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ESA 2 -Rhianna > Cardiovascular > Flashcards

Cardiovascular Flashcards

0
Q

Which germ layer does the cardiovascular system originate from?

A

Haemangioblasts which form in ‘blood islands’ in the splanchnic mesoderm

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1
Q

What embryological process puts the veins of the heart behind the arteries?

A

Looping of the primitive heart tube

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2
Q

What primitive structures develop into the right atrium?

A

Most of the primitive atrium and the sinus venosus

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3
Q

What primitive structures develop into the left atrium?

A

Sinus venosus and some of the primitive atrium.

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4
Q

Where is the oblique pericardial sinus found?

A

The cul de sac of the pericardium underneath the heart formed by the process of looping.

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5
Q

Where is the transverse pericardial sinus found and what is it useful for clinically?

A

Where the pericardial sac meets at the top of the heart, between the superior vena cava and the aorta/pulmonary artery.
Clamp to put the heart on bypass.

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6
Q

What is the ductus arteriosus and where can it be found?

A

It is a fetal shunt that allows blood to bypass the lungs during gestation. It connects the pulmonary artery to the proximal descending aorta.

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7
Q

Which embryological aortic arch develops into the mature aortic arch?

A

Arch 4

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8
Q

Why does the laryngeal nerve descend further down on the left than the right?

A

Descends to t4/5 on the left and only t1/2 on the right because on the left it has to go around the ductus arteriosus but on the right apoptosis of the primitive aortic arches allows it to be shorter.

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9
Q

Name the three types of artery and how you would identify them in a histological slide.

A

Elastic - thick Tunica media with lots of elastin
Muscular - thick tunica media with lots of smooth muscle
Arterioles - thin tunica media

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10
Q

Name three types of capillary and give an example of where they can be found.

A

Continuous - skeletal muscle
Fenestrated - endocrine glands
Sinusoidal - liver, spleen

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11
Q

What are the layers of a blood vessel from superficial to deep?

A

Tunica adventitia - connective tissue
Tunica media - extra cellular elastic
Tunica intima - 1 cell thick with internal elastic lamina

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12
Q

Which type of blood vessels contain valves?

A

Veins and venules

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13
Q

What are venae comitantes and give an example of where they can be found?

A

A pair of veins that follow an artery, encapsulated in a sheath of fascia eg brachial artery

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14
Q

What are vasa vasorum?

A

Blood vessels that supply and drain other large vessels such as the aorta. Found in the tunica adventitia.

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15
Q

What are the atrioventricular valves called?

A

Left - mitral, bicuspid valve

Right - tricuspid valve

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16
Q

Describe the seven phases of the cardiac cycle.

A 
1. Atrial contraction
SA node fires to AV node
2. Isovolumetric contraction
Septum, bundle of His, inner to outer surface of the ventricles contract
3. Rapid ejection
4. Reduced ejection
5. Isovolumetric relaxation
6. Rapid ventricular filling
7. Reduced ventricular filling
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17
Q

Distinguish systole from diastole.

A

Systole - contraction

Diastole - relaxation

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18
Q

During which phases are both the mitral valve and the aortic valve closed?

A

Isovolumetric contraction and isovolumetric relaxation.

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19
Q

Why is a small amount of valve regurgitation normal?

A

A small amount of blood must regurgitate back to close the valve.

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20
Q

At what stage of the cardiac cycle does the aortic valve open?

A

Rapid ejection

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21
Q

At what stage of the cardiac cycle does the mitral valve open?

A

Rapid ventricular filling

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22
Q

What is the first stage of septation in the development of the cvs and where does it occur?

A

Formation of emdocardial cushions in the atrioventricular canal

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23
Q

Describe the process of septation of the atria.

