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My ESA 2 > CVS > Flashcards

CVS Flashcards

1
Q

Describe the 3 factors that affect diffusion rate

A

Area: determined by capillary density
Diffusion Resistance: determined by the nature of the barrier & molecules diffusing, distance required to travel
Concentration Gradient: determined by flow of blood through the capillary.

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2
Q

What’s the average range of blood flow through the entire system?

A

5.0 l/min (rest) to 25.0 l/min (strenuous exercise)

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3
Q

What’s the level of blood flow that must be maintained to the brain at all times?

A

0.75 l/min

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4
Q

Where does the blood lie in our body?

A

65% veins
20% heart and lungs
10% peripheral arteries
5% capillaries

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5
Q

What’s the difference between arterioles and metarterioles?

A

In metarterioles the smooth muscle layer is not continuous, only present at sphincters

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6
Q

Name the 3 major types of artery

A 
Elastic conducting (widest)
Muscular distributing (intermediate diameter)
Arterioles (narrowest, diameter
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7
Q

Name the 3 layers of the walls of arteries and veins

A 
Tunica intima (next to lumen)
Tunica media (intermediate)
Tunica adventitia (outermost)
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8
Q

Is vasoconstriction of muscular arteries controlled by sympathetic or parasympathetic nerve fibres?

A

Synpathetic

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9
Q

What is an end artery?

A

A terminal artery supplying all or most of the blood to a body part without significant collateral circulation. If occluded there is insufficient blood supply to the dependent tissue

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10
Q

Describe the 3 types of capillaries

A

Continuous - (most common) cells joined by tight or occluding junctions
Fenestrated - little interruptions exist across thin parts of the endothelium (in parts of gut, endocrine glands)
Sinusoidal (discontinuous) - larger diameter, slower blood flow. Gaps exist in the walls allowing whole cells to move between blood and tissue (in liver, spleen and bone marrow)

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11
Q

What do pericytes do?

A

Form a branching network on the outer surface of the endothelium. Capable of dividing into muscle cells, fibroblasts, during angiogenesis, tumour growth or wound healing

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12
Q

What are 3 possible routes of transport across the endothelial wall of a fenestrated capillary?

A
  1. Direct diffusion
  2. Diffusion through intercellular cleft
  3. Diffusion through fenestration
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13
Q

Where is the preferred emigration site of leukocytes from the blood?

A

Postcapillary venules

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14
Q

What are venae comitantes?

A

Deep paired veins that accompany one of the smaller arteries. The pulsing of the artery promotes venous return within the adjacent, parallel, paired veins. The 3 vessels are wrapped together in one sheath. E.g. brachial, ulnar, tibial comitantes

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15
Q

Why do we need a cardiovascular system?

A

Most cells far away from source of O2 and nutrients, a system is required to carry such to cells and carry waste products away.

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16
Q

Define systole

A

Contraction and ejection of blood from the ventricles

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17
Q

Define diastole

A

Relaxation and filling of the ventricles

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18
Q

For how long does a cardiac action potential last?

A

~280ms

Lasts the duration of a single contraction of the heart

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19
Q

Where is the tricuspid valve located?

A

Between the right atrium and the right ventricle

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20
Q

Where is the mitral valve located?

A

Between the left atrium and the left ventricle

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21
Q

Where is the pulmonary valve located?

A

Between the right ventricle and the pulmonary artery

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22
Q

Where is the aortic valve located?

A

Between the left ventricle and the aorta

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23
Q

What are the cusps of the mitral and tricuspid valves attached to?

A

Attached from the valves to papillary muscles via chordae tendineae (prevents inversion of valves on systole)

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24
Q

Name 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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25
Q

Why does atrial pressure initially decrease during rapid ejection?

A

Atrial base is pulled downwards as ventricle contracts

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26
Q

Give 3 things which may lead to congenital heart defects

A
  1. Genetics (Marian’s, downs, turners syndromes)
  2. Environmental (teratogenicity from drugs, alcohol ect.)
  3. Maternal infections (rubella, toxoplasmosis, diabetes)
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27
Q

How are congenital heart defects classified?

