Overview of the Cardiovascular System

Basic Anatomy and Function of the Heart

The heart is a muscular organ responsible for pumping blood throughout the body, consisting of four chambers: right atrium, right ventricle, left atrium, and left ventricle.

The heart's structure includes valves (tricuspid, pulmonary, mitral, and aortic) that ensure unidirectional blood flow.

The heart is divided into two sides: the right side pumps deoxygenated blood to the lungs, while the left side pumps oxygenated blood to the body.

The heart's electrical system, primarily the SA node, initiates the heartbeat and regulates the cardiac cycle.

The heart is surrounded by a protective sac called the pericardium, which contains fluid to reduce friction during heartbeats.

The Cardiac Cycle

The cardiac cycle consists of a sequence of events that occur with each heartbeat, including systole (contraction) and diastole (relaxation).

Each cycle is initiated by an action potential generated by the SA node, leading to changes in pressure and blood flow within the heart.

The cycle can be divided into phases: atrial diastole, atrial systole, ventricular systole, and ventricular diastole.

The cycle is crucial for maintaining blood circulation and ensuring that oxygenated blood reaches tissues while deoxygenated blood is sent to the lungs for oxygenation.

Mechanical Events in the Cardiac Cycle

Phases of the Cardiac Cycle

Atrial Diastole: Blood fills the atria from the superior and inferior vena cavae and pulmonary veins, increasing atrial pressure and opening the tricuspid and mitral valves, allowing passive blood flow into the ventricles.

Atrial Systole: Atrial contraction pushes an additional 30% of blood into the ventricles, contributing to the end-diastolic volume (EDV) of 120-130 mL.

Ventricular Systole: Ventricles contract, causing a rapid increase in pressure that closes the atrioventricular valves (producing the first heart sound,

LUP”), and opens the aortic and pulmonary valves to eject blood into the aorta and pulmonary artery, respectively.

Ventricular Diastole: Following contraction, the ventricles relax, leading to a decrease in pressure, closure of the aortic and pulmonary valves (producing the second heart sound,

DUP”), and the beginning of the filling phase again.

Pressure Changes During the Cardiac Cycle

Pressure in the heart chambers and major blood vessels changes throughout the cardiac cycle, rising during systole and falling during diastole.

Atrial pressure remains relatively low, only rising slightly during late diastole (6 mmHg in RA, 8 mmHg in LA).

Ventricular pressure experiences significant changes: 25 mmHg in RV and 120 mmHg in LV during systole, while diastolic pressures drop to 0 mmHg in RV and 2 mmHg in LV.

Aortic pressure is 120 mmHg during systole and 80 mmHg during diastole, while pulmonary artery pressure is 25 mmHg during systole and 10 mmHg during diastole.

Cardiac Output and Its Regulation

Definition and Importance of Cardiac Output

Cardiac output (CO) is defined as the amount of blood ejected from either ventricle into the aorta or pulmonary artery per minute, typically around 5 L/min at rest.

CO is calculated using the formula: CO = Stroke Volume (SV) x Heart Rate (HR).

Stroke volume is the amount of blood ejected by each ventricle during a single contraction, while heart rate is the number of beats per minute.

During exercise, CO can increase significantly (up to 25 L/min) to meet the body's increased oxygen demands.

Factors Affecting Cardiac Output

Stroke Volume: Influenced by factors such as preload (the degree of stretch of the heart muscle), afterload (the resistance the heart must overcome to eject blood), and contractility (the strength of the heart's contraction).

Heart Rate: Regulated by the autonomic nervous system (sympathetic increases HR, parasympathetic decreases HR) and hormonal influences (e.g., adrenaline).

Changes in either stroke volume or heart rate can significantly impact overall cardiac output, allowing the body to adapt to varying levels of activity.

Overview of Cardiac Output

Definition and Importance of Cardiac Output

Cardiac output (CO) is the volume of blood the heart pumps per minute, crucial for maintaining adequate blood flow to meet the body's metabolic demands.

It is calculated as the product of stroke volume (SV) and heart rate (HR): CO = SV × HR.

Normal resting cardiac output is approximately 5 liters per minute, which can increase significantly during exercise.

Components of Cardiac Output

Stroke Volume (SV): The amount of blood ejected by the heart in one contraction, influenced by end-diastolic volume and ventricular contractility.

Heart Rate (HR): The number of heartbeats per minute, regulated by the autonomic nervous system and hormonal influences.