A
  1. Growth of septum primum and the hole underneath it - the ostium primum
  2. Before this is complete, the ostium secundum forms within it by apoptosis.
  3. The septum secundum forms behind it with a hole in it known as the foramen ovale

The process allows blood to constantly flow from right to left which is necessary for intrauterine life. After septation blood flows from the right atrium to through the foramen ovale to the left atrium through the ostium secundum

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24
Q

Describe the process of septation of the ventricles.

A
  1. Muscular growth of the primary inter ventricular foramen

2. Membranous growth of connective tissue, proliferating from the endocardial cushions to fill the gap.

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25
Q

What is the name of the fetal shunt which bypasses the liver and what is the name of its remnant in the adult?

A

Ductus venosus - ligamentum venosum

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26
Q

What is the name of the fetal shunt which bypasses the lungs to prevent deoxy blood missing with oxy. And what is the name of its remnant in the adult?

A

Ductus arteriosus - ligamentum arteriosum

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27
Q

What is the name of the fetal shunt which allows blood flow between the atria in order to bypass the lungs, and what is the name of its remnant in the adult?

A

Foramen ovale - fossa ovalis

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28
Q

What is the name of the fetal shunt which provides nutrients to the fetus and what is the name of its remnant in the adult?

A

Umbilical vein - ligamentum teres

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29
Q

Which arteries originate at the aortic trunk?

A

Right to left
Brachiocephalic
Common carotid
Subclavian

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30
Q

Describe the layout of the coronary arteries.

A

Right coronary - right marginal

Left coronary - left anterior descending, left marginal, left circumflex

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31
Q

What are the names, locations and functions of the two vascular sinuses?

A

Aortic sinus
Opening in the aorta behind the aortic valve
Allows coronary arteries to fill during diastole

Coronary sinus
Drains to the right atrium on the posterior surface
Drainage of the coronary veins

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32
Q

What embryological feature do the cardiac auricles originate from? What is their function in the adult?

A

Embryological atria

Can expand the capacity of the adult atria if required

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33
Q

What causes heart looping to occur?

A

Continual growth of the heart tube in the pericardial cavity which does not stretch or grow.

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34
Q

What is the embryological derivative of the left ventricle?

A

Primitive ventricle

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35
Q

What is the embryological derivative of the right ventricle?

A

Bulbus cordis

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36
Q

What does the process of septation achieve?

A

Divides right and left heart, keeping blood flowing right to left at all times.

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37
Q

Describe the cardiac action potential.

A
  1. Voltage gated Na channels open - depolarisation
  2. Na channels start to inactivate - pointy bit on graph
  3. Voltage gated Ca channels open, balanced with leak K channels - plateau
  4. Ca channels inactivate, delayed voltage gated k channels open - hyperpolarisation
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38
Q

Describe the action potential at the SA node.

A
  1. Hyperpolarisation triggers HCN channels Na slow influx - depolarises to threshold
  2. Voltage gated Ca channels open - full depolarisation
  3. Voltage gated k open - hyperpolisation
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39
Q

What causes the natural automacity of the SA node?

A

The funny current

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40
Q

When the action potential reaches cardiac myocytes, what is the molecular process that causes contraction?

A
  1. Ach release
  2. Beta 1 adrenoceptors - Gs protein - camp pathway - pka activates ca channels - Ca release
  3. Ca - Ca positive feedback via ryanodine receptor
  4. Ca binds to troponin - moves tropomyosin
  5. Myosin binds to actin heads
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41
Q

When the action potential reaches blood vessel smooth muscle cells, what is the molecular process that causes vasoconstriction?

A
  1. Ach release
  2. Alpha 1 adrenoceptor - Gq protein - IP3 pathway - Ca release
  3. Ca activates myosin light chain kinase
  4. MLCK phosphorylates myosin
  5. Myosin binds to actin heads
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42
Q

Which type of heart defects are acyanotic? Which are cyanotic?

A

Acyanotic - left to right shunts

Cyanotic - right to left shunts

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43
Q

Give three examples of congenital heart defects which cause a left to right shunt.

