12.1 High-Performance Cardiopulmonary Resuscitation (CPR) & Automated/Manual Defibrillation

12.1 High-Performance Cardiopulmonary Resuscitation (CPR) & Automated/Manual Defibrillation

Resuscitation Science & The High-Performance CPR Paradigm

Sudden out-of-hospital cardiac arrest (OHCA) represents one of the most time-critical emergencies encountered in Canadian paramedic practice. Under the Canadian Paramedic Competence Framework (CPCF Appendix A #27A), and drawing on the resuscitation guidance published by the Heart and Stroke Foundation of Canada and the International Liaison Committee on Resuscitation (ILCOR), guidelines, resuscitation outcomes depend directly on the delivery of High-Performance CPR (HP-CPR) and rapid electrical defibrillation. HP-CPR transforms cardiac arrest resuscitation from an ad-hoc effort into a highly choreographed, metric-driven pit-crew model designed to maximize myocardial and cerebral perfusion.

Core Quality Metrics of High-Performance CPR

Paramedics must master five interdependent biomechanical parameters during manual chest compressions:

1. Compression Rate: 100 to 120 compressions per minute. Compressing at rates below 100/min generates inadequate cardiac output, while rates exceeding 120/min critically impair diastolic ventricular filling time, diminishing forward stroke volume.
2. Compression Depth: 5 to 6 cm (2 to 2.4 inches) in the average adult. Compressions shallower than 5 cm generate insufficient intrathoracic and intracardiac pressure gradients to open the aortic valve. Depths exceeding 6 cm increase the risk of skeletal trauma (sternal fractures, rib flails) and visceral injury (splenic/liver lacerations) without augmenting forward blood flow.
3. Complete Chest Recoil: Full release of sternal pressure at the upstroke of each compression. Residual leaning on the chest wall elevates baseline intrathoracic pressure, impeding venous return to the right heart, reducing end-diastolic ventricular volume, and drastically lowering coronary perfusion pressure during decompression.
4. Chest Compression Fraction (CCF): The proportion of total resuscitation time dedicated to active chest compressions. HP-CPR mandates a CCF of at least 80% to 85%. Every pause in compressions causes an immediate collapse of intravascular pressure gradients that require 15 to 20 continuous compressions to rebuild.
5. Minimizing Peri-Shock Pauses: The pre-shock pause (time between stopping compressions and shock delivery) must be kept strictly below 5 seconds, and the post-shock pause should be 0 seconds (compressions resume instantly upon shock discharge).

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Biomechanics of Chest Compressions & Coronary Perfusion Pressure (CPP)

During cardiac arrest, forward blood flow is generated by a combination of the cardiac pump mechanism (direct mechanical compression of the ventricles between the sternum and thoracic spine) and the thoracic pump mechanism (cyclical variations in generalized intrathoracic pressure relative to extrathoracic vascular beds).

Myocardial viability and the likelihood of Return of Spontaneous Circulation (ROSC) are governed by Coronary Perfusion Pressure (CPP):

$\text{CPP} = \text{Aortic Diastolic Pressure} - \text{Right Atrial Diastolic Pressure}$

Coronary blood flow occurs almost exclusively during the relaxation (diastolic) phase of CPR. When compressions cease, aortic diastolic pressure immediately decays toward atmospheric pressure. Laboratory and clinical human studies demonstrate that a threshold CPP of at least 15 mmHg is essential to generate sufficient myocardial capillary perfusion to achieve ROSC. Clinicians who rest their hands on the sternum between compressions (incomplete recoil) elevate right atrial pressure, which directly subtracts from aortic diastolic pressure and drives CPP below this critical 15 mmHg threshold.

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Airway Management & Ventilation Dynamics in Resuscitation

Resuscitation protocols establish distinct ventilation strategies based on the airway modality utilized:

The Lethal Hazard of Hyperventilation

Excessive ventilation rates (>10–12 breaths/min) or excessive tidal volumes generate severe hemodynamic harm:

• Elevated Mean Intrathoracic Pressure: High positive pressure compresses the superior and inferior vena cava, drastically curtailing right atrial venous return.
• Decreased Cardiac Output: Reduced right-sided filling translates directly to decreased left ventricular stroke volume and collapsed coronary perfusion.
• Cerebral Vasoconstriction: Rapid washing out of carbon dioxide (hypocapnia, PaCO2 <35 mmHg) induces severe cerebral arterial vasoconstriction, critically diminishing cerebral blood flow and worsening ischemic neurological injury.

