cardiovascular c

Heart and Circulation Overview

• Lecturer: Dr. R. Ahangari

• University: University of Central Florida, Orlando

• Textbook: Human Physiology by Linda S. Constanzo

• Medline Plus: 20000

Myocardial Cells

Types of Myocardial Cells

• Contractile Cells: This type of myocardial cell shares many features with skeletal muscle cells. Each cell contains myofibrils, which are the contractile units, and typically has a single nucleus.

  • Oxygen Efficiency: They are exceptionally efficient at extracting oxygen from the blood, achieving approximately $80\%$ efficiency.

  • Structure: Contractile cells are shorter and branched, allowing for extensive intercellular connections. These cells are physically and electrically linked by specialized structures called intercalated discs.

  • Tight Junctions: Within intercalated discs, tight junctions serve to bind the cells firmly together, providing mechanical stability during contraction.

  • Gap Junctions: Also part of the intercalated discs, gap junctions are crucial for electrical communication. They allow the rapid movement of ions, facilitating the spread of action potentials and electrical current directly between adjacent myocardial cells.

• Nodal/Conducting Cells: These cells have a distinct role compared to contractile cells. They possess very few contractile elements (myofibrils), which means they contract very weakly.

  • Self-Excitability: A unique characteristic of nodal cells is their ability to spontaneously generate action potentials without any external nervous input. This property makes them the originators of the heart's rhythm.

  • Conduction: They are specialized to rapidly conduct these action potentials throughout the heart muscle, ensuring synchronized contraction.

Sinoatrial Node (SA Node)

• Location: The SA node is strategically located in the upper posterior wall of the right atrium.

• Function: It serves as the heart's primary pacemaker, initiating the electrical impulses (action potentials) that dictate the heart rate and rhythm.

• Conduction Pathway: Once an action potential is generated by the SA node, it follows a specific pathway:

  1. It first travels to the atrioventricular node (AV node).

  2. From the AV node, the impulse progresses through the Bundle of His.

  3. Next, it spreads via the Purkinje Fibers.

  4. Finally, it reaches the ventricular muscle, triggering ventricular contraction.

Action Potential Conduction in the Heart

• Atrial Contraction: The action potential generated by the SA node initially spreads throughout the atrial muscle, leading to coordinated atrial contraction.

• Electrical Isolation of Ventricles: The atria are electrically isolated from the ventricles by a fibrous tissue barrier. This anatomical separation is critical because it ensures that the action potential cannot directly pass from the atria to the ventricles; it must first pass through the AV node.

• Ventricular Conduction: After the action potential passes through the AV node, it then travels down the Bundle of His. The Bundle of His branches extensively down toward the apex of the heart, effectively transmitting the action potential via the Purkinje Fibers to the entire ventricular muscle, ensuring a powerful and synchronized ventricular contraction.

Autonomic Nervous System Effects on Heart Rate

Heart Rate Influences

• Chronotropic Effects: These effects specifically refer to changes in the heart rate.

  • Negative Chronotropic Effect: This effect decreases the heart rate, primarily by reducing the frequency of action potential firing from the SA node.

  • Positive Chronotropic Effect: Conversely, this effect increases the heart rate by accelerating the rate of SA node firing.

• Dromotropic Effects: These effects describe changes in the conduction velocity of electrical impulses through the heart, mainly focusing on the AV node.

  • Negative Dromotropic Effect: This decreases the conduction velocity, which can be observed as a prolonged PR interval on an electrocardiogram (ECG).

  • Positive Dromotropic Effect: This increases the conduction velocity, resulting in a shortened PR interval on an ECG.

• Inotropic Effects: These effects relate to changes in the force or strength of myocardial contraction.

  • Negative Inotropic Effect: This leads to a decrease in the strength of cardiac muscle contraction.

  • Positive Inotropic Effect: This results in an increase in the strength of cardiac muscle contraction.

Heart Rate Statistics

• A normal resting heart rate typically ranges between $50-99\text{ BPM}$ (beats per minute).

Arrhythmias

• Arrhythmias are abnormal heart rhythms that arise from disruptions in either the formation or the conduction of electrical impulses within the heart. These abnormalities can lead to irregular, too fast, or too slow heartbeats.

  • Sinus Tachycardia: This condition occurs when the heart rate exceeds $100\text{ BPM}$, while still originating from the SA node and maintaining a generally regular rhythm. It can be caused by various factors such as exercise, fever, stress, or certain medical conditions.

  • Sinus Bradycardia: This refers to a heart rate that falls below $50-60\text{ BPM}$, but still maintains a regular rhythm originating from the SA node. It can be common in highly trained athletes or indicate certain health issues.