A

Just a hole-
Atrial septal defects - eg patent foramen ovale
Ventricular septal defects
Patent ductus arteriosus

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44
Q

Give an example of a congenital heart defect which causes a right to left shunt.

A

Tetralogy of Fallot

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45
Q

What needs to go wrong in the heart for there to be a right to left shunt defect?

A

Hole + increased pressure from the right eg pulmonary stenosis or right sided hypertrophy in heart failure

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46
Q

What are the consequences of a left to right shunt defect?

A

ASD - Blood goes to the lungs twice so increase in pulmonary pressure
Increased preload on right heart. Eventual right heart failure

VSD - (as above plus…) High pressure blood goes to the lungs twice so lung damage and the left heart’s effort is wasted. Cardiac output has to increase so left heart fails.

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47
Q

Describe the 4 defects associated with tetralogy of fallot.

A
  1. Ventricular septal defect
  2. Aorta stems from both ventricles
  3. Pulmonary artery squashed
  4. Right ventricular hypertrophy
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48
Q

Why do people with tetralogy of fallout tend to live for years without diagnosis?

A

Squashed pulmonary artery increases pressure on the right. This balances out the ventricular defect and prevents left to right shunt.

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49
Q

What would be the prognosis for a patient with tetralogy of fallot left untreated? What is the treatment given to a baby?

A

Blood bypasses the lungs, so cyanotic, exercise intolerance, potential for hypoxia and sudden death

Prostaglandin e1 to keep the ductus arteriosus open

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50
Q

Which arteries branch off the celiac trunk? Which vertebra is it level with? What does it supply?

A

Splenic artery
Left gastric artery
Common hepatic artery
At level of t12 to supply the foregut

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51
Q

What is the main process which maintains the venous pressure?

A

Starling’s law - increase vp, increase Stoke volume. More in more out.

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52
Q

What are the main processes which determine the arterial pressure.

A

Total peripheral resistance

Baroreceptors in carotid sinus

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53
Q

Outline Starlings law of the heart.

A

Increase venous pressure, increase filling, increase stroke volume. More is removed from the veins each beat, regulating the venous pressure back down to normal.

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54
Q

Define contractility of the heart.

A

The inherent ability to contract caused by the strength and stretch of bonds between actin and myosin fibres.
Increase contractility with the same venous pressure, increase stroke volume.
But only till the point where the ventricle has been stretched to its maximum.

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55
Q

How do the baroreceptors in the carotid sinus work?

A

Carotid sinus is a weaker wider area of arterial wall that is sensitive to pressure.
Decrease pressure signals to the medulla - increase sympathetic to increase contractility (b1 adrenoceptors) and decrease parasympathetic to increase heart rate (m2 muscarinic)

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56
Q

What is cardiac output made up of?

A

Stroke volume and heart rate

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57
Q

Define total peripheral resistance. Which factors can influence it?

A

Total force opposing blood flow in the vasculature. Mainly produced in the arterioles.
Viscosity of blood, diameter of vessel, turbulent flow.

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58
Q

If my heart rate (only) was artificially increased, how would my body return it to normal?

A

Increase cardiac output, decrease venous pressure, decrease stroke volume, decrease heart rate (starlings law that in equals out)

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59
Q

How does the body regulate against postural hypotension (normally)?

A

Decrease venous pressure, decrease cardiac output, decrease arterial pressure, baroreceptors increase heart rate and increase resistance by vasoconstriction.

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60
Q

Give an example of a situation when the baroreceptors reflex is not beneficial. How does the body deal with that situation?

A

Haemorrhage. Decrease arterial pressure makes the baroreceptors increase hr and vasoconstrict so there is an increase in blood loss.

Instead auto transfusion (shunted out of capacitance vessels) from nearby tissue and veno constriction can help temporarily.

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61
Q

How does the body self regulate blood pressure after light activity or digestion which increase local vasodilation?

