SCIT 1408 Applied Human Anatomy and Physiology II - Heart Chapter 18 B

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Heart Physiology: Intrinsic Conduction System Autorhythmic cells:

1% of cardiac cells (SA node, AV node & bundle, right, left bundle branches, Purkinje fibers)

Have unstable resting potentials called pacemaker potentials

Initiate action potentials- whole muscle contracts Due to gap junctions & rapid ion distribution

Use calcium influx (rather than sodium) for rising phase of the action potential


Heart Physiology: Electrical Events Intrinsic cardiac conduction system

A network of noncontractile (autorhythmic) cells that initiate and distribute impulses to coordinate the depolarization and contraction of the heart


Autorhythmic cells: Action Potentials

Figure 18.13

Ca2+ influx- action potential


Contractile Cells: Action Potential

Figure 18.12


Heart Physiology: Sequence of Excitation 1 Sinoatrial (SA) node – fastest depolarization

Generates impulses about 75 times/min Neural & hormonal influences slow this from

100 to 75/min Sets pace of contraction, rhythm, heart rate

Pacemaker Sinus rhythm

Impulse from SA node thru both atria


AV node receives impulse via internodal path Inferior part of interatrial septum, above AV valve Delays impulse for 0.1 second Atria complete contraction

Impulse returns to top speed thru bundle of His Only electrical connection between atria &

ventricles is bundle of His

Heart Physiology: Sequence of Excitation 2


Bundle of His or AV bundle Only electrical connection between the atria and

ventricles




4. Right and left bundle branches Two pathways in the interventricular septum that

carry the impulses toward the apex of the heart



5. Purkinje fibers Complete the pathway into the apex and

ventricular walls AV bundle and Purkinje fibers depolarize only

30 times per minute in absence of AV node input


Cardiac Intrinsic Conduction

Figure 18.14a


Homeostatic Imbalances1. Dysrhythmias, arrhythmias – abnormal intrinsic conduction

with uncoordinated contraction Cardiogenic shock with dysrhythmia= poor prog.

2. Uncoordinated atrial & ventricular contractions3. Fibrillation- rapid, irregular contractions; no pumping4. Defective SA node may result in

Ectopic focus: abnormal pacemaker takes over If AV node takes over, there will be a junctional rhythm

(40–60 bpm)5. Defective AV node may result in

Partial or total heart block Few or no impulses from SA node reach the ventricles


Extrinsic (Autonomic) Innervation of the Heart Heart stimulated by

sympathetic NS > rate, > force

Heart inhibited by parasympathetic NS (Vagus nerve)

<rate, < force

Vagal tone- > parasympatheic control; if vagus nerve cut, heart rate = 100/min

Figure 18.15

* cardiac center


Electrocardiography Electrocardiogram (ECG or EKG): a composite

of all the action potentials generated by nodal and contractile cells at a given time

Three waves

1. P wave: depolarization of SA node

2. QRS complex: ventricular depolarization

3. T wave: ventricular repolarization


SA node generates impulse;atrial excitation begins

Impulse delayedat AV node

Impulse passes toheart apex; ventricular

excitation begins

Ventricular excitationcomplete

SA node AV node Purkinjefibers

Bundlebranches

Figure 18.17

Heart Excitation Related to ECG

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 18.17

Atrial depolarization, initiatedby the SA node, causes theP wave.

P

R

T

QS

SA node

AV node

With atrial depolarizationcomplete, the impulse isdelayed at the AV node.

Ventricular depolarizationbegins at apex, causing theQRS complex. Atrialrepolarization occurs.

P

R

T

QS

P

R

T

QS

Ventricular depolarizationis complete.

Ventricular repolarizationbegins at apex, causing theT wave.

Ventricular repolarizationis complete.

P

R

T

QS

P

R

T

QS

P

R

T

QS

Depolarization Repolarization

1

2

3

4

5

6


Electrocardiography

Figure 18.16


(a) Normal sinus rhythm.

