chapter 20

Chapter 20

the heart

Anatomy review

Electrical activity of the whole heart (EKG)

Electrical activity of the heart cells

The Cardiac Cycle

Cardiac Input and Output (dynamics)

Heart review

4 chambers2 atria2 ventricles

4 valves2 AV valves2 semilunar valves

2 circuitssystemicpulmonary

receivesend

fig. 20-9

external heart anatomy

fig. 20-6

internal heart anatomy

100 keys (pg. 678)

“The heart has four chambers, two associated with the pulmonary circuit (right atrium and right ventricle) and two with the systemic circuit (left atria and left ventricle). The left ventricle has a greater workload and is much more massive than the right ventricle, but the two chambers pump equal amounts of blood. AV valves prevent backflow from the ventricles into the atria, and semilunar valves prevent backflow from the aortic and pulmonary trunks into the ventricles.”

cardiac conduction system

modified cardiac muscle cells

•SA node (sinoatrial node)wall of RA

•AV node (atrioventricular node)between atrium and ventricle

•conducting cellsAV bundle (of His)conducting fibersPurkinje fibers

fig. 20-12a

conducting system of heart

prepotential

cannot maintain steady resting potentialgradually drift toward threshold

SA node 80-100 bpm

AV node 40-60 bpm

fig. 20-12b

…it controls the heart rate(pacemaker)

but heart rate is normally slower than 80-100 bpm

(parasympathetics)

if SA node is damaged, heart can still continue to beat, but at a slower rate

because SA node is faster…

if heartbeat is slower than normal…

… bradycardia

if heartbeat is faster than normal…

… tachycardia

impulse conduction

fig. 20-13

impulse conduction

SA nodeatria get signal - contractsignal to AV Node

AV node sends signalto ventricles (time delay)

ventricles contractafter atria are done

damage to any part of conducting system may result in abnormalities (EKG)

ECG’sEKG’s

electrocardiagram

recording of the electrical activity of the heart (from the surface of the body)

fig 20-14

ECG’s

different components:

P wave

QRS complex

T wave

depolarization of the atria

depolarization of the ventriclesbiggerstronger signal

repolarization of the ventricles

ECG’s

fig 20-14 EKG

ECG’s

to analyze:

size of voltage changesduration of changestiming of changes

intervals

ECG’s

fig 20-14 EKG

intervals:

ECG’s

P-R interval

from start of atrial depolarization

to start of QRS complex

if longer than 200 msec can mean damage to conducting system

time for signal to get from atrium to ventricles

intervals:

ECG’s

Q-T interval

time for ventricular depolarization and

repolarization(ventricular systole)

if lengthened, may indicate, [ion] disturbances, medications, conducting problems, ischemia, or myocardial damage.

intervals:

ECG’s

T-P interval

from end of ventricular repolarization

to start of next atrial depolarization

the time the “heart” is in diastolethe “isoelectric line”

T-P interval

fig 20-14 EKG

intervals:

ECG’s

abnormalities cardiac electrical activity

= cardiac arrhythmias

some are not dangerous

others indicate damage to heart

100 keys (pg. 688)

“The heart rate is normally established by cells of the SA node, but that rate can be modified by autonomic activity, hormones, and other factors. From the SA node the stimulus is conducted to the AV node, the AV bundle, the bundle branches, and Purkinjie fibers before reaching the ventricular muscle cells. The electrical events associated with the heartbeat can be monitored in an electrocardiagram (ECG).”

99 % of heart is contractile cells

similar to skeletal muscle

AP leads to Ca2+ around myofibrils Ca2+ bind to troponin on thin filaments initiates contraction (cross-bridges)


but there are differences…nature of APlocation of Ca2+ storageduration of contraction

The action potential


resting potential of heart cells~ -90mV

threshold is reached near intercalated discs

signal is AP in an adjacent cell(gap junctions)



review skeletal muscle

fig. 20-15



once threshold is reached the action potential proceeds in three steps.

