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Old curriculum > CVS > Flashcards

CVS Flashcards

1
Q

Describe the parts of an ECG trace and what they represent.

A

P wave - atrial depolarisation
QRS complex - depolarisation of the ventricles
T wave - repolarisation of the ventricles

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2
Q

How can you calculate rate from an ECG trace?

A

Regular rate, 300/RR interval measured in large squares

Irregular rate, QRS complexes in 30 large squares X 10

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3
Q

List the 6 layers of normal arterial structure

A

Endothelium, subendothelial connective tissue, internal elastic lamina, muscular media, external elastic lamina, adventitia

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4
Q

Describe the factors influencing diffusion from capillaries

A

Area: capillary density = max area available for diffusion

Diffusion resistance: path length, size of molecules and what they dissolve in

Gradient: conc. of diffusing substances, rate of flow of blood (I.e. perfusion rate)

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5
Q

To what organs are blood flow maintained to at all times?

A

Brain, heart muscle & kidneys

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6
Q

How is flow control of the CVS achieved?

A

Arterioles (resistance vessels) and pre capillary sphincters

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7
Q

How is perfusion maintained despite changes in cardiac output ?

A

Veins offer capacitance as they contain 67% of the blood volume - this can be used to cope with temporary imbalances in the amount of blood coming back to the heart and the amount needed to pump out.

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8
Q

Describe branches of aortic arch

A

Brachiocephalic
Left common carotid
Left subclavian

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9
Q

How is blood pressure maintained during diastole?

A

Elastic recoil of walls of aorta acts as an auxiliary pump

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10
Q

Describe the 3 types of capillaries

A

Sinusoidal / discontinuous - gaps in walls, larger diameter, slower blood flow
Fenestrated - endothelium has gaps
*Continuous - endothelium has tight or occluding junctions. NB this is the most common

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11
Q

How do the impulses promoting vasoconstriction reach the smooth muscle cells of muscular arteries?

A

Sympathetic parts of unmyelinated nerve fibres in the fibroelastic connective tissue of the tunica media release neurotransmitter which diffuses through the fenestrations in the external elastic lamina. This depolarises some of the superficial smooth muscle cells then this depolarisation is propagated via the gap junctions to produce a co-ordinated contraction.

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12
Q

What’s an end artery?

A

An end artery is a terminal artery supplying all or most of blood to a part of the body w/o significant collateral circulation.

Bonus - eg. *central artery to retina, *labyrinth artery of external ear, coronary artery, splenic artery, renal artery

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13
Q

What’s the function of pre-capillary sphincters and where are they located? (Oh yes, its a double barrelled question .. soz comm skills)

A

Pre-capillary sphincters control the blood flow to capillaries. They are found within the tunica media of meta-arterioles where each cell of the continuous smooth muscle layer encircles the endothelium of a capillary.

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14
Q

What’s the advantage of capillaries having a diameter of 7-10 micrometers?

A

RBCs passing through fill virtually the entire lumen and so the diffusion distance to adjacent tissues is minimised.

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15
Q

Describe & Explain 4 adaptions of capillaries that help them achieve their function.

A
  • Low blood velocity of 0.03cm/s allows time for gas & nutrient exchange.
  • Consist of single layer of endothelium & its basement membrane minimising diffusion distance.
  • 7-10 micrometre diameter - passing RBCs fill virtually entire lumen minimising diffusion path to adjacent tissues.
  • Pericytes form a branching network on outer surface of endothelium. These are capable of dividing into muscle cells of fibroblasts during angiogenesis, tumour growth and healing.
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16
Q

List the routes of diffusion through fenestrated capillaries

A

Pinocytosis
Diffusion through fenestration or inter cellular cleft (gaps between adjacent cells)
Direct diffusion through endothelial cell

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17
Q

What features of post capillary venules help them achieve their function?

A

They have lower pressure than capillaries or surrounding tissue so that fluid tends to drain into them allowing interstitial fluid to re-enter the circulation.They are also very permeable which further facilitates this.

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18
Q

What is the function of the valves in venules and veins?

A

In venules valves restrict the retrograde transport of blood.
In veins valves act together with muscle contractions to propel blood towards the heart.

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19
Q

What are venae comitantes? What’s the point of them?

A

Vena Comitantes are deep paired veins that accompany one of the smaller arteries within the sheath of certain large arteries eg brachial, ulnar or tibial.
This proximity to the pulsing artery promotes venous return.

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20
Q

Name and describe the shape and position of the 4 valves of the heart.

A

Tricuspid valve has 3 leaflets, and is found between R atrium and R ventricle.
Mitral valve is bicuspid (2 leaflets) and is located between the left atrium and ventricles.
Pulmonary valve is semi lunar (3 cusps) found where the pulmonary artery joins the R ventricle.
Aortic valve is also semi lunar and found where the aorta joins the L ventricle.

