Chapter 9 Cardiac Physiology. Outline Comparison of types of muscle tissue Circulatory system overview Anatomy Electrical activity Mechanical events Cardiac

Chapter 9Cardiac Physiology

Outline

• Comparison of types of muscle tissue

• Circulatory system overview

• Anatomy

• Electrical activity

• Mechanical events

• Cardiac output

• Coronary circulation

• The next series of slides compares cardiac, skeletal, smooth muscle cells.

Contraction

Uncovering of cross-bridge binding sites on actin in thin filament

Phosphorylation ofmyosin cross bridgesin thick filament

Series of biochemical events

Physical repositioning of troponin and tropomyosin

Rise in cytosolic Ca2+

(mostly from extracellular fluid)

Rise in cytosolic Ca2+

(entirely from intracellularsarcoplasmic reticulum)

Muscle excitation Muscle excitation

Skeletal muscleSmooth muscle

Contraction

Binding of actin and myosin at cross bridges

Binding of actin and myosin at cross bridges

P i

Fig. 8-31, p. 296

Comparison of the Role of Calcium In Bringing About

Contraction in Smooth, Skeletal, and Cardiac Muscle

Cardiac muscle

Skeletal smooth cardiac

Cardiac Muscle Fibers

• Interconnected by intercalated discs and form functional syncytia• Within intercalated discs – two kinds of membrane junctions

– Desmosomes– Gap junctions

• Ap’s

fig 16-8b, pg 487

Myofibril

Opening of Transversetubule

Intercalateddisc

Transversetubule

Longitudinalsystem

SacrolemmaBasal laminaMyofibrils

Mitochondria

Nucleus

Skeletal Muscle Fiber

fig 16-9a, pg 479

Nucleus

RoughEndoplasmicreticulum

Glycogengranules

Mitochondria

Thin filament

Thick filament

Densebodies

Plasmamembrane

Smooth Muscle Fiber

Outline

• Comparison of types of muscle tissue

• Circulatory system overview

• Anatomy

• Electrical activity


• Cardiac output

• Coronary circulation

Human heart.

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AnatomyHeartHollow, muscular organ about the size of a clenched fistPositioned between two bony structures – sternum and vertebrate

Circulatory System• Three basic components

– Heart• Serves as pump that

establishes the pressure gradient needed for blood to flow to tissues

– Blood vessels• Passageways through which

blood is distributed from heart to all parts of body and back to heart

– Blood • Transport medium within which

materials being transported are dissolved or suspended

• Pulmonary circulation– Closed loop of vessels carrying

blood between heart and lungs• Systemic circulation

– Circuit of vessels carrying blood between heart and other body systems

Circulatory System

• Heart

• Arteries

• Carry blood away from ventricles to tissues

• Veins

• Vessels that return blood from tissues to the atria

• Septum – Continuous muscular partition that prevents mixture of blood from the

two sides of heart• Dual pump

– Right and left sides of heart function as two separate pumps– Divided into right and left halves and has four chambers

• Atria– Upper chambers– Receive blood returning to heart and transfer it to lower

chamber

• Ventricles – Lower chambers which pump blood from heart

Outline

• Internal Anatomy

– Thoracic cavity, base, apex

– AV and semilunar valves

– endothelium, myocardium, epicardium

– cardiac cells, intercalated disks

– Comparison of cardiac cells to skeletal and smooth muscle cells

– pericardium

Heart Valves• Atrioventricular (AV) valves

– Prevent backflow of blood from ventricles into atria during ventricular emptying

– Right AV valve = tricuspid valve– Left AV valve = bicuspid valve or mitral valve– Chordae tendinae

• Fibrous cords which prevent valves from being everted

• Papillary muscles

• Semilunar valves– Aortic and pulmonary valves– Lie at juncture where major arteries leave – ventricles– Prevented from everting by anatomic structure – and positioning of cusps

• No valves between atria and veins– Reasons

• Atrial pressures usually are not much higher than

• venous pressures• Sites where venae cavae enter atria are • partially compressed during atrial

contraction

Endocardium

Myocardium

Epicardium

• 3 layers

• Consists of three distinct layers

– Endothelium• Thin inner tissue• Epithelial tissue which lines entire

circulatory system

– Myocardium• Middle layer• Composed of cardiac muscle• Constitutes bulk of heart wall

