Cardiovascular Physiology Flashcards

1
Q

What is a heart contraction?

A

Electrical impulse that triggers contractile cells

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2
Q

Is a heart contraction intrinsic or extrinsic?

A

intrinsic (arises from within the heart)

nervous system NOT required

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3
Q

What are the nodes?

A

clusters of conducting ells that initiate AP in the heart

they have an unstable resting potential (leaky to Na+)

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4
Q

What is the name for the gradual depolarization of nodal cells

A

prepotential

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5
Q

what happens when threshold is met in the nodal cells?

A

the voltage gated Ca2+ channels open and a spontaneous AP occurs

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6
Q

List the steps of a conducting cell AP

A

1) Na+ enters through leak ch. (slow influx)
2) cell develops a prepotential
3) v. gated ca2+ channels open @ threshold
4) rapid influx of ca2+ causes depolarization which causes an AP
5) ca2+ channels close and voltage gated K+ channels open
6) depolarization occurs

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7
Q

How do the AP’s spread beyond the nodal cells to the contractile cells?

A

gap junctions @ intercalated discs

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8
Q

How are the cells connected?

A

via desmosomes an anchoring protein which prevents separation

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9
Q

explain and list the electrical pathway that the impulse spreads

A

1) Sinoatrial (SA) node -In posterior wall of R. Atrium
* goes across internal pathway
2) Atrioventricular (AV) node - floor of R. Atrium
* AP delayed here to allow time for atria to contract
* impuse transmitted to…
3) AV bundle (in the intertribal septum)
4) L + R Bundle branches (in the inter ventricular septum)
5) Purkinje fibers (walls of ventricles)
* Ventricles contract

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10
Q

what is the contraction rate established by the SA node?

A

100 bpm

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11
Q

so if the SA node wants the heart to beet 100bpm… why doesn’t it?

A

the parasympathetic system innervates the node - Acetylcholine slows the heart

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12
Q

what happens if the sympathetic system innervates the nodes?

A

norepinephrine speeds the heart

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13
Q

What would happen if the SA node stopped working

A

the AV node would fire on its own 40-60bpm

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14
Q

Special aspects of cardiac cell anatomy

A
  • Gap junctions: allow ions to move from cell to cell
  • Desmosomes: prevent separation
  • Mitochondria: are very fatigue resistant
  • Myofibrils: Branch
  • NO Terminal cisternae: T tubules release Ca2+ from sarcoplasmic reticulum
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15
Q

Describe the spread of AP to contractile cells

A

1) Na+ leaks in
2) V. Gated ca2+ ch. open in nodal cells
3) Action potential across nodal cells
4) Cations (+) diffuse into adjacent contractile cells via intercalated discs which house gap junctions
5) this depolarization causes fast v. gated na+ Ch and slow ca2+ channels to open in contractile cells

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16
Q

why are AP slower and more prolonged than in skeletal muscle

A

-V. gated Na+ channels close quickly
-V. Gated K+ Ch = open
**Repolarization is delayed because voltage gated ca2+ channels in the cell membrane are still open and Ca2+ comes in from the ECF
**
This influx also opens ca2+ gated ca2+ channels (like a ligand) in the sarcoplasmic reticulum
**So there is a plateau in membrane potential as ca2+ moves in while K+ moves out
(AP is 30x slower)

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17
Q

Explain the steps of the cardiac muscle cell AP

A

1) Na+ & ca2+ influx through voltage gated ch.
2) na+ ch. close, k+ ch. open
3) ca2+ influx from ECF & SR and K+ influx -plateau
4) Ca2+ ch. close
5) K+ outflow continues
6) v. Gated K+ ch close (repolarized)

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18
Q

What does it mean that contraction of cardiac muscle cells is coupled to excitation

A
  • Ca2+ enters from SR + ECF
  • Ca2+ binds troponin causing tropomyosin to shift
  • This allows the cross bridge to form (Myosin binds actin)
  • the filaments slide which causes a contraction
  • The ca2+ ch are slow to close so the contraction is prolonged
  • eventually the ca2+ pumps will put all the Ca2+ back where it came from and outflux of K+ will repolarize the cell
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19
Q

What is meant by a cardiac cycle?

