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Cardiology > Week 1 aka hell week > Flashcards

Week 1 aka hell week Flashcards

1
Q

Which node does not have a stable membrane potential

A

SA node

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2
Q

What causes the pacemaker potential

A

Decrease in in K+ efflux superimposed on a slow Na+ influx current

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3
Q

What cause the rising phase of the action potential (depolaristation) in the SA node

A

Activation of voltage-gated Ca+ channels > This results in a Ca+ influx

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4
Q

What cause the falling phase of the action potential (repolaristation) in the SA node

A

caused by the activation of K+ channels
> Resulting in a K+ efflux

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5
Q

What is responsible for the rising phase (depolarisation) in ventricular muscle

A
  • Fast Na+ influx
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6
Q

What causes the plateau phase of ventricular muscle

A

influx of Ca+

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7
Q

What causes the falling phase of the action potential (depolarisation)

A

inactivation of Ca+ channels and activation of K+channels causing a K+ efflux

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8
Q

What effect does the Vagus nerve have on heart rate

A

Vagal tone slows the intrinsic HR from 100bpm to sound 70bpm

>Vagal tone dominates under restin conditions

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9
Q

What is a negative/positive chronotropic effect?

A

speeds up/ slows heart rate

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10
Q

What are myofibrils?

A
  • contractile units of muscle. Each muscle cell contains many myofibrils
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11
Q

What are SACROMERES?

A

SACROMERES is the name given to how actin and myocin are arranged within each MYOFIBRIL

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12
Q

How is cardiac muscle tension produced

A

by the sliding of actin filaments on myosin filaments

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13
Q

What switches on the cross bridge formation between muscle fibres

A

Ca+

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14
Q

What element is require to stimulate the release of calcium from the sarcoplasmic reticulum

A

Ca+

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15
Q

What effect does a positive inotropic effect have on the frank starling curve

A

Shifts to the left

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16
Q

How could we regulate the cardiac output?

A

By regulating the stroke volume and Heart rate

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17
Q

What is DIASTOLE

A

Heart ventricles are relaxed and fill with blood

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18
Q

What is systole?

A

the heart ventricles contract and pump blood into the: aorta (LV) and pulmonary artery(RV)

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19
Q

Describe the events of PASSIVE FILLING

A
  • Pressure in atria and ventricles close to zero
  • AV valves open so venous return flows into the ventricles
  • Aortic pressure ~ 80 mmHg, and aortic valve is closed
  • Similar events happen in the right side of the heart, but the pressures (right ventricular and pulmonary artery) are much lower

> Ventricles become ~ 80% full by passive filling (due to a simple pressure gradient)

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20
Q

Describe the events of ATRIAL CONTRACTION

A

The P-wave in the ECG signals atrial depolarisation

The atria contracts between the P-wave and the QRS

> Atrial contraction complete the END DIASTOLIC VOLUME (~ 130 ml in resting normal adult) – the end diastolic pressure is few mmHg)

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21
Q

Describe the events of ISOVOLUMETRIC VENTRICULAR CONTRACTIO

A
  • Ventricular contraction starts after the QRS (signals ventricular depolarisation) in the ECG
  • Ventricular pressure rises
  • When the ventricular pressure exceeds atrial pressure the AV VALVES SHUT
  • This produces the FIRST HEART SOUND (LUB)
  • The aortic valve is still shut, so no blood can enter or leave the ventricle
  • The tension rises around a closed volume “Isovolumetric Contraction”

The ventricular pressure rises very steeply

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22
Q

Describe the events of VENTRICULAR EJECTION

A
  • When the ventricular pressure exceeds aorta/pulmonary artery pressure
  • Aortic/pulmonary valve open
  • Stroke Volume (SV) is ejected by each ventricle, leaving behind the End Systolic Volume (ESV)
  • Aortic pressure rises
  • The T-wave in the ECG signals ventricular repolarisation
  • The ventricles relax and the ventricular pressure start to fall
  • When the ventricular pressure falls below aortic/pulmonary pressure: aortic/pulmonary valves shut
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23
Q

Describe the events of ISOVOLUMETRIC VENTRICULAR RELAXATION

A
  • Closure of aortic/and pulmonary valves signals the start of the isovolumetric ventricular relaxation
  • Ventricle is again a closed box, as the AV valve is shut
  • The tension falls around a closed volume “Isovolumetric Relaxation”
  • When the ventricular pressure falls below atrial pressure, AV valves open (Remember this is a silent event), and the heart starts a new cycle
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24
Q

What causes the first heart sound?

A

closure of mitral and tricuspid valves. It sounds like a “lub”

25
Q

What causes the 2nd heart sound?

A

caused by closure of aortic and pulmonary valves.

It sounds like a “dub”

26
Q

What prevents arterial pressure from falling to zero during diastole?

A

The recoil of the arteries keeps the blood flowing and prevents the pressure from falling

The closure of the aortic valve also contributes to this

27
Q

What drives blood around the systemic circulation?

