Chapter 18 --The Heart

Use the video clip, CH 18 Heart Anatomy for a review of the gross anatomy of the heart

J.F. Thompson, Ph.D. & J.R. Schiller, Ph.D. & G.R. Pitts, Ph.D.

PericardiumThe sac containing the heart

3 Layers Form the Heart’s Wall -

Epicardium (outer)

Myocardium (middle)

Endocardium (inner)

Pericarditis inflammation of the

pericardium painful may damage the lining

tissues may damage

myocardium

fibrinous pericarditisfibrinous pericarditis

Cardiac Tamponade

a buildup of pericardial fluid, or bleeding into the pericardial cavity may result in cardiac failure

Elizabeth, Empress of Austria (d. 1898) by assassination with a hat pin

Internally - 4 compartments

R/L atria with auricles

R/L ventricles Interatrial septum

separates atria Interventricular

septum separates ventricles

Left ventricular wall is much thicker because it must pump blood throughout the body and against gravity

Chambers of the Heart

RALA

LVRV

Blood Flow through the Heart

Right atrium (RA) - receives deoxygenated blood from three sources superior vena cava

(SVC) inferior vena cava

(IVC) coronary sinus (CS)

(CS

SVC

IVC

RA

Right ventricle (RV) receives blood from RA pumps to lungs via

Pulmonary Trunk (PT) Pulmonary Trunk (PT) -

from RV branches into the pulmonary arteries (PA)

Pulmonary arteries deoxygenated blood from

the heart to the lungs for gas exchange

right and left branches for each lung

blood gives up CO2 and picks up O2 in the lungs

Pulmonary veins (PV) - oxygenated blood from the lungs to the heart

Blood Flow through the Heart

RA

PT

PA PA

RV

Pulmonary Circulation

Left atria receives blood from

PV pumps to left ventricle

Left ventricle (LV) sends oxygenated

blood to the body via the ascending aorta

aortic arch curls over heart three branches off of it

feed superior portion of body

thoracic aorta abdominal aorta

LA

LV

Aorticarch

PV PV

Blood Flow through the Heart

Schematic of Circulation

Know the namesof the valvesindicated here.

Schematic of Circulation

ReviewRoutes

Myocardial Blood Supply Myocardium has its

own blood supply coronary vessels simple diffusion of

nutrients and O2 into the myocardium is impossible due to its thickness

Collateral circulation = duplication of supply routes and anastomoses (crosslinked connections)

Heart can survive on 10-15% of normal arterial blood flow

Arteries first branches off the

aorta blood moves more

easily into the myocardium when it is relaxed between beats during diastole

blood enters coronary capillary beds

[note the collateral circulation]

Myocardial Blood Supply

Coronary veins deoxygenated blood

from cardiac muscle is collected in the coronary veins and then drains into the coronary sinus

deoxygenated blood is returned to the right atrium

Myocardial Blood Supply

Coronary Circulation Pathologies

Compromised coronary circulation due to:

emboli: blood clots, air, amniotic fluid, tumor fragments

fatty atherosclerotic plaques

smooth muscle spasms in coronary arteries

Problems ischemia (decreased

blood supply) hypoxia (low supply of

O2) infarct (cell death)

Pathologies (cont.) Angina pectoris - classic chest pain

pain is due to myocardial ischemia – oxygen starvation of the tissues

tight/squeezing sensation in chest labored breathing, weakness, dizziness,

perspiration, foreboding often during exertion - climbing stairs,

etc. pain may be referred to arms, back,

abdomen, even neck or teeth silent myocardial ischemia can exist

Pathologies (cont.) Myocardial infarction

(MI) - heart attack thrombus/embolus in

coronary artery some or all tissue distal

to the blockage dies if pt. survives, muscle

is replaced by scar tissue

Long term results size of infarct, position pumping efficiency? conduction efficiency,

heart rhythm

Pathologies (cont.)

Treatments clot-dissolving agents angioplasty (bypass surgery)

Reperfusion damage re-establishing blood flow may damage tissue

oxygen free radicals - electrically charged oxygen atoms with an unpaired electron

radicals indiscriminately attack molecules: proteins (enzymes), neurotransmitters, nucleic acids, plasma membrane molecules

further damage to previously undamaged tissue or to the already damaged tissue

Valve Structure

Dense connective tissue covered by endocardium

AV valves chordae tendineae -

thin fibrous cords connect valves to

papillary muscles

Valve Function

Opening and closing a passive process when pressure low,

valves open, flow occurs

with contraction, pressure increases

papillary muscles contract pull valves together

Valves of the Heart Function to prevent

backflow of blood into/through heart

Open and close in response to changes in pressure in heart

Four key valves: tri- and bi-cuspid (mitral) valves between the atria and ventricles and semi-lunar valves between ventricles and main arteries

Valves also close the entry points to the atria

Tricuspid

Bicuspid(Mitral)

Semi-lunar

Separate the atria from the ventricles bicuspid (mitral)

valve – left side tricuspid valve –

right side note the

feathery edges to the cusps

Atrioventricular (AV) valves

bicuspidtricuspid

anterior

in the arteries that exit the heart to prevent back flow of blood to the ventricles

pulmonary semilunar valves

aortic semilunar valves

Pathologies Incompetent – does not

close correctly Stenosis – hardened,

even calcified, and does not open correctly

Semilunar valves

Normal Action Potential

Review in Chapter 11

Cardiac Muscle Action Potential

Contractile cells near instantaneous

depolarization is necessary for efficient pumping

much longer refractory period ensures no summation or tetany under normal circumstances