Continuous Waveform Capnography (ETCO2) Monitoring

Continuous quantitative waveform capnography is mandatory in all resuscitations involving advanced airways:

• ETCO2 <10 mmHg: Reflects inadequate pulmonary blood flow, signaling ineffective compression biomechanics, compressor fatigue, or severe irreversible metabolic collapse.
• ETCO2 10–20 mmHg: Represents acceptable low-flow cardiac output during high-quality manual CPR.
• Sudden Sustained Rise to 35–45+ mmHg: The most sensitive and immediate physiological indicator of ROSC. When spontaneous circulation returns, accumulated metabolic carbon dioxide is suddenly transported from peripheral tissues back to the pulmonary capillary bed and exhaled.

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Electrical Defibrillation: Waveforms, Vector Alignment & Rhythm Management

Defibrillation delivers a therapeutic dose of electrical energy across the myocardium to depolarize a critical mass of chaotic ventricular myocytes simultaneously, terminating disorganized fibrillatory wavelets and enabling the cardiac intrinsic pacemaker (sinoatrial node) to resume organized rhythmicity.

Shockable vs Non-Shockable Rhythms

• Shockable Rhythms:
  • Ventricular Fibrillation (VF): Chaotic, disorganized ventricular depolarization without organized QRS complexes or mechanical pumping.
  • Pulseless Ventricular Tachycardia (pVT): Rapid, wide monomorphic or polymorphic QRS complexes without a palpable pulse.
• Non-Shockable Rhythms:
  • Asystole: Complete absence of electrical and mechanical ventricular activity (ventricular standstill).
  • Pulseless Electrical Activity (PEA): Organized or semi-organized electrical activity on the cardiac monitor in the absence of a palpable central pulse.

Defibrillation Energy Levels & Waveforms

Modern prehospital defibrillators employ biphasic waveforms (Biphasic Truncated Exponential [BTE] or Rectilinear Biphasic), which reverse current polarity midway through discharge. Biphasic shocks achieve superior first-shock termination efficacy at significantly lower energy levels compared to obsolete monophasic sinusoidal shocks (which required 360 J).

• Biphasic Defibrillation: 120 J to 200 J initially (manufacturer-specific; e.g., 120–150 J rectilinear or 200 J truncated exponential). Subsequent shocks should be delivered at equal or escalating energy levels (e.g., 200 J–300 J–360 J).
• Automated External Defibrillator (AED): Automated voice prompts and rhythm analysis algorithms identify shockable rhythms. In manual mode, primary care paramedics directly interpret the rhythm strip.

Pad Placement & Current Vectoring

Proper pad placement ensures the electrical vector traverses the maximum volume of ventricular myocardium:

• Anterior-Lateral Placement (Standard): One pad placed on the patient's right upper chest (infraclavicular, right sternal border), and the second pad placed over the left 5th–6th intercostal space at the mid-axillary line (lateral to the left breast/nipple apex).
• Anterior-Posterior Placement (Alternative / Refractory): One pad positioned over the left precordium (anterior sternum/apex) and the second pad directly posterior between the left scapula and thoracic spine. This orientation creates an anteroposterior vector that lowers transthoracic impedance and improves current delivery across the posterior and lateral left ventricular walls.
• Implantable Pacemakers / ICDs: Defibrillation pads must be placed at least 2.5 to 5 cm (1 to 2 inches) away from the implanted pulse generator to prevent current shunting, internal circuit burning, or myocardial damage at the lead-tissue interface.

[!IMPORTANT] Immediate Resumption of CPR Post-Shock: Immediately upon shock discharge, compressions must resume instantly for 2 full minutes without pausing for a rhythm check or pulse palpation. Even when electrical termination of VF is successful, the stunned myocardium produces zero effective stroke volume during the initial 60 to 120 seconds. Checking a pulse immediately post-shock deprives the ischemic myocardium of vital perfusion.

