1.1 Chest Compression Mechanics & Performance Metrics

Physiology of Cardiopulmonary Circulation & Dual Mechanical Models

High-quality cardiopulmonary resuscitation (CPR) is the single most critical intervention for restoring systemic organ perfusion during sudden cardiac arrest. To understand why exact compression metrics are mandated, clinicians must understand the underlying hemodynamics of artificial circulation. Manual CPR generates forward blood flow through two distinct, complementary physiological mechanisms: the Cardiac Pump Model and the Thoracic Pump Model.

Under the Cardiac Pump Model, direct mechanical compression of the sternum squeezes the heart between the sternum and the vertebral column. This physical compression increases intraventricular pressure, closing the atrioventricular (mitral and tricuspid) valves and forcing blood out of the ventricles into the aorta and pulmonary artery. Under the Thoracic Pump Model, downward sternal displacement increases overall intrathoracic pressure relative to extrathoracic vascular beds. This generalized pressure gradient propels blood out of the thoracic cavity through the arterial system, while retrograde flow into the venous system is largely prevented by venous valves.

Regardless of which model predominates in a given patient, artificial forward cardiac output during CPR reaches only 25% to 30% of normal physiological cardiac output at best. Because this margin of safety is extremely narrow, minor degradations in CPR mechanics cause profound drops in tissue oxygen delivery, rapidly leading to irreversible hypoxic-ischemic brain injury and myocardial death.

The CPR cycle is divided into two biomechanical phases: the compression phase (systole) and the relaxation or recoil phase (diastole). While the compression phase ejects blood from the thorax, the relaxation phase is equally vital. Complete sternal recoil creates a negative intrathoracic pressure relative to the periphery. This pressure gradient acts as an intrathoracic vacuum, drawing venous blood from the vena cava back into the right atrium and ventricle—a process known as restoring ventricular preload. Furthermore, myocardial perfusion (blood flow supplying the cardiac muscle itself through the coronary arteries) occurs almost exclusively during this diastolic recoil phase. If a rescuer leans on the chest and prevents full recoil, intrathoracic pressure remains persistently elevated, venous return collapses, and coronary perfusion is severely compromised.

Core Performance Metrics: Rate, Depth, and Surface Mechanics

The 2025 American Heart Association (AHA) Guidelines for CPR and Emergency Cardiovascular Care (ECC) emphasize strict quantitative performance boundaries for chest compressions in adults:

1. Compression Rate (100 to 120 compressions per minute): This narrow window balances forward cardiac output with diastolic filling time. Compressions delivered slower than 100/min fail to generate sufficient mean arterial pressure. Conversely, rates exceeding 120/min drastically shorten the diastolic interval. At excessively fast rates, the ventricles do not have adequate time to fill with venous blood between compressions—a phenomenon termed 'empty heart syndrome'. As a result, despite high physical effort, stroke volume plummets and net cardiac output declines sharply.

2. Compression Depth (at least 2.0 inches / 5 cm, max 2.4 inches / 6 cm): Sternal displacement of at least 2 inches is required in adults to generate sufficient intrathoracic pressure and direct ventricular compression. Compressions shallower than 2 inches fail to squeeze the heart adequately, producing sub-therapeutic stroke volumes. However, compressions deeper than 2.4 inches significantly increase the incidence of resuscitation-related trauma, including rib and sternal fractures, flail chest, lung lacerations, pneumothorax, pericardial tamponade, and hepatic or splenic tears.

3. Body Mechanics and Sternal Position: Rescuers must place the heel of one hand on the center of the patient's chest (the lower half of the sternum) with the other hand locked on top. Rescuers should lock their elbows straight, align their shoulders directly over the patient's sternum, and pivot at the hips. Utilizing core body weight rather than arm muscles maximizes mechanical efficiency, ensures consistent compression force, and delays muscle fatigue.

4. Surface Mechanics & CPR Backboards: CPR must be performed on a firm, unyielding surface. When cardiac arrest occurs in a hospital bed or stretcher, soft foam or air mattresses absorb up to 30% to 40% of the downward compression force. In these situations, the patient's torso sinks into the mattress rather than being compressed. Rescuers must deploy a rigid CPR backboard under the patient's chest immediately without interrupting CPR for more than a few seconds, or activate the bed's CPR mode (which rapidly deflates air mattresses) to ensure full sternal displacement.

Hemodynamics, Coronary Perfusion Pressure (CPP), and Physiological Monitoring

The ultimate physiological objective of high-quality chest compressions is maintaining adequate Coronary Perfusion Pressure (CPP) and Cerebral Perfusion Pressure (CerPP). CPP represents the pressure gradient driving oxygenated blood into the coronary arteries during the relaxation phase. It is calculated using the following physiological formula:

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

Extensive human and animal resuscitation data demonstrate that achieving a CPP > 15 mmHg is a mandatory prerequisite for successful Return of Spontaneous Circulation (ROSC). If CPP remains below 15 mmHg during resuscitation, defibrillation attempts will consistently fail, and spontaneous cardiac activity cannot be restored.

Because direct CPP measurement requires central arterial and venous catheters, resuscitation teams utilize real-time non-invasive and invasive surrogates to guide compression quality:

• Quantitative Waveform Capnography (End-Tidal CO2 / ETCO2): In cardiac arrest, exhalation of carbon dioxide is limited entirely by pulmonary blood flow (cardiac output) delivered by CPR. An ETCO2 value < 10 mmHg indicates inadequate CPR quality or a dismal prognosis for ROSC. Rescuers should adjust rate, depth, and recoil to maintain ETCO2 between 10 and 20 mmHg (ideally > 20 mmHg). An abrupt, sustained jump in ETCO2 (e.g., rising sharply from 15 mmHg to 35–40 mmHg) is the earliest physiological indicator of ROSC, reflecting a sudden surge in endogenous cardiac output.
• Invasive Arterial Line Monitoring: In ICU or emergency department settings where an arterial line is already in place, rescuers monitor the diastolic arterial blood pressure (DAP) during CPR. Guidelines recommend maintaining a DAP > 20 mmHg. If the DAP drops below 20 mmHg, the team leader must immediately instruct the compressor to adjust their compression depth and ensure complete recoil.

Clinical Scenario: An adult patient in the intensive care unit experiences sudden pulseless ventricular tachycardia. The patient has an indwelling radial arterial line and an endotracheal tube connected to quantitative capnography. CPR is initiated immediately. The arterial line displays a diastolic blood pressure of 12 mmHg and the ETCO2 reads 8 mmHg. Recognizing sub-therapeutic perfusion, the Team Leader immediately places a backboard under the patient and instructs the compressor to increase depth to 2.2 inches and avoid leaning. Within 15 seconds, the diastolic pressure climbs to 22 mmHg and ETCO2 rises to 18 mmHg, successfully optimizing conditions for subsequent defibrillation.