Heart Anatomy and Function

Heart Overview

• The heart is a four-chambered muscular organ.
• It contracts rhythmically to pump blood into arteries.
• The heart receives blood back through veins, maintaining constant circulation.
• Location of the heart is in the mediastinum.
• The heart is enclosed by the pericardium, which has an outer fibrous layer and an inner serous layer.
• The serous pericardium has two layers, visceral and parietal, separated by the serous cavity.
• The wall of the heart has three layers: epicardium, myocardium, and endocardium.

Heart Chambers

• The heart functions as two separate pumps (right and left), each consisting of an atrium and a ventricle.
• The right atrium receives blood from the superior and inferior vena cavae, and the coronary sinus.
• The left atrium receives blood from the pulmonary veins.
• The right ventricle receives blood from the right atrium, and its function is to sends blood to the lungs.
• The left ventricle receives blood from the left atrium, and it sends blood throughout the body.
• The wall of the left ventricle is notably thicker than that of the right ventricle.

Heart Valves and Circulation

• Heart valves open and close in response to pressure changes during heart contraction and relaxation.
• Right and left atrioventricular valves (mitral and tricuspid valves) prevent backflow from the ventricles into the atria.
• Right and left semilunar valves (aortic and pulmonary valves) prevent backflow from the arteries into the ventricles.

Coronary Circulation

• The myocardium has its own circulatory network.
• Coronary arteries arise from the base of the aorta.
• They branch out to supply oxygen-rich blood to the myocardium via the left and right coronary arteries.
• Anastomoses provide alternative pathways for blood flow, ensuring blood can reach the heart muscle even if a vessel is blocked.
• Coronary veins drain deoxygenated blood from the heart muscle back to the right atrium.
• Restoration of blood flow to tissues after ischemia is called reperfusion. Reperfusion can lead to reactive oxygen species (ROS) production.

Cardiac Muscle Tissue

• Cardiac muscle cells (cardiomyocytes) are branched, involuntary, and striated.
• They are connected by intercalated discs (ID), which synchronize heart contractions.
• Intercalated discs are divided into desmosomes and gap junctions.
• Desmosomes hold cells together and provide mechanical strength during contraction.
• Gap junctions allow ions and small molecules to pass between cells.
• Gap junctions enable the spread of action potentials, allowing the heart to contract as a functional syncytium.
• Cardiac muscle tissue has a high mitochondrial content for continuous ATP production.
• Cardiac muscle tissue has limited regeneration capacity, leading to scar tissue formation.
• Rhythmicity describes the heart's ability to contracts at regular intervals without external stimuli, controlled by the SA node.

Autorhythmic Fibers and Conduction System

• The sinoatrial (SA) node, located in the right atrium, is the heart's natural pacemaker.
• The SA node initiates action potentials at a rate of 70-80 bpm in a resting adult.
• The atrioventricular (AV) node is at the junction between the atria and ventricles.
• It delays the electrical signal slightly to ensure the atria contract before the ventricles.
• The atrioventricular (AV) bundle (Bundle of His) is located in the interventricular septum.
• It carries the action potential from the AV node to the bundle branches.
• Right and left bundle branches conduct electrical impulses toward the heart's apex along the interventricular septum.
• Purkinje fibers spread throughout the ventricles.
• Purkinje fibers rapidly conduct action potentials to the myocardial cells of the ventricles, ensuring coordinated contraction.
• An ectopic pacemaker is a pacemaker elsewhere than the SA node.
• Ectopic pacemakers are caused by rhythmic discharge rate of AV node/Purkinje fibers greater than the SA node, or, a block of impulse transmission from SA node.
• Cardiac muscle cells are self-excitable and autorhythmic.
• Cardiac muscle cells repeatedly generate spontaneous action potentials, triggering heart contractions.
• These cells form the conduction system for propagating action potentials through the heart muscle fibers.
• Autorhythmic fibers in the SA node are the natural pacemaker because they initiate action potentials most often.
• Signals from the nervous system and hormones like epinephrine can modify the heart rate and force of contraction without setting the fundamental rhythm.

