Chapter 20 the heart. Anatomy review Electrical activity of the whole heart (EKG) Electrical activity of the heart cells The Cardiac Cycle Cardiac Input.
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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)
Electrical activity of the heart cells
but there are differences…nature of APlocation of Ca2+ storageduration of contraction
The action potential
Electrical activity of the heart cells
resting potential of heart cells~ -90mV
threshold is reached near intercalated discs
signal is AP in an adjacent cell(gap junctions)
The action potential
Electrical activity of the heart cells
review skeletal muscle
fig. 20-15
The action potential
Electrical activity of the heart cells
once threshold is reached the action potential proceeds in three steps.
The action potential - step 1
Electrical activity of the heart cells
rapid depolarization (like skeletal muscle)
Na+ into cell through voltage-gated channels
(fast channels)
The action potential - step 2
Electrical activity of the heart cells
the plateau
Na+ channels closeCa2+ channels open for a “long” time
(slow calcium channels)Ca2+ in balances Na+ pumped out
The action potential - step 3
Electrical activity of the heart cells
repolarization
Ca2+ channels begin closingslow K+ channels begin openingK+ rushes out restoring resting pot.
The action potential - step 3
Electrical activity of the heart cells
Na+ channels are still inactivecell will not respond to stimulus
= refractory period
repolarization
fig. 20-15a
The role of calcium
Electrical activity of the heart cells
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
Electrical activity of the heart cells
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
Clinical note: Heart attacks
blockage of coronary vessels
due to:CAD (coronary artery disease)
(plaque in vessel wall)
blocked by clot (thrombosis)
Clinical note: Heart attacks
blockage of coronary vessels
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
Clinical note: Heart attacks
anticoagulants (aspirin)clot-dissolving enzymes
quick treatment will help reduce damage due to blockage
Clinical note: Heart attacks
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
ventricular systole (270 msec)
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
ventricular systole (270 msec)
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
ventricular systole (270 msec)
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.”
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