A

Increase in local vasodilation, decrease in total peripheral resistance, increase venous pressure and decrease arterial pressure
Increase cardiac output
Decrease venous pressure and increase arterial pressure

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62
Q

How would an increase in total peripheral resistance affect venous and arterial blood pressures?

A

Arterial pressure increase

Venous pressure decrease

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63
Q

How would an increase in cardiac output affect venous and arterial blood pressures?

A

Increase arterial pressure

Decrease venous pressure

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64
Q

Why can the body not self regulate long term hypertension?

A

Increase venous pressure, increase cardiac output, increase arterial pressure, increase total peripheral resistance, increase arterial pressure, self perpetuating.

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65
Q

What is a normal bp in the aorta?

A

120/80

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66
Q

What is a normal bp in the right atrium?

A

5 (no systolic pressure)

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67
Q

What is a normal bp in the right ventricle?

A

20/5

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68
Q

What is a normal bp in the pulmonary artery?

A

20/10

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69
Q

What is a normal bp in the left atrium?

A

5 (no systolic)

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70
Q

What is a normal bp in the left ventricle?

A

120/5

71
Q

What is a normal bp in the right ventricle ?

A

20/5

72
Q

Why does the diastolic remain higher in the blood vessels than the ventricles?

A

Elastic recoil in the blood vessels maintains the pressure between beats

73
Q

Define the mean arterial pressure. What does it represent? How is it calculated? What is a normal value?

A

Average pressure for a single cardiac cycle. Represents perfusion to tissues.
=2/3diastolic pressure+1/3systolic pressure
=70-110

74
Q

What is the pressure and resistance like in the pulmonary circulation? How is this achieved?

A

Pressure and resistance are low created by lots of capillaries in parallel providing a high surface area.

75
Q

What is hypoxic pulmonary vasoconstriction? Give an example of a causal factor.

A

Physiological process in which less well ventilated alveoli are vasoconstricted so that the blood is redirected to well ventilated alveoli.

Caused by poor ventilated alveoli by eg mucus or infection

76
Q

What is the optimum ventilation/ perfusion ratio?

A

0.8

77
Q

How does an increase in venous pressure cause oedema?

A

Increase venous pressure, increase hydrostatic force out of the capillary so that it is greater than the oncotic force into the capillary.

78
Q

What is the pressure and resistance like in the cerebral circulation? How is this achieved?

A

Pressure and resistance are low created by lots of capillaries in parallel providing a high surface area.

79
Q

What happens if neurones are without oxygen for a small amount of time? Why does this happen?

A

Faint - very sensitive to hypoxia because they constantly need to do oxidative phosphorylation. No glycogen stores, no creatine phosphate stores and can’t use fatty acids as they don’t cross the barrier. Can use ketones.

80
Q

What is myogenic autoregulation?

A

Auto regulation of the pressure in the arterioles without any cvs involvement. Smooth muscle stretches, opens Ca channels, muscle depolarises and contracts.

81
Q

What is distinctive about a true capillary?

A

No smooth muscle

82
Q

What is the function of a precapillary sphincter? Give an example.

A

Block blood from entering the whole capillary bed, saving it for a more urgent purpose.
Eg, in a fight or flight response, pre capillary sphincters in the mesentery block the blood from the intestine so it can go to the muscles.

83
Q

What is cushings reflex seen in response to raised intracranial pressure?

A

Raised intracranial pressure raises pressure of cerebrospinal fluid higher than mean arterial pressure, compressing the arterioles. The reflex attempts to restore blood flow to the ischaemic brain.

  1. Increased sympathetic - increased force of contraction and blood pressure and tachycardia
  2. Baroreceptors respond with an increased parasympathetic - leading to bradycardia but pressure remains high to push into brain
  3. Pressure on brain stem leads to irregular breathing
84
Q

How do the coronary arteries fill?

A

Through the aortic sinus during diastole

85
Q

What causes angina?

A

Hypoxia in the coronary arteries causes pain. It only occurs on exercise because this is when diastole is shortened so the coronary arteries aren’t given long enough to fill.

