolarisation) occurs
                    ↓
BUT inadequate mechanical response
                    ↓
      ┌─────────────────────────────────┐
      │  TWO DISTINCT ENTITIES:         │
      │                                 │
      │  TRUE PEA (EMD)                 │
      │  • No cardiac motion on POCUS   │
      │  • Complete electromechanical   │
      │    dissociation                 │
      │  • No contractile function      │
      │  • Very poor prognosis (below 2%)    │
      │                                 │
      │  PSEUDO-PEA                     │
      │  • Cardiac motion on POCUS      │
      │  • Organised contractility BUT  │
      │  • Inadequate cardiac output    │
      │    to generate palpable pulse   │
      │  • Better prognosis (15-20%)    │
      │  • May respond to treatment     │
      └─────────────────────────────────┘

Pseudo-PEA vs True PEA

Causes of PEA (by Mechanism)

Electromechanical Dissociation Pathway

Cellular ATP depletion (hypoxia, ischaemia)
                    ↓
Failure of calcium-dependent excitation-contraction coupling
                    ↓
Sarcomere cannot contract despite electrical depolarisation
                    ↓
Electrical activity continues (organised ECG) BUT
No mechanical contraction = No cardiac output = No pulse
                    ↓
TRUE PEA (complete dissociation)

Asystole

Definition

Asystole is the complete absence of ventricular electrical activity, appearing as a flat line on the cardiac monitor [3]. It may occur as a primary rhythm or as the final common pathway of untreated cardiac arrest.

Mechanism

                PATHWAYS TO ASYSTOLE
                        ↓
┌──────────────────────────────────────────────────────────┐
│                                                          │
│  PRIMARY ASYSTOLE              SECONDARY ASYSTOLE        │
│  ────────────────              ──────────────────        │
│  • SA node failure             • VF → Fine VF → Asystole │
│  • Complete heart block        • PEA → Asystole          │
│  • Severe hypoxia              • Untreated VF degrades   │
│  • Profound hypothermia          in ~10 minutes          │
│  • Severe hyperkalaemia        • ATP depletion           │
│  • Massive stroke              • Cellular death          │
│  • Drug-induced                                          │
│    (beta-blockers, CCBs,                                 │
│    digoxin, cholinergics)                               │
│                                                          │
└──────────────────────────────────────────────────────────┘

VF Degradation Timeline

UNTREATED VENTRICULAR FIBRILLATION
            ↓
┌───────────────────────────────────────────────────────┐
│  0-5 min:   Coarse VF (high amplitude, 12-15mm)       │
│             - Most responsive to defibrillation       │
│             - "Electrical" phase of arrest            │
│                                                       │
│  5-10 min:  Fine VF (low amplitude, below 5mm)             │
│             - Harder to defibrillate                  │
│             - "Circulatory" phase - needs CPR         │
│             - May mimic asystole (check gain, leads)  │
│                                                       │
│  10-15 min: Very fine VF → Asystole                   │
│             - Myocardial ATP depleted                 │
│             - "Metabolic" phase                       │
│             - Very poor prognosis                     │
│                                                       │
│  greater than 15 min:   Asystole                                  │
│             - Complete electrical silence             │
│             - Irreversible without intervention       │
└───────────────────────────────────────────────────────┘

Confirmation of Asystole (Avoiding Misdiagnosis)

Cellular Pathophysiology in Non-Shockable Arrest

CARDIAC ARREST INITIATED
            ↓
Global hypoxia → Shift to anaerobic metabolism
            ↓
Lactate accumulation → Intracellular acidosis
            ↓
ATP depletion → Ion pump failure (Na+/K+-ATPase)
            ↓
┌─────────────────────────────────────────┐
│  Intracellular:                         │
│  • Na+ accumulation                     │
│  • K+ depletion                         │
│  • Ca2+ accumulation (from SR + ECF)    │
│  • Cell swelling                        │
│  • Mitochondrial dysfunction            │
└─────────────────────────────────────────┘
            ↓
Calcium overload → Hypercontracture → Cell death
            ↓
Electrical silence (asystole) OR
Electrical activity without contraction (PEA)
            ↓
Irreversible injury (neurons: 4-6 min; myocytes: 15-20 min)