A

A Pressure Gradient between the Aorta (AO) and the Right Atrium (RA)

28
Q

A MAP of what pressure is needed to perfuse vital organs?

A

60 mmHg

29
Q

What is the normal mean range for MAP

A

70 —–> 105

30
Q

Where are the two groups of baroceptors located??

A

(1) Aortic Arch
(2) Carotid Sinus

31
Q

How is information relayed to the medulla

A

via the Vagus nerve and glossopharyngeal nerve

32
Q

What stops the firing of baroceptors

A

if high blood pressure is sustained

33
Q

What is responsible for the long term control of MAP

A

Blood Volume

34
Q

What two factors affect extracellular volume

A

Water excess or deficit

Na+ excess or deficit

35
Q

What is - The Renin-Angiotensin- Aldosterone System - RAAS?

A

Plays an important role in the regulation of plasma volume and TPR and hence the regulation of MAP

36
Q

Where does Renin come from and what does it do?

A

Renin is released from the kidneys and stimulates the formation of angiotensin I in the blood from angiotensinogen (produced by the liver)

37
Q

What is the name of the enzyme which converts AngiotensinI into Angiotensin II

A

ACE (produced by pulmonary vascular endothelium)

38
Q

What are the two jobs of ANGIOTENSIN II?

A
  1. stimulates the release of Aldosterone from the adrenal cortex
  2. Causes systemic vasoconstriction - increases TPR
39
Q

What is the function of ALDOSTERONE?

A

a steroid hormone

acts on the kidneys to increase sodium and water retention – increases plasma volume

40
Q

How is the Renin-Angiotensin- Aldosterone System regulated?

A

(1) Renal artery hypotension -caused by systemic hypotension (decreased blood pressure)
(2) stimulation of renal sympathetic nerves
(3) Decreased [Na+] in renal tubular fluid – sensed by macula densa (specialised cells of kidney tubules)

41
Q

What is Atrial Natriuretic Peptide?

A

28 amino acid peptide synthesised and stored by atrial muscle cells (atrial myocytes)

Released in response to atrial distension (hypervolaemic states)

42
Q

What is the primary purpose of ANP?

A

Causes excretion of salt and water in the kidneys, thereby reducing blood volume and blood pressure

Acts as a vasodilator - decreases blood pressure

Decreases Renin release

43
Q

What is ADH?

A

Peptide hormone derived from a prehormone precursor synthesised by the hypothalamus and stored in the posterior pituitary

Secretion stimulated by

1) reduced extracellular fluid volume or
2) increased extracellular fluid osmolarity (main stimulus)

44
Q

What is the normal osmolarity of extracellular fluid?

A

280 milli-osmoles/l

45
Q

What is the function of ADH?

A

ADH acts in the kidney tubules to increase the reabsorption of water (conserve water) - i.e. concentrate urine (antidiuresis)

This would increase extracellular and plasma volume and hence cardiac output and blood pressure

46
Q

What is the function of osmoreceptors?

A

To monitor the plasma osmolality?

47
Q

What is the main site of TOTAL PERIPHERAL RESISTANCE

A

The arterioles

48
Q

What system supplies the vascular smooth muscle?

A

SYMPATHETIC nerve fibers.

The neurotransmitter is NORADRENALINE acting on alpha receptors

49
Q

Define Vasomotor tone

A

Vasomotor tone is the amount of tension in the smooth muscle inside the walls of blood vessels, particularly in arteries

50
Q

What would increase vasomotor tone and thereby causing vasoconstriction

A
  • Increased sympathetic discharge
51
Q

What would decrease vasomotor tone and thereby causing vasodilation

A

Decreased sympathetic discharge

52
Q

What is the effect of adrenaline of alpha receptors?

A

causes vasoconstriction

53
Q

What is the effect of adrenaline of beta receptors?

A

vasodilation

54
Q

what factors cause relaxation of arteriolar smooth muscles resulting in VASODILATATION:

A
  • Decreased local PO2
  • Increased local PCO2
  • Increased local [H+] (decreased pH)
  • Increased extra-cellular [K+]
  • Increased osmolality of ECF
  • Adenosine release (from ATP)
55
Q

Name 3 humoral agents which cause relaxation of arteriolar smooth muscles resulting in VASODILATATION

A
  1. Histamine
  2. Bradykinin
  3. Nitric Oxide (NO) - this is continuously released by endothelial cells of arteries and arteriole
56
Q

Name 3 humoral agents which cause contraction of arteriolar smooth muscles resulting in VASOconstriction

A

Serotonin

Thromboxane A2

Leukotrienes

Endothelin - this is a potent vasoconstrictor released from endothelial cells. Its production is stimulated by various agents which cause vasoconstriction

57
Q

What effecr does increased VENOmotor tone have?

A

Increased venous return, SV and MAP

58
Q
A

Cardiology (2 decks)

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