20
the Chapter 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 chambers 2 atria 2 ventricles receive send
4 valves 2 AV valves 2 semilunar valves 2 circuits systemic pulmonary
external heart anatomy
fig. 209
internal heart anatomy
fig. 206
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 cells AV bundle (of His) conducting fibers Purkinje fibers
conducting system of heart
fig. 2012a
prepotential cannot maintain steady resting potential gradually drift toward threshold SA node AV node 80100 bpm 4060 bpm
fig. 2012b
because SA node is faster... ...it controls the heart rate (pacemaker) but heart rate is normally slower than 80100 bpm (parasympathetics) if SA node is damaged, heart can still continue to beat, but at a slower rate
if heartbeat is slower than normal... ... bradycardia
if heartbeat is faster than normal... ... tachycardia
impulse conduction
fig. 2013
impulse conduction SA node atria get signal contract signal to AV Node AV node sends signal to ventricles (time delay) ventricles contract after atria are done damage to any part of conducting system may result in abnormalities
(EKG)
ECG's EKG's
electrocardiagram
recording of the electrical activity of the heart (from the surface of the body)
fig 2014
ECG's different components: P wave depolarization of the atria QRS complex depolarization of the ventricles bigger stronger signal T wave repolarization of the ventricles
ECG's
fig 2014 EKG
ECG's to analyze: size of voltage changes duration of changes timing of changes
intervals
ECG's
fig 2014 EKG
ECG's intervals: PR interval from start of atrial depolarization to start of QRS complex time for signal to get from atrium to ventricles if longer than 200 msec can mean damage to conducting system
ECG's intervals: QT interval time for ventricular depolarization and repolarization (ventricular systole) if lengthened, may indicate, [ion] disturbances, medications, conducting problems, ischemia, or myocardial damage.
ECG's intervals: TP interval from end of ventricular repolarization to start of next atrial depolarization the time the "heart" is in diastole the "isoelectric line"
fig 2014 EKG
TP interval
ECG's intervals: 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)."
Electrical activity of the heart cells 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 (crossbridges)
but there are differences... nature of AP location of Ca2+ storage duration of contraction
Electrical activity of the heart cells The action potential resting potential of heart cells ~ 90mV threshold is reached near intercalated discs signal is AP in an adjacent cell (gap junctions)
Electrical activity of the heart cells The action potential review skeletal muscle
fig. 2015
Electrical activity of the heart cells The action potential once threshold is reached the action potential proceeds in three steps.
Electrical activity of the heart cells The action potential step 1 rapid depolarization (like skeletal muscle) Na+ into cell through voltagegated channels (fast channels)
Electrical activity of the heart cells The action potential step 2 the plateau Na+ channels close Ca2+ channels open for a "long" time (slow calcium channels) Ca2+ in balances Na+ pumped out
Electrical activity of the heart cells The action potential step 3 repolarization Ca2+ channels begin closing slow K+ channels begin opening K+ rushes out restoring resting pot.
Electrical activity of the heart cells The action potential step 3 repolarization Na+ channels are still inactive cell will not respond to stimulus = refractory period
fig. 2015a
Electrical activity of the heart cells 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
Electrical activity of the heart cells 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
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 enzymes die and release enzymes LDH SGOT CPK CKMB
lactose dehydrogenase serum glutamic oxaloacetic transaminase creatine phosphokinase muscle cardiac creatine phosphokinase
to here 3/26 lec # 31
Clinical note:
Heart attacks
anticoagulants (aspirin) clotdissolving enzymes quick treatment will help reduce damage due to blockage
Clinical note: risk factors:
Heart attacks
smoking high blood pressure high blood cholesterol high [LDL] diabetes male severe emotional stress obesity genetic predisposition sedentary lifestyle
any 2 more than doubles your risk of MI
The cardiac cycle contraction (systole) fluid (blood) moves always moves from higher pressure... ...toward lower pressure relax (diastole)
fig. 2016
The cardiac cycle atrial systole atrial diastole ventricular systole ventricular diastole
together
generic heart rate 75 bpm
fig. 2017
The cardiac cycle atrial systole (100 msec) 1+2
blood in atria is pushed through AV valves into ventricles (follows path of least resistance) "tops off" the ventricles blood in ventricles is called EDV (end diastolic volume)
3...
end of atrial systole ventricular diastole begins
The cardiac cycle ventricular systole (270 msec) ...3
pressure start to rise in ventricle when it is greater than pressure in atria, the AV valves will close
(chordae tendineae and papillary m.)
"lubb" 4
pressure continues to build until it can force open the semilunar valves
The cardiac cycle ventricular systole (270 msec) 4
up until now, ventricles have been contracting but no blood has flowed: isovolumetric contraction ventricular volume has not changed but the pressure has increased
The cardiac cycle ventricular systole (270 msec)
when pressure in ventricle is greater than pressure in the arteries, the semilunar valves will open
5
ventricular ejection stroke volume some blood left behind end systolic volume (ESV)
The cardiac cycle ventricular systole (270 msec) 6
as pressure drops below that of arteries, the semilunar valves will close again
"Dupp"
The cardiac cycle ventricular diasatole (430 msec) 7
semilunar valves are shut AV valves are shut too (temporarily) isovolumetric relaxation
8
when pressure gets below atrial pressure, AV valves will open and ventricle will begin to fill passively
fig. 2017
Heart sounds auscultation stethoscope
lubb
DUPP
lubb
DUPP
Heart sounds lubb closing of the AV valves as ventricular contraction begins
Heart sounds DUPP closing of the semilunar valves as ventricular relaxation begins
Heart dynamics cardiac output heart rate stroke volume variation & adjustments
Heart dynamics EDV
definitions
end diastolic volume ventricle is full beginning to contract ESV end systolic volume ventricle is done contracting (a little blood left inside) Stroke volume SV = EDV ESV
Heart dynamics
definitions
cardiac output (CO) CO = HR (heart rate) x SV how much blood the heart pumps in a minute both the SV and the HR can vary
Heart dynamics both the SV and the HR can vary
fig. 2020
Heart dynamics variation in HR autonomics dual innervation to SA node
Heart dynamics parasympathetics
HR
releases ACh opens K+ channels lowers the resting potential (hyperpolarize cell) slows heart rate controlled by cardioinhibitory centers in the medulla oblongatat
Heart dynamics parasympathetics
HR
controlled by cardioinhibitory centers in the medulla oblongata
reflexes
hypothalamus
Normal:
Parasympathetics:
fig 2022
Heart dynamics sympathetics
HR
releases NE binds to beta1 receptors opens Na+/Ca2+ channels depolarize cell speeds up heart rate
Heart dynamics sympathetics
HR
controlled by cardioacceleratory centers in the medulla oblongata
reflexes
hypothalamus
Normal:
Sympathetics:
fig 2022
Heart dynamics
HR
atrial (Bainbridge) reflex...