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2 CVS > CVS 3,4,8,9,10,12,14 > Flashcards

CVS 3,4,8,9,10,12,14 Flashcards

1
Q

What are the 7 phases of the cardiac cycle?

A
  1. Atrial contraction
  2. Isovolumetric contraction
  3. Rapid ejection
  4. Reduced ejection
  5. Isovolumetric relaxation
  6. Rapid filling
  7. Reduced filling
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2
Q

In which side of the heart are valve pathologies most common and why?

A

Left side

Higher pressure

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3
Q

Give 3 causes of Aortic valve stenosis.

A
  1. Degeneration (old age-senile calcification/fibrosis)
  2. Congenital eg bicuspid aortic valve
  3. Chronic rheumatic fever- inflammation
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4
Q

What happens as a result of aortic valve stenosis?

A
  • Less blood getting through
    • Increased left ventricular pressure
      • LV hypertrophy
    • Left sided heart failure
      • Syncope (fainting)
      • Angina (not enough blood to coronary arteries)
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5
Q

Give 2 causes of aortic valve regurgitation.

A
  • Valve damage- endocarditis
  • Aortic root dilation
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6
Q

What happens as a result of aortic valve regurgitation?

A

Blood flows back into LV during diastole- RBCs lyse (Microangiopathic haemolytic anaemia)

Increase Stroke Volume

Increased systolic pressure

  • Bounding pulse
  • Heading bobbing
  • Quinke’s sign- nail beds flush w./ heart beat

LV hypertrophy

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7
Q

Name some causes of mitral valve regurgitation.

A
  • Myxomatous degeneration (CT disorder)
    • Weak chordae tendinae
    • Weak papillary muscle
      • Causing prolapse
  • Damge to papillary muscles after heart attack
  • Left sided heart failure- LV dilation
  • Rheumatic fever
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8
Q

What causes mitral valve stenosis in 99.9% of cases?

A

Rheumatic fever

Commissural fusion of valve leaflets

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9
Q

What happens as a result of mitral valve stenosis?

A
  • Increase LA pressure
    • Pulmonary oedema
      • Difficulty breathing
      • Pulmonary hypertension
        • RV hypertrophy
    • LA dilation
      • Artial fibrillation
        • Thrombus
      • Oesaophagus compression
        • Dysphagia (difficulty swallowing)
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10
Q

Complete the equations:

CO= SV x …..

…..= EDV - ESV

A

CO= SV x HR

SV = EDV - ESV

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11
Q

What is the typical stroke volume of a 70kg man?

A

70ml (=about 67% of normal EDV)

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12
Q

What does the ventricular compliance curve show?

A

Relationship between how much ventricles fill and LV pressure

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13
Q

What is the Frank-Starling law of the heart?

A

More the heart fills, harder it contracts

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14
Q

What are cardiac muscle cells increasingly sensitive to as the muscles are stretched?

A

Ca2+ ions

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15
Q

What type of stimulation affects the contractility of the heart?

A

Sympathetic/adrenaline

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16
Q

What is aortic impedence?

A

LV afterload

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17
Q

Why is the jugular venous pulse used clinically?

A

Direct colum of blood into right atrium

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18
Q

What conditions will increase the Jugular venous pulse?

A
  • Right side of heart- not pumping blood out properly
  • Vol overload with IV infusion
  • Something impairing heart filling eg stap wound
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19
Q

Label the follwing waves and describe what produces them:

  • A
  • C
  • X-descent
  • V
  • Dicrotic notch
  • Y-descent
A
  • A: Atrial systole
  • C: Closing mitral valve
  • X-descent: Atrial pressure initially decreases
  • V: Atrial pressure rising- venous return from lungs
  • Dicrotic notch: Aortic valve closing
  • Y-descent: Opening of mitral valve- ventricular filling
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20
Q

In what unit is BP measured?

A

mmHg (milimetres of mercury)

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21
Q

What is the normal/ideal BP?

A

90/60 mmHg and 120/80mmHg

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22
Q

What are the values of Blood pressure for:

  • Stage 1 hypertension
  • Stage 2 hypertension
  • Severe hypertension
A
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23
Q

What’s the difference between primary and secondary hypertension?

A
  1. Primary= cause unknown (95% cases)
  2. Secondary= cause defined
24
Q

Give some examples of secondary causes of hypertension

A
  • Renovascular disease
  • Chronic renal disease
  • Hyperaldosteronism
  • Cushing’s syndrome
25
Q

What can hypertension lead to? (5)

A
  1. Heart failure
  2. MI
  3. Stroke
  4. Renal failure
  5. Retinopathy
26
Q

What are the 4 neurohumoral pathways controlling circulating volume and BP?

A
  1. RAAS
  2. Sympathetic nervous system
  3. ADH
  4. ANP (Atrial natriuretic peptide)
27
Q

What are the actions of angiotensin II?