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21
Q

How does the organisation of cardiac muscle fibres facilitate the heart’s function?

A

Cells joined by low electrical resistance connections facilitating the spread of action potentials
Cardiac action potentials are very long facilitating sustained contractions of the muscle fibres
Pacemaker cells located in sino-atrial node, allowing spread of excitation down the septum and into the myocardium at the apex of the heart, allowing ventricles to contract from apex up, pushing blood out through the semi-lunar valves.

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22
Q

State equation and units for cardiac output.

A

C.O (l/min) = stroke volume (ml) x heart rate (beats per minute)

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23
Q

What happens to systole and diastole when heart rate increases?

A

Systole occurs more frequently as diastole becomes shorter.

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24
Q

What is the function of the heart valves?

A

Enable unidirectional transport of blood allowing heart to be a reciprocating pump so that ventricles fill from veins during diastole and ventricles them pump blood into arteries in systole.

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25
Q

What causes heart values to open or close?

A

Mainly hydrostatic pressure gradients between the 2 regions they separate.
But also .. small but important amount of backflow which pushes leaflets of valve together.

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26
Q

When do the outflow valves of the heart open?

A

Towards the end of ventricular systole

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27
Q

When do the a/v (atrio-ventricular) valves open?

A

Once filling of atrium with a/v valves closed causes atrial pressure > intra-ventricular pressure

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28
Q

Roughly, how long is the “rapid filling phase” of the cardiac cycle?

A

200-300ms

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29
Q

When is diastasis achieved in the cardiac cycle?

A

When intra-ventricular pressure reaches atrial pressure.

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30
Q

What would happen if there was no atrial systole?

A

Heart would continue to pump normally.

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31
Q

When do the atrioventricular valves of the heart close?

A

During ventricular systole, once the intra-ventricular pressure rises above the atrial pressure, after a very brief period of backflow.

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32
Q

What is the “rapid ejection phase” of the cardiac cycle?

A

The period of time during ventricular systole that the aortic pressure rises slightly above that of the ventricle before both pressures peak.

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33
Q

What causes the first and second heart sounds?

A

The closing of the atrioventricular and outflow valves closing, respectively.

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34
Q

How could you measure the length of systole and diastole?

A

By listening to the heart sounds and timing the interval between the 1st and 2nd heart sounds for systole, and that between the 2nd and 1st heart sounds for diastole.

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35
Q

What would happen if the valves on each side of the heart do not close simultaneously?

A

Heart sounds may become split if valves of right and left heart do not close simultaneously.

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36
Q

Describe the extra heart sounds that may be heard in normal hearts.

A

Always heard in diastole (between S2 and S1).
3rd sound - early in diastole due to rapid expansion of the ventricles, often in very thin people
4th sound - due to atrial systole, often in kids

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37
Q

When is an extra heart sound a murmur?

A

If it is heard between the normal sounds 1 and 2.

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38
Q

What causes a heart murmur?

A

Extra sounds are heard in the heart due to a turbulent flow of blood caused by stenosis or incompetence of heart valves.

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39
Q

When would you hear the murmur of aortic stenosis?

A

In the rapid ejection phase of the cardiac cycle (“lub whoosh dup”)

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40
Q

Name the 6 parts of the primitive heart tube

A

Aortic roots, truncus artiosus, bulbous cordis, ventricular, atrium, sinus venous.

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41
Q

How does the primitive heart tube become the cardiac loop?

A

Heart tube undergoes continued elongation in the restricted space of the endocardial cavity, causing it to bend. The cephalic portion folds ventrally, caudally and to the right while the Caudill portion folds dorsally, cranially and to the left.

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42
Q

Why does the left recurrent laryngeal nerve extend all the way down to T4/5?

A

During embryological remodelling of the aortic arches the primitive heart descends and, as the recurrent laryngeal nerve is associated with the 6th aortic arch, it is dragged down with it. In the foetal circulation there is a need for a shunt between the pulmonary trunk and the aorta to bypass the lungs, namely the ductus arteriosus. The L laryngeal nerve becomes hooked round this and so is dragged down further than the nerve on the R side which instead becomes hooked around the R subclavian artery.

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43
Q

What is the first stage of septation in the developing heart of the embryo?

A

Growth of endocardial cushions in the atrioventricular region, to become a platform of tissue dividing the heart into right and left chambers.

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44
Q

Describe how blood flow from the R to L atria is maintained during the embryological process of atrial septation.

A

First the septum primum appears as a sickle shaped crest and grows down towards the endocardial cushions. Before the gap (known as ostium primum) between the two is closed, perforations in the septum primum formed by cell death coalesce to form the ostium secundum. Then as the septum secundum forms it remains crescent shaped, leaving the hole known as the foramen ovale.