Supraventricular Arrhythmia

• Supraventricular arrhythmias are a type of arrhythmia caused by an atrial or nodal extrasystole (ES), which means a premature or extra beat originating from above the ventricles (in the atria or AV node).

  • Ectopic Impulses: Abnormal or ectopic impulses can arise from various locations within the atria or AV node, disrupting the normal sinus rhythm initiated by the SA node.

  • Atrial ES: In an atrial extrasystole, an ECG often shows a deformed P wave (representing atrial depolarization), but the QRS complex (representing ventricular depolarization) typically remains normal.

  • Nodal Extrasystole: In a nodal extrasystole, the impulse originates in the AV node region. This can lead to retrograde stimulation of the atria, potentially resulting in a negative P wave on the ECG (if observable).

Ventricular Extrasystole (VPCs)

• Ventricular Premature Complexes (VPCs), also known as Premature Ventricular Contractions (PVCs), are ectopic impulses that originate from areas within the ventricles, distal to the His-Purkinje system.

• Common mechanisms that lead to VPCs include:

  1. Automaticity: This occurs when new sites within the ventricles spontaneously depolarize and generate action potentials. This can be triggered by various factors, such as electrolyte abnormalities (e.g., low potassium or magnesium) or myocardial ischemia (reduced blood flow to the heart muscle).

  2. Reentry Circuits: These occur when an electrical impulse travels in a circular path through cardiac tissue due to regions of slow-conducting tissue adjacent to normal-conducting tissue. This can cause the impulse to re-excite areas that have already recovered, leading to extra beats.

Symptoms of PVCs

• Individuals experiencing frequent PVCs may report several symptoms, including:

  • Chest pain or discomfort

  • A faint feeling or lightheadedness

  • Fatigue or general tiredness

  • Hyperventilation

• It is important to note that frequent PVCs can sometimes be a precursor to more severe and potentially life-threatening ventricular arrhythmias, such as ventricular tachycardia (VT).

Treatment of Ventricular Extrasystole

Potassium Balance

• A fundamental approach to managing ventricular extrasystole, especially when linked to electrical instability, involves restoring the proper balance of key electrolytes, such as magnesium and calcium, in addition to potassium.

Pharmacological Agents

Pharmacological treatment often involves antiarrhythmic drugs, categorized into different classes based on their primary mechanism of action:

1. Class I Agents: These drugs act as sodium channel blockers. By blocking fast sodium channels, they slow the rate of depolarization and conduction velocity, particularly in the ventricles. Examples include Lidocaine and Phenytoin.

2. Class II Agents: These are beta blockers, such as Atenolol, Propranolol, and Metoprolol. They primarily work by blocking beta-adrenergic receptors, which results in a decrease in heart rate and a reduction in conduction velocity, especially through the AV node.

3. Class III Agents: These agents exert their effects by blocking potassium channels. This action prolongs the repolarization phase of the cardiac action potential, thereby increasing the effective refractory period. Sotalol is an example of a Class III agent.

4. Class IV Agents: These drugs are calcium channel blockers, including Verapamil and Diltiazem. They primarily act on L-type calcium channels, leading to a decrease in conduction velocity (especially in the SA and AV nodes) and a reduction in myocardial contractility.

Tachycardia

Atrial and Ventricular Tachycardia

• Atrial Tachycardia: This is an arrhythmia where the heart rate originates from the atria but is abnormally fast, typically ranging from $100-250\text{ BPM}$.

• Ventricular Tachycardia: This severe arrhythmia is characterized by a rapid sequence of electrical impulses originating from an ectopic focus within the ventricles. The heart rate in ventricular tachycardia is usually between $120-250\text{ BPM}$.

Cardiac Cycle

Phases of the Cardiac Cycle

The cardiac cycle describes the sequence of events that occurs during one complete heartbeat. It is often understood by analyzing the pressure and volume changes within the ventricles:

1. Isovolumetric Contraction (Step 1-2): This is the initial phase of ventricular contraction. During this short period, both the mitral and aortic (or tricuspid and pulmonary on the right side) valves are closed. The ventricles contract, but no blood is ejected because the pressure inside is not yet sufficient to open the outflow valves. Consequently, ventricular volume remains constant, while pressure rapidly increases. The closure of the mitral valve marks the beginning of this phase.

2. Ventricular Ejection (Step 2-3): As ventricular pressure surpasses the pressure in the aorta (or pulmonary artery), the aortic valve (or pulmonary valve) opens, and blood is forcefully ejected from the ventricles into the arteries. The volume of blood ejected during this phase is defined as the stroke volume. This phase concludes when the ventricular muscle begins to relax, and the pressure starts to fall.

