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Physiology of Cardiopulmonary Resuscitation (CPR)
1. Physiological Basis: What Happens at Cardiac Arrest
Sudden cardiac arrest (SCA) sets off a cascade of haemodynamic events. Forward systemic arterial blood flow continues briefly after arrest until the pressure gradient between the aorta and right heart equilibrates. As the arteriovenous gradient diminishes, left heart filling decreases, right heart filling increases, and the venous capacitance vessels become progressively distended. When arterial and venous pressures reach equilibration — approximately 5 minutes after no-flow arrest — coronary and cerebral perfusion stop entirely.
Brain ATP is depleted within 4–6 minutes of absent blood flow, but returns to near-normal within 6 minutes of effective CPR. Studies suggest acceptable neurologic outcomes may still be possible after 10–15 minutes of normothermic arrest if good circulation is promptly restored.
CPR is therefore symptomatic therapy aimed at:
- Maintaining oxygen and blood supply to vital organs (brain, heart)
- Restoring spontaneous circulation
- Minimising post-resuscitation organ injury
2. Mechanisms of Blood Flow During Chest Compressions
Two dominant theories explain how closed-chest compressions generate blood flow:
A. Cardiac Pump Mechanism
Direct compression of the heart between the sternum and the vertebral column causes pulsatile ejection of blood. During the compression phase:
- The mitral and tricuspid valves close
- Ventricular volumes decrease, ejecting blood into the arterial system
- During the decompression (relaxation) phase, the pressure gradient between the systemic venous system and thoracic cavity allows refilling of cardiac chambers
The clinical implication is that adequate compression depth (≥5 cm / 2 inches in adults) is essential to maximise stroke volume, and full chest recoil is equally essential to allow adequate filling. Younger patients with more compliant chest walls are more affected by this mechanism.
B. Thoracic Pump Mechanism
Described after a patient in cardiac catheterisation developed VF and maintained arterial pressure with cough-hiccups (Criley et al., 1976). According to this theory:
- Sternal depression raises intrathoracic pressure equally across all thoracic structures
- This pressure differential forces blood out of the thorax into the extrathoracic circulation
- Retrograde venous flow is prevented by valves in the subclavian and internal jugular veins and by dynamic compression of veins at the thoracic outlet
- Arterial walls are thicker and less compressible, favouring arterial outflow
- The heart acts as a passive conduit, with AV valves remaining open
- Because there is a pressure difference between the carotid artery and jugular vein, blood flow to the head is preferentially maintained
- Below the diaphragm, the inferior vena cava lacks valves, so there is nearly equal pressure in arteries and veins, resulting in minimal subdiaphragmatic organ perfusion
Older patients with less compliant chest walls are more affected by this mechanism.
In clinical practice, the predominant mechanism varies between patients and may even shift during the resuscitation attempt, depending on chest wall compliance, heart size, arrest duration, compression force, and other factors.
3. Distribution of Blood Flow During CPR
Regardless of mechanism, total body cardiac output during CPR is reduced to only 10–33% of normal.
| Vascular Bed | Perfusion During CPR |
|---|---|
| Cerebral | 50–90% of normal |
| Myocardial | 20–50% of normal |
| Abdominal viscera / lower extremities | ~5% of normal |
Total flow tends to decrease with time during CPR. Nearly all flow is directed to organs above the diaphragm. Epinephrine further augments brain and heart perfusion while leaving subdiaphragmatic flow unchanged or further reduced.
4. Physiology of Ventilation During CPR
Gas Transport and the Unique Acid-Base State
During CPR's low-flow state, CO₂ excretion (mL CO₂/min in exhaled gas) falls proportionally to the reduction in cardiac output, primarily due to shunting of blood away from the lower body. This creates a paradoxical acid-base picture:
- Arterial blood: Respiratory alkalosis (low PaCO₂, due to maintained ventilation with markedly reduced cardiac output)
- Venous blood: Respiratory acidosis with a markedly elevated arteriovenous CO₂ difference
The elevated venous PvCO₂ arises because:
- Reduced tissue perfusion causes CO₂ accumulation in tissues, raising tissue PCO₂ and increasing venous CO₂ content
- Buffering of metabolic acid reduces bicarbonate, raising the partial pressure for the same CO₂ content
End-tidal CO₂ (EtCO₂) correlates poorly with arterial CO₂ during CPR (because many alveoli are unperfused and contribute dead space), but correlates excellently with cardiac output — making it the gold-standard non-invasive monitor of CPR quality. An abrupt sustained rise in EtCO₂ to ≥40 mmHg signals return of spontaneous circulation (ROSC).