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45
Q

What normally happens to the foramen ovale at birth?

A

It closes becoming the fossa ovalis when the L atrial pressure rises above that of the R atrium, which presses the septum together.

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46
Q

Describe the embryological process of ventricular septation in the developing heart.

A

Muscular tissue grows upwards towards the fused endocardial cushions. This leaves a small gap (primary interventricular foramen) which is closed by connective tissue from the endocardial cushions, thus forming the membranous part of the septum.

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47
Q

Describe how the aoticopulmonary septum is formed in the developing heart.

A

Endocardial cushions appear in a staggered formation within the truncus arteriosus. These then grow towards each other twisting as they do so to form a spiral septum separating the aorta and pulmonary trunk.

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48
Q

Describe what happens to the foetal circulatory shunts once the baby is born.

A

The smooth muscle of the ductus arteriosus contracts immediately after the first breath is taken. It slowly becomes a strand of connective tissue known as the ligamentum arteriosum.
The baby’s first breaths also cause the L atrial pressure to rise above the R which closes the foramen ovale, leaving an indentation known as the fossa ovalis.
The ductus arteriosus closes as placental support is removed and becomes the ligamentum venosum.

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49
Q

How common is congenital heart disease?

A

Relatively common (6-8 / 1000 births)

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50
Q

Name the 5 most common acynotic congenital heart defects.

A

Patent foramen ovale, ventricular septal defect, atrial septal defect, patent ductus arteriosus, coarction of the aorta.

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51
Q

When might a patent foramen ovale cause problems?

A

If the R atrial pressure increases even transiently eg when scuba diving, the PFO could allow a venous clot to enter the systemic circulation - known as a paradoxical embolism.

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52
Q

What is Eisenmenger syndrome?

A

Eisenmenger syndrome refers to any untreated congenital cardiac defect with intracardiac communication that leads to pulmonary hypertension, reversal of flow, and cyanosis.

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53
Q

Name the 3 most common cyanotic congenital heart defects.

A

Tetralogy of Fallot - severity varies
Transposition of Great arteries - requires shunt of ductus artiosus and/or ASD to survive until can be surgically corrected
Hypoplastic left heart - lethal without surgical correction

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54
Q

What are the 4 congenital cardiac lesions that occur in Tetralogy of Fallot?

A

Ventral septal defect, overiding aorta, pulmonary stenosis & R ventricular hypertrophy

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55
Q

What is the main contributor to the resting membrane potential?

A

RMP set largely due to the permeability of the cell membrane to potassium ions while at rest through leaky K+ channels.

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56
Q

Describe how the ionic permeability of the ventricular cardiac myocytes changes during an action potential.

A

At 200ms V gated Na+ channels open.
Then V gated Ca2+ and some K+ channels open.
At around 500ms the Ca2+ inactivate and all of the K+ channels are open.

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57
Q

Describe the pacemaker potential of cardiac myocytes at the sino-articular node.

A

Slow depolarisation to threshold due to influx of Na+ through HCN channels.

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58
Q

Briefly describe excitation-contraction coupling in the heart.

A

Electrically active cardiac myocytes respond to action potentials so that their cytosolic concentration of Ca2+ increases. This allows actin and myosin to interact leading to contraction. Cells are electrically coupled via gap junctions of the intercalculated discs allowing syncronised contraction across the heart.

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59
Q

How is cytosolic calcium increased in cardiac myocytes when stimulated?

A

Depolarisation opens the L type (V gated) Ca2+ channels in the t tubule system, this localised Ca2+ entry opens CICR channels of the endoplasmic reticulum which provide the majority of Ca2+ entry into the cytosol.

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60
Q

How does increased cytosolic calcium allow actin and myosin filaments to interact?

A

Ca ions bind to troponin C, causing a conformation change which shifts tropomyosin to reveal the myosin binding site on actin filaments.

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61
Q

How is the autonomic nervous system unique in its structure?

A

It requires a 2 neurones in sequence in the efferent pathway, where the cell body of one of these is located outside the CNS in ganglia.

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62
Q

Where are the cell bodies of the pre-ganglionic nerve fibres found in each branch of the autonomic nervous system?

A

Parasympathetic - cranial and sacral region of spinal cord.

Sympathetic - thoracic and lumbar regions of spinal cord.

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63
Q

Where are the ganglia of the autonomic nervous system located?

A

Parasympathetic ganglia tend to be located close to or within the structures they innervate.
While sympathetic ganglia are mostly found next to the spinal cord within the sympathetic or paravertebral chain.

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64
Q

Under basal conditions which branch of the autonomic nervous system is more active?

