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biology 153 > cardiovascular physiology > Flashcards

cardiovascular physiology Flashcards

cardiovascular physiology

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1
Q

what is heart contraction? - impulse? -extrinsic or intrinsic? -nervous system?

A

ELECTRICAL impulse that TRIGGERS contraction of cardiac muscle cells is INTRINSIC
- stimulation from nervous system is NOT required

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2
Q

conducting cells?

A

part of INTRINSIC conducting system

-special cardiocytes that INITIATE and DISTRIBUTE AP in heart muscle

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3
Q

what are nodes?

A

part of intrinsic condonducting system

-CLUSTERS of conducting cells that initiate AP in heart

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4
Q

INTRINSIC conducting system has what kind of potential?

A

UNSTABLE resting potential (NA+ leaks in)

gradual depolarization occurs

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5
Q

what happens when gradual depolarization occurs in intrinsic conducting system?

A

“prepotential” develops

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6
Q

at threshold of intrinsic conducting system, what happens? CONDUCTING cells

A

opening of CA 2+ channels (Ca 2+ rushes in from ECF–> spontaneous action potential!

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7
Q

first step of intrinsic conducting pathway

A

NA + enters thru leak channels

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8
Q

steps of intrinsic pathway after NA+ leaks in

CONDUCTING CELLS

A

2) cell develops prepotenial
3) voltage gated Ca2+ channels open at threshold
4) Ca2+ influx causes depolarization (AP)!
5) Ca2+ channels close, and voltage gated channels open
6) K+ efflux causes repolarization

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9
Q

resting potential in intrinsic pathway is NEVER..

A

a flat line

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10
Q

what are action potentials spread along conducting pathways through?

A

GAP junctions at intercalated discs

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11
Q

where is A.P initiated

A

PACEMAKER (sinoatrial node S.A)

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12
Q

how many times does the SA node depolarize every minute?

A

approximately 100 times

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13
Q

pathway of the AP starting in SA node

A

1) SA node (pacemaker) in posterior wall of r.a
2) atrioventricular node in floor of r.a
3) atrioventricular bundle in interatrial septum
4) right and left bundle branches in interventricular septum
5) purkinje fibres in walls of ventricles

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14
Q

where is the AP delayed?

A

the atrioventricular node TO allow time for atria to contract

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15
Q

why is heart rate slower than the pacemaker contraction rate 100 bpm?

A

parasympathetic innervates nodes, acetylcholine shows down heart

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16
Q

how does heart rate increase

A

sympathetic innervates nodes, norepinephrine speeds heart up

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17
Q

the a.v node also has an intrinsic firing rate.. purpose?

A

it is 40-60bpm and takes over if the SA node fails

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18
Q

why does the pacemaker firing trigger ALL-OR-NONE contraction of whole heart?

A

all cells are connected by gap junctions at intercalated discs

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19
Q

what are gap junctions?

A

allow ions to move from cell to cell

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20
Q

what are desmosomes?

A

anchoring proteins prevent separation of contracting cells

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21
Q

many mitochondria function in cardiac muscle cell?

A

very fatigue resistant

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22
Q

myofibrils in cardiac muscle cell

A

myofibrils branch

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23
Q

is there terminal cisternae in cardiac muscle cells?

A

NO.

-t-tubules release calcium from sarcoplasmic reticulum

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24
Q

where does the AP in nodal conducting cells spread to?

A

contractile cells

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25
Q

steps of the spread from nodal conducting cells to contractile cells..

A

IN conducting cells:
1) Na+ leaks in
2) voltage gated Ca2+ ch open in nodal cell
3) A.P
4) Cations diffuse into adjacent contractile cells (intercalated discs with gap junctions)
IN contractile cells:
5) fast voltage gated Na+ channels and slow Ca2+ channels open in contracticle cells

26
Q

AP in cardiac muscles are ______ and more ______ than in skeletal muscle

A

SLOW and MORE PROLONGED

27
Q

steps of AP in cardiac muscle cells (CONTRACTILE)

A

1) VOLTAGE gated Na+ channels close quickly and then K+ channels open BUT repolarization is delayed because…
2) change in membrane potential also OPENS CALCIUM gate Ca2+ channels in cell membrane–> INFLUX of ca2+ from ECF
3) Ca2+ influx opens gated Ca2+ in ST—> influx of Ca2+ from SR
4) THIS CAUSES A PLATEAU IN membrane potential AS Ca2+ movies in WHILE K+ moves out
* **A.P 30x more in cardiac cells than in skeletal muscle

28
Q

EXCITATION- CONTRACTION COUPLING–>

AP triggers contraction steps..? (LIKE SKELETAL MUSCLE)

A

1) membrane depolarization OPENS calcium gated Ca2+ channels in the S.R and the cell membrane of the cardiac muscle cells
2) Ca2+ enters cytoplasm from S.R and ECF
3) Ca2+ binds to troponin causing tropomyosin to shift
4) Allows crossbridges to form between actin and myosin (FILAMENTS SLIDE= contraction)
5_ Ca2+ channels SLOW to close, contraction pronglonged

29
Q

what is the cardiac cycle

A

one complete contraction and relaxation of the heart

30
Q

systole=?

