CVS Flashcards

1
Q

Which feature of cardiac muscle cells allows all cells to contract in unison (so that blood can be pumped in unison throughout the body)?

A

Intercalated discs

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2
Q

Cardiomyocytes have a Membrane Potential, what is this?

A

The difference in electrical potential between the inside and outside of the cell (due to different conc. of ions)

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3
Q

At rest the membrane potential of the heart is usually +ve/-ve?

A

Negative (-ve)

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4
Q

Cardiomyocytes contract in response to Action Potentials, where are these generated?

A

Pacemaker cells of SinoAtrial Node (SAN) in the Right Atrium. Natural pacemaker of the heart.

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5
Q

What does the membrane potential of cardiomyocytes have to do with contraction in response to Action Potentials?

A

It is the change in the membrane potential of cardiomyocytes, triggered by the AP, which causes contraction.

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6
Q

Why do cardiac muscle cells contain T-tubules and sarcoplasmic reticulum?

A

For calcium release

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7
Q

Which feature of cardiac cells allows the current to flow rapidly from SA node throughout the heart by cell-cell conduction?

A

Gap Junctions

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8
Q

Between Action POtentials pacemaker cells have a varying permeability to K+, what is this called and what does this cause?

A

Spontaneous pacemaker potential - Causes spontaneous depolarisation.

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9
Q

What is the order of conduction from the SAN to the ventricles?

A

SAN –> (Atria and) AVN –> Bundle of His –> branches –> purkinje fibres

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10
Q

Why is spread of the AP delayed at the AV node ?

A

To protect the ventricles from contracting before they are filled with blood from the atria.

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11
Q

What is the resting membrane potential of a pacemaker cell?

A

UNSTABLE, doesnt rest but because of spontaneous pm potential.varies around -60m.

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12
Q

Depolarisation occurs in A) pacemaker cells and B) cardiomyocytes because of Fast influx of what?

A

A) Ca++

B) Na++

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13
Q

Parasympathetic vagal tone is continously exerted on the heart what is the effect of its neurotransmitter ACh on
A) the SAN
B) AVN
?

A

A) reduced HR

B) Increased AV nodal delay

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14
Q

How does ACh prolong (flatten) the pacemaker potential phase?

A

It increases permeability to K+ => increases K+ efflux, slowing the rise in membrane potential

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15
Q

The Sympathetic action of NA on the SAN and AVN opposes the parasympathetic effects exerted continually by the vagus nerve (increases HR and decreases AVN delay), what additional sympathetic effect does NA have on the heart?

A

acts on myocytes to increase contractility.

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16
Q

When and why does spontaneous depolarisation of SA node cells occur?

A

When threshold is reached (-40mV) as a result of slow influx of Na+ and Ca++ (and decreased efflux of K+)

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17
Q

Through which channels does Ca++ rapidly influx to the SAN cells during depolarisation to create an AP?

A

L-Type Ca++ channels.

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18
Q

What happens in the repolarisation phase of both SAN cells and cardiomyocytes?

A

K+ Efflux

Ca++ Influx STOPS

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19
Q

APs are generated automatically from the SAN in absence of external stimuli. What aspect of the AP can be altered by external stimuli?

A

The RATE OF DEPOLARISATION CAN INCREASE OR DECREASE Iin response to external Influences

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20
Q

Why is Atropine used in Bradycardia?

A

It is a competitive inhibitor of ACh => stops ACh binding to the pacemaker cells to decrease the rate of depolarisation

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21
Q

Why does the plateau phase of the cardiomyocyte AP occur when K+ is moving out?

A

Because Ca++ is moving in simultaneous to balance the K+ Efflux therefore maintaining the high membrane potential. When the Ca++ stop coming in this loses balance and negative outweighs the positive and repolarisation occurs.

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22
Q

Why is the whole duration of an action potential of a cardiomyocyte known as the Absolute Refractory Period?

A

It is the period in which the generation of a 2nd AP is not possible.

23
Q

How are the ventricles prevented from contracting before they are filled?

A

AV nodal delay –> ensures that Atrial systole precedes ventricular systole

24
Q

Which feature of the intercalated discs ensures
A) cell-cell conduction of impulses
B) tension is transmitted form cell to cell

A

A) - Gap Junctions - protein channels between cells for electrical communication
B) Desmosomes - mechanical adhesives between adjacent cells

25
Q

What is Starlings law?