A

Parasympathetic

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65
Q

What type of neurotransmitter receptors are found on the ganglionic cell bodies of the ANS?
Which neurotransmitter do they respond to?

A

Nicotinic

Acetylcholine

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66
Q

Which chemical transmitter do most parasympathetic post ganglionic fibres release on stimulation?
Which receptors does this act on?

A

Acetylcholine

G protein coupled muscarinic receptors

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67
Q

Membranes & Receptors How does a G Protein Coupled Receptor work?

A

Receptor binding leads to conformational change which activates GDP/GTP exchange in G proteins. Activated G proteins then can trigger the increased production of various second messenger molecules.

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68
Q

Which chemical transmitter do most sympathetic post ganglionic neutrons release when stimulated?

A

Noradrenaline

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69
Q

What type of receptors are involved in mediating vasoconstriction?

A

Alpha 1 adrenoreceptors

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70
Q

How is control of the distribution of blood flow and total peripheral resistance achieved, physiologically?

A

By a balance between the sympathetic vasomotor tone and the action of vasodilator substance

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71
Q

How is increased blood flow to the skeletal muscle achieved during exercise?

A

Mostly by the local release of vasodilator metabolites such as adenosine, K+, H+ and increased partial pressure of CO2.
The specialised vasodilator response of Beta 2 adrenoreceptors in response to circulating adrenaline also contributes.

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72
Q

What direct effect does the parasympathetic nervous system have on blood vessels?

A

None, except in erectile tissue where it causes dilation.

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73
Q

Without the basal activity of the autonomic nervous symptom on the SA and AV nodes, what would the resting heart rate be and why?

A

Around 100bpm because the parasympathetic innervation normally dominates at rest.

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74
Q

How does the autonomic nervous system affect pacemaker potentials in the heart?

A

The sympathetic branch increases cAMP which increases the rate of depolarisation.
While the parasympathetic branch increases K+ conductance and decreases cAMP, decreasing the rate of depolarisation.

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75
Q

In the heart, what types of receptors are affected by the autonomic nervous system?

A

Beta 1 adrenoreceptors and Muscarinic type 2 cholinergic receptors

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76
Q

Explain the effect of noradrenaline on the force of contraction of the heart.

A

Noradrenaline has a positive inotropic effect as it acts on beta 1 receptors to increase cAMP which in turn activates protein kinase A. This increases the phosphorylation of CA2+ channels, increasing the entry of Ca2+ during action potentials, the uptake of Ca2+ into the sarcoplasmic reticulum and the sensitivity of contractile machinery to Ca2+.

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77
Q

Explain the effect of activation of the beta 2 adrenoreceptors of vascular smooth muscle.

A

Increases cAMP which activates PKA which opens K+ channels and inhibits MLCK. This causes the cells to relax bringing about vasodilation.

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78
Q

Explain the effects of activating the alpha 1 adrenoreceptors of vascular smooth muscle.

A

Stimulates IP3 production which increases intracellular concentration of Ca2+ causing contraction and thus vasoconstriction.

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79
Q

When flow through a tube is constant how would the velocity change if the tube got fatter or thinner (i.e. cross-sectional area changed)?

A

Velocity would vary inversely with cross-sectional area (when one increases the other decreases and vice versa)

80
Q

Explain why average velocity of flow is higher in more viscous fluids. (I.e. Why are thick, sticky fluids not very runny?)

A

In laminar flow adjacent layers of fluid are moving along the tube at different velocities and so must slide over each other. This is more difficult in viscous fluids as the layers are harder to separate. Thus the faster central layers are slowed down by the outer layers, reducing the average velocity.

81
Q

Given that each capillary in a capillary bed is very small, why is their collective resistance relatively low?

A

Collective resistance of capillaries is low despite their high individual resistances because many are combined in parallel and as such it is their combined size which needs to be taken into account.

82
Q

What are 2 advantages for blood vessels being distensible (stretchy)?

A
  1. As pressure increases, walls will stretch and so resistance falls, allowing adequate flow to be maintained even at high pressures.
  2. Distensible tubes have capacitance.
83
Q

How is blood flow maintained during diastole?

A

By the elastic recoil of distensible arteries, which causes the volume of blood in the arteries to increase when pressure is high during systole, leaving a reservoir which flows when pressure decreases during diastole.

84
Q

How do you calculate the mean arterial blood pressure?

A

2/3 of the diastolic pressure + 1/3 of the systolic pressure

85
Q

What factors affect how far pressure rises in systole?

A

Force of contraction of the heart, total peripheral resistance & compliance of arteries

86
Q

What is central venous pressure?

A

The pressure in the great veins supplying the heart

87
Q

Explain why “reactive hyperaemia” occurs

A

If blood flow is not sufficient for an organ’s metabolic rate, vasodilator metabolites such as H+, K+ and adenosine accumulate. This causes local arterioles to dilate, leading to increased blood flow.