– Epicardium • Thin external layer which covers the heart

• Pericardium– the fluid filled sac that surrounds the heart

Outline

• Electrical activity of the heart

– Autorhymicity

– Pacemaker (function, ions)

– Conductive system (SA, AV, bundle of His, Purkinje fibers)

– Abnormal rhythms

– Spread of cardiac excitation

– Cardiac cell action potentials• Characteristics vary by location

Electrical Activity of Heart

• Heart beats rhythmically as result of action potentials it generates by itself (autorhythmicity)

• Two specialized types of cardiac muscle cells– Contractile cells

• 99% of cardiac muscle cells, do mechanical work of pumping,normally do not initiate own action potentials

– Autorhythmic cells • Do not contract but send electrical signals to the contractile cells,

specialized for initiating and conducting action potentials responsible for contraction of working cells


• Locations of noncontractile cells capable of autorhymicity– Sinoatrial node (SA node)

• Specialized region in right atrial wall near opening of superior vena cava

• Pacemaker of the heart– Atrioventricular node (AV node)

• Small bundle of specialized cardiac cells located at base of right atrium near septum

– Bundle of His (atrioventricular bundle)• Cells originate at AV node and enters interventricular septum• Divides to form right and left bundle branches which travel

down septum, curve around tip of ventricular chambers, travel back toward atria along outer walls

– Purkinje fibers• Small, terminal fibers that extend from bundle of His and

spread throughout ventricular myocardium

(a) Specialized conduction system of the heart

Atrioventricular(AV) node

Right atrium Left atrium

Interatrialpathway

Left ventricle

Right branchof bundleof His

Internodalpathway

Sinoatrial(SA) node

Right ventricle

Purkinjefibers

Left branchof bundleof His

Fig. 9-8a, p. 312


• Cardiac impulse originates at SA node

• Action potential spreads throughout right and left atria

• Impulse passes from atria into ventricles through AV node (only point of electrical contact between chambers)

• Action potential briefly delayed at AV node (ensures atrial contraction precedes ventricular contraction to allow complete ventricular filling)

• Impulse travels rapidly down interventricular septum by means of bundle of His

• Impulse rapidly disperses throughout myocardium by means of Purkinje fibers

• Rest of ventricular cells activated by cell-to-cell spread of impulse through gap junctions

Pacemaker potentialand

Action potential in autorhythmic cells

• Pacemaker activity - slow depolarization or drift towards threshold

• Increased inward Na movement

• Decreased outward K movement

• Inward Ca movement

Fig. 9-7, p. 311

Physiology of pacemaker cells

End of repol opens funny channels

Na channels that open upon hyperpolarization

Conduction between atria and ventricles

• AV nodal delay 100 msec allows ventricular filling

• Purkinje cell transmission in 30 msec

• Some spreading thru gap junctions

Action potential of cardiac contractile cell

• Different than nodal pacemaker cell (conductive cell)

• Rp = -90mv

• K channel subtypes– Leak channel keeps -90 mv– Peak potential efflux channels (brief repol)

(fast transient); Cessation of efflux plus Ca influx creates plateau

– Ordinary k channels repolarize


• Atria contract as single unit followed after brief delay by a synchronized ventricular contraction

• Action potentials of cardiac contractile cells exhibit prolonged positive phase (plateau) accompanied by prolonged period of contraction– Ensures adequate ejection time– Plateau primarily due to activation of slow L-type

Ca2+ channels


• Ca2+ entry through L-type channels in T tubules triggers larger release of Ca2+ from sarcoplasmic reticulum– Ca2+ induced Ca2+ release leads to cross-bridge cycling and

contraction

• Because long refractory period occurs in conjunction with prolonged plateau phase, summation and tetanus of cardiac muscle is impossible– Ensures alternate periods of contraction and relaxation which

are essential for pumping blood– Refractory= unresponsive to stimulus

Relationship of an Action Potential and the Refractory Period to the Duration of the Contractile Response in Cardiac Muscle

Physiology of contractile cell

(b) Spread of cardiac excitation

Bundleof His

Interatrialpathway

SA node

Right atrium

Right ventricle

Electricallynonconductivefibrous tissue

Interatrialpathway

Left atrium

Left ventricle

AV node

Purkinjefibers

Fig. 9-8b, p. 312

fig. 18-13; pg: 568

Milliseconds

SA nodepacemaker

Atrial muscle

Atrioventricular

Bundle branch

Purkinje fibers

Ventricularmuscle

Coordination of noncontractile and contractile cells

Electrocardiogram (ECG)

