The Heart - Chapter 20

Cardiac Muscle Tissue

• Intercalated Discs:

  • Plasma membranes of adjacent cardiac muscle cells intertwine.

  • Bound together by desmosomes and gap junctions.

  • Allow the entire tissue to "pull together" as one enormous muscle cell.

  • Cardiac muscle is called a functional syncytium (fused mass of cells).

Location of Heart and Superficial Anatomy

• Pericardial Sac (Fibrous Pericardium):

  • Surrounds the heart.

  • Composed of a dense network of collagen fibers.

  • Attaches to the central tendon of the diaphragm and sternum.

  • Stabilizes the position of the heart.

• Pericardial Cavity:

  • Area between the parietal pericardium and visceral pericardium.

  • Contains 10–15 mL of pericardial fluid secreted by pericardial membranes.

  • Pathogenic infection may cause pericarditis.

• Cardiac Tamponade:

  • Condition in which movement of the heart is restricted.

  • Fluid accumulates in the pericardial cavity.

  • The heart is unable to expand to fill with blood.

  • Can be caused by:

    • Injuries to the pericardium or chest wall.

    • Acute pericarditis.

Coronary Circulation

• Coronary Arteries:

  • Anterior view shows the Left Coronary Artery branching into the Anterior Interventricular (left anterior descending) artery and the Circumflex artery.

  • The Right Coronary Artery gives rise to Marginal arteries.

  • Posterior view shows Right Coronary Artery branching into Marginal artery and Posterior Interventricular artery.

  • Arterial anastomoses exist between anterior and posterior interventricular arteries.

Overview of Blood Flow Through the Heart

• Key Structures:

  • Superior vena cava, Inferior vena cava

  • Right Atrium: Fossa ovalis, Pectinate muscles

  • Right Ventricle: Right AV valve (tricuspid), Chordae tendineae, Papillary muscles, Trabeculae carneae, Moderator band, Pulmonary semilunar valve

  • Pulmonary trunk

  • Left Atrium: Opening of the coronary sinus

  • Left Ventricle: Left AV valve (bicuspid; mitral), Aortic semilunar valve

  • Interventricular septum

• Structural Differences Between Ventricles:

  • Left ventricle has a thick wall, while the right ventricle has a thin wall.

  • Fat is present in the anterior interventricular sulcus.

Heart Valves

• Position of heart valves during ventricular relaxation: Aortic and Pulmonary valves (closed), Left and Right AV (tricuspid) valves (open).

• Position of heart valves during ventricular contraction: Aortic and Pulmonary valves (open), Left and Right AV (tricuspid) valves (closed).

• Key:

  • Chordae tendineae are loose during ventricular relaxation and tense during ventricular contraction.

  • Papillary muscles are relaxed during ventricular relaxation and contracted during ventricular contraction.

• Semilunar Valve Function:

  • Open and Closed states affect how blood flows through the heart.

Coronary Artery Disease

• Coronary Artery Disease (CAD):

  • Areas of partial or complete blockage of coronary circulation.

  • Produces decreased blood flow to the area (coronary ischemia).

  • The usual cause is atherosclerosis but may also arise from an associated blood clot (thrombus).

• Myocardial Infarction (Heart Attack):

  • Death of a tissue due to lack of oxygen as a result of circulatory blockage.

  • Most commonly results from CAD.

The Conducting System

• Conducting System:

  • Network of specialized cardiac muscle cells.

  • Responsible for initiating and distributing the stimulus to contract.

  • Can do so on their own (without neural or hormonal stimulation).

  • Property called automaticity (or autorhythmicity).

• Cells:

  • Pacemaker cells

  • Conducting cells

• Located in various locations creating the conudcting system

• Pacemaker Cells:

  • Sinoatrial (SA) node.

  • Atrioventricular (AV) node.

• Conducting Cells:

  • Internodal pathways.

  • AV bundle and bundle branches.

  • Purkinje fibers.

• Sequence of Conduction:

  • Action potential generated at SA node; atrial activation begins.

  • Stimulus spreads across atrial within internodal pathways to AV node.

  • 100-msec delay occurs at AV node.

  • Impulse travels along interventricular septum within AV bundle & bundle branches to Purkinje fibers.

  • Ventricular contraction begins.

  • Impulse distributed by Purkinje fibers throughout ventricular myocardium; ventricular contraction completes.

