Heart Decks Flashcards
made of desmosomes that connect the cells to each other and gap junctions that allow for the movement of ions
intercalated discs
What are intercalated discs made of?
desmosomes that connect the cells to each other and gap junctions that allow for the movement of ions
What makes the heart behave as a single unit (functional syncytium)?
gap junctionsthey coordinate the movement of ions through the heart
Does cardiac muscle need neuronal stimulation?
no
What are the 2 main types of cells cardiac muscle contains?
cardiac pacemaker cells (aka autorhythmic cells) contractile cardiac muscle cells
these cells make up the intrinsic conduction system of the heart and do not contract
cardiac pacemaker cells (autorhythmic cells)
do cardiac pacemaker cell contract?
no
these cells do contract
contractile cardiac muscle cells
can alter the heart rate but if disconnected the heart still beats
ANS
3 facts about the cardiac pacemaker cells
- do not have stable resting potential 2. set the rhythm 3.form a conduction pathway
Cardiac pacemaker cells: 1. Do not have stable resting potential.
The are always close to threshold with a changing membrane potential (pacemaker potential)
Cardiac pacemaker cells: 2. set the rhythm
they set the rhythm of the heart, they are the pacemaker
Cardiac pacemaker cells: 3. Form a conduction pathway…..
that propagates the action potential of the heart from one area to another
What are the 5 steps of the intrinsic cardiac conduction system in order of propagation.
- sinoatrial (SA) node 2. atrioventricular (AV) node 3. AV bundle (bundle of His) 4. right and left bundle branches 5. subendocardial conduction network (Purkinje fibers)
Intrinsic cardiac conduction system (in order of propagation):located in the right atrium just below the superior vena cava
- sinoatrial (SA) node aka natural pacemaker
Intrinsic cardiac conduction system (in order of propagation):Where is the sinoatrial (SA) node aka natural pacemaker located?
right atrium just below the superior vena cava
Intrinsic cardiac conduction system (in order of propagation):Where does the action potential normally start?
sinoatrial (SA) node aka natural pacemaker
Intrinsic cardiac conduction system (in order of propagation):Where does the action potential go after its start at the sinoatrial (SA) node?
it travels to both atriathe atria contract as a result of this action potential
Intrinsic cardiac conduction system (in order of propagation):The atria contracts as a result of the action potential that starts at the SA node. How many action potential (AP’s) are initiated per minute?
90-100 at rest 75 at rest
Intrinsic cardiac conduction system (in order of propagation):Normally the action potentials from the SA node are about 90-100 per minute whereas at rest they are about 75 per minute, why is this?
because the heart rate is decreased due to the effects of the parasympathetic NS
Intrinsic cardiac conduction system (in order of propagation):located in the lower portion of the interatrial septum. The impules travels via the internodal pathway and is momentarily delayed at this point.
- atrioventricular (AV) node
Intrinsic cardiac conduction system (in order of propagation):Where is the atrioventricular (AV) node located?
in the lower portion of the interatrial septum
Intrinsic cardiac conduction system (in order of propagation):In 2. where does the impulse travel and where is it delayed?
the impulse travels via the internodal pathways and is momentarily delayed at the AV node
Intrinsic cardiac conduction system (in order of propagation):What is the rate of action potentials at the AV node?
50-60 action potentials per minute
Intrinsic cardiac conduction system (in order of propagation):located in the upper portion of the interventricular septum. This part of the conduction pathway connects the atria to the ventricles.
- AV bundle (bundle of His)
Intrinsic cardiac conduction system (in order of propagation):Where is the 3. AV bundle (bundle of His) located?
in the upper portion of the interventricular septum
Intrinsic cardiac conduction system (in order of propagation):What does the 3. AV bundle (bundle of His) connect?
the atria to the ventricles
Intrinsic cardiac conduction system (in order of propagation):located in the respective sides of the interventricular septum, conduct the action potentials from the interventricular septum to the apex of the heart.
- right and left bundle branches
Intrinsic cardiac conduction system (in order of propagation):Where is the 4. right and left bundle branches located?
in the respective sides of the interventricular septum
Intrinsic cardiac conduction system (in order of propagation):Where does the 4. right and left bundle branches conduct action potentials?
from the interventricular septum to the apex of the heart
Intrinsic cardiac conduction system (in order of propagation):branches that are located in the lateral sides of the ventricles, conducts impulses to the ventricles
- subendocardial conduction network (Purkinje fibers)
Intrinsic cardiac conduction system (in order of propagation):Where are 5. subendocardial conduction network (Purkinje fibers) located and where do they conduct impulses?