Factors Influencing Stroke Volume

End-Diastolic Volume (EDV)

EDV is the volume of blood in the ventricles at the end of diastole, directly affecting stroke volume.

Increased venous return leads to higher EDV, resulting in greater myocardial stretch and forceful contractions, as described by the Frank-Starling law.

The relationship between EDV and stroke volume is illustrated by the Starling curve, showing that increased EDV leads to increased SV up to a physiological limit.

Ventricular Muscle Contractility

Contractility refers to the heart's intrinsic ability to contract and generate force, independent of EDV.

Sympathetic nervous system activation increases contractility through the release of catecholamines (adrenaline and noradrenaline), enhancing calcium influx in myocardial cells.

Positive inotropic effects result in stronger contractions and increased stroke volume, even with unchanged EDV.

Regulation of Heart Rate

Mechanisms of Heart Rate Control

Heart rate is primarily regulated by the sinoatrial (SA) node, which generates action potentials that initiate heartbeats.

The autonomic nervous system modulates heart rate: sympathetic stimulation increases HR (positive chronotropy), while parasympathetic stimulation decreases HR (negative chronotropy).

Influences on Heart Rate

Autonomic Nervous System: Sympathetic innervation increases HR by enhancing depolarization rates at the SA node, while parasympathetic innervation decreases HR through hyperpolarization.

Hormonal Factors: Hormones such as adrenaline and thyroxine can increase heart rate, while body temperature also plays a role, with higher temperatures generally increasing HR.

Summary of Cardiac Output Regulation

Key Takeaways

Cardiac output is influenced by both stroke volume and heart rate, which are modulated by various physiological factors.

The two primary determinants of stroke volume are end-diastolic volume and ventricular contractility, both of which can be altered by the autonomic nervous system and venous return.

Understanding the interplay between these factors is crucial for comprehending cardiovascular physiology and responses to exercise.

Cardiac Vocabulary

Contractility: The intrinsic ability of cardiac muscle to develop force for a given muscle length.

Preload: The degree of stretch of the ventricular muscle prior to contraction, primarily determined by end-diastolic volume.

Afterload: The resistance the ventricle must overcome to eject blood, influenced by arterial pressure.

Discussion questions1 of 6

What are the key phases of the cardiac cycle, and how do they contribute to the overall function of the heart?

Difficulty: Easy

How does the autonomic nervous system influence heart rate and stroke volume during physical activity?

Difficulty: Medium

Discuss the Frank-Starling law of the heart and its significance in regulating stroke volume.

Difficulty: Medium

What are the physiological changes that occur in cardiac output during exercise, and what mechanisms facilitate these changes?

Difficulty: Hard

Explain the relationship between end-diastolic volume, stroke volume, and ejection fraction in cardiac function.

Difficulty: Medium

How do pressure changes in the heart chambers and major blood vessels influence the cardiac cycle?

Difficulty: Hard

Show example answer

The cardiac cycle consists of two main phases: systole, where the heart contracts and ejects blood, and diastole, where the heart relaxes and fills with blood. These phases ensure efficient blood flow through the heart and maintain circulation throughout the body.

During physical activity, the sympathetic nervous system increases heart rate and stroke volume by releasing neurotransmitters that enhance myocardial contractility and venous return. This results in a significant increase in cardiac output to meet the heightened oxygen demand of the body.

The Frank-Starling law states that the stroke volume of the heart increases in response to an increase in the end-diastolic volume, due to the stretching of the ventricular myocardium. This intrinsic mechanism allows the heart to adjust its output based on the volume of blood returning to it, ensuring efficient circulation.

During exercise, cardiac output can increase significantly due to elevated heart rate and stroke volume, facilitated by sympathetic nervous system activation, venoconstriction, and enhanced skeletal muscle pump. These mechanisms work together to increase venous return and myocardial contractility, allowing the heart to meet the increased metabolic demands of the body.

End-diastolic volume (EDV) is the total volume of blood in the ventricles at the end of diastole, and stroke volume (SV) is the amount of blood ejected during systole. The ejection fraction, calculated as SV divided by EDV, reflects the efficiency of the heart's pumping ability, with a normal value around 60%, indicating that a healthy heart ejects a significant portion of the blood it receives.

Pressure changes in the heart chambers and major blood vessels are crucial for the opening and closing of heart valves, which directs blood flow during the cardiac cycle. As the heart contracts, ventricular pressure rises, leading to valve closure and the ejection of blood, while during relaxation, pressure drops, allowing for filling and the subsequent cycle to begin anew.