LEC EXAM #3 CHP 11 Flashcards
Cardiac muscle tissue characteristics: (4)
- automaticity
- extended contraction time
- long absolute refractory period
- nervous system alters contraction force and rate
Automaticity:
- contraction without neural stimulation
- controlled by pacemaker cells (SA node)
In what way does cardiac muscle tissue have a long absolute refractory period?
Prevention of wave summation and tetanic contractions of cell membranes
Does cardiac or skeletal muscle tissue have a longer contraction time?
Cardiac
2 kinds of cardiac cells:
- pacemaker cells (auto rhythmic/myogenic cells)
- contractile cells
Intercalated discs:
Hold cells together
Gap junctions:
Ports that allow ions to spread from one cell to another
Pacemaker cells are found:
- SA node (sets pace/rate)
- AV node
- Bundle of HIS
- Purkinjee fibers
- Bundle branches
What do pacemaker and contractile cells have in common?
difference?
- both rely on K+, Ca2+, Na+, and CI-
- different AP’s
4 characteristics of pacemaker cells:
- spontaneously depolarize
- slow to depolarize/hit threshold
- autorhythmic
- do NOT contract
Pacemaker cell AP
Phase 0: (2)
- Ca rushes in
- increases depolarization
Pacemaker cell AP
Phase 3:
K leaves
Pacemaker cell AP
Phase 4:
Na rushes in
Pacemaker cells depolarized by:
Ca rushing in
Contractile cells characteristics:
- low RMP= -96 mv
- gets impulse from pacemaker cells via gap junctions
- depolarize-> contract
- long absolute refractory period
Do pacemaker cells or contractrile cells have a longer absolute refractory period (depol)?
Contractile
Why do contractile cells have a longer absolute refractory period?
Because Ca is rushing in at the same time as K is leaving, leading to a plateau PHASE 2
Cardiac muscle cell contraction occurs:
In contractile cells only
Provides Ca for cardiac muscle contraction:
important bitch
ECF and SR
Main function of sarcoplasmic reticulum?
To store Ca
Less Ca (in cardiac muscle cell contraction) =
less force generated
Heart failure channel blocker would be:
Calcium
What is the secondary active transport in cardiac muscle cell relaxation?
Calcium being forced out by Na coming in
sodium-calcium antiport
Cardiac tissue is innervated by:
Autonomic nervous system at SA node
What is absolute refractory period responsible for?
Not generating an AP
How do contractile cells communicate?
SA node spreads through the atria
AV node is responsible for what during contraction?
Takes the impulse from the atria to the ventricles
Why do we need relaxation to occur?
To refill with enough blood
Once contractile cells get an impulse, what happens?
- Ca from skeletal muscle is released from endoplasmic reticulum
- binds troponin to move tropomyosin out of the way
- myosin binds to active site
Where do we get Ca for skeletal muscle contraction?
Sarcoplasmic reticulum
Alpha and beta adrenergic cardiac tissue receptors bind:
Nor-epi + Epi (hormone) and increase depolarization of pacemaker cells
Epi has higher affinity for:
Beta adrenergic receptors
What happens to your HR when nor-epi and epi bind to alpha and beta receptors?
- increase in HR
- increase in SV
- increase in CO
Nor-epi has higher affinity for:
Alpha adrenergic receptors
Sympathetic hormones:
receptors:
Parasympathetic hormones:
receptors:
NE + Epi
Alpha + Beta adrenergic
Ach
Muscarinic cholinergic
What happens to your HR when Ach bind to muscarinic cholinergic receptors?
- decrease in HR
- decrease in SV
- decrease in CO
Phenoxybenzamine:
Antagonistic drug that binds to alpha adrenergic receptors
Propranolol:
Antagonistic drug that binds to beta adrenergic receptors
Atropine:
(from deadly night shade)
antagonistic drug that binds to muscarinic cholinergic receptor
How would phenoxybenzamine effect HR?
Unable to bind to alpha adrenergic receptor to nor-epi so slight decrease in HR
Lead 1:
RA (-) LA (+)
How would atropine effect HR?
blocks Ach and causes an increase in HR
How would propranolol effect HR?
