MTC.AP2.Ch18.Heart

The Cardiovascular System: The Heart

Learning Objectives

• Describe the gross and microscopic anatomy of the heart.

• Describe the blood flow through the heart including chambers, valves, vessels, and circuits.

• Compare and contrast cardiac and skeletal muscle contraction.

• Describe the electrical conduction system of the heart including physiology of pacemakers and contractile muscle fibers.

• Recognize a normal vs abnormal ECG and identify the events represented by each wave and their intervals.

• Explain the events of the cardiac cycle.

• Explain the cardiac cycle by defining cardiac output, stroke volume, and cardiac reserve, explaining factors that regulate cardiac output.

The Heart

• Cardiac = heart

• Pumps blood through the body.

• Located in the thoracic cavity in the mediastinum, between the lungs.

• Base: wide, superior portion of the heart where large vessels attach.

• Apex: tapered inferior end, tilts to the left.

The Heart Overview

• Heart is a transport system consisting of two side-by-side pumps.

• Pulmonary Circuit: Carries blood to the lungs for gas exchange and back to the heart.

• Systemic Circuit: Supplies oxygenated blood to all tissues of the body and returns it to the heart.

The Heart Overview (Chambers)

• Receiving chambers:

  • Right atrium: Receives blood returning from the systemic circuit.

  • Left atrium: Receives blood returning from the pulmonary circuit.

• Pumping chambers:

  • Right ventricle: Pumps blood through the pulmonary circuit.

  • Left ventricle: Pumps blood through the systemic circuit.

The Heart Overview (Tissues)

• Composed of different tissue types:

  • Valves: connective tissue

  • Lining: epithelial tissue

  • Myocardium: muscle, connective tissue, nervous tissue

The Serous Membrane: The Pericardium

• Pericardium: double-walled sac that encloses the heart.

  • Anchored to the diaphragm inferiorly and sternum anteriorly.

• Parietal pericardium: pericardial sac.

  • Superficial fibrous layer of connective tissue.

  • Deep, thin serous layer.

• Visceral pericardium (epicardium): serous membrane covering the heart.

• Pericardial cavity: space inside the pericardial sac filled with 5 to 30 mL of pericardial fluid.

Clinical Applications - Pericardium

• Pericarditis:

  • Inflammation of the pericardium.

  • Roughens membrane surfaces, causing pericardial friction rub (creaking sound) heard with a stethoscope.

• Cardiac tamponade:

  • Excess fluid that leaks into the pericardial space.

  • Can compress the heart’s pumping ability.

  • Treatment: fluid is drawn out of the cavity, usually with a syringe.

The Heart Wall

• Heart wall has three layers:

  • Epicardium (visceral pericardium)

  • Endocardium

  • Myocardium (cardiac muscle with cardiac skeleton)

The Heart Wall Details

• Epicardium (visceral pericardium):

  • Serous membrane covering the heart.

  • Adipose in a thick layer in some places.

  • Coronary blood vessels travel through this layer.

• Endocardium:

  • Smooth inner lining of the heart continuous with the endothelium of blood vessels.

  • Covers the valve surfaces.

The Heart Wall - Myocardium

• Myocardium:

  • Layer of cardiac muscle proportional to workload.

  • Muscle spirals around the heart, which produces a wringing motion.

• Cardiac skeleton: framework of collagenous and elastic fibers.

  • Provides structural support and attachment for cardiac muscle and anchor for valve tissue.

  • Electrical insulation between atria and ventricles; important in timing and coordination of contractile activity.

Gross Anatomy Internal Features

• Interatrial septum: separates atria.

  • Fossa ovalis: remnant of foramen ovale of the fetal heart.

• Interventricular septum: separates ventricles.

Gross Anatomy - Surface Features

• Auricles: appendages that increase atrial volume.

• Coronary sulcus (atrioventricular groove):

  • Encircles junction of atria and ventricles.