88
Q

How is stroke volume calculated?

A

Difference between end diastolic volume and end systolic volume

89
Q

What would cause end diastolic volume to increase?

A

Increased venous pressure

90
Q

What is Starling’s law?

What does the gradient of the Starling curve represent?

A

If all other things are equal, increases in venous pressure will lead to increases in stroke volume.
The contractility of the ventricle.

91
Q

What 2 factors directly determine the force of contraction of the heart?

A

Contractility and end diastolic volume

92
Q

What effect do noradrenaline and adrenaline have on the heart?

A

Positive inotropic (increase contractility)

93
Q

Where are baroreceptors located?

A

Walls of arch of aorta and carotid sinus

94
Q

What is the function of baroreceptors?

A

To monitor arterial blood pressure so that adequate perfusion to the tissues can be even maintained despite changes in total peripheral resistance.

95
Q

How do baroreceptors achieve their function?

A

Via modulation in the cardiovascular centres of the medulla, detected falls in arterial pressure stimulate the autonomic nervous system to increase both the contractility of the heart and the heart rate.

96
Q

Mathematically, how is total peripheral resistance related to the total metabolic need for blood flow?

A

Inversely proportional

97
Q

Explain when standing up might trigger a faint in a patient

A

The increased effect of gravity on the superficial veins of the lower extremities, increases transmural pressure causing an increase in the blood volume in these vessels. This change causes central venous pressure to drop, reducing cardiac output and thus arterial pressure. If total peripheral resistance does not rise quickly enough in reaction to this, adequate perfusion to the brain may not be maintained and a syncope can occur.

98
Q

Describe the pattern in which action potentials spread through the heart

A

Atria depolarise -> 120-200ms delay at atrioventricular node -> activity spreads through inter-ventricular septum to excite ventricular myocardium from endocardial to pericardial surface at the apex of the heart -> excitation spreads up towards the base

99
Q

Where is the electrical axis of the heart?

A

Slightly left to the line of the inter-ventricular septum

100
Q

Why does a ventricular action potential generate TWO electrical signals on an ECG?

A

Signals only detected during change in membrane potential - i.e. Twice during each action potential - once during depolarisation and again during repolarisation

101
Q

Name all the leads of an ECG

A

Lead I, aVL, Lead II, avF, Lead III, aVR, V1, V2, V3, V4, V5 & V6

102
Q

What does absent P waves on an ECG suggest?

A

Atrial Fibrillation

103
Q

How big should the PR interval on an ECG of a healthy heart?

A

3-5 small squares / 0.12-0.2 seconds

104
Q

Which lead on an ECG should have the biggest QRS complex and why?

A

Lead II, this view normally parallel to the electrical axis of the heart therefore picks up the biggest signal

105
Q

What should the ST segment look like?

What does it suggest if it looks different?

A

Flat, completely horizontal

Damage to myocardium

106
Q

What does ST depression suggest?

A

Angina or NSTEMI

107
Q

What are the major differences between the systemic and pulmonary circulations?

A

Pulmonary is supply driven and must accommodate entire cardiac output whereas systemic is demand led.
Pulmonary is a low resistance, low pressure system.

108
Q

What’s the normal mean arterial pressure in the pulmonary circulation?

A

12-15 mmHg

109
Q

What’s the normal capillary pressure in the pulmonary circulation?

A

9-10mmHg

110
Q

What’s the normal mean venous pressure in the pulmonary circulation?

A

5mmHg

111
Q

Why is tissue fluid not normally formed in the lungs?

A

Pulmonary capillary pressure is normally less than the colloid osmotic pressure

112
Q

Explain what ventilation-perfusion matching is

A

The physiological mechanisms that allow effective gas exchange in the lungs by ensuring there is high blood flow (perfusion) to areas that have good air flow (ventilation) and vice versa. Blood is generally directed away from areas where O2 uptake is reduced by hypoxic pulmonary vasoconstriction. If there is a ventilation-perfusion mismatch, hypoxia will occur.

113
Q

Why is diastole important for the coronary circulation?

A

Coronary blood flow is almost exclusively diastolic especially for the left ventricle. This is because during systole the tension in the walls compresses the coronary vessels.

114
Q

How is flow through coronary circulation controlled?

A

Almost entirely by action of local vasodilator metabolites

115
Q

Why do minor problems with the coronary circulation only become apparent at higher heart rates?

A

Diastole is significantly shortened at higher heart rates and so peak flow must be able to rise rapidly to maintain adequate flow.

116
Q

What happens if there isn’t enough blood supply to the brain?

