Chapter 18 The heart

Heart function 

Heart function 

• This system brings oxygen and nutrients to the many cells in the body and carries wastes away to be disposed of 

• The cardiovascular system provides the machinery that keeps blood continuously circulating 

• The heart is the Transport system pump that keeps blood circulating, while the blood vessels are the delivery routes 

Pulmonary circuit

• The right side of the heart pumps blood to the lungs to pick up oxygen and dispel carbon dioxide.

• Blood returns to the heart 

Systemic circuit 

• The left side of the heart receives blood from the lungs and pumps it throughout the body.

• Blood returns to the heart 

The heart is enclosed in a double-walled sac called the…

• Pericardium

  • Peri = around 

  • Cardi = heart 

Pericardium: Fibrous layer 

• The outer layer of the pericardium, made of tough dense connective tissue

• Protects the heart, anchors it to surrounding structures, prevents overfilling of the heart with blood

Pericardium: Serous pericardium 

• Thin two-layer serous membrane

  1. Parietal pericardium

  2. Visceral pericardium (epicardium)

• Between the two layers is the pericardial cavity which functions to reduce friction

Layers of the heart wall

• Epicardium 

• Myocardium

• Endocardium 

Epicardium 

• The visceral pericardium 

• Is most superficial 

Endocardium

• Inner layer, which is a glistening white sheet of endothelium (squamous epithelium)

• Lines the heart chambers and covers fibrous skeleton valves 

Myocardium 

• The cardiac muscles that make up the heart

• Forms the bulk of the heart 

• This is what contracts when the heart beats 

• Cardiac muscle bundles have a circular and spiral arrangement that links all parts of the heart together 

• Also contains connective tissue fibers 

  • They form a cardiac skeleton of sorts 

  • One important role of connective tissue is it limits the speed of action potentials to specific pathways  

Chambers and vessels of the heart 

• Two atria and two ventricles 

• The right ventricle forms most of the anterior surface of the heart

• The left ventricle forms anteroposterior aspects and forms the heart's apex

The structure that separates right and left sides of the heart 

• Interatrial septum

• Interventricular septum 

The surface of the heart 

• Right atrium 

• Right ventricle 

• Left atrium 

• Left ventricle 

• Apex 

Atria - the receiving chambers 

• Have small appendages called auricles (these increase atrial volume)

• Blood enters the right atrium via 3 veins 

  1. Superior vena cava

  2. Iinferior vena cava

  3. Coronary sinus 

• Blood enters the left atrium via pulmonary veins (there are four of them)

Pulmonary veins 

• 4 veins that bring blood from the lungs back to the heart

• Called right and left pulmonary veins 

• These are the only veins in the body that carry oxygenated blood 

Ventricles - the pumping chambers 

• Make up most of the volume of the heart 

• Internal structure is not smooth. Contains ridges of muscles called trabeculae carneae

• Also contains papillary muscles which play a role in valve function 

• Right ventricle pumps into pulmonary trunk (lungs)

• Left ventricle pumps into aorta 

Right vs. left ventricle 

• They pump equal volumes of blood

• Walls of the left ventricle are 3 times thicker than the right ventricle and its cavity is circular

• The right ventricle cavity is flattened and partially encloses the left ventricle 

Right ventricle 

• Part of pulmonary circuit, which is very short and therefore has low blood pressure

Left ventricle 

• Part of the systemic circuit, which is a very long pathway with considerably more resistance to blood flow 

Blood flow through the heart 

• Blood flows in one direction

  • From atria to ventricles and out the great arteries 

• One-way traffic is ensured by 4 valves that open and close in response to differences in blood pressure on their 2 sides 

  1. Atriovascular valves (2)

  2. Semilunar valves (2)

Atrioventricular (AV) valves

• Tricuspid valve (right AV valve)

• Mitral valve (left AV valve, bicuspid valve)

• Chordae tendineae 

Tricuspid valve (right AV valve)

• Made up of three cusps and lies between right atria and ventricle 

Mitral valve (left AV valve, bicuspid valve)

• Made up of two cusps and lies between left atria and ventricle 

Chordae tendineae 

• Anchor cusps of AV valves to papillary muscles that function to:

  • Hold valve flaps in closed position 

  • Prevent flaps from everting back into atria 

AV valves: Pressure opens them

• Blood returning to the heart fills atria, pressing against the AV valves. The increased pressure forces AV valves to open 

• As ventricles fill, AV valve flaps hang limply into ventricles 

• Atria contract, forcing additional blood into ventricles 

• Atrial pressure greater than ventricular pressure 

AV valves: Pressure closes them

• Ventricles contract forcing blood against AV valve cusps

• AV valves close 

• Papillary muscles contract and chordae tendineae tighten, preventing valve flaps from everting into atria 