• Anterior interventricular sulcus: anterior position of the interventricular septum.

• Posterior interventricular sulcus: landmark on the posteroinferior surface.

Gross Anatomy - Atria

• Atria (receiving chambers):

  • Thin-walled- do not propel blood much.

  • Ridges called pectinate muscles in some regions.

• Three Veins of Right Atria:

  • Superior vena cava (SVC): returns blood from body regions above the diaphragm.

  • Inferior vena cava (IVC): returns blood from body regions below the diaphragm.

  • Coronary sinus: returns blood from coronary veins.

• Four Veins of Left Atria:

  • Four pulmonary veins return blood from lungs.

Gross Anatomy - Ventricles

• Ventricles (discharging chambers):

  • Make up most of the volume of the heart.

  • Right ventricle: most of the anterior surface. Pumps blood to pulmonary trunk.

  • Left ventricle: posteroinferior surface. Pumps blood into the aorta (largest artery in the body).

• Trabeculae carneae: irregular ridges of muscle on ventricular walls.

• Papillary muscles: project into the ventricular cavity.

  • Anchor chordae tendineae that are attached to heart valves.

Heart Valves

• Valves ensure one-way flow of blood through the heart.

• Open and close in response to pressure changes.

• No valves between major veins and atria (heart contractions compress venous openings).

• Atrioventricular (AV) valves: prevent backflow into the atria when ventricles contract.

  • Right AV valve has three cusps (tricuspid valve).

  • Left AV valve has two cusps (mitral valve, formerly ‘bicuspid’).

  • Chordae tendineae: anchor cusps of AV valves to papillary muscles that function to:

    • Hold valve flaps in the closed position.

    • Prevent flaps from everting back into the atria.

Heart Valves - Semilunar

• Semilunar valves: prevent backflow from major arteries back into the ventricles.

  • Pulmonary semilunar valve: located between the right ventricle and the pulmonary trunk.

  • Aortic semilunar valve: located between the left ventricle and the aorta.

Clinical Applications - Valves

• Two conditions severely weaken the heart:

  • Incompetent valve:

    • Blood backflows, so the heart repumps the same blood over and over.

  • Valvular stenosis:

    • Stiff flaps that constrict the opening.

    • The heart needs to exert more force to pump blood.

• A defective valve can be replaced with a mechanical, animal, or cadaver valve.

Pathway of Blood Through the Heart

• The right side of the heart:

  • Superior vena cava (SVC), inferior vena cava (IVC), and coronary sinus → Right atrium → Tricuspid valve → Right ventricle → Pulmonary semilunar valve → Pulmonary trunk → Pulmonary arteries → Lungs

• The left side of the heart:

  • Four pulmonary veins → Left atrium → Mitral valve → Left ventricle → Aortic semilunar valve → Aorta → Systemic circulation

• Blood pathway travels from the right atrium through the pulmonary circuit, then the systemic circuit (through the body) and back to the starting point.

Blood Flow

• Equal volumes of blood are pumped to pulmonary and systemic circuits (and between sides).

• Pulmonary circuit is short, low-pressure circulation.

• Systemic circuit is long, high-friction circulation.

• The anatomy of ventricles reflects differences:

  • Left ventricle walls are 3x thicker than the right, thus pumps with greater pressure.

Coronary Circulation

• Coronary circulation:

  • Functional blood supply to the heart muscle itself.

  • Needs abundant oxygen and nutrients.

  • Delivered when the heart is relaxed.

  • Left ventricle receives most of the coronary blood supply.

  • The heart receives 5% of the body’s blood supply.

Coronary Arteries

• Both left and right coronary arteries arise from the base of the aorta and supply arterial blood to the heart.

• Branching of coronary arteries varies among individuals.

• Arteries contain many anastomoses (junctions) to provide additional routes of blood delivery. Cannot compensate for coronary artery obstruction.