The action potential - step 1


rapid depolarization (like skeletal muscle)

Na+ into cell through voltage-gated channels

(fast channels)



the plateau

Na+ channels closeCa2+ channels open for a “long” time

(slow calcium channels)Ca2+ in balances Na+ pumped out



repolarization

Ca2+ channels begin closingslow K+ channels begin openingK+ rushes out restoring resting pot.



Na+ channels are still inactivecell will not respond to stimulus

= refractory period

repolarization

fig. 20-15a

The role of calcium


extracellular Ca2+ enters cells during the plateau phase (20%)

Ca2+ entering triggers release of Ca2+ from sarcoplasmic reticulum

... heart is highly sensitive to changes in [Ca2+] of the ECF

The role of calcium


in skeletal muscle, refractory period ended before peak tension developed…

…summation was possible

…tetanus.

in cardiac muscle refractory period lasts until relaxation has begun…

…no summation…no tetanus.

Clinical note: Heart attacks

blockage of coronary vessels

myocardium without blood supply…

…cells die(infarction)

myocardial infarction (MI) = heart attack



due to:CAD (coronary artery disease)

(plaque in vessel wall)

blocked by clot (thrombosis)



as O2 levels fall, cardiac cells will:

accumulate anaerobic enzymesdie and release enzymes

LDHSGOTCPKCK-MB

lactose dehydrogenase

serum glutamic oxaloacetic transaminase

creatine phosphokinase

cardiac muscle creatine phosphokinase

to here 3/26lec # 31


anticoagulants (aspirin)clot-dissolving enzymes

quick treatment will help reduce damage due to blockage


risk factors:

smokinghigh blood pressurehigh blood cholesterolhigh [LDL]diabetesmalesevere emotional stressobesitygenetic predispositionsedentary lifestyle

any 2more than

doublesyour risk

of MI

The cardiac cycle

contraction(systole)

relax(diastole)

fluid (blood) moves

always moves from higher pressure…

…toward lower pressure

fig. 20-16

The cardiac cycle

atrial systoleatrial diastole

ventricular systoleventricular diastole

generic heart rate 75 bpm

together

fig. 20-17

The cardiac cycle

atrial systole (100 msec)

blood in atria is pushed through AV valves into ventricles

“tops off” the ventriclesblood in ventricles is called EDV

(end diastolic volume)

(follows path of least resistance)

1+2

3… end of atrial systoleventricular diastole begins

The cardiac cycle

ventricular systole (270 msec)

pressure start to rise in ventriclewhen it is greater than pressure in atria, the AV valves will close

(chordae tendineae and papillary m.)

pressure continues to build until it can force open the semilunar valves

“lubb”

…3

4

The cardiac cycle


up until now, ventricles have been contracting but no blood has flowed:

isovolumetric contraction

ventricular volume has not changedbut the pressure has increased

4

The cardiac cycle


when pressure in ventricle is greater than pressure in the arteries, the semilunar valves will open

ventricular ejection

stroke volume

some blood left behindend systolic volume (ESV)

5

The cardiac cycle


as pressure drops below that of arteries, the semilunar valves will close again

“Dupp”

6

The cardiac cycle

ventricular diasatole (430 msec)

semilunar valves are shutAV valves are shut too (temporarily)

isovolumetric relaxation

7

when pressure gets below atrial pressure, AV valves will openand ventricle will begin to fill passively

8

fig. 20-17

Heart sounds

lubbDUPP

lubbDUPP

auscultation

stethoscope

Heart sounds

lubb

closing of the AV valvesas ventricular contraction begins

Heart sounds

DUPP

closing of the semilunar valvesas ventricular relaxation begins

Heart dynamics

cardiac output

heart rate

stroke volume

variation &adjustments

Heart dynamics definitions

EDV end diastolic volume

ESV end systolic volume

Stroke volume

ventricle is fullbeginning to contract

ventricle is done contracting(a little blood left inside)