A

After a few seconds of cerebral ischeamia -> syncope (faint)

If reduced blood flow is due to raised intracranial pressure -> Cushing’s reflex: impaired blood flow to vasomotor control regions leads to increased sympathetic vasomotor activity, increasing arterial BP and thus maintaining cerebral blood flow.

After 3-4 minutes significant blood flow reduction-> permanent neuronal damage -> death

117
Q

What is the main function of cutaneous circulation and how is this controlled?

A

Thermoregulation, controlled by the sympathetic nervous system’s effects on arteriovenous anastomoses

118
Q

What increases blood flow to the muscles when we exercise?

A

Vasodilator nervous activity and local metabolites acting on capillaries to reduce tonic sympathetic vasoconstrictor tone

119
Q

Name 4 types of anti-ayrrhymic drugs

A

Volatage gated sodium ion channel blockers
Beta blockers
Potassium ion channel blockers
Calcium ion channel blockers

120
Q

What’s the main type of drug used in heart failure?

A

ACE inhibitors

121
Q

Name 5 types of drugs that are used in heart failure

A 
ACE inhibitors
Diuretics
Beta blockers
Cardiac glycosides 
Beta adrenergic agonists
122
Q

What does an atrial flutter look like on an ECG?

A

Saw tooth pattern

123
Q

Give 3 causes of arrhythmia

A

Ectopic pacemaker activity from damaged myocardium, after depolarisations and re-entry loops

124
Q

What do beta blockers do with regards to the heart?

A

Block sympathetic action as they are antagonists of the cardiac beta 1 receptors
Decreasing slope of pacemaker potential in sino-atrial node, slowing conduction at AV node and reducing O2 demand.

125
Q

Why are K+ channel blockers not generally used?

A

They can be pro-arthymic as they prolong action potentials

126
Q

Give a typical use for Amiodarone (antiarrhythmic with mainly K+ channel blocking actions)

A

Treating the tachycardia associated with Wolff-Parkinson-White syndrome

127
Q

What’s an advantage of administering IV adenosine for arrhythmia ?

A

It has a very short half life and so can be given to “reset” rythmn

128
Q

Give 4 key features of heart failure

A

Oedema
Reduced to tissue perfusion
Reduced force of contraction
Reduced cardiac output

129
Q

Which categories of drugs are the best to use long term in heart failure and why?

A

Diuretics, beta blockers and ACE inhibitors because they all reduce the workload of the heart

130
Q

How does digoxin increase the heart’s force of contraction?

A

Digoxin blocks Na+/K+ ATPase leading to a rise in intracellular sodium which in turn decreases the activity of the Na+Ca2+ exchanger protein. This then increases the intracellular concentration of Ca2+ increasing the amount stored in the sarcoplasmic reticulum. There is then more Ca2+ available to be released upon stimulation by an action potential and then act on troponin. More Ca2+ troponin binding means more myosin heads can make their power stroke along actin and thus the force of contraction produced by the cardiac myocytes is greater.

131
Q

Why do diuretics help in heart failure?

A

They reduce the blood volume which reduces the workload on the heart

132
Q

What 3 categories of drugs are used to treat angina?

A

Organic nitrates
Calcium channel antagonists
Beta adrenoreceptor blockers

133
Q

What’s the active ingredient of GTN spray?

A

Glyceryl trinitrate - an organic nitrate

134
Q

How do organic nitrates cause vasodilation of coronary arteries and also venodilation?

A

React with thiols (SH groups) causing nitrite release which is then reduced to nitric oxide. Nitric oxide activates guanylate cyclase which increases cyclic GMP which then lowers intracellular calcium ion concentrations. This causes the relaxation of vascular smooth muscle.

135
Q

Give 3 heart conditions that carry an increased risk of thrombus formation

A

Atrial fibrillation
Acute myocardial infarction
Mechanical prosthetic heart valves

136
Q

What 2 types of drugs are used in thrombosis?

A

Anti-platelet drugs and Anti-coagulants

137
Q

How does heparin work?

A

Thrombin inhibition, thus reducing clotting of the blood

138
Q

How does warfarin work?

A

It antagonises the action of vitamin K which is involved in prothrombin and factor X formation

139
Q

What 4 categories of drugs are used most commonly in hypertension?

A

Diuretics, ACE inhibitors, Alpha 1 adrenoreceptor antagonists and Calcium channel blockers selective fopr vasuclar smooth muscle

140
Q

Give 3 pulmonary causes of chest pain?

A

Pneumonia, Pulmonary embolism, Pneumothorax

141
Q

What does tearing chest pain suggest?

A

Aortic dissection

142
Q

Give two gastrointestinal causes of chest pain

A

Cholecystisis

Reflux oesophagitis

143
Q

What’s a CABG?

A

Coronary artery bypass graft - where vessel harvested from internal mammary artery, radial artery or saphenous vein and used to repair coronary circulation

144
Q

What’s a PCI?