A

CONTRACTION phase-

blood PUSHED OUT of chamber

31
Q

diastole=?

A

RELAXATION phase-

chambers FILLED WITH blood

32
Q

what is the ECG (electrocardiogram)

A

recording of electrical currents (APs in heart muscle cells) during cardiac cycle

33
Q

why is there NO ECG wave recorded before atrial repolarization

A

QRS WAVE takes over, occurs at same time as ventricular depolarization

34
Q

do the ECG waves represent muscle contraction?

A

NO. these electrical events trigger muscle contraction

35
Q

P wave?

A

atrial depolarize THEN atrial systole occurs

36
Q

QRS complex?

A

ventricles depolarize THEN ventricular systole occurs

37
Q

T wave?

A

ventricles repolarize THEN ventricular diastole occurs

38
Q

what are the events during the cardiac cycle/

A
  1. atrial systole
  2. ventricular systole
  3. ventricular diastole
  4. atrial diastole
39
Q

atrial systole=?

A
  • S.A node depolarizes, A.P spreads to A.V node
  • right and left atria contract
  • right and left a.v valves forced forced open as pressures rises
  • blood pushed into ventricles
40
Q

ventricular systole?

A
  • electrical impulse spreads to A.V bundle, r.l bundle branches, purkinje fibers
  • isovolumetric contraction phase AS right and left ventricles begin to contract NO blood yet ejected
  • pressure rises in ventricles, s.l valves forced open
  • ejection phase as blood ejected into aorta and pulmonary trunk
41
Q

ventricular diastole?

A
  • semilunar valves CLOSE (as pressures rises in aorta and pulmonary trunk)
  • isovolumetric relaxation phase (just ESV in ventricles)
42
Q

passive ventricular filling

A
  • low pressure in ventricles pulls blood from atria through A.V valves
  • ventricles fill as they relax until 70% full
43
Q

active ventricular filling

A
  • atria contract and push an addition 30% blood into ventricles
  • A.V valves close
  • blood in ventricles at maximum (EDV-end diastolic volume)
44
Q

atrial diastole

A
  • passive filling of atria as they relax

- occurs during ventricular systole and ventricular diastole

45
Q

what is cardiac output?

A

volume of blood pumped by heart each minute
EQUATION:
heart rate (# of beats per minute) X stroke volume

46
Q

cardiac output increases in response to demand.. HOW?

A
  • altering heart rate

- altering stroke volume

47
Q

how is the heart rate regulated?

A

intrinsic contraction rate cam be altered by ANS (extrinsic control)
-ANS fibers innervate the nodal cells.. adjust pacemaker activity by altering ion permeability

48
Q

medulla oblongata-> cardiac centers–> sympathetic?

A

sympathetic divison increases heart rate by norepinephrine binding to beta receptors

49
Q

medulla oblongata-> cardiac centers–> parasympathetic?

A

parasympathetic division (vagus nerve) decreases heart rate by acetylcholine binding to M2 receptors

50
Q

dominant infuence is which system?

A

parasympathetic; heart exhibits vagal tone due to vagus nerve

51
Q

what is the equation for STROKE volume

A

stroke volume= volume of blood left ventricle expels during contraction
EQUATION:
SV= EDV-ESV

52
Q

what is end diastolic volume?

A

volume of blood left in ventricle at end of diastole

53
Q

what is end systolic volume?

A

volume of blood in left ventricle after systole

54
Q

SV is more commonly expressed as the ejection fraction.. explain?

A

ejection fraction= fraction of blood ejected from ventricle with each contraction
SV/EDV X 100

55
Q

3 factors affecting SV

A

1) preload
2) contractility
3) afterload

56
Q

preload is?

A

AMOUNT the ventricles are STRETCHED by contained blood
preload= stretch= increased force of contraction
-stretch increase sacromere length, more crossbridges of myosin and actin

57
Q

factors that increase speed or volume or venous return will increase preload.. like?

A

increased venous return= increased EDV heart fills more

increased EDV= increased stretch, increased force, decreased ESV

58
Q

how is venous return increased?

A
  • skeletal muscle pump (contraction squeezes veins)

- respiratory pump (diaphragm relaxes and contracts. plunger affect)

59
Q

does the heart rate increase or decrease in response to venous return?

A

increases

  • atrial reflex (bainbridge reflex)
  • stretch receptors in wall of r.a detect rising atrial pressure, trigger a reflexive
  • helps to bump blood out of heart
60
Q

what is contractility?

A

increase in contractile force INDEPENDENT of preload and EDV

  • increased force of contraction = decreased ESV and increased SV
  • more blood pushed OUT, less blood left behind if heart contracts MORE
  • ion flow affects contractility (Ca2+ increases contractility)
61
Q

what is afterload?

A

pressure exerted by arterial blood on s.l valves; MUST be overcome to EJECT blood into systemic circulation
AFTERLOAD= high, heart must work HARDER

62
Q

what effect would hypertension have on afterload?

A

Enlarged heart. High B.P forces heart to work harder to pump blood

biology 153 (17 decks)

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