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48 Cards in this Set

  • Front
  • Back
Autorhythmic cell action potential
**There is no resting membrane potential

If "funny channels" open; permeable to Na+ and K+
• Na+ influx exceeds K+ efflux (= slow depolarization)

Initial depolarization causes T-type (transient) Ca²+ channels to open

Further depolarization causes L-type (long lasting) Ca²+ channels to open (= rapid depolarization)

Depolarization causes K+ channels to open; K+ exits cell
• Repolarization of cell to −60mV; K+ channels close
Electrical Activity in a Pacemaker Cell
Orange: spontaneous depolarization
• K+ exiting; Na+ entering cell
Yellow: later spontaneous depolarization
• Ca+ entering
Green: rapid depolarization
• Ca²+ entering
Pink: depolarization
• K+ existing
Contractile cell action potential
**Resting membrane potential (-90mV); depolarizes only when stimulated

• Stimulus opens voltage-gated Na+ channels
• Rapid inflow of Na+ into cell

• Action potential peak at +30mV
• Na+ gates close quickly

• Delayed opening of V-G Ca²+ channels
• EC Ca²+ enters & binds to ligand-gated Ca²+ channels on sarcoplasmic reticulum
• 2nd wave of Ca²+ binds to troponin → contraction

• K+ channels open; K+ exits cell
• Ca²+ channels close; Ca²+ transported back into SR
• Repolarization
AP of Contractile Cell
0) V-G Na+ channels open (when stimulated)
1) Action potential peaks, slight depolarization, V-G sodium channels close
2) V-G channels Ca²+ open; EC Ca²+ enters & binds to ligand-gated channels on SR, 2nd Ca²+ wave → contraction
3) K+ channels open, K+ exits cell, Ca²+ channels close, Ca²+ returns to SR
4) Repolarization
Electrical activity of heart is recorded by _____.
electrocardiogram (ECG)
P wave
corresponds to atrial depolarization
QRS complex
corresponds to ventricular depolarization
T wave
corresponds to ventricular repolarization
Atrial repolarization is masked by larger ________.
QRS complex
Heart Excitation Related to ECG
SA node generates impulse; atrial excitation begins
Impulse delayed at AV node
Impulse passes to heart apex; ventricular excitation begins
Ventricular excitation complete
Cardiac Cycle
all the events associated with a single heartbeat (w/ respect to L Ventricle)
contraction of heart muscle
relaxation of heart muscle
What are the four phases of the cardiac cycle?
1) ventricular filling (mid-late) diastole
2) isovolumetric contraction (beginning of systole)
3) ventricular ejection: (mid-late systole)
4) isovolumetric relaxation (beginning of diastole)
What occurs during ventricular filling?
• low pressure in ventricles
• AV valves open
• ventricles passively fill with blood

At the end of phase one…
• atria depolarize (P wave), then…
• atria contract → remaining blood enters ventricles
What occurs during isovolumetric contraction?
• ventricle depolarize (QRS)
• ventricles begin to contract
∙ ↑ ventricular pressure
∙ closes AV valves ("Lub" - 1st heart sound)
• semilunar valves remain closed = isovolumetric Contraction (constant volume in ventricles)
What occurs during ventricular ejection?
• ↑ ventricles to maximal pressure
∙ forces semilunar valves open
• blood ejected into great vessels
∙ ↓ ventricular volume
What occurs during isovolumetric relaxation?
• low pressure in ventricles
• SL valves open ("Dup" - 2nd heart sound)
• AV valves still closed ...until...

