lecture Heart and Circulation Physiology Review

Flashcards covering myocardial cell types, cardiac conduction, autonomic effects, arrhythmias, cardiac cycle, contractility, blood flow dynamics, and common heart conditions like atherosclerosis and atrial fibrillation.

What are nodal or conducting cells in the heart?

These are specialized myocardial cells that contract weakly, contain few contractile elements, and can spontaneously generate and rapidly conduct action potentials without nervous input.

What is the pacemaker of the heart?

The sinoatrial node (SA node), located in the upper posterior wall of the right atrium.

What is the typical path of an action potential through the heart's conducting system?

SA node -> Atria -> AV node -> Bundle of His -> Purkinje Fibers -> Ventricular muscle.

What prevents the action potential from directly jumping from the atria to the ventricles?

The atria are electrically isolated from the ventricles by fibrous tissue, requiring the action potential to pass through the AV node.

What are chronotropic effects?

Changes in heart rate, either decreasing (-ve) or increasing (+ve) the SA node firing rate.

What are dromotropic effects?

Changes in conduction velocity, primarily in the AV node, affecting the speed of action potential transmission from atria to ventricles.

What are inotropic effects?

Changes in the force of myocardial contraction, either decreasing (-ve) or increasing (+ve).

What are the sympathetic effects on the heart's chronotropic, dromotropic, and inotropic properties?

Positive chronotropic, positive dromotropic, and positive inotropic effects via β1-receptors.

What are the parasympathetic effects on the heart's chronotropic, dromotropic, and inotropic properties?

Negative chronotropic and negative inotropic effects.

What is an arrhythmia?

An abnormality in impulse formation or conduction in the heart, leading to changes in the sinus rhythm.

What is sinus tachycardia?

A regular heart rhythm where the sinus frequency rises above 100 beats/min.

What is sinus bradycardia?

A regular heart rhythm where the sinus frequency drops below 50-60 beats/min.

What is a supraventricular arrhythmia due to atrial or nodal extrasystole (ES)?

When abnormal impulses originate in the atria or AV node, transmitted to the ventricle, throwing it out of sinus rhythm.

How do ECGs differ for atrial ES versus nodal extrasystole?

In atrial ES, the P wave is deformed but the QRS complex is normal. In nodal extrasystole, the P wave is negative and either masked by the QRS or appears shortly after it.

What are Ventricular premature complexes (VPCs) or infranodal extrasystole?

Ectopic impulses originating from an area distal to the His-Purkinje system, affecting ventricular rhythm with a deformed QRS complex.

What are two common mechanisms for VPCs?

Automaticity (new site of depolarization in nonnodal ventricular tissue) and reentry circuit (slow-conducting tissue adjacent to normal tissue).

List some possible causes of Premature Ventricular Contraction (PVC).

Ischemia, certain medicines (e.g., digoxin), myocarditis, cardiomyopathy, hypoxia, hypercapnia, mitral valve prolapse, smoking, alcohol, drugs (e.g., cocaine), caffeine, magnesium/potassium deficiency, calcium excess, thyroid problems, and heart attack.

What can frequent episodes of continuous PVCs lead to?

Ventricular tachycardia (VT), a rapid heartbeat with an extra electrical impulse causing an extra ventricular contraction.

How can PVCs often be resolved non-pharmacologically?

By restoring the balance of magnesium, calcium, and potassium within the body.

What do Class I antiarrhythmic agents do and give examples?

They are sodium channel blockers, which affect cardiac action potentials. Examples include Lidocaine and Phenytoin.

What do Class II antiarrhythmic agents do and give examples?

They are beta blockers; they block β1-adrenergic receptors, decreasing sympathetic activity and slowing AV node conduction. Examples include Atenolol, Propranolol, and Metoprolol.

What do Class III antiarrhythmic agents do and give an example?

They block potassium channels, prolonging repolarization without decreasing conduction velocity. An example is Sotalol.

What do Class IV antiarrhythmic agents do and give examples?

They are calcium channel blockers; they decrease AV node conduction and shorten the plateau phase of the cardiac action potential, reducing contractility. Examples include Verapamil and Diltiazem.

What is Atrial Tachycardia?

A rhythm disturbance arising in the atria, with heart rates typically ranging from 100-250 bpm, and usually a regular atrial rhythm.

What is Ventricular Tachycardia and its potential danger?

A rapid sequence of ectopic ventricular impulses, with rates between 120 and 250 bpm, which can lead to decreased ventricular filling, reduced cardiac output, and even ventricular fibrillation (uncoordinated twitching), potentially as dangerous as cardiac arrest.