located in the lateral sides of the ventricles conducts impulses to the ventricles
sometimes there is an extra bundle of cardiac pacemaker cells (an extra node) that can produce occasional extra beats or even take over the SA nodes natural rhythm.
ectopic pacemaker
What triggers the ectopic pacemaker?
caffeine, nicotine, hypoxia, and electrolyte imbalances
Where do the action potentials propegate fastest and then where do they get slower?
fastest from SA node to the AV nodeand then slower after that due to smaller diameter of fibers past AV node
What results from the faster propagation from SA node to AV node then slower after AV node?
atria contracts fully before the ventricles are stimulated to contract
What happens if the SA node quits working?
another node bundle can take over at a lower rate (slower than normal) so then an artificial pacemaker will need to be put in place to return the heart back to a normal higher pace
What is an ECG/EKG?
a means of recording all of the action potentials of the heart
What in our tissues is used for the ECG/EKG?
electrolytes in our tissues carry the charges to the surface where they can be measured
How many leads are used and why?
12 leads each in a slightly different position relative to the heart
What 5 things can the ECG/EKG be used to diagnose?
-if the intrinsic conduction pathway is working -if the heart is enlarged -if the heart is damaged -if there is an electrolyte imbalance -if there are arrhythmias (irregular rhythms)
What does each wave in the tracing represent?
an event
PQRST completion time =
one heart beat
atrial depolarization, the atria usually contracts shortly after the P wave begins (enlarged P indicates enlarged atria)
P wave
What is the P wave?
atrial depolarization
In P wave when does the atria usually contract?
shortly after the P wave begins
What does an enlarged P wave indicate?
enlarged atria
ventricular depolarization; atria repolarization is occurring but is masked, the ventricles contract shortly after the depolarization
QRS complex
What does the QRS complex indicate?
ventricular depolarization
In the QRS complex when do the ventricles contract?
shortly after the depolarization
What is happening with the atria in the QRS complex?
the atria is repolarizing but it’s masked
ventricular repolarization
T wave
What is the T wave?
ventricular repolarization
When an ECG is performed during exercise, increasing the demand for oxygen makes it easier to detect blockages and changes in the tracing.
stress test
Why is an ECG performed during exercise for a stress test?
because increasing the demand for oxygen makes it easier to detect blockages and changes in the tracing
abnormal rhythm, can be too slow or too fast or erratic
arrhythmia (dysrhythmia)
What is arrhythmia (dysrhythmia)?
abnormal rhythm can be too fast, slow, or erratic
too slow (less than 60 bpm)
bradycardia
too fast (greater than 100bpm)
tachycardia
What is bradycardia?
too slow less than 60 bpm
What is tachycardia?
too fast greater than 100 bpm
an interruption in the conduction system, AV block is most common
heart block
What is a heart block?
an interruption in the conduction system
What is the most common heart block?
AV block
What are the 5 types of heart blocks?
1st degree 2nd degree 3rd degree atrial fibrillation (AFib) ventricular fibrillation (VF)
delay in propagation of the action potential from the SA node to AV node, detected as an increase in the P-R interval.
1st degree
1st degree is a delay in the propagation of the action potential from the ___ node to ___ node.
SA to AV node
Where in the interval is the 1st degree block detected?
P-R interval
sometimes the action potential gets to the AV node and sometimes it doesn’t. The ratio of P:QRS is 2:1 or 3:1 or 4:1
2nd degree
What is a 2nd degree heart block?
sometimes the action potential gets to the AV node and sometimes it doesn’t
What is the ratio of P:QRS for a 2nd degree heart block?
2:1, 3:1, or 4:1
complete heart block, the AP ventricles and atria do not contract in the proper sequence
3rd degree
complete heart block
3rd degree
What happens with a 3rd degree heart block?
the AP ventricles and atria do not contract in the proper sequence
cardiac muscle within the atria are not contracting in sync. (This is usually seen as a missing P wave for one heart beat.)
atrial fibrillation (AFib)
What is happening with the cardiac muscles with atrial fibrillation?
the cardiac muscle within the atria are not contracting in sync
How is AFib usually seen?
as a missing P wave for one heart beat
cardiac muscle within the ventricles is not contracting in sync
ventricular fibrillation (VF)
What is ventricular fibrillation (VF)
cardiac muscle within the ventricles is not contracting in sync
Where does the cardiac action potential start and spread?
starts in the SA node and the action potential spreads form one contractile cell to another via gap junctions
What are the 4 key differences between cardiac action potential and the skeletal muscle action potential? (shortened)
- cardiac muscles don’t require outside innervation 2. cardiac muscles contract as an entire unit 3. cardiac action potential typically 15-300 msec 4. very long absolute refractory period
- Why don’t cardiac muscles require outside innervation?