86
Q

Give three possible mechanisms of arrhythmia.

A
  1. Ectopic pacemaker activity - ischaemic area spontaneously depolarises
  2. After depolarisations - extra depolarisation during the action potential. Can be early or late.
  3. Re entry loops - conduction damage leads to abnormal route of excitation.
87
Q

What increases the risk of delayed after polarisations?

A

High cellular calcium

88
Q

What increases the risk of early after polarisations?

A

A long action potential - eg long qt syndrome

89
Q

What type of arrhythmia can be caused by ectopic pacemaker activity?

A

Ectopic beats

90
Q

What type of arrhythmia can be caused by delayed afterpolarisations?

A

Ectopic beats

91
Q

What type of arrhythmia can be caused by early depolarisations?

A

Flutter/fibrillation

92
Q

What type of arrhythmia can be caused by re entry loops?

A

Flutter/fibrillation

93
Q

Define heart failure.

A

Chronic failure of the heart to provide sufficient output to keep the body perfused due to muscle weakness/stenosis

94
Q

How do beta blockers work? What do they treat?

A

Antagonists of beta 1 adrenoceptors. Decrease ionotropy in the AV node. Decrease the rate of activation of the funny current at the SA node, decrease heart rate and therefore cardiac output.

Treat hypertension and supra ventricular tachycardia.

95
Q

How do Calcium channel blockers work? What do they treat?

A

Decrease the calcium in the cell, Decrease the slope at the SA node, decrease heart rate and cardiac output.
Also decreases force of contraction by decreasing the ryanodine positive feedback loop.
Treat hypertension and angina. Also diastolic heart failure

96
Q

How would K channel blockers work? Why are they not used?

A

Theoretically Lengthen the refractory period of the action potential, preventing any extra depolarisations.
But increase length of the action potential increases risk of early depolarisation so pro arrhythmic.
(Except amiodarone)

97
Q

How would Na channel blockers work? Why are they not used?

A

Blocks inactive Na channels so that the refractory period is maintained and there are no mistake depolarisations. Eg lidocaine.
Too many side effects

98
Q

How do cardiac glycosides work? What do they treat? What is a better option?

A

Eg digoxin. Block Na K ATPase so that the driving force for Na ca exchange is decreased and there is a build up of Ca which is perpetuated by the ryanodine loop - increase force of contraction.

Treat heart failure but don’t flog a dying horse - better to decrease the afterload with ace inhibitors

99
Q

How do ace inhibitors work? What do they treat?

A

Prevent angiotensin 1 to 2
Decrease Na and water reabsorption and vasodilation
Treat heart failure by reducing the load on the heart

100
Q

How do organic nitrates work? What do they treat?

A

Increase veno dilation to treat angina

101
Q

What is the relationship between blood pressure, cardiac output and total peripheral resistance?

A

Bp = co x tpr

102
Q

How do loop diuretics work? What do they treat?

A

Block NaKCl co transporter in the loop of Henle. Stops reuptake of these salts so stops water following. Increases water content of urine. Treats Hypertension.

103
Q

How would you interpret an ecg?

A
  1. Rate
  2. Rhythm
  3. Axis
  4. P wave - missing?
    - related to QRS?
  5. PR segment length - 3-5 small squares
  6. QRS length - 1-3 small squares
  7. QT length - less than half r-r
  8. T wave - elevation?
    - depression
104
Q

What do movements in the heart do the ecg letters PQRS and T refer to?

A 
P - SA node, atria contract
Q - septum, ventricular endocardium contracts
R - main ventricular contraction
S - contraction spreads up the ventricle
T - relaxation of ventricles
105
Q

What is the pathophysiology of atrial fibrillation?

A

SA node starts to fire randomly (caused by ectopic pacemaker activity, after depolarisation, re entry loops), random contractions. So sometimes AV node takes over ventricular contractions.

106
Q

How would you identify atrial fibrillation on an ecg?