What is AV node block?

A condition resulting from damage to the AV node, causing slowing or blockage of impulse conduction, reflected by changes in the PR interval.

Describe First-degree AV node block.

The PR interval exceeds 0.20 seconds, indicating slowed conduction through the AV node.

Describe Second-degree AV node block.

Severe AV node damage where only some atrial electrical waves pass to the ventricles, resulting in P waves without associated QRS waves on an ECG.

Describe Third-degree, or complete, AV node block.

None of the atrial waves can pass through the AV node to the ventricles, resulting in bradycardia.

What are the two principal types of myocardial cells?

Contractile cells (similar to skeletal muscle cells) and nodal/conducting cells (similar to nerve cells).

How do cardiac contractile cells differ from skeletal muscle cells?

Cardiac cells have only one nucleus, more mitochondria (1/3 volume), are shorter and branched, and are joined by intercalated discs containing tight junctions and gap junctions.

What is the function of intercalated discs, tight junctions, and gap junctions in contractile cells?

Intercalated discs bind cells, tight junctions hold them together, and gap junctions allow ion movement and action potential conduction from cell to cell without nerves.

Describe the key steps in excitation-contraction coupling in myocardial cells.

AP spreads into T tubules, Ca2+ enters from extracellular fluid, triggering Ca2+ release from SR (Ca2+-induced Ca2+ release), which increases intracellular Ca2+, leading to Ca2+ binding to troponin C, removal of tropomyosin inhibition, actin-myosin binding, filament sliding, and contraction.

How does relaxation occur in myocardial cells?

Relaxation occurs when Ca2+ is reaccumulated by the sarcoplasmic reticulum (SR) via an active Ca2+-ATPase pump.

What is contractility (inotropism)?

The intrinsic ability of the cardiac muscle to develop force at a given muscle length, related to intracellular Ca2+ concentration.

How is contractility estimated?

By the ejection fraction (stroke volume/end-diastolic volume), which is normally 0.55 (55%).

List factors that increase contractility (positive inotropism).

Increased heart rate, sympathetic stimulation, and cardiac glycosides (e.g., digitalis).

What is a major factor that decreases contractility (negative inotropism)?

Parasympathetic (Ach) stimulation via muscarinic receptors, which decreases the inward Ca2+ current in the atria.

Define Preload in the context of ventricles.

Preload is equivalent to end-diastolic volume, related to right atrial pressure, and increases with venous return, stretching ventricular muscle fibers.

Define Afterload for the left and right ventricles.

For the left ventricle, afterload is equivalent to aortic pressure. For the right ventricle, it is equivalent to pulmonary artery pressure. Increases in these pressures increase afterload.

How does sarcomere length affect contraction?

It determines the maximum number of cross-bridges that can form between actin and myosin, thus determining the maximum tension or force of contraction.

What is the Frank-Starling relationship?

It describes how increases in venous return or end-diastolic volume lead to increases in stroke volume and cardiac output, matching cardiac output to venous return based on ventricular fiber length.

How do changes in contractility affect the Frank-Starling curve?

Increased contractility shifts the curve upward (increased CO for any given preload), while decreased contractility shifts it downward (decreased CO).

Describe the Isovolumetric ventricular contraction phase (1-2) of the cardiac cycle.

Ventricular depolarization (QRS) and contraction increase ventricular pressure, closing the mitral valve. All valves are closed, so no blood is ejected, and ventricular volume remains constant.

Describe the Ventricular systole (ejection period) phase (2-3) of the cardiac cycle.

Left ventricular pressure exceeds aortic pressure, opening the aortic valve, and blood is ejected into the aorta. Ventricular volume decreases, and the ejected volume is the stroke volume.

Describe the Early ventricular diastole (isovolumetric relaxation) phase (3-4) of the cardiac cycle.

The ventricle relaxes, ventricular pressure drops below aortic pressure, closing the aortic valve. All valves are closed, so ventricular volume remains constant.

Describe the Late ventricular diastole (ventricular filling) phase (4-1) of the cardiac cycle.

Left ventricular pressure drops below left atrial pressure, opening the mitral (AV) valve, and the ventricle fills with blood, increasing its volume to the end-diastolic volume.

How does increased preload affect the pressure-volume loop?

It increases end-diastolic volume, leading to an increase in stroke volume (Frank-Starling effect), reflected by an increased width of the loop.

How does increased afterload affect the pressure-volume loop?

