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Cardiovascular System > Session 4 > Flashcards

Session 4 Flashcards

1
Q

What sets the resting membrane potential of cardiac myocytes?*

A
  • K+ permeability (background K+ channels, not voltage-gated)
  • Membrane is permeable to K+ ions but impermeable to other ion species
  • K+ ions move out of the cell down the concentration gradient: makes inside negative with respect to outside
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2
Q

Why does the resting membrane potential not equal equilibrium potential of calcium ions?

A
  • Net outflow of K+ only continues until K+ is reached, and then there is no outflow
  • There is a very small permeability to other ions at rest , so it is -90 to -85mV
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3
Q

What is the function of cardiac myocytes?

A
  • Firing action potentials
  • APs trigger increase in cytosolic Ca2+
  • Allows actin-myosin interaction = contraction
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4
Q

What do cardiac and sino-atrial action potentials look like?*

A

They are much longer (especially cardiac ventricle)

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5
Q

Describe the ventricular action potential.*

A
  • Opening of voltage gated Na+ ion channels by depolarisation drives the potential towards the sodium membrane potential
  • Rapid initial repolarisation due to Na/K exchange (outward K+ current)
  • Opening of voltage-gated Ca2+ channels and influx allows for plateau as it balances with K+ efflux
  • Ca2+ channels inactivate and several different K+ channels open, allowing full K+ efflux

LASTS ABOUT 300ms

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6
Q

Describe the SA node action potential.*

A
  • Funny current causes slow, long depolarisation
  • Opening of voltage-gated Ca2+ channels (Na+ aren’t involved as they’d just be inactivated)
  • Then repolarisation by voltage-gated K+ channels
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7
Q

Describe the pacemaker potential in more detail.

A
  • Funny current to threshold
  • More negative = more activation
  • HCN channels allow influx of Na+ ions which cause depolarisation
  • T-type and L-type Ca2+ channels involved
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8
Q

What are HCN channels?

A
  • Hyperpolarisation-activated cyclic nucleotide-gated channels (sensitive to cAMP)
  • More hyperpolarisation = higher current as more channels are activated
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9
Q

What is a unique feature of the SAN potential?

A
  • Does not need nervous input/stimulus

- Unstable membrane potential (heart beats when denervated without need for neurotransmitter)

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10
Q

Why is the SAN fastest to depolarise?*

A
  • Sets rhythm (pacemaker)

- Spreads throughout atria

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11
Q

Why is there a delay in the AVN?*

A

Allows atria to finish contracting before the ventricles do.

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12
Q

What happens if action potentials fire too slowly?

A

Bradycardia (below 60bpm)

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13
Q

What happens if action potentials fail?

A

Asystole (no contraction)

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14
Q

What happens if action potentials fire too quickly?

A

Tachycardia (above 100bpm)

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15
Q

What happens if the action potentials become random?

A

Atrial fibrillation or Ventricular fibrillation (no cardiac output if VF)

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16
Q

What is hypokalaemia?

A

Plasma concentration of K+ is too low (below 3.5 mmol.L)

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17
Q

What is hyperkalaemia?

A

Plasma concentration of K+ is too high (> 5.5 mmol.L)

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18
Q

What is the normal concentration of potassium in plasma?

A

3.5 - 5.5 mmol/L

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19
Q

Why are cardiac myocytes so sensitive to potassium changes?

A
  • K+ permeability dominates the resting membrane potential

- Variance in K+ conc will cause a variation in RMP

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20
Q

What is the effect of hyperkalaemia?*

A
  • Depolarises myocytes
  • Slows down AP upstroke
  • Ek less negative and membrane potential depolarises slightly, which inactivates some voltage-gated Na+ channels
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21
Q

What are the risks of hyperkalaemia?

A
  • Asystole (initial increase in excitability)

- Severe hyperkalaemia (above 6.5 mmol/L will inactivate more channels and slow down the heart.

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22
Q

What is the treatment for hyperkalaemia?

A
  • Calcium gluconate: membrane becomes less excitable
  • Insulin and glucose: potassium enters cells to lower plasma concentrations

Won’t work if heart stops

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23
Q

What is the effect of hypokalaemia?*

A
  • Lengthens action potential
  • Delays repolarisation as some potassium channels respond to a decrease in K+ by reducing current further
  • ELONGATED POTENTIAL
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24
Q

What is the problem with prolonged hypokalaemia?*

A

Can lead to early after depolarisations (EAD).

  • Oscillations in membrane potentials
  • Can result in VF (minimum CO)
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25
Q

What is the process of excitation-contraction coupling?*

A
  • Depolarisation opens L-type Ca2+ channels in T-tubule system
  • Opens calcium-induced calcium release channels in SR
  • 75% from SR, 25% from sarcolemma

Calcium entry needed to open CICR.

