Ch 20 Heart Physiology Flashcards
Cardiac muscle tissue
Sarcomere- striated
Intercalated disc, one nuclei, lots of mitochondria ( ATP) , sarcolemma, no tendons- intercalated discs
Contractile cells - heart muscle cell
99% of cardiac muscle cells
Mechanical work, pumping
Do not initiate own action potential
Auto rhythmic cells- cardiac muscle
Do not contract
Initiating and conducting action potential responsible for contraction of working cells
No sarcomeres- no actin or myosin
Generate and discharge electrical impulse
Autorhythmicity
Heart beats rhythmically as a result of action potential it generates
Contract on its own, don’t need nervous system
Intercalated disc
Allow electrical impulse to travel quick to contract as unit
Structural elements of contractile cells
Sarcolemma, sarcoplasm, within plasm- myofibrils ( actin myosin), sarcoplasmic riticulum ( Swiss cheese) ,transverse tubule
Sarcomere
Basic contractile unit of cardiac ( and skeletal) muscle
Composed of long fibrous proteins that slide past each other when muscle contracts/relaxes- sliding filament
Part of sarcomere- myosin
Thick filament
Long fibrous tail and globular head, binds to actin
Part of sarcomere- actin
Thin filament
Thanks
Two additional proteins present in sarcomere
Trope in and tropomyosin
Sarcomere has boundary line on left and right
Z disc (line) made of actin and myosin ( in between actin)- made of
Thin (actin) made of 3 proteins
Actin
Tropomyosin- regulatory protein
Troponin- regulatory protein
Thick (mysosin) made up of
Myosin
Regulate interaction between actin and myosin
Tropomyosin
Troponin
Excitation contraction coupling mechanism
Motor neuron sends action potential down, releasing AcH in junction
Sodium generates electrical current- travels over sarcolemma, finds transverse tubules then to sarcoplasmic reticulum- opens pores allowing Ca to exit reticulum
Ca binds to troponin- cross bridge firmed- myosin heads will move actin
Ca is coupling agent
Excitation contraction coupling
AP over cardiac muscle membrane— reaches interior through T tubules—- t tubule AP acts on longitudinal sarcoplasmic reticulum—- release of Ca ions into sarcoplasm— Ca ions catalyze sliding of actin-myosin filaments
Cardiac and skeletal share mechanism of contraction but
They don’t work the same- skeletal takes less time from contraction to relaxing- bell shape
Cardiac elongated contraction- sustained contraction( plateau phase) - 250-300 millisecond -
Everything of heart is made to
Maximize cardiac output with least number of beats
More efficient to hold contraction
Action potential of skeletal muscle is caused by opening fast sodium channels
Action potential in cardiac muscle is caused by fast sodium channels and slow calcium channels
Troponin
3 polypeptide found in striated muscle fibers
One peptide binds to actin (Tnl) another binds to tropomyosin (TNT) a third binds to calcium (Tnc)
When____ ions bind to troponin, the troponin change shape forcing tropomyosin away from actin filaments. This allows myosin cross-bridges to attach onto actin enabling contraction
Calcium
Troponin holds on to ____ in cardiac muscle, giving longer contraction
Calcium
Cardiac troponin serves as a potent and specific marker for
Cardiac disease
Heart attack- cell membranes rupture- release of cardiac troponin into blood stream.
Cardiac muscle does not go in to
Tetany
Heart muscle in tetany is called what
Cardiac flutter and fibrillation- later can lead to death
Tetany is a condition where
A muscle cell goes into elongated contraction (spasm)
In order for the heart to pump it has to
Fill with blood
The heart can only fill with blood when it is
Relaxed
Refractory period is what
Time where cell is stimulated but doesn’t react
Refractory period is very short in skeletal
Resting period- longer than contraction in cardiac muscle
When sarcomere shorten they use
ATP, producing carbon dioxide (acting like an acid) .