A

Absent p wave

Irregular rhythm

107
Q

What is the difference between 1st, 2nd and 3rd degree heart block?

A
  1. SA struggles to transmit to AV but no AV takeover - prolonged PR
  2. SA sometimes fails, AV sometimes takes over, regularly irregular - erratic PR, missed QRS
  3. SA never transmits to AV, AV takes over completely - no relationship between P and QRS.
108
Q

How would you identify heart block on an ecg?

A

Prolonged PR interval or lack of relationship between P and the rest of the wave.

109
Q

What is the difference between heart block and bundle branch block?

A

Heart block is a block in conduction between the SA and AV nodes so is noted at the p wave. Bundle branch block occurs at the septum so it noted at the q wave.

110
Q

How would you identify bundle branch block on an ecg?

A

Rabbit ear QRS because two attempts made at getting through the block in the septum.

111
Q

How would you identify angina/ myocardial ischaemia on an ecg?

A

ST depression because the block is during diastole.

112
Q

How would you identify MI on an ecg?

A

ST elevation
Rabbit ear Q wave
Inverted T

113
Q

What is the common cause of left axis deviation?

A

Defects of the conduction system

114
Q

What is the common cause of right axis deviation?

A

Right ventricular hypertrophy

115
Q

If a patient had an abnormally short PR interval what would be a likely cause?

A

Wolf Parkinson White - an extra pathway known as the bundle of Kent is present.

116
Q

If there was ST elevation in leads II III and aVF where would the MI be?

A

Inferior

117
Q

If there was ST elevation in leads V3 and V4 where would the MI be?

A

Anterior

118
Q

If there was ST elevation in leads V1 and V2 where would the MI be?

A

Septal

119
Q

If there was ST elevation in leads I, aVL, V5, V6 where would the MI be?

A

Lateral

120
Q

What is sinus rhythm?

A

A p wave precedes every QRS complex

121
Q

What is the difference between Mobitz type 1 and type 2 second degree heart block?

A

Type 1 - delay gets longer and longer till there is a skipped QRS
Type 2 - irregular pattern

122
Q

What does it mean if there are tall peaked T waves?

A

If seen in all leads it is hyperkalaemia. Can be an early sign of MI.

123
Q

Give three possible cvs causes of chest pain

A

Ischaemic heart disease
Pericarditis
Aortic dissection

124
Q

What is ischaemic heart disease?

A

Occurs when 02 supply cannot meet demand of coronary arteries and they can become ischaemic.

125
Q

Give four causes/precipitants of ischaemic heart disease. Identify the most common one.

A 
Decreased supply:
1. Tachycardia - shortened diastole
2. Anaemia
Increased demand:
1. Atheroma MOST COMMON
2. Aortic stenosis
126
Q

Which area of the heart is most vulnerable to ischaemia?

A

Endocardium, because it is the last area the blood flow of the coronary arteries reaches.

127
Q

What are the four types of ischaemic heart disease caused by atheroma?

A

Stable angina
Unstable angina
NSTEMI
STEMI

128
Q

What is crescendo angina?

A

Stable angina that becomes unstable.

Pain no longer transient
Increasing severity
More often, longer duration

129
Q

What is the difference between stable and unstable angina?

A

Severe: Occlusion more severe, can no longer cope at rest.

130
Q

What is the difference between unstable angina and an NSTEMI?

A

NSTEMI develops necrosis so biomarkers become positive.

131
Q

What is the difference between an NSTEMI and a STEMI?

A

Occlusion of the artery becomes complete so there is full thickness infarction.

132
Q

What are the classic ecg markers for a STEMI?

A

St elevation
Q enlarges
T inverts

133
Q

What are the classic ecg markers for stable angina?

A

Normal ecg at rest

ST depression during stress test

134
Q

What are the classic ecg markers for unstable angina?

A

ST depression

135
Q

What are the classic ecg markers for an NSTEMI?