A

1 complete contraction & relaxation

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20
Q

What is systole

A

contraction phase (blood pushed out of chamber)

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21
Q

what is diastole

A

Relaxation phase (chamber fills with blood)

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22
Q

What does an electrocardiogram do?

A

Records electrical currents (AP’s) during the cardiac cycle

DOES NOT measure muscle contractions: just the electrical events that trigger it

23
Q

what causes the p wave

A

atria depolarization then atrial systole occurs in space after

24
Q

What causes QRS Complex

A

Ventricles depolarize then after the ventricular systole occurs
(@ same time atria is repolarizing and atrial diastole)

25
What is causes the T wave
ventricles repolarize then ventricular diastole occurs
26
What is happening at atrial systole
SA node depolarizes to AV node both atria contract both AV valves are forced open the blood is pushed into the ventricles
27
What is happening at ventricular systole
The electrical impulse to AV bundle to R +L Bundle branches to purkinje fibers -The isovolumetric contraction phase occurs as pressure rises the SL valves open the ejection phase
28
What is the isovolumetric contraction phase
both ventricles contract but blood has not been ejected yet
29
what is the stroke volume
amount ejected from left ventricle
30
what is the end systolic volume
the amount of blood remaining in ventricles after systole
31
What is happening at ventricular diastole
- Semilunar valves close - isovolumentric relaxation phase (only the ESV is in ventricle) - passive filling - active filling
32
What is passive filling
low pressure pulls blood from atria through av valve the ventricles fill 70% w/o the atria even contracting
33
What is active filling
The atria contract and push 30% more blood in | the av valves close
34
What is end diastolic volume
blood in ventricles @ max
35
what is happening during atrial diastole
- Passive filling of atrial as the relax | - occurs during ventricular systole and diastole
36
What are the muscles doing @ P wave
passive ventricular filling & atrial contraction
37
what are the muscles doing @QRS complex
isovolumetric contraction
38
What happens just after QRS complex
ventricular ejection phase
39
what happens in muscles at T wave
isovolumetric relaxation
40
What is the equation for cardiac output
HR X SV
41
Explain the regulation of heart rate
Intrinsic contraction rate is altered by the ANS | ANS fibers innervate nodal cells (adjust pacemaker activity) by altering ion permeability
42
Explain what the cardio accelerator centers do
- Sympathetic - Increase heart rate - Norepinephrine binds to beta 1 receptors
43
Explain what the cardio inhibitory enters do
- parasympathetic - vagus nerve - decrease heart rate - Acetylcholine binds to M2 recepters
44
What is the dominant influence on regulation of heart rate
Parasympathetic | The vagus nerve fibers release ACH which opens K+ ch in conducting cells to decrease HR
45
Steps of parasympathetic regulation of HR
1) cardio inhibitory center 2) Vagus nerve 3) ach. decrease hr on SA+AV node
46
steps of sympathetic regulation of HR
1) cardioacceleratory center 2) sympathetic chain ganglion 3) sympathetic cardiac nerve - NE increase HR & Contractile force 4) can go to the nodes and the muscle cells
47
Equation for stroke volume
SV = EDV - ESV
48
what is ejection fraction
fraction of blood ejected from ventricles with each contraction
49
equation for ejection fraction
SV / EDV x 100
50
What are the 3 factors affecting stoke volume
1) Preload 2) Contractility 3) Afterload
51
Explain preload
Amount the ventricles are stretched by contained blood Increased preload causes harder heart contractions *Increased stretch increases sarcomere length, more cross bridges can form between actin & Myosin *Factor that increase venous return will increase preload *Hr will also increase in response to venous return (atrial reflex)
52
Explain the atrial reflex
Strech receptors in all or right atrium detect pressure and increase HR to get blood out of the heart
53
Explain contractility
Increase in contractile force - Decreased ESV and increased SV - regulated by hormones * NE, THYROXINE, EPINEPHRINE - increase Ca2+ entry into cardiac cells
54
Explain after load
pressure exerted bu arterial blood on SL valves must overcome to eject blood into systemic circulation ventricles must over come this resistance to circulate blood