• Atrial pressure less than ventricular pressure 

Semilunar valves

• Between ventricles and great vessels 

• Called aortic (between left ventricle and aorta) and pulmonary (between right ventricles and pulmonary trunk) 

Semilunar valves: pressure opens them

• As ventricles contract and intraventricular pressure rises, blood is pushed up against semilunar valves, forcing them to open 

Semilunar valves: Pressure closes them

• As ventricles relax and intraventricular pressure falls, blood flows back from arteries, filling the cusps of semilunar valves and forcing them to close 

Entrances to the atria

• There are no valves in these locations - there is some backflow of blood into these vessels but this is minimized by:

  • Inertia of the blood

  • When the atria contract it compresses these venous entry points, collapsing then somewhat to minimize backflow of blood 

The cardiac cycle 

• Consist of the events that occur during one heartbeat

  1. Ventricular filling

  2. Isovolumetric contraction phase

  3. Ventricular ejection phase

  4. Isovolumetric relaxation phase

Systole

• Contraction of either atria or ventricles is occurring 

Diastole

• Relaxation is occurring

Ventricular filling mid-to-late diastole

• Pressure in the heart must be low in order for blood to flow into the ventricles 

• Around 80% of the blood enters the ventricles during this period of relaxation.

• It is 100% passive - the AV valves are open and blood flow from the atria to the ventricles 

• The atria then contract (atrial systole), pumping the remaining 20% of the blood into the ventricles

• When this is done ventricles have maximum volume of blood (end-diastolic volume)

• Atria relax and ventricle depolarize in preparation for ventricular contraction 

Isovolumetric contraction Ventricular ejection 

• Iso = equal

• A phase when the volume of the ventricles is not changing but they are contracting 

  • The ventricles are contracting but all the valves (AV valves and SL valves) are closed

Ventricular ejection

• Once the SL valves open, blood rushes from ventricles into the aorta and the pulmonary trunk

• The pressure in the aorta normally reaches 120mmHg

Isovolumetric relaxation: early diastole 

• The ventricles relax

• Blood left in the ventricles is referred to as end-systolic volume (ESV)

• This blood is no longer under pressure, so the blood in the aorta and pulmonary trunk flows back into the ventricles, closing the SL valves

• Because the AV and SL valves are closed, the ventricles are a closed chamber, thus isovolumetric relaxation 

• When ventricles were in systole the atria were in diastole (relaxed) and began filling with blood. When the pressure on the atrial side exceeds the pressure on the ventricular side the AV valves open and the cycle starts again 

Cardiac cycle summary 

• Cardiac cycle lasts for ~ 0.8 seconds (0.1s of atrial contraction and 03.s of ventricular contraction)

• Remaining 0.4 is a period of total heart relaxation (the quiescent period)

• Blood flow through the heart is controlled entirely by pressure changes 

• Blood flows down a pressure gradient through any available openings

• The pressure is created by the contraction of cardiac muscle 

• The right and left sides of the heart are both pumps, however, differ in the pressure they generate 

  • The right side is much less

    • Systolic = 24mmHg

    • Diastolic = 10mmHg

  • Left side 

    • Systolic = 120mmHg

    • Diastolic = 80 mmHg

Cardiac muscle 

• Is striated

• Adjacent cells are connected via intercalated discs 

  • Prevent them from separating during contraction

  • allow ions to pass through (so action potentials can travel between cells)

Cardiac vs. skeletal muscle cell contraction

1. Some cardiac cells are self excitable 

2. The heart contracts as a unit 

3. The influx of calcium from extracellular fluid triggers calcium release from the SR

4. Tetanic contraction cannot occur in cardiac muscle 

5. The heart relies almost exclusively on aerobic respiration 

Some cardiac cells are self-excitable

• Most cardiac muscle cells are contractile cardiac muscle cells

• A small number are non-contractile cardiac muscle cells called pacemaker cells. These cells can spontaneously depolarize (automaticity or autorhythmicity). Because all heart cells are connected, these pacemaker cells can stimulate all other cells to contract with no neural input 

The heart contracts as a unit

• Either all cells in the heart contract or none of them contract 

• This ensures effective pumping of the heart 

The influx of calcium from extracellular fluid triggers calcium release from the SR

• Calcium is extremely important for heart function 

The heart relies almost exclusively on aerobic respiration 

• It must have oxygen in order to create ATP

• Therefore, the cardiac muscles must have oxygen in order to have the ATP required for contraction 

Skeletal muscle: structure

• Striated, long, cylindrical, multinucleated

Skeletal muscle: Pacemaker cells present

• No

Skeletal muscle: Tetanus possible

• Yes

Skeletal muscle: Supply of ATP

• Aerobic and anaerobic (fewer mitochondria)

Cardiac muscle: structure

• Striated, short, branched, one of 2 nuclei per cell

Cardiac muscle: Pacemaker cells present

• Yes

Cardiac muscle: Supply of ATP

• Aerobic only (more mitochondria)

Cardiac muscle: Tetanus possible

• No

Heart muscle blood supply 

• In order to contract continuously the heart muscle needs oxygen and nutrients and needs to get rid of waste.