(c) Second-degree heart block. Some P waves are not conducted through the AV node; hence more P than QRS waves are seen. In this tracing, the ratio of P waves to QRS waves is mostly 2:1.

(d) Ventricular fibrillation. These chaotic, grossly irregular ECG deflections are seen in acute heart attack and electrical shock.

(b) Junctional rhythm. The SA node is nonfunctional, P waves are absent, and heart is paced by the AV node at 40 - 60 beats/min.


Heart Sounds Two sounds (lub-dup) associated with closing of

heart valves First sound occurs as AV valves close and signifies

beginning of systole Second sound occurs when SL valves close at the

beginning of ventricular diastole

Heart murmurs: abnormal heart sounds most often indicative of valve problems


Tricuspid valve sounds typically heard in right sternal margin of 5th intercostal space

Aortic valve sounds heard in 2nd intercostal space atright sternal margin

Pulmonary valvesounds heard in 2ndintercostal space at leftsternal margin

Mitral valve soundsheard over heart apex(in 5th intercostal space)in line with middle ofclavicle


Cardiac Cycle Cardiac cycle refers to all events associated with

blood flow through the heart Systole – contraction of heart muscle Diastole – relaxation of heart muscle


Phases of the Cardiac Cycle

1. Ventricular filling – mid-to-late diastole Blood enters atria flows into ventricles SL valves closed AV valves are open Atrial systole at end- remaining 20% blood to

ventricles from atria EDV- End diastolic volume; The vol. of blood in

ventricles just before they contract = max vol they will have



2. Ventricular systole Atria relax Rising ventricular pressure results in closing of AV

valves Isovolumetric contraction phase – all valves closed Ventricular ejection phase opens semilunar valves (ESV) End systolic volume: volume of blood

remaining in each ventricle



3. Isovolumetric relaxation – early diastole Ventricles relax Backflow of blood in aorta and pulmonary trunk

closes semilunar valves Dicrotic notch – brief rise in aortic pressure caused

by backflow of blood rebounding off semilunar valves

PLAY InterActive Physiology ®: Cardiac Cycle, pages 3–18


Cardiac Cycle


Cardiac Output (CO) and Reserve CO - amt blood pumped by each ventricle/minute

CO = HR X SV

HR - heart beats/minute SV - amt blood pumped out from ventricle/beat Cardiac reserve maximal CO minus resting CO Cardiac Reserve- improves with exercise


Cardiac Output: Example CO (ml/min) = HR (75 beats/min) x SV (70

ml/beat) CO = 5250 ml/min (5.25 L/min)


Regulation of Stroke Volume SV = end diastolic volume (EDV) minus end

systolic volume (ESV); how much ventricles can hold minus what is left over after

contraction

EDV = amount of blood collected in a ventricle during diastole

ESV = amount of blood remaining in a ventricle at the end of systole (after contraction)


Factors Affecting Stroke Volume Preload – amount ventricles are stretched by blood

just before systole (contraction) Contractility – cardiac cell contractile force due to

factors other than EDV Afterload – back pressure exerted by blood in the

large arteries leaving the heart; pressure that ventricles must overcome to open SL valves


Preload and Afterload

Figure 18.21


Frank-Starling Law of the Heart Preload, or degree of stretch, of cardiac muscle

cells before they contract is the critical factor controlling stroke volume

Slow heartbeat (>time for ventricular filling) and exercise (>HR) increase venous return to the heart, increasing SV

Blood loss and extremely rapid heartbeat decrease SV


Regulation of Stroke Volume SV = EDV – ESV Three main factors affect SV

1. Preload – degree of stretch before contracting;

2. Contractility

3. Afterload


Extrinsic Factors Influencing Stroke Volume Contractility - > contractile strength, independent of stretch

and EDV Increased contractility from:

Increased sympathetic stimuli Hormones (thyroxine, glucagon, and epinephrine) Ca2+ and some drugs

Decrease contractility from: Acidosis Increased extracellular K+

Calcium channel blockers


Regulation of Heart Rate Positive chronotropic factors > HR Negative chronotropic factors < HR