Why Defibrillation Doesn't Work for Non-Shockable Rhythms

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Rhythm Recognition

PEA - ECG Characteristics

ECG Clues to PEA Aetiology

Asystole - ECG Characteristics

Fine VF vs Asystole

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ARC/ANZCOR Non-Shockable Algorithm (Guideline 11)

Non-Shockable Rhythm Algorithm

┌─────────────────────────────────────────────────────────────────────────────┐
│                            CARDIAC ARREST                                    │
│                  Unresponsive, not breathing normally                        │
│                         DRSABCD approach                                     │
└─────────────────────────────────────────────────────────────────────────────┘
                                     ↓
┌─────────────────────────────────────────────────────────────────────────────┐
│                              CALL FOR HELP                                   │
│               000/111 or MET call, request defibrillator                    │
└─────────────────────────────────────────────────────────────────────────────┘
                                     ↓
┌─────────────────────────────────────────────────────────────────────────────┐
│                            START CPR 30:2                                    │
│          Attach defibrillator pads when available                           │
│     Rate 100-120/min | Depth 5-6cm | Full recoil | Minimise pauses          │
└─────────────────────────────────────────────────────────────────────────────┘
                                     ↓
┌─────────────────────────────────────────────────────────────────────────────┐
│                          ANALYSE RHYTHM                                      │
│                  Minimise pause for analysis (below 5 sec)                        │
│                  If asystole: Check 2 leads, gain, connections              │
└─────────────────────────────────────────────────────────────────────────────┘
                                     ↓
┌─────────────────────────────────────────────────────────────────────────────┐
│                         NON-SHOCKABLE RHYTHM                                 │
│                        Asystole or PEA                                       │
│                                                                              │
│                  ╔═════════════════════════════════════╗                    │
│                  ║  NO SHOCK - Resume CPR immediately  ║                    │
│                  ║  for 2 minutes                      ║                    │
│                  ╚═════════════════════════════════════╝                    │
│                                                                              │
│             ┌──────────────────────────────────────────────┐                │
│             │  ADRENALINE 1mg IV/IO IMMEDIATELY            │                │
│             │  As soon as vascular access obtained         │                │
│             │  Then every 3-5 minutes                      │                │
│             │  (Do NOT wait - differs from shockable!)     │                │
│             └──────────────────────────────────────────────┘                │
└─────────────────────────────────────────────────────────────────────────────┘
                                     ↓
┌─────────────────────────────────────────────────────────────────────────────┐
│                          DURING CPR                                          │
│                                                                              │
│  • Ensure high-quality CPR (100-120/min, 5-6cm depth, full recoil)         │
│  • Plan actions before rhythm check (minimise pause)                        │
│  • Vascular access (IV or IO) - prioritise early                           │
│  • Airway management (advanced airway when appropriate)                     │
│  • Waveform capnography (ETCO2 monitoring)                                  │
│  • POCUS during brief rhythm check (look for cardiac motion, tamponade)    │
│  • Consider and TREAT REVERSIBLE CAUSES                                     │
│                                                                              │
│        ┌────────────────────────────────────────────────────────────┐       │
│        │                 REVERSIBLE CAUSES                          │       │
│        │                                                            │       │
│        │   4Hs:                     4Ts:                            │       │
│        │   • Hypoxia                • Tension pneumothorax          │       │
│        │   • Hypovolaemia           • Tamponade (cardiac)           │       │
│        │   • Hypo/Hyperkalaemia     • Toxins                        │       │
│        │   • Hypothermia            • Thrombosis (PE or MI)         │       │
│        │                                                            │       │
│        │   ★ Non-shockable rhythms = FOCUS ON FINDING CAUSE ★       │       │
│        └────────────────────────────────────────────────────────────┘       │
└─────────────────────────────────────────────────────────────────────────────┘
                                     ↓
                         After 2 minutes of CPR
                                     ↓
┌─────────────────────────────────────────────────────────────────────────────┐
│                        RE-ANALYSE RHYTHM                                     │
│                                                                              │
│     ┌───────────────┐              ┌───────────────────────────────┐        │
│     │  Still PEA/   │              │  Rhythm change to             │        │
│     │  Asystole     │              │  VF/pVT (Shockable)           │        │
│     └───────┬───────┘              └───────────────┬───────────────┘        │
│             │                                       │                        │
│             ↓                                       ↓                        │
│     Resume CPR                              DEFIBRILLATE                     │
│     Continue adrenaline                     Switch to shockable              │
│     every 3-5 min                           pathway                          │
│     Treat reversible                                                         │
│     causes                                                                   │
└─────────────────────────────────────────────────────────────────────────────┘
                                     ↓
                          CONTINUOUS LOOP until:
                                     ↓
┌─────────────────────────────────────────────────────────────────────────────┐
│                               OUTCOMES                                       │
│                                                                              │
│  ┌─────────────────────────────┐    ┌────────────────────────────────────┐  │
│  │         ROSC                │    │     Consider Termination           │  │
│  │                             │    │                                    │  │
│  │  • Palpable pulse           │    │  • Asystole throughout            │  │
│  │  • Rising ETCO2             │    │  • No reversible cause found      │  │
│  │  • Arterial waveform        │    │  • Duration greater than 30-40 min            │  │
│  │  • Patient movement         │    │  • ETCO2 persistently below 10 mmHg    │  │
│  │                             │    │  • No bystander CPR + prolonged   │  │
│  │  → Post-resuscitation care  │    │    downtime                       │  │
│  │  → Treat precipitating      │    │  • Cardiac standstill on POCUS    │  │
│  │    cause                    │    │                                    │  │
│  │  → TTM if comatose          │    │  → Team leader decision           │  │
│  │  → ICU admission            │    │  → Document reason                 │  │
│  └─────────────────────────────┘    └────────────────────────────────────┘  │
└─────────────────────────────────────────────────────────────────────────────┘