• The blood that is pumped by the heart provides little nourishment to the heart tissue

• The heart's blood supply comes from the Coronary circulation (the shortest circulation in the body) 

Coronary arteries 

• Left and right coronary arteries arise from base on the aorta 

  • Encircle heart in coronary sulcus

  • Provide oxygenated blood and nutrients to heart tissue

• Right coronary supplies right atrium and most of right ventricle 

• Left coronary artery supplies left atrium, most of the left ventricles and the interventricular septum 

Blockage of coronary arteries leads to…

• tissue death and myocardial infarction (heart attack)

Coronary veins 

• De-oxygenated is collected by the coronary veins whose path roughly follows the coronary arteries.

• These veins join to form a larger vein called the coronary sinus which empties into the right atrium

Heart rhythm 

• Heartbeat is controlled/influenced in 2 ways:

  1. Intrinsic control system 

  2. Autonomic nervous system 

Intrinsic control system 

• Pacemaker cells 

Autonomic nervous system 

• Can alter the basic rhythm that is established by the intrinsic control system 

Intrinsic conduction system 

• Cardiac pacemaker cells spontaneously (with no nervous system stimulation) generate action potentials

  1. Pacemaker potentials 

  2. Depolarization 

  3. Repolarization

Intrinsic conduction system: Pacemaker potentials 

• This slow depolarization is due to both opening of Na+ channels and closing of K+ channels. Notice that the membrane potential is never a flat line.

Intrinsic conduction system: Depolarization 

• This action potential begins when the pacemaker potential reaches a threshold. Depolarization is due to Ca+ influx through Ca+ channels 

• Note

  • Calcium not sodium 

Intrinsic conduction system: Repolarization

• Repolarzation is due to Ca+ channels inactivating and K+ channels opening. This allows K+ efflux, which brings the membrane potential back to its most negative voltage 

• Once A/P occurs the ‘heart beats’

What do Action potentials look like in cardiac muscle cells

1. Depolarization 

2. Plateau phase

3. Repolarization 

What do Action potentials look like in cardiac muscle cells: Depolarization 

• Depolarization is due to Na+ influx through fast voltage-gated channels. A positive feedback cycle rapidly opens many Na+, reversing the membrane potential. Channel inactivation ends this phase 

What do Action potentials look like in cardiac muscle cells: Plateau phase

• Plateau phase is due to Ca+ influx through slow Ca+ channels. This keeps the cell depolarized because most K+ channels are closed 

• Ca+ is key 

What do Action potentials look like in cardiac muscle cells: Repolarization 

• Repolarization is due to Ca+ channels innactivating and K= channels opening. This allows K+ efflux, which brings the membrane potential back to its resting voltage.

Long plateau 

• Ensure contraction long enough to make sure blood ejected effectively from heart 

• Ensure long enough refractory period so tetanus cannot occur 

Once A/P is triggered 

• Pacemaker cells are found:

  • Sinoatrial (SA) node 

  • Atrioventricular (AV) nodules

• SA node typically generates A/Ps around 75 times per minute

• Rhythm that is established by SA node is called sinus rhythm 

• Total time from depolarization at SA node to all muscle fibers being stimulated is 0.22s 

Homeostatic imbalance 

• Defects in intrinsic conduction system may cause:

  • Arrhythmias

  • Uncoordinated atrial and ventricular contractions 

  • Fibrillation 

  • Bradycardia 

  • Tachycardia 

Arrhythmias

• Irregular heart rhythms 

Tachycardia 

• Higher than normal heart rate 

Bradycardia 

• Slower than normal heart rate

Fibrillation 

• Rapid, irregular contractions 

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

• Treatment:

  • Defibrillation interrupts chaotic twitching, giving heart “clean slate” to start regular, normal depolarizations 

Electrocardiography

• We can record the electrical activity that is generated and transmitted through the heart using a device called an electrocardiograph 

• This device records a record that it the net effect of all the action potentials generated by pacemaker and contractile cells at any given time 

Auscultating the heart

• Lub-dub

• These sounds are associated with the heart valves closing 

• First sound 

  • Is the AV valves closing 

• Second sound 

  • Occurs as SL valves snap shut 

• First sounds tend to be louder and longer than the second

What you can hear where: Aortic valve 

• Sounds heard in 2nd intercostal space at right sternal margin 

What you can hear where: Pulmonary valve 

• Sounds heard in 2nd intercostal at left sternal margin 

What you can hear where: Mitral valve 

• Sounds heard over heart apex (in 5th intercostal space) in line with middle of clavicle 