GTP GDP

Inactive protein kinase A

Active protein kinase A

ATP cAMP

GTP

SR Ca2+

channel

Ca2+

Ca2+

bindsto

TroponinEnhancedactin-myosininteraction

Extracellular fluid

Cytoplasm

Adenylate cyclaseCa2+

channel

Ca2+1-Adrenergicreceptor

Norepinephrine

Ca2+

uptakepump

Sarcoplasmicreticulum (SR)

Cardiac muscleforce and velocity

1

3

2

Heart Contractilityand Norepinephrine Sympathetic

stimulation releases norepinephrine and initiates a cyclic AMP second-messenger system

Figure 18.22

Basis of Beta blockers/Calcium channel blockers


Atrial (Bainbridge) Reflex Sympathetic reflex from > blood in the atria Increased blood in atria:

Stimulates SA node Stimulates stretch receptors in atria Together, these stimulate SNS, > HR

Basis of BP control via SNS reflex control of HR


ESV- end systolic vol


Chemical Regulation of the Heart Hormones: epinephrine, thyroxine > HR

hyperthroidism

Electrolyte balance required for normal cardiac function

< or > Ca2+ < function < or > K+ life threatening

PLAY InterActive Physiology ®: Cardiac Output, pages 3–9


Other Factors that Influence Heart Rate Age Gender Exercise Body temperature


Homeostatic Imbalances Tachycardia: abnormally fast heart rate

(>100 bpm) If persistent, may lead to fibrillation

Bradycardia: heart rate slower than 60 bpm May result in grossly inadequate blood circulation May be desirable result of endurance training


Congestive Heart Failure (CHF) CO insufficient to supply body; caused by:

Coronary atherosclerosis- < blood to supply heart Persistent high blood pressure- >>hypertrophy Multiple myocardial infarcts Dilated cardiomyopathy (DCM) – over-stretched ventricles

Ca2+ mediated hypertropy; progressive Alcohol, cocaine, chemo, hyperthyroidism,

inflammation Idiopathic


Left Heart failure Right Heart failure Blood backs up into lungs Right side of heart pumps to

lungs but left cannot eject to body

Pulmonary edema Death

Blood pools in organs Edema in feet, ankles, fingers

Can be caused by lung dysfunction; Cor pulmonale

Failure of either side eventually leads to failure of both sides.


Developmental Aspects of the Heart Embryonic heart chambers

Sinus venous Atrium Ventricle Bulbus cordis


Developmental Aspects of the Heart

Figure 18.24

3 wks 1. Sinus venosus

2. Atrium

3. Ventricle

4. Bulbus cordis

4a. Truncus arteriosus

Foramen ovale- septum btwn rt & left atrium

Ductus arteriosus- between pulmonary trunk & aortaBypass pulmonary circulation


Occurs inabout 1 in every500 births

Occurs inabout 1 in every 1500 births

Narrowedaorta

Occurs inabout 1 in every 2000births

Ventricular septal defect.The superior part of the inter-ventricular septum fails to form; thus, blood mixes between the two ventricles. More blood is shunted from left to right because the left ventricle is stronger.

(a) Coarctation of the aorta. A part of the aorta is narrowed,increasing the workload of the left ventricle.

(b) Tetralogy of Fallot. Multiple defects (tetra = four): (1) Pulmonary trunk too narrow and pulmonary valve stenosed, resulting in (2) hypertrophied right ventricle; (3) ventricular septal defect; (4) aorta opens from both ventricles.

(c)


Age-Related Changes Affecting the Heart Sclerosis and thickening of valve flaps

mitral murmurs

Decline in cardiac reserve Less able to respond to sudden > demand < sympathetic regulation of heart

Fibrosis of cardiac muscle Healthy cardiac cells replaced with fibrous tissue; valves

Atherosclerosis- DIET

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SCIT 1408 Applied Human Anatomy and Physiology II - Heart Chapter 18 B