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26
Q

How is cardiac myocyte contraction regulated?*

A
  • Ca2+ binds to troponin C
  • Conformational change to remove tropomyosin and reveal myosin binding side
  • Sliding filament mechanism
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27
Q

How do cardiac myocytes relax?

A
  • Most Ca2+ pumped back into SR via SERCA

- Some exits across cell membrane (Ca2+ ATPase, Na/Ca exchangers to bring Ca2+ out

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28
Q

How is smooth muscle arranged in vessels?

A
  • Circular
  • Tunica media
  • Tone controlled by contraction and relaxation of vascular smooth muscle in tunica media
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29
Q

What is the process of excitation-contraction coupling in smooth muscle? * !!!!

A

1) Depolarisation opens VGCCs, Ca2+ into cell
2) Calcium also released from SR
3) 4 x Ca2+ ions bind to calmodulin, which binds to myosin light-chain kinase and can bind to actin filaments (phosphorylation)
4) MLCP always active and causes dephosphorylation to relax it

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30
Q

What is the contribution of alpha-1 receptors in smooth muscle contraction?

A
  • Noradrenaline binds to and activates a-1 receptors
  • Gaq releases IP3 and DAG
  • IP3 causes release of calcium from the SR
  • Causes activation
  • DAG activates protein kinase C and inhibits MLCP
  • Prevents contraction
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31
Q

How does myosin light chain interact with actin?

A

Must be phosphorylated to allow interaction.

32
Q

How is contraction regulated in vascular smooth muscle?

A
  • Ca2+ binds to calmodulin
  • Activates MLCK - phosphorylates the myosin head to allow contraction
  • Relaxation as Ca2+ levels reduce
  • Dephosphorylation of chain by MLCP
  • Phosphorylation of MLCK by PKA inhibits the action of MLCK, so inhibits phosphorylation and contraction
33
Q

What is the genetic aetiology of congenital heart disease?

A

Down’s, Turner’s, Marfan’s syndromes

can also be polygenic

34
Q

What is the environmental aetiology of congenital heart disease?

A

Teratogenic (from drugs, alcohol and smoking that can harm the child in utero)
Maternal obesity, etc

35
Q

What maternal infections can cause congenital heart disease?

A

Rubella, toxoplasmosis

36
Q

What are the normal features of a fully-functioning heart?

A
  1. Right ventricle pumps deoxygenated blood to the lungs
  2. Pulmonary circulation has a lower pressure and resistance
  3. Left ventricle pumps oxygenated blood at a systemic pressure to the aorta
  4. Left ventricle is differently built than RV
37
Q

What is the oxygen saturation of the blood coming back from the body to the heart?*

A

67%

38
Q

What is the oxygen saturation of the blood coming back from the lungs to the heart?

A

99-100%

39
Q

What is the mixed venous pressure in the right atrium?

A

4mmHg (if above 10, then you can see distended jugular vein)

40
Q

What is the pressure in the right ventricle and why?

A

25/3 (diastolic needs to be lower to allow the filling, and systolic created due to the RV creating suction)

41
Q

What is the pressure in the pulmonary trunk and why?

A

25/10 (diastolic higher than in RV due to the pulmonary valve shutting)

42
Q

What is the pressure in the left atrium and why?

A

5 mmHg (RA and LA have same physiology but RA is slightly thicker and tougher so can generate a higher pressure)

43
Q

What is the pressure in the left ventricle and why?

A

80/4 (lower than in LA, and higher systolic to be able to pump blood around the body)

44
Q

What is the pressure in the aorta and why?

A

Around 80/20 (in adults more so 120/80) - higher diastolic pressure due to the pressure causing closure of the aortic valve and due to total peripheral resistance from the arterial smooth muscle

45
Q

What is the threshold for treating high blood pressure?

A

140/90 mmHg

46
Q

What are acyanotic congenital heart defects and what are some examples of those?

A

Acyanotic: defects which do not alter the oxygen content

  • ASD, VSD, PDA (left-right shunts)
  • Obstructive lesions (aortic stenosis due to hypoplasia), pulmonary stenosis, coarctation of the aorta, mitral stenosis
47
Q

What are cyanotic congenital heart defects and what are some examples of those?

A

Cyanotic: defects which lower the systemic O2 levels and leave a lot of haemoglobin unsaturated

  • Transposition of the great arteries
  • Univentricular heart
  • Tetralogy of Fallot
  • Total anomalous pulmonary venous drainage
48
Q

What is the function of a left-to-right shunt and how can it cause issues?

A

Allowing blood from the left heart to be returned to the lungs instead of the body

Increased blood flow and therefore pulmonary artery and venous pressure which can cause damage

49
Q

What is the function of a right-to-left shunt and how can it cause issues?