Electrocardiogram (ECG)

• Electrocardiogram (ECG or EKG):

  • Recording of electrical activities of the heart from the body surface.

  • Used to assess the performance of nodal, conducting, and contractile components.

  • Example: abnormal pattern of conduction shown on an ECG when a portion of the heart is damaged by a heart attack.

  • Appearance varies with placement and number of electrodes or leads.

• Key Components:

  • P wave

  • QRS complex

  • T wave

  • P–R interval

  • Q–T interval

• Cardiac Arrhythmias:

  • Abnormal patterns of cardiac electrical activity.

  • About 5% of the population experiences a few abnormal heartbeats each day.

  • Not a clinical problem unless arrhythmias reduce pumping efficiency of the heart.

• Examples of Arrhythmias:

  • Atrial Fibrillation (AF): Atrial contraction is abnormal.

  • Premature Ventricular Contractions (PVCs).

Cardiac Contractile Cell Contractions

• Three Stages of a Cardiac Action Potential

  • Rapid Depolarization:

    • Similar to the process in skeletal muscle fiber.

    • At threshold, voltage-gated Na^+ channels open.

    • Massive influx of sodium ions.

    • Channels are called fast sodium channels because they open quickly and remain open only a few milliseconds.

  • Plateau:

    • Membrane potential remains near 0 mV.

    • Two opposing factors maintain that value:

      • Fast sodium channels close as membrane potential approaches +30 mV.

        • +30 mV

      • Cell begins actively pumping Na^+ out of the cell.

        • Na^+

      • Voltage-gated calcium channels open, allowing influx of Ca^{2+} (nearly balances loss of Na^+.

        • Ca^{2+}

        • Na^+

    • Called slow calcium channels because open slowly and remain open a relatively long time (~175 msec).

  • Repolarization:

    • Slow calcium channels close.

    • Slow potassium channels open.

    • Potassium ions rush out of the cell.

    • The net result is rapid repolarization.

    • Restores resting potential.

The Cardiac Cycle and Pressure Gradients

• Phases of the Cardiac Cycle (for a heart rate of 75 bpm)

  • Cardiac cycle begins with all four chambers relaxed.

    • Ventricles are partially filled with blood (due to AV valves being open – passive filling).

    • 70% of ventricle filled this way.

  • Atrial Systole (100 msec):

    • Contracting atria fill relaxed ventricles with blood (active filling last 30% of ventricle filled).

    • When ventricles are 100% filled = End Diastolic volume (EDV).

  • Atrial Diastole (270 msec):

    • Continues until the start of the next cardiac cycle (through both phases of ventricular systole).

  • Ventricular Systole—First Phase:

    • Contracting ventricles push AV valves closed.

    • Not enough pressure to open semilunar valves.

    • Called isovolumetric contraction.

    • No change in volume.

  • Ventricular Systole—Second Phase:

    • Increasing pressure pushes open semilunar valves.

    • Blood flows out of ventricles.

    • Called ventricular ejection.

  • There is always a small amount of blood left in ventricles after contraction =

    • End Systolic Volume (ESV)

  • Ventricular Diastole—Early:

    • Ventricles relax, and blood pressure in them drops.

    • Blood flowing back against semilunar valve cusps closes the valves.

  • Isovolumetric Relaxation:

    • Still part of ventricular diastole.

    • Semilunar valves closed; AV valves still closed.

    • No change in ventricular volume.

    • Blood flowing into atria.

  • Ventricular Diastole—Late:

    • All chambers relaxed.

    • AV valves open.

    • Ventricles fill passively to roughly 70%.

    • Ventricular diastole lasts 530 msec

      • 430 msec to the end of the current cardiac cycle

      • 100 msec into the next cardiac cycle.

      • Until next ventricular systole.

• Heart Sounds:

  • S1 (Lub):

    • Marks the start of ventricular contraction.

    • Produced as AV valves close.

    • Lasts longer than the second heart sound.

  • S2 (Dup):

    • Occurs when semilunar valves close.

  • S3 and S4:

    • Very faint and rarely heard in adults.

    • S3 (blood flowing into ventricles).

    • S4 (atrial contraction).

Cardiac Output and the Conducting System

• Cardiac Output (CO):

  • Amount of blood pumped by the left ventricle into the aorta each minute.