Key Differences: Non-Shockable vs Shockable Algorithm

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Reversible Causes in Non-Shockable Rhythms

The 4 Hs

The 4 Ts

Toxin-Specific Management in PEA/Asystole

POCUS for Reversible Causes

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Medications in Non-Shockable Arrest

Adrenaline (Epinephrine)

Mechanism in Cardiac Arrest:

• Alpha-1 agonist effect: Peripheral vasoconstriction → increased SVR → augmented aortic diastolic pressure → improved coronary perfusion pressure (CPP = Aortic diastolic - Right atrial pressure) [29]
• CPP over 15 mmHg associated with ROSC
• Beta effects (chronotropy, inotropy) less relevant during arrest but may increase myocardial oxygen demand

Evidence - PARAMEDIC2 Trial (2018):

• Adrenaline vs placebo in OHCA
• Improved ROSC (36.3% vs 11.7%) and 30-day survival (3.2% vs 2.4%)
• No difference in survival with favourable neurological outcome (2.2% vs 1.9%)
• Benefit more pronounced in non-shockable rhythms
• Remains standard of care per ARC guidelines [30]

Medications NOT Indicated in Non-Shockable Rhythms

Medications for Specific Reversible Causes

Vascular Access Priority

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Point-of-Care Ultrasound in Non-Shockable Arrest

Role of POCUS in PEA/Asystole

Cardiac Standstill and Prognosis

Multiple studies have demonstrated that cardiac standstill (absence of organised myocardial contractility) on POCUS during PEA arrest is associated with extremely poor outcomes [8][28][33]:

• Survival with cardiac standstill: below 2%
• Survival with organised cardiac motion (pseudo-PEA): 15-20%
• Clinical implication: Cardiac standstill may be used as one factor in decisions about termination of resuscitation

Important Note: Caution: Cardiac standstill should NOT be the sole criterion for terminating resuscitation, but should be considered alongside:

