chapter 9 cardiac physiologybiology/.../past-classes/295/chap9_cardiac_physiology.pdfchapter 9...

Chapter 9Chapter 9

Cardiac PhysiologyCardiac Physiologyby Dr. Jay M. Templin

© Brooks/Cole - Thomson Learning

Circulatory System

Heart

Blood Vessels

Blood

Pulmonary and Systemic Circulation

Location of the Heart

Anatomy of the Heart: Chambers

Anatomy of the Heart: Blood Vessels

Blood Flow in the Heart

High pressure, High resistance

Low pressure, Low resistance

Heart Valve Action

Valve System in the Heart

Right atriumRight AV valve

Direction ofbackflow ofblood

Right ventricle

Papillary muscle

Chordae tendineae

Septum

Transverse Heart Structure

© Brooks/Cole - Thomson Learning

Tricuspid valveMitral valve

Semilunar valve

Semilunar valve

Valve SystemNotice:

Valves are found between atria and ventricles or between ventricles and arteries (aorta and pulmonary vein)

No valves between atria and veins (pulmonary vein and vena cava) WHY?

http://www.smm.org/heart/heart/pumping-f.htmMOVIE

http://www.smm.org/heart/heart/pumping-f.htm

http://www.smm.org/heart/heart/pumping-f.htm

Tissue Structure in the Heart

Endocardium-Epithelial tissue

Myocardium-Cardiac muscle tissue

Epicardium-Connective tissue

Pericardial sac and Pericardial fluid

Cell Structure in the MyocardiumPlasma membranes of adjacentcardiac muscle fibers

Desmosome

Actionpotential

Gap junction

Cells in MyocardiumContractile cells

Pacemaker cells

1) Sinoatrial node

2) Atrioventricularnode

3) Atrioventricularbundle

4) Purkinje cells

Function of Pacemaker CellsSelf-inducedaction potential

Slowdepolarization(pacemakerpotential)

Thresholdpotential

http://www.interactivephysiology.com/demo/systems/buildframes.html?cardio/actnpot/01

Pacemaker CellsCell A

Cell B

Complete Heart Block

Premature Beat (Extrasystole)

Spreading of Cardiac Excitation

Cardiac Contraction

1) Atrial excitation should be completed before ventricular excitation

AV nodal delay~100 msec

Cardiac Contraction

2) Each chamber should contract as a unit

Cardiac Contraction

3) Each pairs of atria or ventricles should contract at the same time

Interatrial pathway

Right atrium Left atrium

Right ventricle Left ventricle

SA node

AV node Internodalpathway

Purkinjefibers Bundle

of His

Action Potential in Cardiac Muscle

Plateauphase ofaction potential

Thresholdpotential

http://www.interactivephysiology.com/demo/systems/buildframes.html?cardio/actnpot/01

Action potentialin cardiaccontractile cell

Travels downT tubules

Entry of small amount of Ca2+

from ECF

Release of large amount of Ca2+

from sarcoplasmicreticulum

CytosolicCa2+

Troponin-tropomyosin complex in thin filaments pulled aside

Cross-bridge cycling between thick and thin filaments

Thin filaments slide inward between thick filaments

Contraction

Ryanodinechannels

Dihydropyridinechannels

Actionpotential

Contractileresponse

Refractoryperiod

Refractory Period in Cardiac Muscle

No summation o of contractions in cardiac muscles WHY?

Electrocardiogram (ECG)Lead I:Right arm toleft arm

aVR: right arm

Lead II:Right arm toleft leg

aVF: left leg

aVL: left arm

Lead III:Left arm toleft leg

Ground electrode

ECG reflect the flow of electrical currents during heart contraction

Electrocardiogram (ECG)Single Lead Recording

1 23

4 56

Electrocardiogram (ECG)

R

T

P

QS

PPR ST TP interval

R

T

NORMAL RATE AND RHYTHM

ABNORMALITIES IN RATE Tachycardia

Bradycardia-appositive of Tachycardia

Extrasystole (premature beat)

Ventricular fibrillation

ABNORMALITIES IN RHYTHM

Complete heart block

CARDIAC MYOPATHIES: DAMAGE TO CARDICA MUSCLE FIBERS

Myocardial infarction

Cardiac Cycle: Systole vs. Diastole

1) Ventricular filling

2) Isovolumetricventricular contraction

3) Ventricular ejection

4) Isovolumetricventricularrelaxation

Passive filling duringventricular and atrial diastole Atrial contraction

Rightatrium

Rightventricle

Leftatrium

Leftventricle

BA

Ventricular filling

Isovolumetric ventricular contraction

C

Isovolumetric ventricular relaxationVentricular ejection

Ventricular emptying

ED

Dicrotic Notch

DN represents the closure of the aortic valve during relaxation of ventricles

http://www.interactivephysiology.com/demo/systems/systems/cardio/index.html

Changes in Volume

Stroke volume~70 mL


Cardiac Cycle


Heart Sounds


Laminar vs. Turbulent Flow

Laminar flow (does not create any sound)

Turbulent flow (can be heard)

Cardiac Output at Rest

Cardiac Output: VOLUME of blood pumped by each ventricle per minute

Cardiac Output = Heart Rate X Stroke Volume(CO) = (HR) X (SV)

IF: Average heart rate = 70 beats/minStroke volume = 70 mL

Cardiac Output at Rest ~ 5 L/min

Cardiac Output during ExerciseCardiac Output during Exercise ~ 25 L/min

How does the organism regulate cardiac output?

