Cardiovascular System Control Quiz

Cardiovascular System Control

• The cardiovascular system (CV) transports nutrients, oxygen, and waste products throughout the body.
• It also regulates body temperature (core to skin).
• The CV system buffers body pH and electrolytes.
• It transports hormones, such as adrenaline from the adrenal glands.
• The system assists in response to infection.
• It needs to rapidly respond to changes in metabolic demand.

Intended Learning Objectives

• Describe the sequence of the cardiac cycle.
• Describe how the heart initiates and conducts impulses.
• Identify the parts of the electrocardiogram (ECG).
• Describe the events causing heart muscle contraction.

Basic Cardiac Anatomy

• Aorta: Major artery carrying oxygenated blood away from the heart.
• Superior vena cava: Carries deoxygenated blood from the upper body to the heart.
• Pulmonary artery: Carries deoxygenated blood to the lungs.
• Pulmonary veins: Carry oxygenated blood from the lungs to the heart.
• Left atrium (LA): Receives oxygenated blood from the pulmonary veins.
• Right atrium (RA): Receives deoxygenated blood from the venae cavae.
• Left ventricle (LV): Pumps oxygenated blood to the body.
• Right ventricle (RV): Pumps deoxygenated blood to the lungs.
• Mitral valve: Separates the left atrium and left ventricle.
• Tricuspid valve: Separates the right atrium and right ventricle.
• Aortic valve: Separates the left ventricle and the aorta.
• Pulmonary valve: Separates the right ventricle and the pulmonary artery.
• Pressure readings are in mm Hg (systolic/diastolic)

Heart Valves

• Valves ensure unidirectional blood flow.
• Valve opening/closing is determined by pressure gradients (passive).
• Atrioventricular (AV) valves are between the atria and ventricles.
• Chordae tendinae and papillary muscles prevent AV valve backflow.
• Semilunar valves control blood into the exit arteries (aorta and pulmonary artery).
• Valve insufficiency (e.g., calcification or stenosis) causes blood regurgitation, potentially leading to heart failure.

Cardiac Function

• The heart's function is not further detailed.

The Cardiac Cycle

• The cardiac cycle involves systole (contraction) and diastole (relaxation) of the atria and ventricles.
• The Wiggers diagram plots pressure, volume, and ECG throughout the cardiac cycle.
• The diagram shows seven phases.

Phase 1: Atrial Systole

• The SA node initiates the P wave on the ECG.
• Active filling of ventricles occurs.
• Ventricles receive ~ 10-40% of their filling volume.
• LVEDP- LV end diastolic pressure
• S4 sound is during atrial contraction due to blood turbulence.

Phase 2: Isovolumetric Contraction

• QRS complex marks ventricular depolarization.
• Ventricular and papillary muscles contract.
• AV valves (mitral and tricuspid) close (S1 "lubb" sound).
• Ventricular pressure increases rapidly, but the volume remains constant.
• Ventricles become spherical in shape.

Phase 3: Rapid Ejection

• LVP > aortic pressure – aortic valve opens.
• Small pressure difference is seen.
• Max outflow velocity happens, so maximum blood ejected.
• Atria continue to fill during ejection, with atrial pressure dips.

Phase 4: Reduced Ejection

• T-wave repolarization marks the start of ventricular relaxation.
• Ventricular muscle relaxes.
• Ejection rate decreases.
• Atrial pressure increases due to continuous venous return.

Phase 5: Isovolumetric Relaxation

• LVP falls below aortic pressure – aortic valve closes.
• The short, sharp 'dupp' sound (S2) is heard.
• Blood flow momentarily stops due to elastic recoil.
• LVEDV – LV end diastolic volume.
• LVESV - LV end systolic volume

Phase 6: Rapid Filling

• LVP falls below atrial pressure, and AV valves open.
• Despite continued relaxation, filling occurs rapidly.
• Passive filling due to diastolic suction occurs.
• The S3 sound is if filling turbulence occurs.

Phase 7: Reduced Filling

• Passive filling is almost complete.
• Pressure gradient decreases, and filling slows.
• The ventricles become stiffer.
• The reduced filling phase occurs at rest, more prolonged.

