Anatomy & PhysiologyBio 2402 Lecture

Dr shabeel pn

Review:

Cardiac Cycle Beginning of control system

Review of Cardiac Blood Flow

Be able to trace flow, from start to finish

Sequence of blood flow

Right atrium tricuspid valve right ventricle

Right ventricle pulmonary semilunar valve pulmonary arteries lungs

Lungs pulmonary veins left atrium Left atrium bicuspid valve left ventricle Left ventricle aortic semilunar valve

aorta Aorta systemic circulation

Two systems:

Pulmonary Systemic

Review of Cardiac Blood Flow

Function of chordae tendineae and papillary muscles?

What opens and closes the valves?

New section for today

Control system- Autorhythmic Fibers

See figure 18.14 on page 694 These fibers have an unstable resting

potential due to Na+ & Ca++ leakage in.

Control system- Autorhythmic Fibers

See figure 18.14 on page 694 These fibers have an unstable resting

potential due to Na+ & Ca++ leakage in.

Control system- role of instability of RMP

Sinoatrial node (SA) – Inherent rate of 100 BPM “Sinus Rhythm” – Heart’s pacemaker Location: Upper RA Fastest cells in system

Atrial (Bainbridge) Reflex

Atrial (Bainbridge) reflex – a sympathetic reflex initiated by increased blood in the atria Causes stimulation of the SA node Stimulates baroreceptors in the atria, causing

increased SNS (Sympathetic Nervous System) stimulation

Control system-

Atrioventricular Node (AV) –

Control system-

Atrioventricular Node (AV) – Impulse is delayed here 0.1 second (Why?)

Control system-

Atrioventricular bundle – (Bundle of His)

Control system-

Atrioventricular bundle – (Bundle of His) The only electrical connection between atria

and ventricles Rapidly conducts through Right Bundle

branch, (RBB), Left Bundle Branch (LBB) and Purkinje fibers

Control system-

Right Bundle branch, (RBB), - stimulates septal cells

Left Bundle Branch (LBB) – septal cells Purkinje fibers- most important, stimulates

most of the ventricular walls, and first stimulates the papillary muscles (why?)

Control system-

Time required: 220 ms from SA node to complete depolarization.

Longer time indicates conduction defect

Intrinsic Conduction System

Autorhythmic cells: Initiate action potentials Have unstable resting potentials called

pacemaker potentials Use calcium influx (rather than sodium) for rising

phase of the action potential

Pacemaker and Action Potentials of the Heart

Sequence of Excitation

Sinoatrial (SA) node generates impulses about 75 times/minute

Atrioventricular (AV) node delays the impulse approximately 0.1 second

Impulse passes from atria to ventricles via the atrioventricular bundle (bundle of His)

Sequence of Excitation

AV bundle splits into two pathways in the interventricular septum (bundle branches) Bundle branches carry the impulse toward the

apex of the heart Purkinje fibers carry the impulse to the heart apex

and ventricular walls

Cardiac Intrinsic Conduction

Heart Excitation Related to ECG

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

SA node generates impulse;atrial excitation begins

SA node

Heart Excitation Related to ECG

Impulse delayedat AV node

AV node

Heart Excitation Related to ECG

Impulse passes toheart apex; ventricularexcitation begins

Bundlebranches

Heart Excitation Related to ECG

Ventricular excitationcomplete

Purkinjefibers

Extrinsic Innervation

Heart is stimulated by the sympathetic cardioacceleratory center

Heart is inhibited by the parasympathetic cardioinhibitory center

ECG – What it means

Electrical activity is recorded by electrocardiogram (ECG)

P wave corresponds to depolarization of SA node QRS complex corresponds to ventricular

depolarization T wave corresponds to ventricular repolarization Atrial repolarization record is masked by the larger

QRS complex SEE IP 9 Intrinsic Conduction System pages 3-6

ECG

Heart Sounds - valves

Heart sounds (lub-dup) are associated with closing of heart valves First sound occurs as AV (Tricuspid and Mitral)

valves close and signifies beginning of systole Second sound occurs when SL (Pulmonary &

Aortic) valves close at the beginning of ventricular diastole

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 Cardiac Cycle

Ventricular filling – mid-to-late diastole Heart blood pressure is low as blood enters atria

and flows into ventricles AV valves are open, then atrial systole occurs

Phases of Cardiac Cycle

Ventricular systole Atria relax Rising ventricular pressure results in closing of