A

Percutaneous Coronary Intervention and stenting

145
Q

What is stable angina?

A

Chest pain due to transient ischeamia in times of increased O2 demand such as exertion. There is no myocyte injury or necrosis and the ST segment of the ECG is generally depressed.

146
Q

What is unstable angina?

A

Transient ischeamia in the heart and thus chest pain even at rest. It’s a risk factor for MI.

147
Q

What’s Acute Coronary Syndrome?

A

Acute severe chest pain due to a sudden atheromatous plaque tissue within a blood vessel leading to a thrombus which lodges within the coronary circulation causing ischeamia in the heart tissue.

148
Q

When would chest pain be associated with positive biomarkers?

A

If it’s a STEMI or NSTEMI (negative biomarkers in unstable angina)

149
Q

What can the ST elevation of an ECG in STEMI tell you?

A

Can see the location of ischeamic damage as ST elevated in leads facing infarcted area of the myocardium

150
Q

What are the 4 important modifiable risk factors for Coronary Atheromatous Disease?

A

Hyperlipideamia
Cigarette smoking
Hypertension
Diabetes Mellitus

151
Q

What’s the difference between a stable and an unstable plaque?

A

Stable has small necrotic core and a thick fibrous cap so is less likely to rupture; whereas an unstable plaque has a large necrotic core and a thin fibrous cap

152
Q

Give 6 potential causes of ischeamic heart disease other than atheromatous Coronary Artery Disease

A 
Non-atheromatous causes of CAD
Severe hypertension
Severe anaemia
Aortic stenosis
Tachycardia
Thyrotoxicosis
153
Q

Name the biochemical markers of myocyte damage

A 
Cardiac troponin I & T
Creatine kinase (CKMB)
154
Q

What 3 types of drugs would you use in Acute Coronary Syndrome?

A

Fibrinolytic agents
Anti-platelet drugs
Anti-coagulants

155
Q

Give 8 potential complications of Myocardial Infarction

A 
Ventricular tachycardia / fibrillation 
Atrial fibrillation
Sinus tachycardia 
Cardiogenic shock 
Heart failure
Sinus bradycardia
Heart block
Sudden cardiac death
156
Q

What are the 3 key ECG features in STEMI and in which leads are they seen?

A

Seen in leads facing infarcted area
Q waves
T wave inversion
ST segment elevation

157
Q

Criteria for a pathological Q wave?

A

> 1 small square wide

>25% of QRS complex in height

158
Q

What causes a Q wave to form on an ECG?

A

Infarction causes an area of dead myocardium which gives an electrical window to allow action potentials on the other side of the heart to be detected by the ECG leads facing the infarcted area.

159
Q

Define heart failure

A

State in which the heart fails to meet the needs of the body despite adequate filling pressure

160
Q

What’s the biggest cause of heart failure?

A

Ischeamic Heart Disease

161
Q

If a heart failure patient has symptoms at rest what class of the NHYA Functional Classification would they be in?

A

Class IV

162
Q

Define class II of the NYHA Functional Classification of heart failure.

A

Slight limitation on physical activities where ordinary physical activity causes symptoms. There are no symptoms at rest.

163
Q

State the Frank-Starling law

A

“Force developed in a muscle fibre depends on the degree to which that fibre is stretched”

164
Q

Explain the difference in the Starling curve seen in gross heart failure

A

There is no plateau as the damaged myocardium is no longer able to withstand higher pressures

165
Q

Why does the myocardial wall thin in systolic dysfunctional heart failure?

A

Fibrosis and necrosis in addition to the activity of matrix proteinases.

166
Q

Give 5 features of systolic dysfunction, other than myocardial wall thinning.

A 
Increased L ventricle capacity
Decreased L ventricle cardiac output
Mitral valve incompetence
Cardiac arrhythmias
Neurohormonal activation
167
Q

What changes in cellular structure & function can be seen in systolic dysfunction?

A

Sarcoplasmic reticulum dysfunction
Changes to calcium availability and/or receptor regulation
Myocytolysis and vacuolation of cells
Myocyte hypertrophy

168
Q

What are the 4 main routes of neurohormonal activation involved in heart failure?

A

Sympathetic nervous system
Renin Angiotensin Aldosterone System
Natriuretic Hormones
Anti-Diuretic Hormone

169
Q

How does noradrenaline adversely affect the heart in the later stages of heart failure?

A

Induces the Renin Angiotensin Aldosterone System

Acts on alpha 1 receptors to cause cardiac hypertrophy, myocyte apoptosis and necrosis

170
Q

How does the sympathetic nervous system increase cardiac output in early heart failure?