A

ST depression

136
Q

What would be the diagnosis for a positive result for creatine kinase or troponin?

A

STEMI or NSTEMI

137
Q

How would you treat angina?

A

Aspirin

GTN spray
Statins
Beta/Ca channel blockers
Re vascularise

138
Q

How would you treat a STEMI?

A

Streptokinase
Emergency re vascularisation

GTN spray
Statins
Beta/Ca channel blockers

139
Q

How would you treat an NSTEMI?

A

Heparin

GTN spray
Statins
Beta/Ca channel blockers
Re vascularise

140
Q

What is a bruit? Where might they be found?

A

Audible turbulent flow of blood in an artery due to obstruction eg:

Aneurism
Thrombus

141
Q

What is the relationship between blood flow and radius of the vessel?

A

Flow is proportional to radius to the power of 4.

So decrease radius leads to massive decrease in flow.

142
Q

What are you worried about if the popliteal pulse is easily palpable?

A

Popliteal aneurism

143
Q

What is a cardiac catheter? Where would it be inserted?

A

Entry into heart via blood vessels for therapeutic or diagnostic purposes.

Right heart - femoral vein
Left heart - femoral artery

144
Q

What is venous insufficiency? What is it called when it occurs chronically, following a DVT?

A

Inability of veins to pump blood back efficiently. Leads to pooling in the legs and peripheries.

After DVT - postphlebotic syndrome

145
Q

What is the main difference between left and right heart failure?

A

Left causes lung oedema, right causes peripheral oedema

146
Q

What causes the oedema in heart failure?

A

Increased hydrostatic pressure in the veins

147
Q

Why does hypertension alone not cause oedema?

A

Hypertension refers to arteries. Oedema only released from slow moving veins.

148
Q

What is meant by cardiac asthma?

A

The cough that develops in left heart failure due to constriction of airways by pulmonary oedema.

149
Q

Which two physiological processes cause heart failure to deteriorate even faster?

A

Sympathetic overdrive

Up regulation of renin-angiotensin-aldosterone-system

150
Q

Why does sympathetic overdrive occur in heart failure?

A

Low perfusion to brain
Detected by baroreceptors as low bp
Increased sympathetic drive

Also affected by increased angiotensin from upRegulation of RAAS

151
Q

Why is RAAS (renin angiotensin aldosterone system) upregulated in heart failure?

A

Kidneys underperfused, think low bp
Upregulate RAAS to:
increase aldosterone - increase salt retention
Increase angiotensin 2 - increase water retention, vasoconstriction and sympathetic overdrive

152
Q

Why do increased sympathetic drive and upregulation of RAAS cause increased deterioration of heart failure?

A

Increase: HR, vasoconstriction, salt and water retention

Therefore increased afterload and increased oedema.

153
Q

What is the difference between diastolic and systolic heart failure?

A

Systolic is a failure to pump, diastolic is a failure to fill as well as pump

154
Q

Why is ejection fraction preserved in diastolic heart failure?

A

There is a decrease in both the amount of blood entering the heart and the amount leaving, so the proportion (ejection fraction) stays the same.

In systolic, just the amount leaving decreases, so the ejection fraction also decreases.

155
Q

What is a normal ejection fraction value?

A

Above 50%

156
Q

How would you treat increasingly serious heart failure?

A
  1. Low salt diet
  2. ACE inhibitor to decrease RAAS
  3. Diuretics to decrease oedema
    Aldosterone antagonist to decrease salt retention
    Digoxin to increase contractility
  4. Palliative opioids to ease breathlessness
157
Q

What is ejection fraction?

A

A measure of efficiency of the heart - end diastolic volume/stroke volume

158
Q

What is meant by shock?

A

Acute circulatory failure with inadequate or inappropriate tissue perfusion.

159
Q

Give 5 types of shock

A 
Cardiogenic
Mechanical
Hypovolaemic
Anaphylactic
Septic
160
Q

What causes cardiogenic shock? What colour is the patient? What does their peripheral pulse feel like?