Heart rate

Parasympatheticactivity

Sympatheticactivity(and epinephrine)

Innervate atria via vagus nerve

Innervate atria and ventricles

Regulation of Cardiac Output

Sympathetic

Increase excitability- increase rate of depolarization -decrease AV nodal delay

Increase heart rate

Increase contractionof atrium and ventricles

Increase secretion of adrenaline from adrenal medulla

EyeNasal mucosa

Spinal nerves

Sympathetictrunk

Splanchinonerves

Liver

GallbladderPancreasAdrenal

glandKidney

Smallintestine

ColonRectumUrinary bladderGenitalia

Lung

Heart

Spinalnerves

Cranialnerves

Salivaryglands

Parotid gland

Trachea

Lacrimal gland

Stomach

Spleen

Parasympathetic

Decrease excitability-decrease rate of depolarization-decrease AV nodal delay

Decrease heart rate

Decrease contractionof atrium ONLY

No effect on adrenaline secretion

Sympathetic Regulation of Heart Rate

Thresholdpotential

Decrease K+ permeability

Parasympathetic Regulation of Heart Rate

Thresholdpotential

Increase K+ permeability

Right atrium Left atrium

SA node

AV node

Right ventricle Left ventricle

Sympathetic

Decrease AV nodal delay

Parasympathetic

Increase AV nodal delay

Regulation of Cardiac Output

Heart rate


Sympatheticactivity(and epinephrine)

Innervate atria via vagus nerve

Innervate atria and ventricles

Regulation of Stroke VolumeStroke volume

Strength ofcardiac contraction

Extrinsiccontrol

Intrinsic control

End-diastolicvolume

Intrinsic control

Venous return

Sympathetic activity(and epinephrine)

Frank-Starling LawThe heart will pump out all the blood returned to it

Frank-Starling curve onsympathetic stimulation

Normal Frank-Starlingcurve

Effect of Sympathetic Stimulation on Stroke Volume

End-diastolic volume135 ml

Stroke volume70 ml

End-systolic volume65 ml

Normal SV


Stroke volume100 ml


SV following sympathetic stimulation:

Due to increase Ca2+

influx during muscle fiber depolarization


Stroke volume140 ml


SV following sympathetic stimulation and increase end-diastolic volume

Cardiac output

Heart rate Stroke volume


Sympatheticactivity (andepinephrine)

End-diastolicvolume

Venous return

Extrinsiccontrol

Intrinsic control

Intrinsic control

Heart rate is determined by

the balance between

sympathetic and

parasympathetic stimulation

Notice that at rest

parasympathetic activation

have the dominant

effect

Heart FailureInability of the heart to contract

Normalstrokevolume

Decreasein strokevolume

Strokevolumewithuncompensatedheart failure Normal end-diastolic volume

Normal heart

Failing heart

Heart Failure

Caused by:

1) Damage heart muscle

2) Excess pumping against increased load (for example after hypertension or damaged valves)

Area of cardiacmuscle deprivedof blood supplyif coronary vesselis blocked at point

Area of cardiacmuscle deprivedof blood supplyif coronary vesselis blocked at point

Leftcoronaryartery

Rightcoronaryartery

Leftventricle

Rightventricle

Coronary Blood FlowSupply heart muscle with O2 and nutrients

Coronary Blood Flow

Aortic pressure

Blood flow in leftcoronary artery

Systole Diastole

CARDIAC MYOPATHIES: DAMAGE TO CARDICA MUSCLE FIBERS

Myocardial infarction

Compensatory Measures Against Heart Failure

Increased blood volume by reducing water and Na+ secretion

Compensatory Measures Against Heart Failure: Sympathetic stimulation

Normal end-diastolic volume

Normal heart

Failing heart withsympatheticstimulation

Failing heartwithoutsympatheticstimulation

Normalstrokevolume

Increasein end-diastolicvolume

Interdependence of Blood Flow and Oxygen Need

Metabolic activity of cardiac muscle cells( oxygen need)

Adenosine

Vasodilation of coronary vessels

Blood flow to cardiac muscle cells

Oxygen available to meet oxygen need

Factors that Affect Blood FlowVascular SpamsAtherosclerosis

Thromboembolism

Atherosclerotic PlaqueCollagen-richsmooth musclecap of plaque

Normal bloodvessel wall

Lipid-rich coreof plaque

Endothelium

Plaque

Formation of Atherosclerotic Plaque

Blood vessel damage

Inflammatory response

Deposition and oxidation of low-density lipoprotein (bad cholesterol) (Prevented by Vit E, Vit C, beta-carotene)

Recruitment of macrophes and fibroblasts leading to formation of collagen cap

Ca2+ precipitation and hardening of blood vessels

Formation of ThrombusRupture of collagen cap

Platelet aggregation and formation of blood clot (thrombus)

Thrombus

ThrombormbolismLeading cause of strokes (brain) and myocardial ischemia (heart muscle)

Blood flow

Thrombus

Blood flow

Embolus

Consequences of Thrombormbolism

Blood flow

Embolus

Angina Pectoris or Hear Pain due to narrowing of coronary blood vessels

Heart Attack occurs when blood vessels are completely plugged

chapter 9 cardiac physiologybiology/.../past-classes/295/chap9_cardiac_physiology.pdfchapter 9...

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