• Left coronary artery supplies interventricular septum, anterior ventricular walls, left atrium, and posterior wall of the left ventricle; has two branches:

  • Anterior interventricular artery

  • Circumflex artery

• Right coronary artery supplies the right atrium and most of the right ventricle; has two branches:

  • Right marginal artery

  • Posterior interventricular artery

Coronary Arteries Blood Flow

• Flow through coronary arteries is greatest when the heart relaxes.

• Contraction of the myocardium compresses the coronary arteries and obstructs blood flow.

• Opening of the aortic valve flap during ventricular contraction covers the openings to the coronary arteries blocking blood flow into them.

• During ventricular relaxation, blood in the aorta surges back toward the heart and into the openings of the coronary arteries.

Coronary Veins

• Cardiac veins collect blood from capillary beds.

• Coronary sinus empties into the right atrium; formed by merging cardiac veins.

  • Great cardiac vein of anterior interventricular sulcus.

  • Middle cardiac vein in posterior interventricular sulcus.

  • Small cardiac vein from the inferior margin.

• Several anterior cardiac veins empty directly into the right atrium anteriorly.

Clinical Applications - Coronary Issues

• Angina pectoris: chest pain from partial obstruction of coronary blood flow.

  • Pain caused by ischemia of cardiac muscle.

  • Obstruction partially blocks blood flow.

  • Myocardium shifts to anaerobic fermentation, producing lactic acid and thus stimulating pain.

• Myocardial infarction (MI): sudden death of a patch of myocardium resulting from long-term obstruction of coronary circulation.

  • Atheroma (blood clot or fatty deposit) often obstructs coronary arteries.

  • Cardiac muscle downstream of the blockage dies.

  • Heavy pressure or squeezing pain radiating into the left arm.

  • Some painless heart attacks may disrupt electrical conduction pathways, leading to fibrillation and cardiac arrest.

  • Silent heart attacks occur in diabetics and the elderly.

  • MI is responsible for about 20% of all deaths in the US (CDC, 2022).

Microscopic Anatomy - Cardiocytes

• Cardiocytes: cells of cardiac muscles.

  • Striated, short, thick, branched cells, one (or two) central nucleus surrounded by light-staining mass of glycogen.

  • Large mitochondria consume ~30% cell volume (resistance to fatigue).

  • Many sarcomeres (unit of muscle contraction).

  • Repair of damage to cardiac muscle is almost entirely by fibrosis (scarring).

• Intercalated discs are connecting junctions between cardiac cells that contain:

  • Desmosomes: hold cells together; prevent cells from separating during contraction.

  • Gap junctions: allow ions to pass from cell to cell; electrically joining cells.

    • Allows heart to be a functional syncytium, a single coordinated unit.

Cardiac vs Skeletal Muscle Physiology

• Similarities with skeletal muscle:

  • Muscle contraction is preceded by depolarizing action potential.

  • Depolarization wave travels down T tubules; causes sarcoplasmic reticulum (SR) to release Ca^{2+}.

  • Excitation-contraction coupling occurs.

  • Ca^{2+} binds troponin, causing filaments to slide.

• Differences between cardiac and skeletal muscle:

  • Some cardiac muscle cells are self-excitable.

    • Two kinds of myocytes: Contractile cells (responsible for contraction) AND Pacemaker cells: noncontractile cells that spontaneously depolarize.

  • The heart contracts as a unit. Contraction of all (or none) cardiac myocytes ensures effective pumping action. Skeletal muscles contract independently.

  • Influx of Ca^{2+} from extracellular fluid triggers Ca^{2+} release from SR. Depolarization opens slow Ca^{2+} channels in sarcolemma, allowing Ca^{2+} to enter the cell. Extracellular Ca^{2+} then causes SR to release its intracellular Ca^{2+}. Skeletal muscles do not use extracellular Ca^{2+}.

  • Cardiac muscle fibers have a longer absolute refractory period than skeletal muscle fibers. The absolute refractory period is almost as long as the contraction itself. Prevents wave summation and allows the heart to relax and fill as needed to be an efficient pump.