SV = EDV - ESV

Heart dynamics definitions

cardiac output (CO)

CO = HR (heart rate) x SV

how much blood the heartpumps in a minute

both the SV and the HR can vary

Heart dynamics

both the SV and the HR can vary

fig. 20-20

Heart dynamics

variation in HR

autonomics

dual innervation to SA node

Heart dynamics HR

parasympathetics

releases AChopens K+ channels

lowers the resting potential(hyperpolarize cell)

slows heart rate

controlled by cardioinhibitory centers in the medulla oblongatat

Heart dynamics HR

parasympathetics

controlled by cardioinhibitory centers in the medulla oblongata

reflexes hypothalamus

Normal:

Parasympathetics:

fig 20-22

Heart dynamics HR

sympathetics

releases NEbinds to beta-1 receptors

opens Na+/Ca2+ channelsdepolarize cell

speeds up heart rate

Heart dynamics HR

sympathetics

controlled by cardioacceleratory centers in the medulla oblongata

reflexes hypothalamus

Normal:

Sympathetics:

fig 20-22

Heart dynamics HR

atrial (Bainbridge) reflex

increased venous returnstretches atria

stimulates stretch receptorsstimulates sympathetics

increase HR(and CO)

Heart dynamics HR

hormones

E, NE, thyoid hormoneaffect SA node

speed up HR

to here 3/30/07lec# 33

Heart dynamics

stroke volume (SV)

remember

SV = EDV - ESV

Heart dynamics SV

EDV

the amount of blood in the ventricle at the end of its diastolic phase, just before contraction begins.

Heart dynamics SV

EDV

affected by the filling time&

venous return

preload

Heart dynamics SV

EDV

preload the degree of stretching of the ventricle during diastole

preload is proportional to EDV

preload affects heart muscles ability to generate tension

Heart dynamics SV

EDV

preload

Heart dynamics SV

EDV

preload

“more in = more out”

Frank-Starling principle

fig. 20-23

Heart dynamics SV

ESV

preload

contractility

afterload

Heart dynamics SV

ESV

contractility

amount of force generated with a contraction

increase

decrease

+ inotropic action

- inotropic action

Heart dynamics SV

ESV

contractility

factors that influence:

ANShormones

Heart dynamics SV

ESV

contractility

ANS

sympathetic NS

NE, E

+ inotropic effect

parasympathetic NS

ACh

- inotropic effect

fig. 20-23

Heart dynamics SV

ESV

contractility

hormones(and drugs)

NE, E, glucagon,thyroid hormones

+ inotropic effect

dopamine,dobutamineisoproterenol

digitalis

Heart dynamics SV

ESV

contractility

hormones(and drugs)

propanololtimololetc.,

(beta-blockers)

- inotropic effect

verapamilnifedipine

(Ca2+ blocker)

(hypertension)

fig. 20-23

Heart dynamics SV

ESV

preload

contractility

afterload the amount of tension needed to open semilunar valves and eject blood

Heart dynamics SV

ESV

afterload the amount of tension needed to open semilunar valves and eject blood

greater afterloadlonger isovolumetric contraction

less ejected, larger ESV

Heart dynamics SV

ESV

afterload

restrict blood flow

constrict peripheral vesselscirculatory blockage

inc. afterload

fig. 20-23

Summary

Heart rate

EDV

ESV

SV = EDV-ESV

hormonesvenous return

filling timevenous return

preloadcontractilityafterload

100 keys (pg. 703)

“Cardiac output is the amount of blood pumped by the left ventricle each minute. It is adjusted on a moment-to-moment basis by the ANS, and in response to circulating hormones, changes in blood volume, and alternation in venous return.

Most healthy people can increase cardiac output by 300-500 percent.”

chapter 20

Documents

heart ekgelectrical

av nodeav node

bpmparasympatheticsif

external heart anatomyfig

slower ratebecause sa

internal heart anatomy100

right ventricle

left ventricle