1) Ventricular filling
• ventricular pressure drops below atrial pressure → forces AV valves open
∙ ventricular filling
What is the Dicrotic notch?
rise in the BP in aorta: blood encounters resistance and starts to flow back to ventricle
Blood moves from one place to another because of a _______
Pressure Gradient
isovolumetric contraction
all valves closed, ventricles contracting

volumes of ventricles remain constant & at HIGHEST

End diastolic volume
isovolumetric relaxation
all valves closed, ventricles relaxing

volumes of ventricles remain constant & at LOWEST

End systolic volume
End diastolic volume
amount of blood collected in a ventricle during diastole
End systolic volume
amount of blood collected in a ventricle during systole
Stoke Volume =
End diastolic volume - End systolic volume

Cardiac Output (CO)
volume of blood pumped by one ventricle in 1 minute (ml/min or L/min)

CO = HR x SV
Heart Rate (HR)
heart beats/minute

CO = HR x SV
Stroke Volume (SV)
amount of blood ejected per beat (ml/beat)

at rest 80ml/beat x 75 beats/min = 6000ml/min

Therefore our entire blood supply is circulated in 1 minute
CO is the total blow flow to ________ of the body
CO is the total blood flow to all tissues of the body (systemic circuit); increased demand for O₂ and nutrients must be met by increased CO
Basic heart rate is set by _____; ________ modifies it
Basic heart rate is set by intrinsic conduction system; extrinsic modifies it
Extrinsic control of the heart is controlled by:
endocrine system and nervous system
Endocrine system
influences heart rate & force of contraction via several hormones
e.g. epinephrine, acetylcholine & thyroxine
Nervous System
influences heart rate and force primarily via cardiac centers of medulla oblongata
What are the two cardiac centers of the medulla oblongata?
Cardioacceleratory center and Cardioinhibitory center
Cardioacceleratory Center
Sympathetic Nervous System (SNS)

Increases heart rate
Cardioinhibitory Center
Parasympathetic Nervous System (PNS)

Decreases heart rate
Under resting conditions the PNS and SNS sends signals to _______
the heart
Given the following information:
• Both SNS and PNS sends signals to SA node
• Without nervous system influence → SA node fires at 100 bpm
• Resting heart rate = 70-80 bpm
• If vagus nerves are severed → heart rate increases to 100 bpm

What is the dominant influence of the resting heart rate? PNS? SNS?
PNS is greater because heart rate is less than the natural, spontaneous depolarization of SA node → called Vagal Tone
What are the three main factors that influences stroke volume?
1) Preload
2) Contractility
3) Afterload
What is Preload?
amount ventricles are stretched by contained blood

Preload - how much the ventricle is stretched before contracting ~ how much blood is in the ventricle before systole (EDV)

↑ EDV = ↑ Preload

The more the ventricle is stretched - the more force it generates
EDV (preload) is affected by:
1) Venous return - amount of blood returning to heart & filling ventricles
Note: an increase in CO = increase in VR
2) Filling time - duration of ventricular diastole
Note: an increase in HR = decrease in filling time
What is the Frank-Starling Law of the Heart
heart can pump any additional blood it receives per cardiac cycle (more in = more out)

↑ EDV = ↑ SV

Preload (degree of stretch) is critical factor controlling SV
What is contractility?
cardiac cell contractile force due to factors other than EDV

Contractility - how hard ventricles is squeezing, regardless of how it is stretched

Directly proportional to Ca²+ levels within myocardial cell

↑ Contractility = ↑ SV and ↓ ESV

Contractility increases when:
• Cardioacceleratory activity increases
• Plasma epinephrine levels increases
• Plasma thyroxine levels increases

Contractility decreases when:
• Drugs such as calcium channels blockers increase
Contractility increases when:
• Cardioacceleratory activity increases
• Plasma epinephrine levels increases
• Plasma thyroxine levels increases
Contractility decreases when:
• Drugs such as calcium channels blockers increase
What is afterload?
back pressure exerted by blood in large arteries leaving the heart

Afterload - refers to pressure that must be overcome by the ventricles in order for SL valves to open and blood to be ejected

Any factor that increases resistance (and thus pressure) in the arterial circulation will increase after load

Major problems with increase in after load results from chronic hypertension - heart attempt to compensate - leads to heart failure

↑ Afterload = ↓ SV

Afterload increases with vasoconstriction (reduction in vessel diameter)

Afterload decreases with vasodilation (increase in vessel diameter)
What is the PR interval?
Delay of AV node to allow filling of ventricles
What is the ST Segment?
Beginning of ventricle to depolarization. Should be flat