• Record of overall spread of electrical activity through heart

• Represents

– Recording part of electrical activity induced in body fluids by cardiac impulse that reaches body surface

• Not direct recording of actual electrical activity of heart

– Recording of overall spread of activity throughout heart during depolarization and repolarization

• Not a recording of a single action potential in a single cell at a single point in time

– Comparisons in voltage detected by electrodes at two different points on body surface, not the actual potential

• Does not record potential at all when ventricular muscle is either completely depolarized or completely repolarized

ST segment =Time during whichventricles are contractingand emptying

T wave =Ventricularrepolarization

TP interval =Time during whichventricles arerelaxing and filling

Re

co

rde

d p

ote

nti

al

P

PR segment =AV nodal delay

QRS complex =Ventricular depolarizationatria repolarizingsimultaneously)

P wave =Atrial depolarization

SA nodefires

TPinterval

STsegment

PRsegment

Q

P

S

200 msec

R

T

Fig. 9-14, p. 320

Normal ECG.

Credit: © Mediscan/Visuals Unlimited 3202

Abnormalities in Rhythm and rate

• Rhythm– Regularity or spacing of ECG waves

• Arrhythmia – Variation from normal rhythm and

sequence of excitation of the heart

• Atrial flutter (200-300 BPM)

• Atrial fibrillation

• Ventricular fibrillation

• Heart block

• Tachycardia >100 beats per minute

• Bradycardia < 60 beats per minute

• Damage of the heart muscle– Myocardial ischemia

• Inadequate delivery of oxygenated blood to heart tissue– Necrosis

• Death of heart muscle cells– Acute myocardial infarction (heart attack)

• Occurs when blood vessel supplying area of heart becomes blocked or ruptured

Outline


– Systole, diastole

– animation (volumes, pressures, sounds and EKG)

Specialized Conduction System of Heart

Cardiac Output

• Volume of blood ejected by each ventricle each minute

• Determined by

heart rate times

stroke volume

• Heart rate is varied by altering balance of parasympathetic and sympathetic influence on SA node:

– Parasympathetic stimulation slows heart rate

– Sympathetic stimulation speeds it up

Fig. 9-20a, p. 329

Cardiac Output

• Stroke volume

– Determined by extent of venous return and by sympathetic activity

– Influenced by two types of controls• Intrinsic control

• Extrinsic control

– Both factors increase stroke volume by increasing strength of heart contraction

Frank-Starling Law of the Heart

• States that heart normally pumps out during systole the volume of blood returned to it during diastole

(c) Stroke volume withcombination ofsympathetic stimulationand increased end-diastolic volume

End-systolic volume65 ml

Stroke volume140 ml

End-diastolic volume135 ml

(a) Normal strokevolume

(b) Stroke volumeduring sympatheticstimulation





Stroke volume70 ml

Stroke volume100 ml

Fig. 9-23, p. 331

Coronary circulationNourishing the Heart Muscle

• Muscle is supplied with oxygen and nutrients by blood delivered to it by coronary circulation, not from blood within heart chambers

• Heart receives most of its own blood supply that occurs during diastole

– During systole, coronary vessels are compressed by contracting heart muscle

• Coronary blood flow normally varies to keep pace with cardiac oxygen needs

Coronary Artery Disease (CAD)

• Pathological changes within coronary artery walls that diminish blood flow through the vessels

• Leading cause of death in United States

• Can cause myocardial ischemia and possibly lead to acute myocardial infarction

– Three mechanisms• Profound vascular spasm of coronary arteries

• Formation of atherosclerotic plaques

• Thromboembolism

Collagen-richsmooth musclecap of plaque

Normal bloodvessel wall

Lipid-rich coreof plaque

Endothelium

Plaque

Fig. 9-29, p. 328

Fig. 9-30, p. 330

Left coronaryartery

B

ARight coronaryartery

Area of cardiac muscledeprived of blood supplyif coronary vessel isblocked at point A:

Area of cardiac muscledeprived of blood supplyif coronary vessel isblocked at point B:

Left ventricle

Right ventricle

Fig. 9-31, p. 339

Table 9-4 p339

Documents

Chapter 9 Cardiac Physiology. Outline Comparison of types of muscle tissue Circulatory system overview Anatomy Electrical activity Mechanical events Cardiac