  • The heart relies almost exclusively on aerobic respiration. Cardiac muscle has more mitochondria than skeletal muscle, so it has a greater dependence on oxygen.

Electrical Conduction of the Heart

• Coordinates the heartbeat.

• Composed of an internal pacemaker and nerve-like conduction pathways through the myocardium.

• The heart depolarizes and contracts without nervous system stimulation (rhythm altered by autonomic nervous system).

• Relies on gap junctions connecting cells.

• Generates and conducts rhythmic electrical signals in the following order:

  • Sinoatrial (SA) node: modified cardiocytes.

    • Pacemaker initiates each heartbeat and determines heart rate.

    • Pacemaker in the right atrium near the base of the superior vena cava.

    • Rate: about 75 bpm (sinus rhythm).

    • Signals spread throughout atria.

  • Atrioventricular (AV) node:

    • Located near the right AV valve at the lower end of the interatrial septum.

    • Electrical gateway to the ventricles.

    • Fibrous skeleton: insulator prevents currents from getting to the ventricles by any other route.

  • Atrioventricular (AV) bundle (bundle of His):

    • The bundle forks into right and left bundle branches.

    • Branches pass through the interventricular septum toward the apex.

  • Purkinje fibers:

    • Nerve-like processes spread throughout the ventricular myocardium.

    • Cardiocytes then pass a signal from cell to cell through gap junctions.

Electrical and Contractile Activity

• Electrical activity leads to the contraction of the myocardium.

• Cycle of events in the heart:

  • Systole: contraction.

  • Diastole: relaxation.

• Although “systole” and “diastole” can refer to the contraction and relaxation of either type of chamber, they usually refer to the action of the ventricles.

• Signal from the SA node stimulates two atria to contract almost simultaneously (reaches AV node in 50 ms).

• The signal slows down through the AV node (thin cardiocytes with fewer gap junctions). Delays signal 100 ms which allows the ventricles time to fill.

• Signals travel very quickly through the AV bundle and Purkinje fibers. The entire ventricular myocardium depolarizes and contracts in near unison.

• Ventricular systole progresses up from the apex of the heart. The spiral arrangement of the myocardium twists ventricles slightly; like someone wringing out a towel.

Pacemaker Physiology

• The SA node does not have a stable resting membrane potential, starts at -60 mV and drifts upward due to slow Na^+ inflow.

• Gradual depolarization is called pacemaker potential.

• When it reaches a threshold of −40 mV, the voltage-gated Ca^{2+} channels open (huge influx of positive calcium ions). Faster depolarization occurs, peaking at 0 mV.

• K^+ channels then open and K^+ leaves the cell (cell becomes more negative), causing repolarization.

• Once K^+ channels close, the pacemaker potential starts over.

• When the SA node fires, it sets off the heartbeat. As the internal pacemaker, it typically fires every 0.8 seconds, setting the resting rate at 75 bpm.

Clinical Applications - Conduction System

• Defects in the intrinsic conduction system may cause:

  • Arrhythmias: irregular heart rhythms (uncoordinated atrial and ventricular contractions).

  • Heart becomes useless for pumping blood, causing circulation to cease; may result in brain death.

  • Fibrillation: rapid, irregular contractions.

  • Treatment: defibrillation interrupts chaotic twitching, giving the heart a “clean slate” to start regular, normal depolarizations.

• A defective SA node may cause an ectopic focus, an abnormal pacemaker that takes over pacing.

• If the AV node takes over, it sets a junctional rhythm at 40–60 beats/min.

• If the AV node is defective, it may cause a heart block (few impulses (partial block) or no impulses (total block) reach ventricles). Ventricles beat at their own intrinsic rate, which is too slow to maintain adequate circulation.

• Treatment: artificial pacemaker, which recouples atria and ventricles.