Properties of cardiac muscle
Auto excitable- capability of contract even in the absence of neural control
Autorhythmic- heart beats are extremely regular
Prolonged contraction- hold contraction for longer period
Does not fatigue ( go into tetany), does not get tired
Cardiac cycle
Cardiac events that occur from beginning of one heart beat to the beginning of the next
Each initiated by spontaneous generation of action potential in sinus node
Cardiac cycle
Electrical pressure and volume change in a functional heart between successive heart beats
Diastole
Cardiac cycle phase when myocardium is relaxed
Systole
Phase of cardiac cycle when myocardium contracts
Atrial systole- when atria contract
Ventricular systole when ventricles contract
Fluids move from high pressure to- pressure gradient
Low pressure
Three things happen simultaneously in systolic phased
High pressure phase
Contraction
Emptying - fluid leaving(high pressure to low pressure) volume decreasing
Diastolic has 3 simultaneous events
Low pressure
Muscle relaxed
Filling up( volume increases)
When atrial are in systole ventricles are in
Diastole
End diastolic volume
Volume of blood that fills in ventricles at end of diastolic phase
120-150 ml
Stroke volume
Volume of blood pumped by a ventricle per beat
SV= end diastolic volume minus end systolic volume
70 ml
End systolic volume
Amount of blood remaining in a ventricle after contraction
Ejection fraction
% of edv that is pumped by ventricle
Stroke volume/end diastole volume x100%- should be about 55-60% higher
Ventricular systole
Contraction
High pressure
Fluid leaving (ventricles empty)
Atrial systole opens
Bicuspid and tricuspid valves
Aortic and pulmonary closed
S1- sound 1- lub
Bicuspid and tricuspid close during ventricular systole
Pulmonary and aortic are open
S2- sound 2- dub
Aortic and pulmonary valves closing occurs during atrial systole.
Lub
Recoil of blood against closed AV valve
Dub
Recoil of blood against semilunar valves
Murmur
Defect causing hissing sound when stream of blood squirts backward through valve
Cardiac output
Volume of blood ejected from heart ( left ventricle) every minute
CO= HRxSV =5000 ml/min (5liters)
SV= stroke volume
This is a resting measure
This is our entire volume of blood pumped every min at rest
A drop would be congestive heart failure
Cardiac reserve
Difference between maximum cardiac output and resting cardiac out put
Normal cardiac reserve as a percent
Normal cardiac reserve = 15-20L/min= 200-400%- cardiac reserve of 2-4
Endurance athlete= 35mL=600% - cardiac reserve of 7 times in a min
Cardiac index
CI= cardiac output(CO) /body surface area BSA
Remember CO= HRxSV
Relates cardiac output to the size of the individual
Normal range of CI is 2.6-4.2 L/min per square meter
If CI falls below 1.8 L/min the patient may be in cardiac shock
What are the factors of cardiac output
Inotropic- strength of contraction (stroke volume)
Chronotropic- the heart rate
Cardiotropy is based on
Cardiac muscle properties
Cardiac muscle properties that effect cardiotropy
Chronotropic ( HR)*
Inotropic ( contractility)- stroke volume*
Dromotropic ( conduction velocity)- sends impulse- pace maker surgery
Bathmotropic ( excitability)- electrical field- ions, Na, K— electrolyte embalance, pH balances
Lusitropic ( relaxation)*- heart fills
Any issue will decrease cardiac output
Primary impact on chronotropic factor (HR control)
Autonomic nervous system
Baroreceptors
Monitor heart activity by monitoring BP
Monitor HR through BP
Vagus (x) - (parasympathetic)and glassopharyngeal (IX)
Sensory neurons- electrical impulse CI to medulla-into cardiovascular (CV) integration area—- cardiac inhibitory center or cardiac acceleration center
Reflex circuit-
Reflexes have 5 basic parts
Receptors Sensory neuron Integration center Motor neuron Effector
ANS controls
HR
Speed HR up with_____ slow it down with______
Sympathetic(epinephrine), parasympathetic ( uses acH)
Positive chronotropic
Any chemical that raises HR
Epinephrine
Caffeine is
Negative chronotropic
AcH
Stroke volume - 3 variables effect
Preload-
Contractility
After load
Preload
Volume that stretches the LV( left ventricle) just before contraction ( enters during diastole- end diastolic volume)
Measured by CVP for RV and pAWP for LV
Measures preload of the LV or LVEDP= wedge or paw
Greater the preload the greater the stroke volume and the greater the cardiac….
