Lecture+9+Cardio+2+2025

Cardiovascular Overview

The cardiovascular system is a complex network responsible for the circulation of blood throughout the body, comprising various components, including the heart, blood vessels, and the blood itself. It plays a crucial role in delivering oxygen and nutrients to tissues while removing carbon dioxide and waste products. The efficiency of this system is paramount for maintaining overall health and supporting bodily functions.

ECG/EKG Interpretation

• P Wave: Represents atrial depolarization, which precedes atrial contraction, indicating proper atrial functioning.

• Q Wave: Indicates initial septal depolarization, which is critical for coordinated contraction of the ventricles.

• R Wave: Reflects the depolarization of the ventricles, marking the onset of ventricular contraction (systole).

• S Wave: Signifies depolarization of the upper edges of the ventricles, completing the contraction signal.

• T Wave: Shows ventricular repolarization, in which the ventricles recover and prepare for the next cycle. An inversion or abnormality in this wave can indicate underlying dysfunction.

Intervals:

• P-R Interval: Reflects the delay at the AV node, essential for the timing between atrial and ventricular contractions, with a normal range of 120-200 ms.

• S-T Interval: Represents the contraction phase of the ventricles (systole). It is crucial for assessing myocardial ischemia. During this phase, the ion channels behave as follows: O-Cart(1) channels close, while Kt channels increase, indicating a shift in ion flow that supports ventricular function.

Key Terms in Cardiovascular Function

• Systole: The phase of heartbeat during which heart muscles contract and pump blood from the chambers into the arteries.

• Diastole: The relaxation phase when heart muscles relax, allowing the chambers to fill with blood from the veins.

• End Diastolic Volume (EDV): The volume of blood in the ventricles at the end of the filling phase, significantly influencing stroke volume.

• End Systolic Volume (ESV): The volume of blood remaining in the ventricles after contraction, critical for understanding cardiac efficiency.

• Stroke Volume: Amount of blood pumped out of each ventricle per beat; influenced by preload, contractility, and afterload.

• Ejection Fraction: The percentage of blood ejected from the ventricle with each heartbeat, typically measured as a key indicator of heart function.

• Isovolumetric Contraction: The phase when the ventricle contracts without change in volume, critical for generating pressure before blood ejection.

• Isovolumetric Relaxation: The phase when the ventricle relaxes without change in volume, marking the transition to diastole.

Wiggers Diagram

This diagram illustrates the synchronization of:

• EKG: Provides a visual representation of the heart's electrical activity during the cardiac cycle.

• Heart Sounds: Valuable for assessing valve function and overall cardiac health.

• Pressures: Evaluated in the aorta, left ventricle, and left atrium, highlighting the dynamic changes during the cardiac cycle.

• Volume: Changes occurring within the left ventricle, showing how the heart pumps blood effectively.

Key Points:

• Pressure curves crossing indicates valve state changes, essential for understanding cardiac mechanics.

• Most filling of ventricles is passive, occurring in the first third of diastole, involving movement of blood from the atria into the ventricles.

• Most emptying occurs in the first third of systole, illustrating efficient ejection of blood from the ventricles.

Pressure-Volume Relationships

This section visually illustrates the relationship between left ventricular pressure and atrial pressure and volume. Key measurements include:

• Aortic Pressure: 130 mmHg, critical for understanding systemic circulation.

• Left Atrial Pressure: 50 mmHg, provides context on atrial filling and function.

• Left Ventricular Pressure: 110 mmHg, reflects the pressure required for effective ejection of blood.

Visual Representation:

• Demonstrates end-diastolic and end-systolic volumes, fundamental in calculating stroke volume and evaluating cardiac function.

Frank-Starling Mechanism

A fundamental mechanism in cardiac physiology where:

• Increased filling of the ventricle stretches cardiac myocytes, consequently enhancing the force of contraction through the length-tension relationship.

• Questions arise regarding the optimal length-tension relationship in cardiac myocytes, as they typically operate at shorter lengths than 2.0 µM, a critical aspect for heart function.

Length-Tension in Skeletal Muscle

Passive stretching increases tension at higher lengths due to elastic resistance, underscoring the importance of muscle conditions in various physiological states.

• Graphically represents the relationship between sarcomere length and active tension generated, offering insights into muscle mechanics.

Cardiac Stretch-Sensitivity

Increasing stretch on cardiac myocytes activates stretch-sensitive Ca++ channels, leading to an influx of intracellular calcium which enhances force production, a significant distinction from skeletal muscle contraction dynamics.

Review of Mechanisms

The Frank-Starling mechanism is vital in determining cardiac output, especially regarding the relationship between blood filling and heart muscle stretching.

Mechanisms of Crossbridge Formation

Enhanced calcium sensitivity in troponin due to increased stretch conditions promotes the formation of more cross-bridges during each cardiac cycle, impacting contraction strength.

Frank-Starling Effect Mechanisms

Optimal alignment of myosin and actin during the cardiac cycle increases the potential for cross-bridge formation, crucial for effective heart contractions. Key mechanisms that lead to increased intracellular calcium concentrations include:

• Stretch sensitivity in calcium channels

• Altered affinity of troponin/tropomyosin

Stroke Volume Dynamics

Understanding stroke volume is essential as it is influenced by multiple factors, including contractility and sympathetic stimulation:

• A graphical representation displays the increase in contractility leading to variations in stroke volume corresponding to increased end-diastolic volume.

Sympathetic Influence on Cardiac Functions

Heightened sympathetic stimulation results in:

• Increased intracellular calcium levels

• Enhanced contractile force generation

• More rapid contractile responses, thus reducing plateau phases during action potentials, which can impact heart rhythms.

Pressure Volume Loop Analysis

The analysis correlates the left ventricular volume changes with contraction efficiency and stroke volume, illustrating the importance of preload and afterload in cardiac mechanics.

Pressure-Volume Curves

Illustrates both active (systolic) and passive (diastolic) tension within a pressure-volume loop, fundamental for understanding the heart's efficiency.

Afterload and Cardiac Work

Increased sympathetic tone raises afterload, subsequently affecting cardiac output and the dynamics of end-diastolic and end-systolic volumes, crucial for evaluating heart function.

Effects of Increased Preload

Elevating preload can significantly enhance stroke volume, identifying the relationship between EDV and contractility processes, relevant for patients with heart failure.

Consequences of Decreased Contractility

A reduction in contractility leads to decreased stroke volume, adversely impacting overall cardiac output and efficiency, emphasizing the need for interventions in cases of heart dysfunction.

Impact of Increased Afterload

An increase in afterload can stress stroke volume, which in turn, reduces the efficiency of blood pumping, highlighting the critical balance in cardiac workload.

Determinants of Cardiac Output

Cardiac Output (CO) is defined by the formula: CO = Heart Rate x Stroke Volume.

• Heart Rate: Modulated by sympathetic and parasympathetic nervous systems.

• Stroke Volume: Influenced by several factors including contractility and the vascular resistance state, essential for predicting cardiopulmonary health.

Mechanisms Influencing Stroke Volume and Heart Rate

Explores the complex interactions between preload, afterload, and the states of vascular resistance, providing insights into cardiovascular physiology.