Autonomic Innervation of the Heart

• The intrinsic heartbeat is 100 bpm.

• Heartbeat is modified by the ANS via cardiac centers in the medulla oblongata.

  • Cardioacceleratory center: sends signals through the sympathetic trunk to increase both rate and force, stimulates SA and AV nodes, heart muscle, and coronary arteries.

  • Cardioinhibitory center: parasympathetic signals via the vagus nerve to decrease rate, inhibits SA and AV nodes via vagus nerves.

• Gives the normal heartbeat of 75bpm (vagal tone).

Electrical Behavior of the Myocardium

• Contractile muscle fibers have a stable resting potential of −90 mV and depolarize only when stimulated.

• Three phases to cardiocyte action potential:

  • Depolarization.

  • Plateau.

  • Repolarization.

Myocardium- Depolarization

• Stimulus opens voltage-regulated Na^+ channels (Na^+ rushes in), membrane depolarizes rapidly.

• Action potential peaks at +30 mV.

• Na^+ gates close quickly

Myocardium- Plateau

• Plateau phase lasts 200 ms, sustains contraction for expulsion of blood from the heart.

• Voltage-gated slow Ca^{2+} channels open, admitting Ca^{2+} which triggers the opening of Ca^{2+} channels on the sarcoplasmic reticulum (SR).

• Ca^{2+} (mostly from the SR) binds to troponin and triggers contraction.

Myocardium- Repolarization

• Ca^{2+} channels close, K^+ channels open, and rapid diffusion of K^+ out of the cell returns it to resting potential.

• Has a long absolute refractory period of 250 ms (compared to 1 to 2 ms in skeletal muscle).

• Prevents wave summation and tetanus, which would stop the pumping action of the heart.

• Longer contraction time ensures efficient ejection of blood.

The Electrocardiogram (ECG or EKG)

• Detects electrical currents generated by the heart.

• Is a graphic recording of electrical activity.

• Composite of all action potentials at a given time, not a tracing of a single AP.

• Electrodes are placed at various points on the body to measure voltage differences.

ECG Waves and Intervals

• P wave: depolarization of the SA node and atria.

• QRS interval: ventricular depolarization and atrial repolarization.

• T wave: ventricular repolarization.

• P-R interval: beginning of atrial excitation to the beginning of ventricular excitation.

• S-T segment: entire ventricular myocardium depolarized.

• Q-T interval: beginning of ventricular depolarization through ventricular repolarization.

ECGs: Normal and Abnormal

• Changes in patterns or timing of ECG may reveal diseased or damaged heart, or problems with the heart’s conduction system:

  • Myocardial infarction (MI)

  • Heart enlargement

  • Electrolyte and hormone imbalances

Cardiac Arrhythmias

• Ventricular fibrillation: a serious arrhythmia caused by electrical signals traveling randomly. The heart cannot pump blood; no coronary perfusion. Hallmark of a heart attack (MI) and kills quickly if not stopped.

• Defibrillation: strong electrical shock with intent to depolarize the entire myocardium and reset the heart to sinus rhythm. Not a cure for artery disease, but may allow time for other corrective action.

The Cardiac Rhythm - Heart Block

• Heart block: failure of conduction system to conduct.

• Premature ventricular contraction: extra beats due to a ventricular ectopic focus.

Reading an ECG

• Small box= 0.04 sec

• Big box= 0.2 sec

• 5 big boxes= 1 sec

• BPM calc methods-

  • R-R time= sec per 1 beat → inverse= BPM

  • Count # beats/ count time, convert to beats per min

The Cardiac Cycle

• Systole: period of heart contraction.

• Diastole: period of heart relaxation.

• Cardiac cycle: blood flow through the heart during one complete heartbeat.

• Atrial systole and diastole are followed by ventricular systole and diastole.

• Cycle represents series of pressure and blood volume changes.

• Mechanical events follow electrical events seen on the ECG.

Principles of Pressure and Flow

• Two main variables govern fluid movement: pressure causes flow, and resistance opposes it.