they are self-stimulatory aka they have automaticity or autorhythmicity provided by the pace maker cells
- The cardiac muscles of the heart contract as an entire unit (a functional syncytium) rather than what?
rather than as a motor unit
- How does the cardiac action potential differ from the skeletal muscle action potential?
cardiac action potential = 15 to 300 msec in length skeletal muscle action potential = 1-5 msec in length
- What is the difference between the absolute refractory period of the cardiac and skeletal muscle?
absolute refractory period of cardiac muscle is ver long 200 msec compared to 1-2 msec of skeletal muscle
What is the resting membrane potential of the cardiac muscle cell?
about -90mV
The resting membrane potential of the cardiac muscle cell is about -90mV. Just as we saw in the action potential of the neuron it involves depolarization and repolarization of the cell. What are the 3 steps?
- rapid depolarization 2. plateau 3. repolarization
fast voltage-gated sodium channels open increasing the permeability of the cells for sodium. The flow of sodium into the cell makes the cell more positive than the resting membrane potential hence depolarizing the cell (to+30mV). The channels only stay open for a short period of time.
- rapid depolarization
In 1. rapid depolarization fast voltage-gated sodium channels open and what does this increase?
the permeability of the cells for sodium
In 1. rapid depolarization fast voltage-gated sodium channels open increasing the permeability of the cells for sodium. What does the flow of sodium into the cell do?
it makes the cell more positive than the resting membrane potential hence depolarizing the cell (to +30mV).
In 1. rapid depolarization fast voltage-gated sodium channels open increasing the permeability of the cells for sodium. The flow of sodium into the cell makes the cell more positive than the resting membrane potential hence depolarizing the cell (to+30mV). How long do the channels stay open?
they only stay open for a short period of time.
the depolarzied state is maintained for 175 msec because of a dramatic influx of calcium. This is due to the opening of slow sodium channels that in turn triggercalcium sensitive channels in the sarcoplasmic reticulum which open to release calcium.
- plateau
In 2. plateau how long and why is the depolarized state maintained?
175 msec because of a dramatic influx of calcium
What is 2. plateau due to?
the opening of slow sodium channels that in turn trigger calcium sensitive channels in the sarcoplasmic reticulum which open to release calcium
the overall negativity of the cell is restored when voltage-gated potassium channels open resulting in the flow of potassium out of the cell. At about the same time, the calcium channels close.
- repolarization
In 3. repolarization when is the overall negativity of the cell restored?
when the voltage-gated potassium channels open resulting in the flow of potassium out of the cell
In 3. repolarization the overall negativity of the cell is restored when voltage-gated potassium channels open resulting in the flow of potassium out of the cell. What else is happening at the same time?
the calcium channels close
What happens in the excitation-contraction coupling of cardiac muscle (similar to skeletal muscle)?
calcium binds to troponin which allows actin and myosin to slide past one another.
This is very long, a new contraction does not start until after the first contraction has finished. A short one of these follows.
absolute refractory period
For relative refractory period when does a new contraction start and what follows?
a new contraction does not start until after the first contraction has finished, a short relative refractory period follows
What is not possible because wave summation is not possible?
tetanus
What does the lack of tetanus ensure?
that the atria contract fully before the ventricles contract
Pacemaker potentials aka prepotentials: Why don’t the cardiac pacemaker cells (usually at the SA node) not have a stable resting potential?
due to the opening of sodium channels and the closing of potassium channels at the same time
Pacemaker potentials aka prepotentials: What are the cardiac pacemaker cells (usually at the SA node) continually fluctuating toward?
the threshold of about -40 mV
Pacemaker potentials aka prepotentials: The cardiac pacemaker cells (usually at the SA node) are continually fluctuating toward the threshold of about -40 mV. What do these pacemaker potentials trigger?
the action potential for the pacemaker cells
Pacemaker potentials aka prepotentials: when threshold of -40mV is reached, calcium channels open (rather than sodium for cardiac action potential)
depolarization
Pacemaker potentials aka prepotentials: for depolarization what happens when the threshhold of -40mV is reached?
calcium channels open rather than sodium (in cardiac action potential)
Pacemaker potentials aka prepotentials: calcium channels close and potassium channels open
repolarization
Pacemaker potentials aka prepotentials: what happens in repolarization?
calcium channels close and potassium channels open
one heart beat =
cardiac cycle
How does blood flow in the cardiac cycle?
from high to low pressure
contraction of the heart, it usually refers to the ventricles unless otherwise noted
systole
what does systole usually refer to unless otherwise noted?
the ventricles
relaxation of the heart (usually ventricles relaxing)
diastole
How many phases is the cardiac cycle?
