Cardiac Cycle and Hemodynamics
The cardiac cycle describes how the heart fills with blood and pumps it out in a repeating sequence of contractions and relaxations. Understanding this cycle is essential in pharmacology because many cardiac drugs target specific phases of this process, alter blood flow dynamics, or change how hard the heart has to work.
Phases of Cardiac Pumping Action
The heart alternates between two states: systole (contraction) and diastole (relaxation). Both the atria and ventricles go through their own systole and diastole, and the timing between them is what keeps blood moving in one direction.
- Systole (contraction)
- Atrial systole: The atria contract, pushing their remaining blood into the ventricles. This "atrial kick" accounts for only about 20% of ventricular filling, since the other 80% already flowed in passively during ventricular diastole.
- Ventricular systole: The ventricles contract, sending oxygen-poor blood from the right ventricle into the pulmonary artery and oxygen-rich blood from the left ventricle into the aorta.
- Diastole (relaxation)
- Atrial diastole: The atria relax and refill with blood from the veins. The superior and inferior vena cava drain into the right atrium; the pulmonary veins drain into the left atrium.
- Ventricular diastole: The ventricles relax and fill with blood from the atria. About 80% of ventricular filling happens passively during this phase, driven by the pressure gradient between atria and ventricles.

Key Events in the Cardiac Cycle
Here's the sequence of events in order, along with what the valves are doing at each step:
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Atrial systole
- The atria contract, delivering the final 20% of blood into the ventricles.
- The AV valves (tricuspid on the right, mitral on the left) are open, allowing blood to pass from atria to ventricles.
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Ventricular systole
- The ventricles contract, generating enough pressure to push blood into the pulmonary artery (right) and aorta (left).
- The AV valves snap shut to prevent backflow into the atria. This closure produces the first heart sound, S1 ("lub").
- The semilunar valves (pulmonary and aortic) open once ventricular pressure exceeds arterial pressure, allowing blood to eject into the arteries.
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Ventricular diastole
- The ventricles relax, and pressure inside them drops.
- The semilunar valves close as arterial pressure now exceeds ventricular pressure, preventing blood from flowing back into the ventricles. This closure produces the second heart sound, S2 ("dub").
- The AV valves reopen once ventricular pressure falls below atrial pressure, and blood begins flowing passively from the atria into the ventricles (80% of filling).
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Atrial diastole
- The atria relax and fill with venous blood (vena cava → right atrium; pulmonary veins → left atrium).
- Blood continues to flow passively through the open AV valves into the ventricles, driven by the pressure gradient.

Blood Flow Dynamics in the Cardiovascular System
Blood flow through the cardiovascular system follows a simple relationship: blood moves from areas of higher pressure to areas of lower pressure, and anything that resists that flow slows it down.
- Blood flow equation:
- = blood flow, = pressure gradient (difference in pressure between two points), = resistance
- A larger pressure gradient increases flow (e.g., during ventricular systole, the ventricle generates high pressure to push blood out).
- Greater resistance decreases flow (e.g., narrowed or constricted vessels make it harder for blood to pass through).
- Pressure gradient across the circulation:
- Pressure is highest in the aorta and drops progressively through arteries → arterioles → capillaries → venules → veins.
- Pressure is lowest in the vena cava as blood returns to the heart.
- Resistance factors: Three things determine vascular resistance:
- Blood vessel diameter is the most powerful factor. Small changes in diameter cause large changes in resistance.
- Blood viscosity (thickness of the blood) also affects resistance. More viscous blood flows more slowly.
- Total vessel length contributes, though this doesn't change much in a given person.
- Vasoconstriction (vessel narrowing) increases resistance and decreases blood flow.
- Vasodilation (vessel widening) decreases resistance and increases blood flow.
- Autoregulation: Tissues can locally adjust their own blood flow to match metabolic demand.
- Active tissues (e.g., exercising skeletal muscle) release vasodilators like nitric oxide, which widen local blood vessels and increase flow.
- Less active tissues experience vasoconstriction, redirecting blood toward the tissues that need it most.
Cardiac Performance Factors
Several factors determine how effectively the heart pumps. These are the terms you'll see repeatedly when studying cardiac drugs:
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Preload: The volume of blood stretching the ventricles at the end of diastole (right before contraction). More blood in the ventricle means more stretch on the muscle fibers.
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Afterload: The pressure the ventricles must push against to eject blood. Higher arterial blood pressure means higher afterload, which makes the heart work harder.
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Stroke volume (SV): The amount of blood ejected from one ventricle in a single contraction. A normal resting stroke volume is roughly 70 mL.
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Ejection fraction (EF): The percentage of blood in the ventricle that actually gets pumped out per beat. A normal EF is about 55–70%. An EF below 40% generally indicates heart failure.
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Frank-Starling law: As preload increases (more blood fills the ventricle), the heart muscle stretches more and contracts more forcefully, increasing stroke volume. Think of it like stretching a rubber band further before releasing it. This mechanism lets the heart automatically adjust its output to match venous return.
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Cardiac output (CO): The total volume of blood the heart pumps per minute. It's calculated as:
where is stroke volume and is heart rate. At rest, a typical cardiac output is about 5 L/min (70 mL × 72 beats/min ≈ 5,040 mL/min).