A

Dysfunction of heart itself eg. MI, acute heart failure
Leads to decreased cardiac output, decreased bp
Pale, sweating, cold
Weak pulse

161
Q

What causes mechanical shock? What colour is the patient? What does their peripheral pulse feel like?

A

Restriction of the heart’s normal action
Eg. Pulmonary embolism or cardiac tamponade
Decreased filling (PE left only) decreased output, decreased bp
Baroreceptors compensate with HR and TPR
But while block still there, still no blood!
Pale, sweating, cold
Pulse weak
Like

162
Q

What causes hypovolaemic shock? What colour is the patient? What does their peripheral pulse feel like?

A 
Blood loss decreases venous pressure. 
Decrease cardiac output, decrease arterial pressure. 
Baroreceptors compensate with HR and TPR
But this just exacerbates blood loss
Pale, cold, sweating
Weak pulse
163
Q

What causes anaphylactic shock? What colour is the patient? What does their peripheral pulse feel like?

A 
Histamine, prostaglandins, bradykinin, leukotrines respond to allergen. 
( bronchoconstriction so can get blue)
Smooth muscle relaxes
Decrease TPR, decrease arterial pressure
Baroreceptors compensate with HR and TPR
But capillary leakage 
Puffy and red
Fast bounding pulse
164
Q

What causes septic shock? What colour is the patient? What does their peripheral pulse feel like?

A 
Endotoxins from g neg bacteria
Or interleukin 1 from tumour
Relax smooth muscle decrease arterial pressure
Baroreceptors compensate with HR and TPR
But capillary leak 
Fast bounding pulse
165
Q

How would you treat shock in general?

A

High pressure oxygen
Fluid (crystalloid if capillary leak)
Adrenalin for anaphylaxis only

166
Q

Describe the conduction pathway of the heart.

A

SA node - atria contract - AV node - 120ms - septum contracts - ventricles contract endocardium to epicardium through purkinje fibres - ventricles relax

167
Q

What is a common side effect of ACE inhibitors? What is it caused by?

A

Bradykinin causes fatal stimulation - dry cough

168
Q

Why does aspirin cause stomach ulcers?

A

It is an NSAID. Blocks COX 1 which encourages mucus production.

169
Q

What is the difference between pulmonary oedema and pleural effusion?

A

Pulmonary oedema fill the lung interstitium and the alveoli

Pleural effusion fills the space between the pleura

170
Q

Why is oxygen not administered automatically after an MI?

A

If sats are not below 94 then no need. Can cause oxygen toxicity which is like reperfusion injury, causes increased production of reactive oxygen species.

171
Q

Name 3 modifiable risk factors of heart disease and 3 non modifiable factors.

A

Non Modifiable: increasing age, male sex, South Asian ethnicity, familial hyperlipidaemia

Modifiable: low exercise, high fat diet, type 2 diabetes, alcohol, smoking

172
Q

What is levine’s sign?

A

Clenched right fist over chest implies ischaemic chest pain.

173
Q

What is meant by compensation and decompensation of the heart?

A

If it is compensated, it can function in spite of stressors or defects. Eg baroreceptors and RAAS maintain fluid, and increase heart rate and bp.

It becomes decompensated when this is no longer able to maintain adequate circulation. Eg increased HR and bp lead to worse peripheral perfusion and shock.

174
Q

What is meant by a paradoxical embolism?

A

An embolus that crosses the heart via an ASD or a VSD. So venous can go to the brain/other arteries and arterial can go to the lungs.

175
Q

Describe the evolution of the ecg pattern in an MI.

A

Minutes - tall T waves
Hours - ST elevation
Days - pathological Q waves

176
Q

Describe the venous drainage of a drug travelling by first pass metabolism.

A

Superior mesenteric vein - portal vein
Or
Inferior mesenteric vein - splenic vein - smv - portal vein

ESA 2 -Rhianna (7 decks)

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