• Fluid will only flow if there is a pressure gradient (pressure difference). Fluid flows from a high-pressure point to a low-pressure point. Pressure is measured in mm Hg with a manometer (sphygmomanometer for BP).

• The volume of a space and pressure are inversely related (assuming the amount of material within remains constant).

Example Pressures in the Cardiac Cycle

• Ventricles relax.

  • Pressure drops inside the ventricles.

  • Semilunar valves close as blood attempts to back up into the ventricles from the vessels.

  • AV valves open.

  • Blood flows from atria to ventricles.

• Ventricles contract.

  • AV valves close as blood attempts to back up into the atria.

  • Pressure rises inside the ventricles.

  • Semilunar valves open, and blood flows into great vessels.

Phases of the Cardiac Cycle

• Ventricular filling (during diastole).

• Isovolumetric contraction (during systole).

• Ventricular ejection (during systole).

• Isovolumetric relaxation (during diastole).

Ventricular Filling

• Ventricles expand, and their pressure drops below that of the atria. AV valves open, and blood passively flows into the ventricles.

• Atrial depolarization triggers systole (P wave), atria contracts, pushing remaining blood into ventricles.

• End diastolic volume (EDV): volume of blood in each ventricle at the end of ventricular diastole.

• Depolarization spreads to ventricles (QRS wave), atria finish contracting and return to diastole while ventricles begin systole.

Isovolumetric Contraction

• Atria repolarize, relax, and remain in diastole for the rest of the cardiac cycle. Ventricles depolarize and begin to contract.

• The volume of ventricles decreases, and pressure increases. AV valves close as ventricular blood surges back against the cusps. Heart sound S1 occurs at the beginning of this phase.

• “Isovolumetric” because although ventricles contract, they do not eject blood, as the pressures in the aorta and pulmonary trunk are still greater than those in the ventricles.

• Myocardium exerts force, but with all four valves closed, the blood cannot go anywhere. very brief!

Ventricular Ejection

• Begins when ventricular pressure exceeds arterial pressure and semilunar valves open.

• Blood is ejected from ventricles into great vessels. Pressure peaks in the left ventricle at about 120 mm Hg and 25 mm Hg in the right.

• Ejection lasts about 200 to 250 ms - corresponds to the plateau phase of the cardiac action potential. T wave of ECG occurs late in this phase.

Isovolumetric Relaxation

• T wave ends, and ventricles begin to expand. increasing the volume of ventricles à decreases pressure

• Blood from the aorta and pulmonary trunk briefly flows backward, filing cusps and closing semilunar valves. Creates pressure rebound that appears as a dicrotic notch in the graph of artery pressure. Heart sound S2 occurs.

• “Isovolumetric” because semilunar valves are closed and AV valves have not yet opened. Ventricles are therefore taking in no blood.

• When AV valves open, ventricular filling begins again.

Cardiac Cycle - Resting Person

• In a resting person:

  • Atrial systole lasts about 0.1 second.

  • Ventricular systole lasts about 0.3 second.

  • The quiescent period, when all four chambers are in diastole, lasts about 0.4 second.

• The total duration of the cardiac cycle is therefore 0.8 seconds in a heart beating 75 bpm.

Heart Sounds

• Auscultation: listening to sounds made by the body.

• Two sounds (lub-dup) are associated with the closing of heart valves.

  • The first sound is the closing of AV valves at the beginning of ventricular systole.

  • The second sound is the closing of SL valves at the beginning of ventricular diastole.

  • The pause between lub-dups indicates heart relaxation.

• The mitral valve closes slightly before tricuspid, and aortic closes slightly before the pulmonary valve. Differences allow auscultation of each valve when a stethoscope is placed in four different regions.

Clinical Application - Heart Murmurs

• Heart murmurs: abnormal heart sounds heard when blood hits obstructions, which usually indicate valve problems.