3. Isovolumetric Relaxation (Step 3-4): Following ejection, the ventricles relax, and both the aortic/pulmonary valves and the mitral/tricuspid valves close. For a brief moment, all valves are closed, and the ventricular volume remains constant as the muscle continues to relax. Ventricular pressure drops rapidly during this phase.

4. Ventricular Filling (Step 4-1): Once ventricular pressure falls below atrial pressure, the mitral valve (or tricuspid valve) opens, allowing blood to flow from the atria into the ventricles. This phase includes both passive filling (due to pressure gradient) and active filling (atrial contraction). The ventricle fills to an approximate end-diastolic volume, often around $140\text{ ml}$.

Changes in Ventricular Pressure-Volume Loop

Influencing Factors

The ventricular pressure-volume loop graphically illustrates the changes in ventricular pressure and volume during one cardiac cycle. It is influenced by several factors:

• Increased Preload: Preload refers to the stretch of the ventricular muscle fibers at the end of diastole (just before contraction). An increased preload means a greater end-diastolic volume. According to the Frank-Starling relationship, an increased end-diastolic volume leads to enhanced stroke volume, as the heart can contract more forcefully when its fibers are stretched to an optimal length.

• Increased Afterload: Afterload represents the resistance the ventricle must overcome to eject blood. This is primarily determined by aortic pressure (or pulmonary artery pressure). A higher aortic pressure (increased afterload) makes it harder for the heart to eject blood, resulting in a decrease in stroke volume and an increase in end-systolic volume (more blood remaining in the ventricle after contraction).

• Increased Contractility: Contractility is the intrinsic ability of the heart muscle to contract, independent of preload and afterload. Higher myocardial tension (increased contractility) means the heart can pump more efficiently. This leads to an increased stroke volume (more blood ejected) and a decreased end-systolic volume (less blood remaining in the ventricle after contraction).

Metrics of Cardiac Function

Several key metrics are used to quantify cardiac function:

1. Stroke Volume (SV): This is the volume of blood ejected from the ventricle with each single heartbeat.
   $SV = \text{End-diastolic volume} - \text{End-systolic volume}$

2. Cardiac Output (CO): This represents the total amount of blood pumped by the heart per minute. It is a crucial indicator of the heart's overall pumping effectiveness.
   $CO = SV \times \text{Heart rate}$

3. Ejection Fraction (EF): This is the fraction or percentage of the end-diastolic volume that is ejected from the ventricle during each contraction. It is a critical measure of ventricular pump function.
   $EF = \frac{SV}{\text{End-diastolic volume}}$
   A normal ejection fraction is roughly $0.55$ (or $55\%$).

Cardiac O2 Consumption

• Cardiac oxygen consumption is directly proportional to the amount of tension generated by the cardiac muscle. The more work the heart does, the more oxygen it requires.

• Oxygen consumption is increased by several factors, which enhance cardiac workload:

  • Increased afterload (higher resistance to blood ejection)

  • Increased heart size (larger muscle mass requires more oxygen)

  • Increased contractility (stronger contractions require more energy and oxygen)

  • Increased heart rate (more beats per minute means more frequent contractions and higher oxygen demand)

Measurement of Cardiac Output by Fick Principle

The Fick Principle is a method used to measure cardiac output, based on the principle of conservation of mass. It states that the total uptake or release of a substance by an organ is the product of the blood flow to the organ and the arteriovenous concentration difference of the substance. For cardiac output, oxygen is often used:

$CO = \frac{\text{O}<em>2 \text{ consumption}}{\text{O}</em>2 \text{ pulmonary vein} - \text{O}_2 \text{ pulmonary artery}}$

In this formula:

• $\text{O}_2 \text{ consumption}$ is the total oxygen consumed by the body per minute.

• $\text{O}_2 \text{ pulmonary vein}$ is the oxygen content of blood in the pulmonary veins (representing arterial systemic blood).

• $\text{O}_2 \text{ pulmonary artery}$ is the oxygen content of blood in the pulmonary artery (representing mixed venous blood).

Heart Sounds

Heart sounds are produced by the turbulent flow of blood when heart valves close. They are typically heard using a stethoscope.

• 1st Heart Sound (S1): This sound is generated by the closure of the atrioventricular (AV) valves (mitral and tricuspid valves) at the beginning of ventricular systole. It is characterized by a relatively low pitch and a longer duration, often described as a "lubb" sound.

• 2nd Heart Sound (S2): This sound is produced by the closure of the aortic and pulmonary semilunar valves at the end of ventricular systole. It typically has a higher pitch and a shorter duration compared to S1, often described as a "dupp" sound.

• 3rd Heart Sound (S3): This sound is caused by the rapid inflow of blood into the ventricles during early diastole, when the ventricular walls are rapidly expanding. It is typically a low-pitched sound and is often difficult to hear in healthy adults. In some cases, it can be indicative of volume overload or heart failure.