A

Allows blood flow from the right ventricle to the left ventricle (needs a distal obstruction too) and therefore allows deoxygenated blood to enter the systemic circulation and bypass the lungs

50
Q

What are the shunts present in the heart?*

A

Held closed by increased pressure

  • Atrial
  • Ventricular
  • Atrio-ventricular
  • Aorto-pulmonary (ductal)
51
Q

What can cause atrial-septal defects?*

A
  • Sinus venous defect and primum atrial defects

can cause larger holes for blood flow

52
Q

What are the haemodynamic effects of atrial septal defects?

A
  1. Increased pulmonary blood flow
  2. RV overload but at a low pressure, so pulmonary hypertension is rare
  3. Eventual RV failure
53
Q

What do ventricular septal defects do?*

A

Allow the blood to go around the body quicker

54
Q

What are the haemodynamic effects of ventricular septal defects?

A
  1. Left to right shunt allowing LV overload
  2. Pulmonary venous congestion (lung damage)
  3. Eventual pulmonary hypertension
55
Q

What causes atrio-ventricular septal defects?

A

Endocardial cushions do not migrate to separate ventricles, which can lead to a common valve and holes

56
Q

What are the complications of aortic stenosis?*

A
  • Ventricular hypertrophy (heart has to pump harder due to a narrow valve)
  • Heart can stop
57
Q

What is coarctation of the aorta?*

A

A narrowing of the aorta caused by the duct fibrosing as it closes, and taking bits of the aorta with it

58
Q

What are the complications of the coarctation of the aorta?

A
  • Increased BP
  • Strokes
  • Reduced lower body blood flow
59
Q

How is the coarctation of the aorta treated?

A

Bypass surgery

60
Q

What is tetralogy of Fallot?*

A

A combination of four congenital cardiac abnormalities:

1) Pulmonary stenosis
2) Overriding aorta
2) Ventricular septal defect (aorta above septum prevents the correct septal formation)
4) Right ventricular hypertrophy (caused by pulmonary stenosis)

61
Q

What are the complications of tetralogy of Fallot?

A

Progressive RV hypertrophy that can progress into right-sided heart failure

Treatment = surgery

62
Q

What is tricuspid atresia?*

A

A congenital cardiac defect where the tricuspid valve (between RA and RV) is completely absent as the blood can flow normally in the embryo and it does not form.

63
Q

What is the pathophysiology of tricuspid atresia?

A
  • No RV inlet
  • R to L atrial shunt of the entire venous return
  • Blood flow to lungs via VSD or a patent ductus arteriosus as there is no valve to let blood through
64
Q

What are the complications of tricuspid atresia?

A

Underdeveloped right ventricle and cyanosis

65
Q

What is transposition of the great arteries?*

A

A congenital cardiac defect where the great vessels do not rotate at all (pulmonary trunk connected to right ventricle and aorta connected to right side of heart)

  • There are 2 independent circulations
  • Not viable with life unless the 2 circuits can communicate (via a shunt that failed to close after birth)
66
Q

How is transposition of the great arteries treated?

A

Surgery that allows the RV to pump blood to the body, but the right ventricle can fail later as it is not adapted to this function

67
Q

What is the complication of the transposition of the great arteries?

A

There are 2 independent circuits so blood cannot travel to the lungs to pick up oxygen, so the child will go very blue very quickly

68
Q

What is a hypoplastic left heart?*

A
  1. Underdeveloped left ventricle
  2. Ascending aorta small
  3. Blood cannot get to the LV so systemic circulation via RV
  4. Right to left shunt
69
Q

What is needed to do for a hypoplastic left heart to work?

A

The duct must remain open (eg. by prostaglandin) to allow the systemic circulation to continue as the left ventricle is too small and cannot function
(MUST have an ASD and a patent ductus arteriosus to allow blood from the PA to enter the aorta)

70
Q

What is an univentricular heart?*

A

A congenital cardiac defect that can occur with or without transposition of the great arteries (septum does not form)

71
Q

How do atrial septal defects present?

A
  • Usually asymptomatic until late adulthood

- Late onset arrhythmia and heart failure

72
Q

How do ventricular septal defects present?

A
  • Present in infancy (left heart failure)

- Can lead to inoperable pulmonary hypertension

73
Q

How does tetralogy of Fallot present?

A
  • Cyanotic spells in infancy/early childhood

- Mild cases compatible with adulthood

74
Q

Which conditions are neonatal emergencies?

A
  • Transposition of the great arteries
  • Hypoplastic left heart
  • Pre-ductal coarctation
  • Pulmonary atresia
    Often due to reduced pulmonary blood flow and therefore cyanosis
75
Q

How does the adult variety of coarctation of aorta present?

A
  • Left ventricular hypertrophy

- Associated aortic valve stenosis

Cardiovascular System (11 decks)

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