• Incompetent (or insufficient) valve: fails to close completely, allowing backflow of blood, causing a swishing sound as blood regurgitates backward from the ventricle into atria.

• Stenotic valve: fails to open completely, restricting blood flow through the valve, causing a high-pitched sound or clicking as blood is forced through the narrow valve.

Cardiac Output

• Cardiac output (CO): amount of blood pumped out by each ventricle in 1 minute.

• CO = heart rate \, (HR) \times stroke volume \, (SV)

  • Stroke volume (SV): volume of blood pumped out by one ventricle with each beat.

  • About 4 to 6 L/min at rest

  • Vigorous exercise increases CO to 20-25 L/min for a fit person and up to 35 L/min for a world-class athlete.

  • Cardiac reserve: the difference between a person’s maximum and resting CO. Increases with fitness and decreases with disease.

Stroke Volume Details

• Stroke \, Volume = end \, diastolic \, volume \, (EDV) - end \, systolic \, volume (ESV)

  • EDV is affected by the length of ventricular diastole and venous pressure (~120 ml/beat).

  • ESV is affected by arterial BP and force of ventricular contraction (~50 ml/beat).

    • Normal SV = 120 ml - 50 ml = 70 ml/beat

• Three main factors that affect SV: Preload, Contractility, Afterload

Stroke Volume - Preload

• Preload: the degree of stretch of the heart muscle before contraction, increased preload causes increased force of contraction.

• The most important factor in preload stretching of cardiac muscle is venous return: amount of blood returning to the heart. Slow heartbeat and exercise increase venous return.

• Increased venous return distends (stretches) ventricles and increases contraction force, cardiocytes generate more tension during contraction.

Stroke Volume - Contractility

• Contractility refers to how hard the myocardium contracts, increased contractility lowers ESV.

• Caused by Sympathetic epinephrine release stimulates increased Ca^{2+} influx, leading to more cross bridge formations

• Positive inotropic agents increase contractility: Thyroxine, glucagon, epinephrine, digitalis, high extracellular Ca^{2+}.

• Decreased by negative inotropic agents: Acidosis (excess H+), increased extracellular K+, calcium channel blockers.

Stroke Volume - Afterload

• The pressure that ventricles must overcome to eject blood.

• The largest part of afterload is blood pressure in the aorta and pulmonary trunk which opposes the opening of semilunar valves and limits stroke volume.

• Hypertension increases afterload and opposes ventricular ejection.

Heart Rate

• If SV decreases as a result of decreased blood volume or weakened heart, CO can be maintained by increasing HR and contractility.

• Positive chronotropic factors increase heart rate, and negative chronotropic factors decrease heart rate.

• Heart rate can be regulated by the autonomic nervous system, chemicals, and other factors.

Autonomic NS Regulation of Heart Rate

• Does not initiate the heartbeat, it modulates rhythm and force.

• Cardiac centers in the medulla oblongata initiate autonomic output to the heart.

• The sympathetic nervous system can be activated by emotional or physical stressors. Norepinephrine causes the pacemaker to fire more rapidly, increasing HR and contractility of the heart.

• The parasympathetic nervous system opposes sympathetic effects. Acetylcholine hyperpolarizes pacemaker cells- slows HR. Vagal Tone- parasympathetic influence on heartrate. Decreases intrinsic pacemaker activity by 25 bpm.

• Atrial (Bainbridge) reflex: sympathetic reflex initiated by increased venous return, increased HR to eject more blood.

Medulla Oblongata Factors

• Inputs to cardiac centers in medulla oblongata from:

  • Cerebral Cortex, Limbic System, Hypothalamus (sensory info and emotional stimuli).

  • Proprioceptors- in muscles, and joints inform cardiac centers about changes in activity, so HR increases before metabolic demands on muscle arise.

  • Baroceptors- pressure sensors in the aorta and carotid arteries Blood pressure decreases, signal rate drops, the cardiac center increases heart rate.