4
What are the 4 phases of the cardiac cycle?
ventricular filling isovolumetric contraction ventricular ejection isovolumetric relaxation
Occurs mid to late diastole when the pressure in the atria is greater than the pressure in the ventricles, the AV valves open. Initially, the filling of the ventricles is due to gravity and passive (rapid filling- 2/3 of the volume), then a pause and then the atria contract (active) to push out the last 1/3.
- ventricular filling
When does 1. ventricular filling occur?
mid-to-late diastole when the pressure in the atria is greater than the pressure in the ventricles
What does the filling in mid-to-late diastole when the pressure in the atria is greater than the pressure in the ventricles cause?
the AV valves to open
In 1. ventricular filling what happens with the initial filling?
the initial filling of the ventricles is due to gravity and passive and it fills 2/3 of the volume
- ventricular filling what happens after the passive filling of the first 2/3?
there is a pause and then the atria contracts (active) to push out the last 1/3
this occurs during early systole- all 4 valves are closed, the ventricles contract increasing the pressure with no change in volume
- isovolumetric contraction
When does 2. isovolumetric contraction occur?
during early systole
How many valves are closed during 2. isovolumetric contraction?
all 4
In 2 isovolumetric contraction what happens with regards to pressure and volume?
the ventricles contract increasing the pressure with no change in volume
Occurs during late systole- when the pressure in the ventricles is greater than the pressure in the major vessel (aorta or pulmonary artery), then the SL valves open
- ventricular ejection
When does 3 ventricular ejection happen?
during late systole when the pressure in the ventricles is greater than the pressure in the major vessel (aorta or pulmonary artery)
- ventricular ejection Occurs during late systole- when the pressure in the ventricles is greater than the pressure in the major vessel (aorta or pulmonary artery), then what opens?
the SL valves
all 4 chambers are resting, all 4 valves are closed
- isovolumetric relaxation
What happens in 4 isovolumetric relaxation?
all 4 chambers are resting, all 4 valves are closed
How long are all chambers in diastole?
0.4 sec
How long are the atria in systole?
0.1 sec
How long are ventricles in systole?
0.3 sec
What is the total time on average for one cardiac cycle?
0.8 seconds
the act of listening to sounds within the body
auscultation
How many heart sounds are there?
4
How many heart sounds are loud enough to be heard? and why?
2 are loud enough to be heardthese 2 are a result of blood turbulence from the closing of the valves
the 1st heart sound is the turbulence from the closing of the AV valves. It is described as a lubb sound.
S1
What is S1?
the first heart sound which is the turbulence from the closing of the AV valves. It’s the lubb sound.
2nd heart sound is turbulence from the closing of the SL valves. It is described as a dubbings sound.
S2
What is S2?
2nd heart sound turbulence from the closing of the SL valves. dubb sound
Where are heart sounds best heard?
above a valve
rapid ventricular filling
S3
atrial contraction
S4
abnormal heart sound usually before or in between heart sounds. They are often a result of valve abnormality.
heart murmurs
What are the 3 common causes of heart murmurs?
stenosis valvular insufficiency MVP (mitral valve prolapse)
a narrowing of the valvular opening form scarring or a birth defect
stenosis (common cause of heart murmurs)
valve doesn’t close quite right so there is back flow into the cavity just before the valve
valvular insufficiency (common cause of heart murmurs)
when a portion of the valve is pushed up into the atrium when the ventricles contract. Only in extreme cases does leakage occur.
MVP-mitral valve prolapse (common cause of heart murmurs)
the volume of blood that is ejected from either right or left ventricle in one minute
CO (cardiac output)
The CO is the volume of blood that is ejected from either right or left ventricle in…..
one minute
the volume of blood ejected in one contraction of a ventricle
SV or stroke volume
What is the SV or stroke volume?
the volume of of blood ejected in one contraction of a ventricle
the end volume in the ventricle after ventricular diastole
EDV or end diastolic volume
What is EDV or end diastolic volume?
the end volume in the ventricle after ventricular diastole
the volume in the ventricle after ventricular systole
ESV or end systolic volume
ESV + SV =
EDV
EDV - ESV =
SV
SV x HR =
CO
CO =
70 ml/beat x 70 beats/min = 4900 ml/min
When can CO be measured?
at rest or during exercise
What is the CO reserve?
the ratio of the CO (max) divided by the CO (rest)
What is the ratio of the CO reserve normally?