It increases aortic pressure, causing the ventricle to eject blood against higher resistance, resulting in a decrease in stroke volume (decreased width of loop) and an increase in end-systolic volume.

How does increased contractility affect the pressure-volume loop?

The ventricle develops greater tension, causing an increase in stroke volume and a decrease in end-systolic volume.

How is stroke volume calculated?

Stroke volume = End-diastolic volume - End-systolic volume.

How is cardiac output calculated?

Cardiac output = Stroke volume × Heart rate.

What is ejection fraction and its normal value?

Ejection fraction (EF) is the fraction of end-diastolic volume ejected in each stroke volume, related to contractility, and is normally 0.55 (55%). EF = Stroke volume / End-diastolic volume.

What factors increase cardiac O2 consumption?

Increased afterload (aortic pressure), increased heart size, increased contractility, and increased heart rate.

State the Fick principle formula for cardiac output.

Cardiac output = O2 consumption / (O2 pulmonary vein - O2 pulmonary artery).

When does the aortic valve open during the period of ejection?

The aortic valve opens when the pressure in the left ventricle rises above the pressure in the aorta (typically 80 mmHg).

What indirectly produces the first heart sound?

The closure of the AV valves (mitral and tricuspid).

What indirectly produces the second heart sound?

The closure of the aortic and pulmonary semilunar valves.

What causes the third heart sound, if present?

Blood flowing with a rumbling motion into the almost filled ventricles during mid-diastole.

What is the normal cardiac output at rest, and how does it change during vigorous exercise?

At rest, CO is roughly 5 liters/minute. During vigorous exercise, it can increase up to 20 l/min in normal individuals and 35-40 l/min in highly trained athletes.

How is an increase in cardiac output achieved during exercise?

By increasing either heart rate, stroke volume, or both.

How do the parasympathetic and sympathetic nervous systems control heart rate?

The PSYN decreases heart rate and force of contraction by affecting SA and AV nodes. The SNS increases heart rate and force of contraction with stronger innervation to ventricular muscle.

What is the heart's natural rhythm if all autonomic nervous system influences are removed?

Approximately 100 beats per minute (bpm).

Why is the resting heart rate typically 70 bpm instead of the heart's natural rhythm of 100 bpm?

Because there is constant activity from the parasympathetic nervous system at rest, keeping the heart rate slowed to roughly 70 bpm.

What is atherosclerosis?

A disease involving patchy intimal plaques (atheromas) in medium and large arteries, containing lipids, inflammatory cells, smooth muscle cells, and connective tissue, caused by arteries getting blocked by fats and cholesterol.

What are common risk factors for atherosclerosis?

Dyslipidemia, diabetes, cigarette smoking, family history, sedentary lifestyle, obesity, and hypertension.

What are the key components of an atherosclerotic plaque?

Lipids (intracellular and extracellular cholesterol and phospholipids), inflammatory cells (e.g., macrophages, T cells), smooth muscle cells, connective tissue (e.g., collagen), thrombi, and Ca++ deposits.

What are common symptoms and complications of atherosclerosis?

Symptoms include shortness of breath and tightening chest pain. Complications include strokes, and damage to muscles, body organs, and blood vessels.

What is thought to have a primary role in the initiation of atherosclerosis?

Endothelial injury and dysfunction.

How do monocytes and lipids contribute to atherosclerosis development?

Monocytes migrate to the subendothelium, transform into macrophages, and produce enzymes that digest the fibrous cap. Lipids (LDL, VLDL) bind to endothelial cells and are oxidized in the subendothelium.

What is the key difference between atrial fibrillation and atrial flutter?

In atrial flutter, the atria beat regularly but faster than the ventricles. In atrial fibrillation, the heart beat is completely irregular, with very quick and irregular atrial muscle contractions.

What are potential complications of atrial fibrillation?

Blood pooling and clot formation due to incomplete ejection from the atria, which can lead to stroke.

What are common causes and symptoms of atrial fibrillation and flutter?

Causes include many types of heart disease, stress/anxiety, caffeine, alcohol, tobacco, diet pills, open heart surgery, pericarditis, chest trauma/surgery, pulmonary disease, and certain medications.

What are heart murmurs?

Sounds generated by turbulent flow of blood, which may be physiological (benign) or pathological (abnormal).

What two pathological conditions can cause abnormal heart murmurs?

Stenosis (restricting the opening of a heart valve) and valve insufficiency (or regurgitation, allowing backflow of blood when the valve should be closed).