Cardiac Muscle Action Potential

electrochemicalevents

Cardiac Muscle Action Potential

sarcolemma’s ion permeabilities

opening fast Na+ channels initiates depolarization near instantaneously

opening CA++ channels while closing K+ channels sustains depolarization and contributes to sustaining the refractory period closing Na+ and

Ca++ channels while opening K+ channels restores the resting state

repolarization

Cardiac Muscle Action Potential

long absolute refractory period permits forceful contraction followed by adequate time for relaxation and refilling of the chambers

inhibits summation and tetany

Pacemaker Potentials leaky membranes spontaneously

depolarize creates

autorhythmicity the fact that the

membrane is more permeable to K+ and Ca++ ions helps explain why concentration changes in those ions affect cardiac rhythm

Conduction System and Pacemakers

Autorhythmic cells cardiac cells repeatedly fire

spontaneous action potentials

Autorhythmic cells: the conduction system

pacemakers SA node

origin of cardiac excitation fires 60-100/min

AV node conduction system

AV bundle (Bundle of His) R and L bundle branches Purkinje fibers

It’s as if the heart had only two motor units: the atria and the ventricles!

Conduction System and Pacemakers

Arrhythmias irregular rhythms: slow (brady-) & fast

(tachycardia) abnormal atrial and ventricular contractions

Fibrillation rapid, fluttering, out of phase contractions – no

pumping heart resembles a squirming bag of worms

Ectopic pacemakers (ectopic focus) abnormal pacemaker controlling the heart SA node damage, caffeine, nicotine, electrolyte

imbalances, hypoxia, toxic reactions to drugs, etc. Heart block

AV node damage - severity determines outcome may slow conduction or block it

Conduction System and Pacemakers

SA node damage (e.g., from an MI) AV node can run things (40-50

beats/min) if the AV node is out, the AV bundle,

bundle branch and conduction fibers fire at 20-40 beats/min

Artificial pacemakers - can be activity dependent

Atrial,Ventricular Excitation Timing

Atrial,Ventricular Excitation Timing

Sinoatrial node to Atrioventricular node about 0.05 sec from SA to AV, 0.1 sec to

get through AV node – conduction slows allows atria time to finish contraction and

to better fill the ventricles once action potentials reach the AV

bundle, conduction is rapid to rest of ventricles

Extrinsic Control of Heart Rate

basic rhythm of the heart is set by the internal pacemaker system

central control from the medulla is routed via the ANS to the pacemakers and myocardium sympathetic input -

norepinephrine parasympathetic

input – acetylcholine

Electrocardiogram measures the

sum of all electro-chemical activity in the myocardium at any moment P wave QRS complex T wave

Electrocardiogram

Cardiac Cycle Relationship between electrical and

mechanical events Systole Diastole Isovolumetric contraction Ventricular ejection Isovolumetric relaxation

Cardiac Output Amount of blood pumped by each

ventricle in 1 minute Cardiac Output (CO) = Heart Rate x

Stroke Volume HR = 70 beats/min SV = 70 ml/beat CO = 4.9 L/min *

*Average adult total body blood volume = 4-6 L

Cardiac Reserve Cardiac Output is variable Cardiac Reserve = maximal output

(CO) – resting output (CO) average individuals have a cardiac

reserve of 4X or 5X CO trained athletes may have a cardiac

reserve of 7X CO heart rate does not increase to the

same degree

Regulation of Stroke Volume SV = EDV – ESV

EDV End Diastolic Volume Volume of blood in the heart after it fills 120 ml

ESV End Systolic Volume Volume of blood in the heart after contraction 50 ml

Each beat ejects about 60% of the blood in the ventricle

Regulation of Stroke Volume Most important factors in regulating SV:

preload, contractility and afterload

Preload – the degree of stretching of cardiac muscle cells before contraction

Contractility – increase in contractile strength separate from stretch and EDV

Afterload – pressure that must be overcome for ventricles to eject blood from heart

Preload Muscle mechanics

Length-Tension relationship? fiber length determines number of cross bridges cross bridge number determines force

increasing/decreasing fiber length increases/decreases force generation

Cardiac muscle How is fiber length determined/regulated? Fiber length is determined by filling of heart –

EDV Factors that effect EDV (anything that effects

blood return to the heart) increases/decreases filling

Increases/decreases SV

Preload Preload – Frank-Starling Law of

the Heart Length tension relationship of heart Length = EDV Tension = SV

As the ventricles become overfilled, the heart becomes inefficient and stroke volume declines.

“cardiac reserve”

Contractility Increase in contractile strength

separate from stretch and EDV

Do not change fiber length but increase contraction force? What determines force? How can we change this if we don’t

change length?

Sympathetic Stimulation Increases the number

of cross bridges by increasing amount of Ca++ inside the cell

Sympathetic nervous stimulation (NE) opens channels to allow Ca++ to enter the cell

Positive Inotropic Effect

increase the force of contraction without changing the length of the cardiac muscle cells

Afterload if blood pressure is high, it is difficult

for the heart to eject blood

more blood remains in the chambers after each beat

heart has to work harder to eject blood, because of the increase in the length/tension of the cardiac muscle cells

Regulation of Heart Rate

Intrinsic

Pacemakers

Bainbridge effect Increase in EDV increases HR Filling the atria stretches the SA node

increasing depolarization and HR

Regulation of Heart Rate

Extrinsic Autonomic Nervous System

Sympathetic - norepinephrine Parasympathetic – acetyl choline

hormones – epinephrine, thyroxine ions (especially K+ and Ca++) body temperature age/gender body mass/blood volume exercise stress/illness

Regulation of Heart Rate

Overview

End Chapter 18