The Cardiac Cycle, Cardiac Output, and Hemodynamics

The Cardiac Cycle

The cardiac cycle is the sequence of mechanical and electrical events that occurs with every heartbeat. Each cycle has two main phases: systole (contraction) and diastole (relaxation). Understanding these phases is essential for respiratory therapists because pulmonary blood flow — and therefore gas exchange — depends directly on the heart's ability to pump blood through the lungs.

Phases of the Cardiac Cycle

1. Isovolumetric Contraction

After the ventricles receive an electrical signal, they begin to contract. All four valves are closed at the start of this phase, so ventricular volume does not change yet. Ventricular pressure rises sharply. This phase ends when rising left ventricular pressure exceeds aortic pressure, forcing the aortic valve open.

2. Ejection

Once the aortic and pulmonic valves open, blood is ejected into the systemic and pulmonary circulations. Pressure peaks during this phase (systolic pressure). The volume remaining in the ventricle after ejection is the end-systolic volume (ESV). The volume ejected per beat is the stroke volume (SV).

3. Isovolumetric Relaxation

The ventricles begin to relax. The aortic and pulmonic valves close (producing the S2 heart sound), and pressure falls rapidly. Because the mitral and tricuspid valves are also still closed, ventricular volume again does not change.

4. Ventricular Filling

When ventricular pressure falls below atrial pressure, the mitral and tricuspid valves open and blood flows passively into the ventricles. Most filling is passive; a smaller additional volume is delivered by atrial contraction (the "atrial kick"). The volume in the ventricle at the end of filling is the end-diastolic volume (EDV).

Cardiac Output and Its Determinants

Cardiac output (CO) is the volume of blood the heart pumps per minute:

> CO = HR × SV

• HR = heart rate (beats per minute)
• SV = stroke volume (mL per beat)
• Normal resting CO is approximately 4–8 L/min in adults.

Stroke volume itself is controlled by three factors:

Preload — the stretch of the ventricular wall at end-diastole, which corresponds to EDV. The Frank-Starling law states that within physiological limits, greater stretch produces a more forceful contraction and a larger SV. Fluid loading increases preload; hemorrhage or excessive diuresis decreases it.

Afterload — the resistance the ventricle must overcome to eject blood. For the left ventricle this is largely systemic vascular resistance (SVR); for the right ventricle it is pulmonary vascular resistance (PVR). Elevated afterload (e.g., hypertension, pulmonary hypertension) reduces SV.

Contractility — the intrinsic strength of myocardial contraction independent of preload and afterload. Positive inotropic agents (dopamine, dobutamine) increase contractility; myocardial infarction and acidosis decrease it.

Hemodynamics and Pulmonary Perfusion

Hemodynamics refers to the forces and flows that govern blood movement. Key parameters a respiratory therapist will encounter include:

• Blood pressure (BP) — systolic/diastolic; mean arterial pressure (MAP) = diastolic + 1/3 (pulse pressure)
• SpO2 — peripheral oxygen saturation, a surrogate for arterial oxygenation
• Pulmonary artery pressure — elevated when right ventricular afterload is high (pulmonary hypertension, ARDS, PE)

Pulmonary perfusion (blood flow through the lungs) equals right ventricular output, which under normal steady-state conditions equals left ventricular output. When CO falls, pulmonary blood flow decreases, reducing the blood available for gas exchange and causing V/Q mismatch. This is why patients in cardiogenic shock become hypoxemic even when ventilation is adequate.

Cardiogenic Shock: The Respiratory Perspective

Cardiogenic shock occurs when the heart cannot maintain sufficient CO to meet metabolic demands. Early signs include tachycardia, hypotension, decreased urine output, and rising respiratory rate as the body attempts to compensate. Pulmonary consequences include:

• Decreased mixed venous oxygen content (tissues extract more O2 from a smaller flow)
• Pulmonary edema if left ventricular failure raises left atrial pressure and fluid backs up into the lungs
• Worsening hypoxemia requiring supplemental oxygen or mechanical ventilatory support

Respiratory therapy interventions in this context are ordered by the physician and may include supplemental oxygen to correct hypoxemia, non-invasive positive pressure ventilation (e.g., CPAP or BiPAP) to reduce work of breathing and improve oxygenation, and preparation for invasive mechanical ventilation if the patient deteriorates. Positive pressure ventilation also reduces left ventricular afterload, which can transiently improve CO in a failing left ventricle — an important physiological rationale.

Safety Notes

• Always monitor SpO2 and work of breathing continuously in any patient with reduced CO; deterioration can be rapid.
• Positive pressure ventilation reduces venous return (preload), which may worsen hypotension in a volume-depleted patient — communicate immediately with the medical team if BP drops after initiating ventilatory support.
• Scope of practice: respiratory therapists anticipate and prepare interventions but do not independently initiate vasoactive medications or fluid boluses; these are physician-ordered.
• Document all assessments and interventions accurately to support the care team's hemodynamic management decisions.