A

The greater the EDV, the greater the Stroke Volume during Systole

26
Q

In Cardiac muscle optimal muscle length is achieved at rest? T/F

A

F. Thats for skeletal muscle.

In Cardiac optimal length is achieved through STRETCHING

27
Q

What is the effect of After load on Stroke volume?

A

If Afterload increases Stroke Volume decreases because full the full volume of blood cannot be ejected.

28
Q

If the afterload is continually increased (i.e untreated hypertension) how will the heart compensate?

A

Ventricular muscle mass will INCREASE to cope with extra resistance.
F-S law will partially compensate by increasing EDV (in response to decreased SV)

29
Q

How is a positive inotropic effect mediated through sympathetic firing to the heart?

A

Once NorAdrenaline reaches B1 receptors on cardiac muscle, calcium influx occurs increasing contractility.

30
Q

What is the effect of positive inotropy on the frank-starling curve?

A

SHIFTS LEFT.

For any given EDV, the contractility increases –> increased SV.

31
Q

What must be regulated to regulate the cardiac output?

A

Stroke Volume and Heart Rate.

32
Q

Why is parasympathetic tone sometimes called vagal tone?

A

Vagus nerve is the main nerve of the parasympathetic system.

33
Q

Failure of what reflex causes postural hypotension to occur?

A

Baroreceptor reflex

34
Q

Baroreceptors can respond to consistently high blood pressure? T/F

A

FALSE baroreceptors only respond to ACUTE changes in Bp

35
Q

How is MAP regulated in the long term?

A

Through control of blood volume (extracellular fluid)

36
Q

Why can untreated hypertension lead to ventricular hypertrophy?

A

Hypertension increases the afterload so the ventricles have to work harder to eject the blood into this high pressure. Over time this increased work results in thickening of the ventricular muscle.

37
Q

What is the rate limiting step for the REnin-Angiotension-Aldosterone-System (RAAS) ?

A

Renin secretion from kidney

38
Q

What are the three hormones that work to increase blood pressure through retaining water and sodium?

A

ADH, Angiotensin 2, Aldosterone

39
Q
Which hormones that work to increase blood pressure come from the 
A) Adrenal cortex
B) posterior pituitary
C) liver
??
A

A) Aldosterone
B) ADH
C) Angiotensin 2

40
Q

When is ADH released?

A

In response to high plasma osmolarity (low bp) detected by osmoreceptors in hypothalamus which stimulates posterior pituitary to release ADH

41
Q

How does ADH act on the
A) Kidney
B) blood vessels
to increase blood pressure?

A

A) Acts on collecting duct of kidneys to increase water reabsorption => increasing ECF and PV and => incresing CO and Bp
B) Vasoconstriction

42
Q

Which ion is proportional to ECF volume?

A

Na+ (Water follows salt)

43
Q

Which hormone opposes the effects of RAAS and is released from atrial myocytes?

A

Atrial NAtiuretic Peptide.

44
Q

Renin is an enzyme secreted from which cells?

A

Juxtaglomerular granular cells in kidney.

45
Q

baroreceptor response can trigger renin release T or F?

A

T. In response to low blood pressure baroreceptors increase sympathetic firing which stimulates granular cells to release renin.

46
Q

Why does MAP = ((2X dBp) + sBp)/ 3 ?

A

Because diastole is 2X longer than systole.

47
Q

When arterial blood pressure is measured by a sphygmomanometer the systolic and diastolic pressures measured are representative of the pressure within which artery?

A

Brachial Artery

48
Q

At what point (in measuring blood pressure) does blood flow change from laminar (normal flow, inaudible through stethescope) to turbulant?

A

When external pressure applied is between systolic and diastolic.

49
Q

What is the name for the partial constriction of vascular smooth muscle at rest due to tonic discharge of the SYMPATHETIC system?

A

VASOMOTOR TONE

50
Q

Innervation of vascular smooth muscle = mainly SYMPATHETIC or PARASYMPATHETIC?

A

SYMPATHETIC

51
Q

How is cerebral flow autoregulated to remain constant over a wide range of pressures?

A

It is not affected by the baroreceptor reflex and instead autoregulated by a MYOGENIC response. If MAP increases vasoconstriction occurs and if MAP decreases then vasodilation occurs (to increase flow)

52
Q

Why does hyperventilation lead to fainting?

A

Reduced pCO2 –> cerebral vasodilation

53
Q

Why do tumours or head injuries result in reduced cerebral flow?

A

They increase intracranial pressure which results in a decrease in cerebral perfusion pressure to keep the overall pressure constant.

54
Q

Which matter within the brain is more sensitive to hypoxia?

A

GRey matter