What you can hear where: Tricuspid valve 

• Sounds heard in right sternal margin of 5th intercostal space

Regulation of heart rate (HR): Heart can be regulated by

• Autonomic nervous system 

• Chemicals 

• Other factors 

Autonomic nervous system regulation of heart rate: Sympathetic nervous system activity 

• Norepinephrine is released causing pacemaker to fire more rapidly increasing heart rate 

Autonomic nervous system regulation of heart rate: Parasympathetic activity 

• Acetylcholine is released. This opposes sympathetic activity, reducing heart rate when stressful events end 

Impact of other sensory input on HR

• Baroreceptors

  • Sensory receptors that respond to changes in blood pressure

• Atrial (Bainbridge) reflex 

  • Sympathetic reflex initiated by increased venous return, hence increased atrial filling 

    • Atrial walls are stretched with increased volume 

    • Stimulates SA node, which increases HR

    • Also stimulates atrial stretch receptors that activate sympathetic reflexes 

Vagal tone

• At rest both sympathetic and parasympathetic divisions send impulses to SA node - dominant influence is inhibitory 

• Inhibitory signals - parasympathetic division - fibers run in vagus nerve thus this is referred to as vagal tone 

Chemical regulation of HR

1. Hormones 

   • Epinephrine 

   • Thyroxin 

2. Ions 

   • Calcium levels 

   • Potassium levels 

Chemical regulation of HR: Epinephrine 

• Enhances HR and contractility 

Chemical regulation of HR: Thyroxin 

• When released in large quantities it causes a sustained increase in HR. 

• Acts directly on heart and enhances effects of epinephrine and norepinephrine 

Chemical regulation of HR: Calcium levels 

• Are extremely important for heart function

Chemical regulation of HR: Potassium levels 

• High or low potassium is particularly dangerous and are associated with several clinical conditions 

Other factors that regulate HR

• Age, gender and body temp also include HR (less important than neural factors)

• HR is fastest in fetus (140 - 160 bpm), and decreases through lifespan 

• HR is generally faster in females (72-80 bpm), than males (64-72 bpm)

• Exercise increases HR

• The more conditioned you are the lower your resting HR (heart becomes a better pump, so SV increases and lower HR needed)

• Heat increases HR because heat increases the metabolic rate of cardiac cells 

Stroke Volume 

• The volume of blood pumped by 1 ventricle with each beat 

• = end-diastolic volume - (minus) end-systolic volume 

End diastolic volume’ (EDV)

• The amount of blood that will be pumped out of a ventricle is more or less equal to the amount of blood that flows into the ventricle when it is relaxed 

End systolic volume’ (ESV)

• Once the ventricle contracts it will pump most of its blood to great vessels, however, the ventricle will never be completely empty and blood remains

Preload and stroke volume 

• In a healthy heart, the higher the preload the higher the stroke volume. (Frank-Starling law of the heart)

• Stretching cardiac muscles places the muscle cells near their optimal length for force production - this results in greater contractile force 

• The most important factor for stretching cardiac muscle is venous return 

Factors that influence venous return: Exercise 

• Exercise (by increased sympathetic activity, increased skeletal muscles and respiratory pumps)

• Increased venous return 

• Increased EDV (preload)

• Increased stroke volume (SV)

Factors that influence venous return: Increased ventricular filling time

• Increased ventricular filling time (due to decreased heart rate)

• Increased venous return 

• Increased EDV (preload)

• Increased stroke volume (SV)

Three main factors that impact SV, by alternating either EDV or ESV 

1. Preload 

2. Contralility 

3. Afterload 

Contractility and stroke volume

• Contractility is defined as the contractile strength achieved at a given muscle length

  • It is independent of muscle stretch and EDV

• Enhanced contractility means more blood is ejected from the heart so ESV is lower and SV will be higher 

• Contractility is enhanced when more calcium enters the cytoplasm.

  • Increase in calcium is triggered by

    • hormones (epinephrine, glucagon, thyroxin), drugs - (digitalis) and high extracellular levels of calcium 

      • Bloodborne epinephrine, thyroxine, excess Ca+

      • Increased Contractility

      • Decreased  ESV

      • Increased stroke volume

Afterload and stroke volume 

• Afterload is the pressure that the ventricles must overcome to eject blood 

• It is determined by the pressure in the arteries (normally 80 mm Hg in aorta and 10 mm Hg in pulmonary trunk)

• Afterload is not a determining factor of SV in healthy individuals. It becomes a factor when blood pressure is elevated 

• In people with hypertension, it is harder for the ventricles to eject blood, so ESV increases , resulting in a decrease in SV