Output
Ventricular preload is the
End diastolic volume, generally dependent on ventricular filling
Relationship between cardiac output and ventricular end diastolic volume is known as
Starlings law of the heart
Increase end diastolic volume
Cardiac wall now stretches, stronger contraction- starling law
Sterling law (sling shot analogy)
Greater the length of cardia fibers, the greater the strength of contraction
Describes how heart changes it’s force of contraction, stroke volume, in response to venous blood return
Greater Venus blood return results in an increase in ventricular filling and preload . In turn
Length of cardiac muscle fibers increases- stretch as heart fills with blood, resulting in greater strength of contraction
If preload increases so does
Cardiac output CO
More sarcomere the _____
Stronger the contraction
Increase stretch increases contraction which increases….
Stroke volume
Left and right must pump the ____ amount of fluid
Same
Factors increasing end diastolic volume
Respiratory pump Cardiac pump Muscle pump Blood volume Sympathetic discharge Standing body position Resistance to venous return
Cardiac output
Preload -starling
Contractility-starling mech.
After load
Chronotropic
Contractility
Intrinsic ability of the myocardium to pump in the absence of changes to preload or after load
Can be altered by neural, humoral, pharmacological influences-
Sympathetic nervous system activity normally has the most important effect on contractility
Myocardial contractility is depressed by anoxia, acidosis, depletion of catecholamine stores within heart and loss of functioning muscle mass as a result of ischemia or infarction
Most anesthetic and anti arrhythmic agents are negative inotropes ( they decrease contractility )
Contractility
Intrinsic ability of cardiac muscle
Inotropism, inotropy
Related to intracellular ca2+
Force generated by myocardium when ventricular muscle fibers shorten
Inotropic agents
Positive: increase contractility - epinephrine
Negative: decrease contractility-AcH
How much calcium in muscle cells- increase Ca, increase strength and vice versa
Increase sarcomere numbers that increase
Increase contraction strength
Contractility is affected by
Drugs
Oxygen levels within myocardium
Cardiac muscle damage
Electrolyte imbalance
After load
Amount of resistance the heart must pump against when ejecting blood
3 components that affect stroke volume
Preload- increase this, increase SV
Contractility- increase this, increase SV
After load - resistance LV runs into when pushing blood in sorta, main resistance is aortic valve
Opening aortic valve
- 90 units
- Additional 20 units
- Contract with additional 10 units of pressure strength
120/80- becomes blood pressure
Normal valve has back pressure ( 80 units)- keeps valve closed. LV has to open valve, 79 units won’t open valve. Has to contract over 80 units. ( usually 90’units) to open as far as it will
Large volume of blood through small opening- additional 20 units to pump into aorta
Push far enough in to aorta to give valve time to close- kinetic (velocity) energy
Preload that LV has to work against is the diastolic ( bottom-80)
Pressure of BP against the valve
Higher pressure, more work on LV
Decrease after load
That will increase stroke volume
Top number systolic is function of
Diastolic- bottom increase, top increase vice versa
Pulse pressure (40)
Difference between systolic (120) and diastolic (80)
Heart will try to keep systolic (top)
50% higher than bottom
Treating hypertension
Get bottom number to drop, top number will follow
LV tries to keep pulse pressure
50% of bottom number
Pre load
Always is a volume
After load
Pressure (BP)
Decrease after load to increase
Stroke volume