Cardiac Cycle Definition

• Cardiac cycle: sequence of alternating contraction and relaxation of atria and ventricles.
• The cardiac cycle is responsible for pumping blood throughout the body.
• Cardiac cycle starts at the beginning of one heartbeat and ends at the beginning of another.
• Events of one heartbeat: electrical events, pressure changes, heart sounds, volume changes, and mechanical events.

Cardiac Cycle Phases

• Atrial Systole (Atrial Contraction): The atria contract to push remaining blood into the ventricles.
• AV valves (tricuspid and mitral) are open, semilunar valves (pulmonary and aortic) are closed.
• Atrial systole ends when ventricles are filled to their maximum volume, known as the end-diastolic volume (EDV).
• Ventricular Systole (Ventricular Contraction): Consists of Iso-volumetric Contraction and Ventricular Ejection stages.
  • Iso-volumetric Contraction: Ventricles start to contract, increasing pressure inside the ventricles.
  • AV valves (tricuspid and mitral) close to prevent backflow of blood into the atria.
  • Semilunar valves (pulmonary and aortic) remain closed initially; ventricular pressure has not exceeded arterial pressure.
  • Ventricular Ejection: Ventricular pressure exceeds arterial pressure, and the semilunar valves open.
  • Ejection: Blood is ejected from the ventricles into the pulmonary trunk (right ventricle) and aorta (left ventricle).
  • At the end of the ejection phase, the ventricles reach their lowest volume: end-systolic volume (ESV).
• Ventricular Diastole (Ventricular Relaxation): Consists of Isovolumetric Relaxation and Ventricular Filling.
  • Isovolumetric Relaxation: The ventricles begin to relax, causing a decrease in pressure.
  • Semilunar valves close to prevent blood from flowing back into the ventricles. AV valves remain closed.
  • Ventricular Filling: Ventricular pressure continues to drop, and the AV valves (tricuspid and mitral) open.
  • Blood flows passively from the atria into the ventricles.
  • Atrial contraction (atrial systole) finishes filling the ventricles.

Cardiac Cycle Duration and Values

• The cardiac cycle lasts about 0.8 seconds at a resting heart rate of 75 beats per minute.
• The cardiac cycle ensures synchronized filling and emptying of heart chambers.
  • Systole is the phase when the heart contracts and pumps blood out.
  • Diastole is the phase when the heart relaxes and fills with blood.
• End-Diastolic Volume (EDV): The maximum volume of blood in the ventricles after atrial systole.
• End-Systolic Volume (ESV): The volume of blood remaining in the ventricles after ventricular systole.
• Stroke Volume (SV): The volume of blood ejected from the ventricles during ventricular systole (EDV - ESV).
• Cardiac Output (CO): the amount of blood the heart pumps, in one minute (CO = SV × heart rate).
• Normal values:
  • EDV = 110-120ml
  • ESV = 40-50ml
  • SV = 70ml/beat.

Auscultation and Heart Sounds

• Auscultation is the act of listening to sounds within the body using a stethoscope.
• Each cardiac cycle produces four heart sounds.
• S1 and S2 are normally heard through a stethoscope.
• S1 corresponds to the closure of the AV valves (mitral and tricuspid) at the beginning of ventricular contraction (systole),;"lub" sound.
• S2 corresponds to the closure of the semilunar valves (aortic and pulmonary) at the end of ventricular contraction; "dub" sound.

Stroke Volume Regulation

• Three main factors can effect/regulate Stroke volume: preload, contractility, and afterload.

Preload

• Preload is the degree of stretch of the heart muscle fibers before contraction.
• Preload is influenced by venous return.