Measuring Systolic Function

• Stroke Volume (SV): End diastolic volume (EDV)- End systolic volume(ESV)
• Cardiac output (CO): SV x heart rate (HR)
• Cardiac index: CO/body surface area
• Ejection fraction: SV/EDV x100

Electrical Conduction

• SAN initiates impulses, spreading over the atria.
• AVN slows conduction, creating a delay before ventricular contraction.
• Impulses spread through the ventricles via the bundle of his and purkinje fibres.
• Depolarisation occurs leading to muscle contraction.

SA Node Action Potential

• These cells spontaneously depolarize at a rate of ~1/s (automaticity).
• Sympathetic stimulation increases HR by increasing Ca2+ influx
• Parasympathetic stimulation decreases HR by increasing K+ permeability.

Action Potentials in Other Regions

• AVN action potential is similar to SAN, but with a different threshold.
• Purkinje action potential is relatively prolonged.
• Ventricular action potential also has a plateau phase.

Electrocardiogram (ECG)

• Detects changes in potential difference between electrodes on the heart surface.
• The body acts as a volume conductor.
• Used to diagnose arrhythmias, myocardial infarction, and other disorders.

Typical ECG

• P-wave: Atrial depolarization.
• QRS-complex: Ventricular depolarization.
• T-wave: Ventricular repolarization.
• P-R interval: Delay through the AV node.
• S-T interval: Plateau phase of the action potential.

Clinically Relevant ECG Results

• Sinus rhythm (normal healthy heart)
• Sinus bradycardia (slow heart rate)
• Atrial fibrillation (chaotic atrial rhythm)
• Ventricular fibrillation (chaotic ventricular rhythm).
• Bundle branch blocks and 2nd degree AV blocks
• Ventricular tachycardia
• ST-Elevation Myocardial Infarction (STEMI)

What Happens in Cardiac Muscle Cells

• Sliding filament theory describes muscle contraction.
• Excitation-contraction coupling involves Ca2+ and myofilament interactions.
• Myosin hydrolyzes ATP to form cross bridges.

Excitation-Contraction Coupling in Cardiomyocytes

• Action potentials trigger membrane depolarization.
• Ca2+ enters through L-type calcium channels.
• Calcium-induced calcium release (CICR) from SR.
• Cross-bridge cycling causes contraction.
• Ca2+ removal from cytoplasm causes relaxation

Regulation by Adrenoceptors

• Heart contains primarily β1 receptors.
• These receptors are activated by norepinephrine and epinephrine (adrenaline).
• Increased intracellular Ca2+ causes positive inotropy, chronotropy, dromotropy, and lusitropy.
• Agonists (e.g., dobutamine) support the heart, whilst antagonists (e.g., β-blockers) reduce workload.

Determinants of Ventricular Function

• Contractility (Inotropy)
• Preload
• Afterload
• Heart rate
• These factors affect stroke volume and cardiac output.

Afterload

• The load against which the heart works to eject blood.
• Determined by aortic pressure, aortic compliance, and peripheral resistance.
• High afterload increases workload.

Preload

• Myocyte stretch prior to contraction.
• Marked by end-diastolic volume or pressure (EDV/EDP).
• Higher sarcomere overlap increases force.
• Determined by venous return, and LV compliance and functionality.

Frank-Starling Law

• The heart contracts more forcefully when it is filled to a greater extent.
• Ventricular stretch increases force of ejection.
• Important in balancing both ventricular output.
• Failing hearts have impaired Frank-Starling responses.

Example of Frank-Starling Mechanism

• Myocyte stretch increases force generation.
• Higher venous return stretches myocytes, increasing ejection force.
• Critical for balancing ventricular output and contractility.

Summary

• The cardiac cycle phases are detailed using a Wiggers diagram.
• Systolic function parameters like cardiac output are vital.
• Autonomic nervous system and electrical conduction (SAN, AVN, Purkinje) are included.
• ECG abnormalities and typical waveforms are reviewed.
• Excitation-contraction coupling, and how it leads to heart muscle contraction is examined along with the roles of Ca2+.
• Regulation by adrenoceptors is considered.
• The effects and determinants of ventricular function, such as preload and afterload, are explained.
• The Frank-Starling law is crucial for understanding preload's effect on heart function.