4-5 and 7-8 for conditioned athletes
What are the 3 factors that regulate stroke volume?
preload contractility afterload
the stretch of the heart before the contraction which is the EDV (end diastolic volume). Venous return is the primary factor that affect this
preload
What is preload?
the stretch of the heart before the contraction which is the EDV (end diastolic volume)
What is the primary factor that affects preload?
venous return
the forcefulness of the contraction will increase SV(stroke volume) (can be increased with regular cardiovascular conditioning)
contractility
With contractility what will increase the SV (stroke volume)?
the forcefulness of the contraction
What can contractility be increased by?
regular cardiovascular conditioning
the threshold of pressure that must be reached to open the SL valves and eject blood out of the ventricles (provided by the contraction of the heart)
afterload
The afterload is the pressure that must be reached to open what?
the SL valves and eject blood out of the ventricles (provided by the contraction of the heart)
Frank-Starling Law of the Heart: The heart has its own autoregulation that alters the force of contraction, what does this prevent?
blood from pooling in the ventricles
Frank-Starling Law of the Heart: What does the autoregulation of the heart do?
it alters the force of contraction prevents blood from pooling in the ventricles
Frank-Starling Law of the Heart: What is an example?
if the EDV increases (preload) than the force of the contraction increases to increase the SV and maintain ESV (end systolic volume).
Frank-Starling Law of the Heart: For example if the EDV increases (preload increases) then what happens?
the force of the contraction increases to increase the SV and maintain ESV.
Congestive Heart Failure (CHF): Why is there a limit to the increase in preload that the heart can compensate for?
because the increased force of contraction ultimately leads to more and more stretch in the heart which can lead to weakening of the heart
Congestive Heart Failure (CHF): What happens if the left side of the heart fails?
blood pools in the pulmonary circuit and results in pulmonary edema eventually making it impossible to breathe
Congestive Heart Failure (CHF): What happens if the right side of the heart fails?
peripheral edema results
What does the cardiovascular center in the medulla oblongata do for the regulation of heart rate?
it alters the heart rate to increase of decrease cardiac output to match the demands of the body
Why are receptors needed?
to detect the change in demand
What are the 2 types of receptors needed?
chemoreceptors baroreceptors
monitor the blood composition (e.g. pH, oxygen, hormones, calcium, potassium)
chemoreceptors
What are some examples of chemoreceptors monitoring the blood composition?
pH oxygenhormonescalciumpotassium
monitor blood pressure in major arteries by monitoring the change in diameter
baroreceptors
What is the cardioacceleratory center?
sympathetic division of the ANS
Sympathetic division of the ANS is the cardioacceleratory center. Where do nerves travel?
the SA node
Sympathetic division of the ANS is the cardioacceleratory center. Nerves travel to the SA node and what do they release?
norepinephrine
Sympathetic division of the ANS is the cardioacceleratory center. Nerves travel to the SA node and release Norepinephrine which has what 2 effects?
- increases the rate of depolarization (and therefore increases HR) 2. Increases the influx of calcium, thereby increasing the force of the contraction and SV (to a point)
Parasympathetic division of the ANS is the __________ center. Vagus nerves release acetylcholine which slows the rate of depolarization.
cardioinhibitory
Parasympathetic division of the ANS is the cardioinhibitory center. What do Vagus nerves released what does it do?
acetylcholine which slows the rate of depolarization.
How does age affect heart rate?
higher in infants HR decreases as we age
How does gender affect HR?
males have larger hearts and therefore slower heart rates
How does conditioning affect HR?
it decreases the resting HR due to increased efficiency of the heart
How does temperature affect HR?
decrease in temperature means a decrease in HR and vice versa. This is due to metabolic changes in the cardiac cells
Why does a decrease in temperature decrease HR or an increase in temperature increase HR?
due to the metabolic changes in the cardiac cells
factors that affect the HR
chronotropic
factors that affect the force of contraction
inotropic
too much sodium, usually asymptomatic
hypernatremia
What happens in extreme cases of hypernatremia?
blood volume increases which increases the HR
too low sodium, usually asymptomatic
hyponatremia
What happens in extreme cases of hyponatremia?
plasma levels in the brain increases leading to brain swelling
too much potassium
hyperkalemia
What happens with regard to contraction with hyperkalemia?
decreases the force of contraction of the heart and HR
too low potassium
hypokalemia
How does hypokalemia lower the HR?
too much potassium leaves the cardiac muscle cell during depolarization, lowering the HR
too much calcium
hypercalcemia
increases length of plateau phase increases force of contraction decreases HR causes heart to become out of sync
hypercalcemia
too low calcium
hypocalcemia
How does hypocalcemia increase the HR?
decreases the force of contraction and increases HR