Effect of Stretching (Frank-Starling Law)

• The Frank-Starling Law states that as the heart muscle fibers are stretched (increased preload), the strength of contraction increases.
• The optimal overlap of actin and myosin filaments results in greater stroke volume.
• This allows the heart to adjust its output based on venous return and meet the body's demands effectively.

Contractility

• Contractility is the inherent strength of the heart's contraction.
• Contractility is affected by factors such as calcium levels and sympathetic stimulation.
• Inotropic Effect: Refers to changes in the strength or force of heart muscle contraction.
  • Positive inotropic effect (+ve) increases the force of contraction. Example: Increased intracellular calcium ions (Ca²⁺)
  • Negative inotropic effect (-ve) decreases the force of contraction. Example: Elevated levels of potassium ions (K⁺)

Afterload

• Afterload is the resistance the heart must overcome to eject blood.
• Afterload is influenced primarily by arterial pressure.
• Conditions that can increase afterload include hypertension and atherosclerosis.

Heart Rate Regulation

• Terminology: Chronotropic Effect: refers to changes in heart rate
• Positive chronotropic effect (+ve) increases heart rate.
• Negative chronotropic effect (-ve) decreases heart rate.
• Heart rate regulation involves autonomic regulation, chemical regulation, and other factors.

Autonomic Regulation of HR

• The sympathetic nervous system releases norepinephrine, which binds to beta-adrenergic receptors in the heart,.
• The Sympathetic nervous system increases HR and contractility.
• It is activated during stress or exercise.
• The parasympathetic nervous system primarily through the vagus nerve.
• The Parasympathetic nervous system releases acetylcholine, which slows down the HR.
• The parasympathetic nervous system predominates during rest and relaxation.

Chemical Regulation of HR

• Hormones:
  • Epinephrine and Norepinephrine: Increase heart rate and contractility during stress.
  • Thyroid Hormones: Can increase heart rate and enhance the heart's sensitivity to catecholamines.
• Ions:
  • Calcium (Ca²⁺): Increases heart rate and contractility when levels are high.
  • Potassium (K⁺): High levels can lead to decreased heart rate and contractility; low levels can increase heart rate.
  • Sodium (Na⁺): Influences action potentials and can affect heart rate.

Other Factors Affecting Heart Rate

• Age: Heart rate tends to decrease with age.
  • Adults: 70-80 beats per minute
  • Children: 95-100 beats per minute
• Fitness Level: Athletes often have lower resting heart rates due to increased vagal tone and cardiac efficiency.
• Temperature: Increased body temperature (fever) can increase heart rate, decreased temperature can lower it (hypothermia). Heart rate regulation can be effected by emotional state.
• Emotional State: Stress, anxiety, or excitement can activate the sympathetic nervous system, increasing heart rate.

Heart Rate Terminologies

• Bradycardia: Heart rate < 50 beats per minute
• Tachycardia: Heart rate > 100 beats per minute
• Cardiomegaly: Increase in heart size/muscle
  • Physiological: Example athlete's heart
  • Pathological: Hypertension (HTN), Congestive Heart Failure (CHF)

Help For Failing Heart

• Lifestyle Changes:
  • Diet: Low-sodium, heart-healthy diet to manage weight and blood pressure.
  • Exercise: Regular, moderate physical activity as tolerated to improve cardiovascular fitness.
• Medications:
  • Diuretics, ACE Inhibitors, Beta-Blockers, Digoxin.
• Surgery:
  • Heart Valve Repair/Replacement: Addresses valve dysfunction contributing to heart failure.
  • Coronary Bypass Surgery: Restores blood flow to the heart muscle in cases of coronary artery disease.
  • Heart Transplant: Considered for end-stage heart failure when other treatments are ineffective.
• Devices and Procedures:
  • Pacemakers: Help regulate heart rhythm and improve heart function.
  • Implantable Cardioverter-Defibrillators (ICDs): Prevent life-threatening arrhythmias.
  • Biventricular Pacing: Improves coordination of heart contractions in heart failure patients.