AV valves Isovolumetric contraction phase Ventricular ejection phase opens semilunar

valves

Phases of Cardiac Cycle

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

SEE IP9 Cardiac Cycle pages 3-19

Cardiac Output (CO) and Reserve

CO is the amount of blood pumped by each ventricle in one minute

CO is the product of heart rate (HR) and stroke volume (SV)

HR is the number of heart beats per minute SV is the amount of blood pumped out by a

ventricle with each beat Cardiac reserve is the difference between

resting and maximal CO

Cardiac Output (CO) - Example

CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)

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

Stroke Volume

SV = end diastolic volume (EDV) minus end systolic volume (ESV)

EDV = amount of blood collected in a ventricle during diastole

ESV = amount of blood remaining in a ventricle after contraction

What affects Stroke Volume?

Preload – amount ventricles are stretched by contained blood

Contractility – cardiac cell contractile force due to factors other than EDV

Afterload – back pressure exerted by blood in the large arteries leaving the heart

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 and exercise increase venous return to the heart, increasing SV

Blood loss and extremely rapid heartbeat decrease SV

Preload and Afterload

Chemical Regulation of Heart

The hormones epinephrine and thyroxine increase heart rate

Intra- and extracellular ion concentrations (Ca++, K+, Na+) must be maintained for normal heart function

SEE IP9 – Cardiac Output pages 3-9

Regulation of Heart Rate: Autonomic Nervous System

Sympathetic nervous system (SNS) stimulation is activated by stress, anxiety, excitement, or exercise

Parasympathetic nervous system (PNS) stimulation is mediated by acetylcholine and opposes the SNS

PNS dominates the autonomic stimulation, slowing heart rate and causing vagal tone

Heart Contractilityand Norepinephrine

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

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 cyclase

Ca2+

channel

Ca2+1-Adrenergicreceptor

Norepinephrine

Ca2+

uptakepump

Sarcoplasmicreticulum (SR)

Cardiac muscleforce and velocity

1

3

2

Figure 18.22

Extrinsic Factors Influencing Stroke Volume

Agents/factors that decrease contractility include: Acidosis Increased extracellular K+

Calcium channel blockers

Extrinsic Factors Influencing Stroke Volume

Contractility is the increase in contractile strength, independent of stretch and EDV (End Diastolic Volume)

Increase in contractility comes from: Increased sympathetic stimuli Certain hormones Ca2+ and some drugs

Cardiac Output

The big picture All factors: Key: Be able

to identify whether a factor influences SV or HR, and which direction

Control system- Clinical Applications

Arrhythmias Uncoordinated atrial and ventricular contractions

Control system- Clinical Applications

Ectopic Foci – Depolarization (beat) originates someplace other than SA node. May be triggered by high caffeine or nicotine Most common cause is low oxygen to a region of

the heart Premature Ventricular contractions (PVC’s) most

serious.

Control system- Clinical Applications

Ventricular Tachycardia – rapid rate stimulated by ventricular ectopic foci.

Control system- Clinical Applications

Ventricular Fibrillation – This is the quivering of muscle – uncoordinated No pumping is occurring Use of defibrillator is indicated here

Control system- Clinical Applications

Congestive Heart Failure Walls thinning, loss of strength May be on either side (r or l) If on left, fluid builds up in lungs (why?)

Treatment: Digitalis – (From poisonous Foxglove family of

plants) – slows the rate, but increases strength (contractility)

Clinical:What is a “Heart attack”?

(Page 692 Btm Left) Ishemia results in: anaerobic metabolism - lactic acid formation: Rising acidity hinders ATP & cannot pump out

Ca++, then: Gap junctions close - cells electrically isolated,

and: If ischemic area is large, pumping action

impaired.

Clinical Application – CHFCongestive Heart Failure

Congestive heart failure (CHF) is caused by: Coronary atherosclerosis Persistent high blood pressure Multiple myocardial infarcts Dilated cardiomyopathy (DCM)

Age-Related Changes Affecting the Heart

Sclerosis and thickening of valve flaps Decline in cardiac reserve – (max HR) Fibrosis of cardiac muscle – (normal) Atherosclerosis (You are as old as your

arteries)

Developmental Aspects of the Heart

Contraction detectable at 23 days

Developmental Aspects of the Heart

Contraction detectable at 23 days 4 chambers by day 25

Fetal Heart Development

Fetal heart structures that bypass pulmonary circulation Foramen ovale connects the two atria Ductus arteriosus connects pulmonary trunk and

the aorta

Congenital Heart Defects