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Systematic Identification and Management of Reversible Causes (H's and T's)

During PEA and asystole resuscitation, primary care paramedics must methodically investigate and treat underlying reversible conditions:

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Post-Resuscitation Care & Post-ROSC Hemodynamic Optimization

Achieving ROSC is not the end of resuscitation; it begins the fragile phase of Post-Cardiac Arrest Syndrome (PCAS), characterized by brain injury, myocardial dysfunction, systemic ischemia-reperfusion response, and persistent acute pathology. Post-ROSC paramedic care focuses on four pillars:

1. Diagnostic 12-Lead ECG: Must be acquired immediately following hemodynamic stabilization. The presence of ST-elevation myocardial infarction (STEMI) or new LBBB mandates direct transport to a regional Percutaneous Coronary Intervention (PCI) center with prehospital catheterization lab activation.
2. Hemodynamic Maintenance: Maintain Systolic Blood Pressure (SBP) >90 mmHg and Mean Arterial Pressure (MAP) ≥65 mmHg to ensure cerebral autoregulation. Administer titrated isotonic crystalloid fluid boluses (500–1000 mL normal saline). If fluid-refractory, request Advanced Life Support (ALS) intercept for vasopressor/inotropic infusions (e.g., norepinephrine or dopamine).
3. Ventilation & Oxygenation Titration:
   • Oxygenation: Titrate inspired oxygen to achieve an SpO2 of 92% to 98%. Avoid absolute hyperoxia (SpO2 100% or PaO2 >300 mmHg), which triggers excessive reactive oxygen species (ROS) generation, accelerated cerebral lipid peroxidation, and secondary neuronal cell apoptosis.
   • Ventilation: Maintain normoventilation targeting an ETCO2 of 35 to 40 mmHg (PaCO2 35 to 45 mmHg). Prevent hyperventilation-induced cerebral vasoconstriction.
4. Targeted Temperature Management (TTM) & Avoiding Hyperthermia: Actively prevent pyrexia/fever. Every 1°C elevation in core temperature above 37.5°C exponentially increases cerebral metabolic oxygen demand ($CMRO_2$) and worsens neurological morbidity. If the patient is comatose, maintain normothermia (36°C–37.5°C); do not routinely infuse large volumes of ice-cold intravenous fluids in the prehospital setting, as this increases the incidence of pulmonary edema and rearrest.

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Clinical Scenario: Pit-Crew Resuscitation in Refractory Ventricular Fibrillation

Paramedics arrive at an athletic facility where a 52-year-old male collapsed during recreational hockey. Bystander CPR is in progress with an on-site AED that delivered one shock prior to arrival.

1. Choreography & Pit-Crew Setup: Paramedic 1 immediately assumes continuous manual chest compressions with a metronome set to 110 beats/min. Paramedic 2 applies the manual monitor/defibrillator pads in the anterior-lateral position.
2. Rhythm Analysis 1: At the 2-minute mark, the monitor displays coarse Ventricular Fibrillation. The team charges the monitor to 200 J biphasic while compressions continue ('charging during CPR'). Compressions pause for <3 seconds to clear the patient, the shock is discharged, and compressions resume instantaneously without a rhythm or pulse check.
3. Airway & Vascular Access: Paramedic 2 inserts an i-gel supraglottic airway without interrupting compressions, attaches continuous waveform capnography showing an initial ETCO2 of 16 mmHg, and establishes intravenous access.
4. Rhythm Analysis 2 & Reversal of Causes: Following 2 minutes of continuous compressions (CCF calculated at 88%) with asynchronous ventilations at 1 breath every 6 seconds, the rhythm is analyzed: persistent refractory VF. A second biphasic shock (200 J) is delivered, and CPR resumes immediately. Epinephrine 1 mg (1:10,000) IV is administered with a 20 mL saline flush.
5. ROSC Identification: Ninety seconds into the third compression cycle, the continuous capnography waveform jumps abruptly from 18 mmHg to 44 mmHg. At the conclusion of the 2-minute cycle, an organized sinus tachycardia is observed with a strong palpable radial pulse (BP 124/82 mmHg).
6. Post-ROSC Care: An immediate 12-lead ECG demonstrates 3 mm ST elevation in leads II, III, and aVF (inferior STEMI). The paramedic initiates prehospital cath lab bypass, titrates oxygen to 95%, maintains normothermia, and transports directly to the PCI center.

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Exam Pitfalls & High-Yield Resuscitation Pearls

• Checking Pulses Immediately Post-Shock: Never pause compressions immediately after shock discharge. Myocardial stunning prevents pulse generation; resume compressions for the full 2 minutes.
• Leaning on the Chest: Failing to achieve complete recoil elevates right atrial diastolic pressure, drastically collapsing Coronary Perfusion Pressure (CPP).
• Hyperventilating Post-ROSC: Pushing ETCO2 below 35 mmHg severely vasoconstricts cerebral arterioles, causing profound brain ischemia.
• Ignoring Right Ventricular Leads in Inferior STEMI Post-ROSC: If inferior STEMI is identified post-resuscitation, acquire lead V4R before administering any vasodilators if hemodynamics fluctuate.