• Duration of resuscitation
• ETCO2 levels
• Reversible causes addressed
• Patient factors (age, comorbidities, witnessed/unwitnessed)
• Quality of CPR received

Lung Ultrasound

• Absent lung sliding: Suggests pneumothorax - perform finger thoracostomy
• Lung pulse: Cardiac activity transmitted to pleura - rules out pneumothorax
• Barcode sign (M-mode): Confirms absence of lung sliding = pneumothorax

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Prognosis and When to Consider Termination

Survival Outcomes

Factors Associated with Better Outcome in Non-Shockable Arrest

Factors Associated with Poor Outcome

When to Consider Termination of Resuscitation

ETCO2 as Prognostic Indicator

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Special Circumstances

Pregnant Patient with Non-Shockable Arrest

Hypothermic Arrest

Drowning

• Hypoxic aetiology - give 5 rescue breaths initially
• Often presents as asystole or PEA (respiratory cause)
• Hypothermic drowning has better prognosis - continue extended resuscitation
• Cervical spine immobilisation only if diving injury or high-energy mechanism

Dialysis Patient

• Hyperkalaemia: Most common cause - treat empirically with calcium, insulin/glucose
• Fluid overload: May require dialysis post-ROSC
• Electrolyte derangements: Check VBG for K+, Ca2+
• Vascular access: AV fistula should NOT be used for resuscitation drugs (risk of damage)

Massive PE Causing PEA

• Consider if risk factors present (immobility, malignancy, recent surgery)
• POCUS: Dilated RV, D-sign, McConnell's sign
• Treatment: Thrombolysis - alteplase 50mg IV bolus during CPR
• Continue CPR for 60-90 minutes post-thrombolysis to allow drug effect [26]
• Consider ECPR if available

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Indigenous Health Considerations

Important Note: Aboriginal, Torres Strait Islander, and Maori Considerations:

Health Disparities Relevant to Non-Shockable Arrest

Aboriginal and Torres Strait Islander Australians:

• Higher rates of cardiovascular disease at younger ages (10-15 years earlier) [35]
• Higher prevalence of chronic kidney disease → hyperkalaemia risk
• Higher rates of rheumatic heart disease (8-fold higher)
• Increased prevalence of diabetes, hypertension
• Remote communities: delayed EMS response times (over 60 min in some areas)
• Lower rates of bystander CPR in some communities
• Increased likelihood of presenting in non-shockable rhythm (delayed recognition + response)

Maori (New Zealand):

• 2-3 times higher cardiovascular mortality
• Similar disparities in risk factor prevalence
• Rural areas may have delayed access to care

Specific Causes More Common in Indigenous Populations

Cultural Considerations in Resuscitation

Communication During/After Resuscitation:

• Involve Aboriginal Health Workers/Liaison Officers early
• Allow time for extended family to be contacted and arrive
• Understand community elder involvement in major decisions
• Be aware of cultural protocols around death and dying ("Sorry Business")
• Use interpreters for language barriers
• Respect that silence may indicate consideration, not lack of understanding

Post-Resuscitation/Death:

• Discuss sensitively - beliefs about body integrity vary
• Organ donation: discuss with cultural liaison support
• Allow cultural practices (karakia/prayers, family rituals)
• Document family wishes regarding care and decision-making

Maori-Specific:

• Whanau (family) involvement is crucial
• Tikanga Maori (cultural protocols) around death
• Karakia (prayers) may be requested
• Cultural liaison available in major NZ hospitals

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Remote and Rural Considerations

Challenges in Rural/Remote Australia

Modified Approach in Resource-Limited Settings

RFDS and Retrieval Considerations

• Activate RFDS/retrieval service early if ROSC likely
• Telemedicine consultation for complex decisions
• ROSC must be achieved and stable before aeromedical transport in most cases
• Discuss termination decisions with retrieval coordination if uncertain

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Viva Practice

Viva Scenario 1: Basic PEA Management

Viva Scenario 2: Asystole Confirmation

Viva Scenario 3: Hyperkalaemia Causing PEA

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OSCE Scenarios

OSCE Station 1: Non-Shockable Arrest Leadership

Format: Resuscitation leadership station Time: 11 minutes Setting: ED resuscitation bay

Candidate Instructions:

A 55-year-old male is brought in by ambulance in cardiac arrest. CPR is in progress. The monitor shows a regular rhythm but the paramedic states there is no pulse. You are the team leader. Lead the resuscitation.