Ventilation Technique
- Tidal volume of 0.5–0.6 L (visible chest rise) with each breath given over 1 second
- Peak inspiratory pressures must be kept below oesophageal opening pressure (~20 cm H₂O) to avoid gastric insufflation
- 30:2 compression-to-ventilation ratio before advanced airway placement
- After ETT/supraglottic airway: 1 breath every 6 seconds (10 breaths/min) with continuous compressions
- Hyperventilation is harmful — even modest increases in intrathoracic pressure impair venous return, reduce cardiac output, and worsen coronary and cerebral perfusion
5. Coronary Perfusion Pressure — The Critical Target
Coronary perfusion occurs primarily during the relaxation (diastolic) phase of chest compressions, analogous to normal diastolic coronary filling.
- A minimum coronary perfusion pressure (CPP) of 15–25 mmHg is required for ROSC
- CPP = Aortic diastolic pressure − Right atrial diastolic pressure
- The threshold aortic diastolic pressure for critical myocardial blood flow is >40 mmHg
- Minimum myocardial blood flow required for successful resuscitation: 15–20 mL/min/100 g myocardium
When invasive monitoring is available, these targets guide titration of compression technique and vasopressor dosing.
6. Pharmacological Physiology: Vasopressors
Epinephrine
The first-line vasopressor (1 mg IV/IO every 3–5 minutes). Its efficacy lies entirely in its α-adrenergic properties:
- Peripheral vasoconstriction → increases aortic diastolic pressure → increases CPP and myocardial blood flow
- All strong α-agonists (phenylephrine, methoxamine, norepinephrine, dopamine) are equally effective
- β-agonists without α-activity (isoproterenol, dobutamine) are no better than placebo
- α-adrenergic blockade precludes resuscitation; β-blockade has no effect on ROSC
The β-adrenergic effects of epinephrine are potentially deleterious — increasing myocardial oxygen consumption in the fibrillating heart without improving the oxygen supply-to-demand ratio. High-dose epinephrine (>1 mg) has not shown improved long-term neurological outcomes in randomised trials.
Amiodarone / Lidocaine
Antiarrhythmics target refractory ventricular fibrillation/pulseless VT; they do not directly improve cardiac output but facilitate successful defibrillation.
7. High-Quality CPR — The Physiological Standards
| Parameter | Target |
|---|---|
| Compression rate | 100–120/min |
| Compression depth | ≥5 cm (2 in), not >6 cm (2.4 in) |
| Chest recoil | Complete after each compression |
| Compression fraction | >60% of total CPR time |
| Ventilation | Avoid excessive; 1 breath/6 sec with advanced airway |
| EtCO₂ target | ≥10–20 mmHg during CPR; ≥40 mmHg = ROSC |
Interruptions in chest compressions cause an abrupt fall in perfusion pressure that takes multiple subsequent compressions to rebuild. Every interruption must be minimised.
8. Post-Resuscitation Physiology
Following ROSC, a "post-cardiac arrest syndrome" develops comprising:
- Post-resuscitation myocardial dysfunction (stunned myocardium — typically recovers within 24–48 h)
- Systemic ischaemia/reperfusion injury with inflammatory activation
- Neurological injury from global cerebral ischaemia
- Persistent precipitating pathology (e.g., ACS, PE)
Targeted temperature management (TTM) at 32–36°C for ≥24 hours reduces the metabolic demand of recovering cerebral tissue and improves neurological outcomes in comatose post-arrest survivors.
Summary
| Concept | Key Fact |
|---|---|
| Brain ATP depletion | 4–6 min (recovers in 6 min with effective CPR) |
| Cardiac output during CPR | 10–33% of normal |
| Cerebral perfusion | 50–90% of normal |
| Myocardial perfusion | 20–50% of normal |
| Critical CPP for ROSC | 15–25 mmHg |
| EtCO₂ as CPR monitor | Best non-invasive surrogate for cardiac output |
| Primary mechanism of vasopressors | α-adrenergic peripheral vasoconstriction |
Sources: Barash, Cullen & Stoelting's Clinical Anesthesia, 9e (Chapter 58); Miller's Anesthesia, 10e (Chapter 82); Roberts & Hedges' Clinical Procedures in Emergency Medicine, 7e (Chapter 12)
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