A

Increases contractility of the myocardium
Induces tachycardia
Causes arterial and venous vasoconstriction

171
Q

Describe the gross structural changes to the myocardium in heart failure

A

There is muscle loss and uncoordinated abnormal contraction

172
Q

List 4 effects of Angiotensin II on the kidneys in heart failure

A

Reduce GFR
Increase proteinuria
Increase aldosterone
Glomerular sclerosis

173
Q

Why is stroke more likely in a patient with heart failure?

A

RAAS is activated, Angiontensin II causes atherosclerosis and vasoconstriction putting the body into a pro-thrombotic state. If a thrombus embolises into the cerebral circulation it can cause ischeamic stroke.
More likely to be in Atrial fibrillation which is also associated with increased risk of thrombus formation.

174
Q

Why is anaemia common in heart failure?

A 
Varied aetiology:
Chronic inflammatory disease
Increased plasma volume
Effects of ACE inhibitors / aspirin
Iron malabsorption
Chronic renal failure
175
Q

In which groups is diastolic dysfunction most common?

A

Elderly, female and/or patients with history of hypertension / obesity / diabetes

176
Q

State 4 features of diastolic dysfunction

A

Reduced left ventricular compliance
Impaired myocardial contraction
Impaired left ventricle filling
Low cardiac output when heart is unable to compensate by increasing left ventricle end diastolic pressure

177
Q

Give 4 symptoms of left sided heart failure

A

Fatigue
Exertional dyspnoea
Orthopnoea
Paroxysmal nocturnal dyspnoea

178
Q

State 6 signs that you might observe in left sided heart failure

A 
Tachycardia 
Cardiomegaly
3rd or 4th heart sound
Functional mitral regurgitation
Basal pulmonary crackles
Peripheral oedema
179
Q

Give 6 potential causes of right sided heart failure

A 
Left sided heart failure
Chronic lung disease
Pulmonary embolism or hypertension
Pulmonary or tricuspid valvular disease
L-> R shunts such as ASD or VSD
Isolated R ventricular cardiomyopathy
180
Q

What signs are associated with R sided heart failure?

A 
Raised JVP
Tender, smooth hepatomegaly
Dependant pitting oedema 
Ascites 
Oedema 
Pleural effusion
181
Q

What are the 4 main principles of heart failure management?

A

Correct underlying cause
Non-pharmacological measures
Pharmacological therapy for symptom relief, to delay progression and to reduce mortality
Treat complications / associated conditions / cardiovascular risk factors

182
Q

What is the NICE 2003 guideline for heart failure management?

A

Diuretics if required for congestive symotoms / fluid retention
Digoxin if patient in AF or if symptomatic after following steps:
Progress through steps if no relief
1. Start ACE inhibitors and titrate up, or if not tolerated an angiotensin II receptor antagonist
2. Add beta blockers and titrate up
3.

183
Q

Give 4 examples of regional poor perfusion

A

Peripheral Artery Disease
Coronary Artery Disease
Varicose veins
Deep Vein Thrombosis

184
Q

How do the symptoms of unstable angina differ from stable angina?

A

In unstable angina chest pain comes on rapidly and at rest. The pain itself is more central and radiates less.

185
Q

What defines a cardiac arrest?

A

Unresponsive patient with no pulse

186
Q

State 2 arrythmias that can lead to ventricular fibrillation

A

Long QT and Torsades de Pointes

187
Q

Define shock

A

Shock is an acute condition of inadequate blood flow through the body

188
Q

How does administration of adrenaline help in a cardiac arrest?

A

Improves myocardial function and increases peripheral resistance

189
Q

What are the 5 types of shock?

A

Toxic, Anaphylactic, Mechanical, Hypovoleamic and Cardiogenic

190
Q

State 2 causes of mechanical shock

A

Cardiac tamponade

Massive pulmonary embolism

191
Q

3 potential precipitating conditions for cardiogenic shock

A

Myocardial infarction
Serious arrhythmias
Heart failure

192
Q

What happens to the arterial blood pressure in shock?

A

Arterial BP drops dramatically in shock

193
Q

Why might a patient in anaphalaxis have difficulty breathing?

A

High levels of histamine can cause bronchocontriction and laryngeal oedema

194
Q

Define hypertension

A

Hypertension is a sustained increase in arterial blood pressure to values greater than 140/90mmHg

195
Q

Why does hypertension increase the risk of heat failure?

A

It can cause left ventricular hypertrophy which is a risk factor for heart failure.

196
Q

Give 3 non-pharmacological measures for managing hypertension

A

Weight loss, increase physical activity, decrease salt intake

197
Q

What types of drugs might you give a hypertensive patient?

A

Diuretics, Vasodilators, ACE inhibitors, and Beta blockers (if they have had a previous MI)

Old curriculum (12 decks)

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