Resources Available:

• 2 nurses, 1 registrar
• Full resuscitation equipment
• Defibrillator attached
• POCUS available

Expected Actions:

1. Confirm cardiac arrest (no pulse despite organised rhythm = PEA)
2. Take over team leadership with clear role allocation
3. Ensure high-quality CPR continues (minimise interruptions)
4. Establish IV/IO access promptly
5. Give adrenaline 1mg IV immediately (correct timing for non-shockable)
6. DO NOT shock (correctly identifies non-shockable rhythm)
7. Request/perform POCUS during rhythm check to assess for cardiac motion and reversible causes
8. Systematically consider 4Hs and 4Ts verbally
9. Order appropriate investigations (VBG, glucose)
10. Demonstrate closed-loop communication
11. Repeat adrenaline every 3-5 minutes
12. Respond appropriately to rhythm changes

Examiner Instructions:

• Initial rhythm: Regular narrow complex at 70bpm (PEA)
• At 4 minutes: Provide VBG showing K+ 7.2 mmol/L
• At 6 minutes: If candidate treats hyperkalaemia appropriately, can achieve ROSC
• At 8 minutes: If no appropriate treatment, rhythm deteriorates to asystole

Marking Criteria:

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OSCE Station 2: Asystole Confirmation

Format: Resuscitation skills station Time: 8 minutes Setting: ED resuscitation bay with manikin

Candidate Instructions:

A patient is in cardiac arrest. The monitor shows a flat line. Before proceeding with your management, confirm the rhythm. Demonstrate your approach to the examiner.

Expected Actions:

1. Verbalise suspicion of asystole
2. Check monitor gain/amplitude and increase
3. Confirm in second lead (switch from Lead II to Lead III or orthogonal)
4. Check electrode connections - physically inspect
5. Check cable connections
6. Verbalise "confirming asystole is true asystole, not fine VF"
7. Once confirmed, state management approach:
   • CPR, adrenaline immediately, consider reversible causes
   • No defibrillation indicated

Marking Criteria:

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SAQ Practice

SAQ Question 1: Non-Shockable Algorithm (6 marks)

Clinical Scenario: A 68-year-old female is found unresponsive in the hospital ward. The arrest team arrives and finds asystole on the monitor after confirming she has no pulse.

Question: Outline the key elements of the ARC non-shockable rhythm algorithm, including drug therapy and timing.

Time Allocation: 9 minutes

Model Answer:

Confirm non-shockable rhythm (asystole or PEA) after confirming absence of pulse (1 mark)

• For asystole: check in 2 leads, increase gain, check connections

CPR 30:2 immediately, minimise interruptions (1 mark)

• Rate 100-120/min, depth 5-6cm, full recoil
• Rotate compressors every 2 minutes

Vascular access (IV or IO) - priority for drug administration (0.5 mark)

Adrenaline 1mg IV/IO IMMEDIATELY when access obtained (1 mark)

• Then every 3-5 minutes
• Key difference from shockable: do NOT wait for shocks

NO defibrillation for non-shockable rhythms (0.5 mark)

Consider reversible causes (4Hs and 4Ts) actively during resuscitation (1 mark):

• Hypoxia, Hypovolaemia, Hypo/hyperkalaemia, Hypothermia
• Tension pneumothorax, Tamponade, Toxins, Thrombosis

Reassess rhythm every 2 minutes - look for rhythm change to VF/pVT (1 mark)

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SAQ Question 2: Pseudo-PEA (6 marks)

Clinical Scenario: During resuscitation of a patient in PEA arrest, you perform POCUS and observe weak but visible cardiac contractility despite no palpable pulse.