    • If blood pressure increases, the signal rate rises, the cardiac center decreases heart rate. Baroreflexes and chemoreflexes—responses to fluctuation in blood pressure and chemistry—are both negative feedback loops.

  • Chemoreceptors- detect pH, CO2 and O2 levels in the aortic arch, carotid arteries, medulla oblongata More important in respiratory control than cardiac control, but will trigger an increase in heart rate when high CO_2 levels (hypercapnia) lead to acidosis.

    • Also respond to hypoxemia (oxygen deficiency in blood) usually by slowing down the heart.

Exercise and Cardiac Output

• Exercise makes the heart work harder and increases cardiac output.

• Proprioceptors signal cardiac center.

• At the beginning of exercise, signals from joints and muscles reach the cardiac center of the brain. Sympathetic output from the cardiac center increases HR and SV.

• Increased muscular activity increases venous return which increases preload and ultimately cardiac output.

• Exercise produces ventricular hypertrophy. Increased stroke volume allows heart to beat more slowly at rest. Athletes with increased cardiac reserve can tolerate more exertion than a sedentary person.

• Increases in heart rate and stroke volume cause an increase in cardiac output.

Heart Rate Regulation: Hormones & Ions

• Hormones

  • Epinephrine from the adrenal medulla increases heart rate and contractility.

  • Thyroxine increases heart rate; enhances effects of norepinephrine and epinephrine.

• Ions

  • Intra- and extracellular ion concentrations (e.g., Ca^{2+} and K^+) must be maintained for normal heart function; imbalances are very dangerous to the heart.

Clinical Applications - Heart Ion Imbalances

• Hypocalcemia: depresses the heart.

• Hypercalcemia: increases HR and contractility.

• Hyperkalemia: alters electrical activity, which can lead to heart block and cardiac arrest.

• Hypokalemia: results in feeble heartbeat; arrhythmias.

Other Factors Influencing HR

• Age: Fetus has the fastest HR and declines with age.

• Gender: Females have a faster HR than males.

• Exercise: Increases HR, trained athletes can have a slow HR.

• Body temperature: HR increases with increased body temperature.

Clinical Applications - Heart Rate

• Pulse: surge of pressure produced by heartbeat that can be felt by palpating a superficial artery.

  • Infants have an HR of 120 bpm or more.

  • Young adult females average 72 to 80 bpm.

  • Young adult males average 64 to 72 bpm.

  • The heart rate rises again in the elderly.

Clinical Applications - Heart Condition

• Tachycardia: resting adult heart rate above 100 bpm. Is caused by stress, anxiety, drugs, heart disease, or fever and the loss of blood or damage to myocardium. If persistent, may lead to fibrillation.

• Bradycardia: resting adult heart rate of less than 60 bpm. May result in grossly inadequate blood circulation in nonathletes. Is evident in sleep, low body temperature, and endurance-trained athletes

• Congestive heart failure (CHF): results from the failure of either ventricle to eject blood effectively. CO is so low that blood circulation is inadequate to meet tissue needs. Reflects a weakened myocardium caused by:

  • Coronary atherosclerosis: clogged arteries caused by fat buildup impairs oxygen delivery to cardiac cells (heart becomes hypoxic, contracts ineffectively).

  • Persistent high blood pressure: myocardium exerts more force to overcome pressure → weakness.

  • Multiple myocardial infarcts: the heart becomes weak as contractile cells are replaced with scar tissue.

• Either side of the heart can be affected:

  • Left-sided failure results in pulmonary congestion (Blood backs up in lungs).

  • Right-sided failure results in peripheral congestion (Blood pools in body organs, causing edema).

• The failure of either side ultimately weakens other side, which leads to a decompensated, seriously weakened heart.

• Treatment: removal of fluid, drugs to reduce afterload and increase contractility.

Heart Blood Flow Disease

• If the left ventricle pumps less blood than the right, the blood pressure backs up into the