Atherosclerosis

Characteristics

• Atherosclerosis is a specific form of arterial disease characterized by the gradual accumulation of plaque, known as atheromas, within the inner lining of arterial walls. These plaques are primarily composed of fats, cholesterol, calcium, and other substances.

• The buildup of these plaques causes progressive narrowing and hardening of the affected arteries, leading to obstruction of blood flow.

• It predominantly affects medium to large arteries throughout the body, including vital vessels such as the coronary arteries (supplying the heart) and carotid arteries (supplying the brain).

Risk Factors

Several factors significantly increase the risk of developing atherosclerosis:

• Dyslipidemia: Abnormal levels of lipids (fats) in the blood, particularly high levels of LDL (bad) cholesterol and low levels of HDL (good) cholesterol.

• Diabetes Mellitus: High blood sugar levels contribute to endothelial damage and inflammation.

• Smoking: Tobacco smoke chemicals damage the endothelium and promote plaque formation.

• Sedentary Lifestyle: Lack of physical activity contributes to obesity, hypertension, and dyslipidemia.

• Obesity: Excess body fat is linked to inflammation, insulin resistance, and hypertension.

• Hypertension: Chronically high blood pressure places mechanical stress on arterial walls, promoting endothelial injury.

Symptoms & Complications

• Symptoms: Initial symptoms are often vague or absent as the disease progresses gradually. As arteries narrow significantly, symptoms may include shortness of breath (especially during exertion) and chest pain (angina) if coronary arteries are affected.

• Complications: Atherosclerosis is a leading cause of severe cardiovascular complications, including:

  • Strokes: When plaque ruptures or severely narrows carotid or cerebral arteries.

  • Heart attacks: When coronary arteries become severely stenosed or occluded.

  • Damage to organs: Reduced blood flow can lead to chronic damage to kidneys, limbs (peripheral artery disease), and other organs.

Inflammatory Response in Atherosclerosis

• Endothelial Injury and Inflammation: The initiation of atherosclerosis often begins with some form of injury or dysfunction to the endothelial lining of the artery. This injury triggers a chronic inflammatory response within the arterial wall, which is a key process in the formation and progression of plaque.

• Endothelial Dysfunction: This dysfunction involves changes in the properties of endothelial cells, including a reduced production and availability of nitric oxide (NO). Nitric oxide is a crucial vasodilator and anti-inflammatory molecule; its reduction contributes to vasoconstriction and promotes further inflammatory responses, driving plaque growth.

Atrial Fibrillation and Flutter

Characteristics

• Atrial Fibrillation (AFib): This is one of the most common types of sustained arrhythmia. It is characterized by highly irregular heart rhythms and very rapid, disorganized electrical activity and contractions in the atria. Instead of a single, coordinated atrial contraction, the atria quiver chaotically, leading to an irregular and often rapid ventricular response.

• Atrial Flutter: This arrhythmia involves a more organized, but still abnormally fast, electrical activity in the atria. It typically presents with regular, rapid atrial contractions (often at rates of $250-350\text{ BPM}$), which are faster than the ventricular response, leading to a characteristic "sawtooth" pattern on the ECG.

Causes

Both atrial fibrillation and flutter can be triggered or exacerbated by a variety of factors:

• Stress: Emotional or physical stress can sometimes induce or worsen these arrhythmias.

• Caffeine: Excessive consumption of caffeine can act as a stimulant and trigger episodes.

• Alcohol: Alcohol consumption, particularly binge drinking, is a well-known trigger (often referred to as "holiday heart syndrome").

• Heart Disease: Underlying structural heart diseases, such as coronary artery disease, heart failure, or valvular heart disease, are significant risk factors.

• Post-surgery Complications: These arrhythmias can frequently occur after cardiac surgeries or other major surgical procedures.

Heart Murmurs

• Heart murmurs are abnormal sounds generated by turbulent blood flow within or near the heart. They are typically heard with a stethoscope and can range from soft to loud.

• Origin of Turbulence: Murmurs can be either physiological (innocent, often in healthy individuals due to rapid blood flow, without underlying pathology) or pathological (indicative of a structural heart problem).

• Causes of Pathological Murmurs: The primary causes include heart valve abnormalities:

  • Valve Stenosis: This occurs when a heart valve is narrowed or stiff, impeding the forward flow of blood. Blood must then flow at a higher velocity through the restricted opening, creating turbulence.

  • Valve Insufficiency (Regurgitation): This occurs when a heart valve does not close completely, allowing blood to leak backward (regurgitate) during the cardiac cycle. This backflow of blood also creates turbulent flow and a characteristic murmur.

Both stenosis and insufficiency lead to abnormal patterns of blood flow that produce audible sounds.