A
28
Q

Give an example of an ACE inhibitor.

A

Captopril

29
Q

Is bradykinin a vasodilator or vasoconstrictor?

A

Vasodilator

Bradykinin= inflammatory mediator

Releases nitric oxide + others to cause vasodilation

30
Q

What effects does hyperkalaemia have on myocytes and their ability to fire APs?

A
  1. Slows upstroke
  2. Inactivates some Na+ channels as Ek is now more negative
31
Q

What can happen to the heart as a result of hyperkalaemia?

A

Asystole (heart stops)

may initially get some increased excitiability

32
Q

What is the normal plasma concentration of K+?

A

3.5-5.5 mmol/L

33
Q

How is hyperkalaemia treated?

A
  • Calcium gluconate
  • Insulin and glucose- enhance potassium uptake

(won’t work if heart already stopped)

34
Q

How can hypokalaemia cause ventricular fibrillation?

A
  1. Longer action potential
  2. Delays repolarisation
  3. Causes early after depolarisations
  4. Oscillations in membrane potential
  5. Ventricular fibrillation
35
Q

How does an action potential in the cardiac myocyte result in contraction?

A
  • L-type Ca2+ channels= open
  • Ca2+ opens CICRs
  • Ca2+ binds to troponin C
  • Tropomyosin reveals myosin binding site for actin filament
36
Q

What is MLCK?

A

Myosin light chain kinase

Phosphorylates myosin light chains

Phosphorylated to allow binding to actin

37
Q

What enzyme inhibits contraction by inhibiting MLCK

A

PKA (protein kinase A)

Phosphorylates myosin itself

38
Q

How does vascular smooth muscle contract?

A
  • alpha-adrenoceptors depolarised/activated
  • Increased intracellular Ca2+
  • Ca2+ binding to calmodulin
  • Activation of MLCK
  • Phosphorylates myosin light chain
39
Q

What is the affect of sympathetic stimulation of β1 receptor in the heart?

A

Increase rate and force of contraction

40
Q

What is the effect of parasympathetic stimulation of the M2 muscarinic receptors in the heart?

A

Decreased rate

(Released ACh)

41
Q

The parasympthetic nervous system influences the heart via which nerve?

A

Vagus nerve

(10th cranial nerve)

Innervates SA node and AV node

42
Q

How does the sympathetic nervous system influence the heart?

A
  • Post ganglionic fibres from sympathetic trunk
  • Innervates SA node, AV node, myocardium
  • Releases noradrenaline–> β1 receptors
43
Q

What is the If funny current?

A

Slow Na+ conductance- slow depolarisation of pacemaker potential

44
Q

Arteries and veins can receive sympathetic stimulation via α1 adrenoreceptors.

Coronary and skeletal muscle blood vessels also have what other type of receptor?

A

β2 adrenoreceptors

45
Q

If sympathetic output to α1 adrenoreceptors is increased- what will occur in the blood vessels?

A

Increased output= vasoconstriction

46
Q

What is caused by the activation of β2 adrenoreceptors?

A

Vasodilation

47
Q

What effect do local metabolites have on vasodilation in active tissue?

A

Active tissue- increases metabolites

Increase vasodilation

48
Q

How do baroreceptors work?

A

In carotid sinus and aortic arch

  1. Increase in arterial pressure- stretches receptors
  2. Vagus nerve- to medulla
  3. Parasympathetic stimulation
  4. Bradycardia and vasoldilation to counteract increased mean arterial pressure
49
Q

What drug may be given for cardiogenic shock? (pump failure)

A

Dobutamine β1 agonist

50
Q

How does Salbutamol work?

A

β2 agonist

51
Q

What is the muscarinic agonist Pilocarpine used to treat?

A

Gluacoma

(Optic nerve damaged- due to pressure of fluid inside eye)

52
Q

How does sympathetic stimualtion cause renin release?

A

Renal blood flow decreases

Sympathetic stimulation of cells in afferent arteriole to release renin

(Renin release increase Angiotensin II levels)

53
Q

What effect do prostaglandins have on BP?

A

Lower BP

= vasodilators

= enhance glomerular filtration rate

= reduce Na+ reabsorption

Locally acting

54
Q

What effect does dopamine have of blood pressure?

A

Lower BP

Formed locally in kidney

Dopamine receptors in renal blood vessels

Reduce reabsorption of NaCl

55
Q

Explain how renovascualr disease can cause high BP.

A
  1. Occlusion of renal artery
  2. Fall in perfusion pressure- kidney
  3. Activation of RAAS
  4. Vasoconstriction and Na+ retention in other kidney
56
Q

Explain how renal parenchymal disease causes high BP?

(Chronic kidney disease)

A

Initially less vasodilator substances

Later Na+ retention

57
Q

What is Conn’s syndrome?

A

Aldosterone secreting adenoma

Hypertension and hypokalaemia

2 CVS (16 decks)

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