    • CO = HR \times SV

  • Measured in ml/min.

  • Depends on:

    • Heart rate (beats per minute).

    • Stroke volume (SV).

      • Amount of blood pumped out of the ventricle during a single heartbeat.

        • SV= EDV-ESV

Autonomic Effects on Heart Rate

• Cardiac Centers of Medulla Oblongata:

  • Cardioacceleratory Center:

    • Controls sympathetic neurons.

    • Sympathetic innervation in the heart arrives in postganglionic fibers within cardiac nerves.

  • Cardioinhibitory Center:

    • Controls parasympathetic neurons.

    • Parasympathetic innervation arrives through the vagus nerve and synapses in the cardiac plexus.

• Normally, the resting heart rate is slower than the intrinsic rate because parasympathetic innervation dominates.

• Pacemaker Potential:

  • Pacemaker cells in SA and AV nodes cannot maintain a stable resting potential.

  • After repolarization, the membrane gradually drifts toward the threshold.

  • Gradual spontaneous depolarization is called a prepotential or pacemaker potential.

  • SA node cells do this the fastest (80–100 times per minute).

    • Establishes heart rate.

  • Impulse from SA node brings AV nodal cells to threshold before they would do so on their own

• Parasympathetic Influence

  • Any factor that changes the rate of depolarization and repolarization will change the time to reach the threshold.

  • Parasympathetic Stimulation:

    • Binding of ACh from parasympathetic neurons.

    • Opens K^+ channels in the plasma membrane.

      • K^+

    • Slows the rate of spontaneous depolarization.

    • Extends duration in repolarization.

    • Results in decreased heart rate.

• Sympathetic Influence

  • Sympathetic Stimulation:

    • Binding of norepinephrine to beta-1 receptors leads to the opening of ion channels.

    • Increases the rate of depolarization.

    • Shortens duration in repolarization.

    • Results in increased heart rate.

• Resting Heart Rate:

  • Varies with age, general health, and physical conditioning.

  • Normal range is 60–100 bpm.

  • Bradycardia:

    • Heart rate slower than normal (<60 bpm).

  • Tachycardia:

    • Heart rate faster than normal (>100 bpm).

Factors Affecting Stroke Volume

• Stroke Volume Analogy:

  • Stroke volume can be compared to pumping water with a manual pump.

  • The amount pumped varies with pump handle movement.

  • Even though there are two pumps (ventricles) to the heart, they pump the same volume.

  • Can use a single pump as a model.

    • SV = EDV – ESV

    • EDV = End Diastolic Volume

    • ESV = End Systolic Volume

• Influences on EDV:

  • Venous Return:

    • Amount of venous blood returned to the right atrium.

    • Affected by:

      • Blood volume

        • Reduced with significant drop in volume.

      • Muscular activity

        • Increased with increased contractions, compressing veins.

      • The rate of blood flow through peripheral tissues

        • Increased with increased flow.

  • Filling Time:

    • Duration of ventricular diastole.

    • Slowing heart rate (increasing filling time) increases EDV.

    • Increasing heart rate (less filling time) decreases EDV.

  • Preload:

    • Amount of myocardial stretching.

    • Greater EDV = larger preload = greater stroke volume.

    • Called the Frank-Starling law of the heart.

    • Increased filling stretches sarcomeres of ventricular muscle cells to optimal length.

    • Contract more efficiently.

    • Produce more powerful contractions.

    • Eject more blood.

• Influences on ESV:

  • Contractility:

    • Amount of force produced during a contraction at a given preload.

    • Varies with autonomic stimulation as well as with many hormones and drugs.

    • Increased by: sympathetic stimulation, many hormones (epinephrine, norepinephrine, thyroid hormone, glucagon).

    • Reduced by “beta blockers” and calcium channel blockers.

  • Afterload:

    • Tension necessary for ventricular ejection.

    • Greater afterload = decreased stroke volume.

    • Increases period of isovolumetric contraction to build enough tension.

    • Decreases the duration of ventricular ejection.

    • Increased by any factor that restricts arterial blood flow.

• Example: vasoconstriction

Factors Affecting Cardiac Output

• Cardiac output varies widely to meet metabolic demands.

• Heart Failure:

  • Condition when the heart cannot meet the demands of peripheral tissues.

  • Cardiac output can be changed by affecting either heart rate or stroke volume.