Since we have more beta receptors, greater decrease in HR
Lead 2:
RA (-) and LL (+)
Lead 3:
LA (-) and LL (+)
Which lead shows the bulk of the electrical current?
Lead 2
“0” on an EKG represents:
Isoelectric line= no electrical activity
When waveform deflects up (pos deflection)->
Electrical activity is going towards positive lead (lLL)
When waveform defects down (neg deflection)->
Electrical activity is going towards negative lead (RA)
P wave shows:
Atrial depol
Before the atria depolarizes, what has to depolarize?
SA node
QRS interval shows:
Ventricle depol
T wave shows:
Ventricle repol
Where is the P wave depolarizing towards?
LL
Positive deflection
Interval has ____
Segments have no ____
Waves
If SA node is damaged, can the heart still beat?
Yes, but the rate will be slower and the AV node takes over
Cardiac cycle:
period between the start of one heartbeat and the beginning of the next
Cardiac cycle consists of:
Systole + diastole
Atria cardiac cycle:
- atria passively fill (end of diastole)
- atria contract (start of systole)
- atria eject blood into ventricles (end of systole)
- atria relax (start of diastole)
Ventricular cardiac cycle:
- ventricles passively fill as atria fill and contract (end of diastole)
- atria contract (start of systole)
- atria eject blood into ventricles (end of systole)
- atria relax (start of diastole)
What is happening at diastole?
Blood is filling into the atria and ventricles
What is the “lub” sound in the heart?
Blood hitting the closed AV valves, pressure is built up
What is the “dub” sound in the heart?
Blood hitting the shut semilunar valves
During systole, what happens to BP?
increases
During diastole, what happens to BP?
decreases
Blood flows from:
high -> low pressure
What dictates blood flow throughout the heart?
Contractions and valves
Does all the blood get ejected from the ventricles when it contracts?
NO
Where is pressure higher?
Ventricles
Ventricles contract every:
270 milliseconds (0.2 secs)
Contraction for heart time:
370 milliseconds
How is SV calculated?
EKG, ultrasound, prob into neck
Tachycardia:
Fast rhythm
Bradycardia:
Slow rhythm
Be able to talk through the steps of the Wigger diagram:
- P wave depolarizes
- Increase in atrial pressure-> atrial systole
- blood is pushed into ventricles as a result of the LA contracting
- increase in ventricular volume
- QRS complex causes ventricular depol
- isovolumetric contraction occurs resulting in the AV and semilunar valves closing as the ventricles build up in pressure
- semilunar valve opens causing ejection
- causes a decrease in ventricular volume
- T wave causes ventricles to repolarize
- ventricle relaxation + isovolumetric relaxation
- ventricles able to fill again
Ventricular filling (phase 1)
- blood->relaxed atria->av valves->ventricles
- atria contract-> blood going into ventricles
Isovolumetric contraction (phase 2)
- ventricles begin contracting
- all valves closed
- no blood flowing=same volume
Ventricular ejection (phase 3):
- ventricles contract
- blood ejects into aorta + pulmonary arteries
Isovolumetric relaxation (phase 4)
- semilunar shut
- AV valves open and ventricles passively fill with blood until they contract again
During ventricular contraction the aorta:
Stores energy by stretching (pressure reservoir)
Aortic pressure is higher than ventricular pressure during:
Diastole
During ventricular diastole the aorta:
Releases pressure to maintain blood flow to body
MAP=
profusion pressure to organs
EDV:
End-diastolic volume
ESV:
End-systolic volume
Equation to get SV?
EDV-ESV=SV
Starling’s law:
Increase EDV by increasing venous return via:
- skeletal muscle pump
- respiratory pump
- sympathetic nervous system
- arterial vasoconstriction
Dicrotic notch shows:
Semilunar valves closing
Equation to get CO?
SVxHR=CO
What does increasing venous return result in? (starling’s law cont.)
- increase stretch of cardiac fibers
- increase strength of contraction
- increase SV
Starling’s law causes:
Stroke volume to increase
How do we measure resting HR? (3)
3 sec method
6 sec method
R-R method
PT interval:
heart contracts, systole
PT segment:
heart resting, diastole
Why is an AP not possible during absolute refractory period?
Because Na v.g.v. are sealed shut