Question: a) Define pseudo-PEA and true PEA (2 marks) b) Discuss the clinical significance and prognostic implications (2 marks) c) How does this finding influence your management? (2 marks)

Time Allocation: 9 minutes

Model Answer:

a) Definitions (2 marks):

Pseudo-PEA (1 mark):

• Organised ECG rhythm with visible cardiac mechanical activity on POCUS
• No palpable pulse (very low blood pressure, but some cardiac output present)
• Represents extreme hypotension rather than true electromechanical dissociation

True PEA (1 mark):

• Organised ECG rhythm with NO cardiac mechanical activity on POCUS
• Complete electromechanical dissociation
• Electrical activity present but myocardium unable to contract

b) Clinical significance and prognosis (2 marks):

Pseudo-PEA (1 mark):

• Better prognosis - survival to discharge 15-20%
• Suggests underlying cause may be reversible (hypovolaemia, PE, tamponade)
• May respond to treatment (fluids, vasopressors, treating cause)
• Often has measurable (though very low) arterial pressure with A-line
• ETCO2 typically higher (over 20 mmHg)

True PEA (1 mark):

• Very poor prognosis - survival to discharge below 2%
• Indicates complete failure of excitation-contraction coupling
• Often represents irreversible injury or untreatable cause
• ETCO2 typically very low (below 10 mmHg)

c) Management implications (2 marks):

For pseudo-PEA (1 mark):

• Aggressive search for and treatment of reversible causes
• Higher threshold for termination of resuscitation
• Consider fluid bolus if hypovolaemic picture
• Consider vasopressor if near-ROSC
• Repeat POCUS to monitor response

For true PEA (cardiac standstill) (1 mark):

• Continue resuscitation but recognise poor prognosis
• Cardiac standstill is ONE factor in termination decisions
• Ensure all reversible causes have been addressed
• Earlier consideration of cessation if prolonged with no improvement

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SAQ Question 3: Termination of Resuscitation (8 marks)

Clinical Scenario: You are managing a 75-year-old male in asystolic cardiac arrest. The arrest was unwitnessed with estimated downtime of 15-20 minutes before ambulance arrival. No bystander CPR was performed. After 25 minutes of resuscitation with optimal CPR, multiple adrenaline doses, and treatment of potential reversible causes, the patient remains in asystole with ETCO2 of 8 mmHg. POCUS shows cardiac standstill.

Question: a) List the factors in this case that would support consideration of termination of resuscitation (4 marks) b) Describe the process you would follow to cease resuscitation (4 marks)

Time Allocation: 12 minutes

Model Answer:

a) Factors supporting termination (4 marks, 0.5 each):

1. Asystole throughout - never achieved shockable rhythm
2. Unwitnessed arrest with prolonged downtime (15-20 min)
3. No bystander CPR - prolonged no-flow time
4. Prolonged resuscitation (25+ minutes) without ROSC
5. Persistently low ETCO2 (8 mmHg) despite quality CPR - predicts failure of ROSC
6. Cardiac standstill on POCUS - poor prognostic sign
7. Advanced age (75 years) - though not sole criterion
8. Reversible causes considered/treated without response

b) Process for cessation (4 marks):

Team consultation (1 mark):

• Brief pause in CPR for team discussion
• "I'm considering ceasing resuscitation. Does anyone have additional information or disagree?"
• Ensure all agree that reversible causes have been addressed

Decision and timing (1 mark):

• Team leader makes final decision
• Announce "We will stop resuscitation"
• Note exact time of cessation = time of death
• Continue compressions briefly if family present and wish to be at bedside

Documentation (1 mark):

• Time of death
• Duration of resuscitation
• Interventions attempted
• Drug doses and timing
• ETCO2 values
• Reversible causes considered
• POCUS findings
• Reason for cessation

Post-event care (1 mark):

• Family notification and support
• Involve social work, pastoral care, cultural liaison as appropriate
• Offer team debrief (hot debrief immediately, cold debrief within 48 hours)
• Complete death certification requirements
• Consider referral to coroner if appropriate

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References

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