A

Acyanotic (left to right shunts)

Cyan optic (right to left shunts, complex)

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28
Q

What is the approximate resting membrane potential for a cardiac monocyte

A

-90mV

Ek =-95mV

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29
Q

What’s the major difference between cardiac action potentials and skeletal muscle action potentials?

A

Cardiac action potentials are much longer in duration (100ms compared to 0.5ms in skeletal)

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30
Q

What causes the ‘plateau’ in a cardiac action potential?

A

Opening of voltage gated Ca2+ channels

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31
Q

What causes the upstroke of a cardiac action potential?

A

Opening of voltage-gated Na+ channels

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32
Q

What is If?

A

Funny current!

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33
Q

What is repolarisation due to in the cardiac action potential?

A

Efflux of K+ through voltage-gated K+ channels

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34
Q

What causes the gradual increase in membrane potential of the funny current?

A

Influx of Na+ via HCN (Hyperpolarisation-activated Cyclic Nucleotide-gated channels). The more negative, the more it activates (activated at potentials

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35
Q

What causes the upstroke in the SA node action potential?

A

Opening of voltage gated Ca2+ channels

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36
Q

What causes the downstroke of the SA node action potential?

A

Opening of voltage-gated K+ channels

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37
Q

Give 3 features of cardiac muscle

A 
Striated
Central nuclei
Intercolated discs connecting cells
Gap junctions (permit movement of ions and electrically couple cells)
Desmosomes rivet cells together
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38
Q

Where does Ca2+ come from when it is used to stimulate contraction of muscle?

A

25% enters across sarcolemma

75% released from SR (intracellular stores)

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39
Q

What type of receptor causes initial influx of Ca2+ in muscle upon depolorisation?

A

L-type Ca2+ channels

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40
Q

What occurs after localised Ca2+ entry has occurred upon depolorisation of a muscle cell?

A

Opening of CICR (Calcium-Induced Calcium Release) channels in the SR

There is a close link between L-type channels and Ca2+ release channels

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41
Q

What happens on relaxation of cardiac myocytes?

A

Ca2+ levels are returned to resting levels, mostly by pumping Ca2+ back into SR (via SERCA), some exits across cell membrane

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42
Q

How is contraction of vascular smooth muscle regulated?

A

Ca2+ binds to calmodulin - this activates MLCK (myosin light chain kinase). MLCK then phosphorylates the myosin light chain to permit interaction with actin.

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43
Q

How is relaxation of vascular smooth muscle achieved?

A

Myosin light chain phosphatase dephosphorylates the myosin light chain (constituently active)

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44
Q

What are the respective lengths of the pre and post ganglionic neurones in the parasympathetic (cranio-sacral outflow) system?

A

Pre-ganglionic: long

Post-ganglionic: short

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45
Q

What are the respective lengths of the pre and post ganglionic neurones in the sympathetic (thoraco-lumbar outflow) system?

A

Pre-ganglionic: short

Post-ganglionic: long

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46
Q

What neurotransmitter do preganglionic neurones release?

A

Acetylcholine ACh
Acts on nicotinic ACh receptors on the postganglionic neurone (receptors contain integral ion channel permeable to Na+ and K+)

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47
Q

What neurotransmitter do postganglionic sympathetic neurones usually release?

A

Noradrenaline (so are noradrenergic)

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48
Q

What neurotransmitter do postganglionic parasympathetic neurones usually release?

A

Acetylcholine (so are cholinergic)

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49
Q

Name an exception to the neurotransmitter released by postganglionic sympathetic neurones?

A

Innervation of sweat glands by postganglionic release of ACh which acts on muscadine can ACh receptors)

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50
Q

What do chromaffin cells of the adrenal medulla release?

A

Adrenal chromaffin cells release adrenaline into the blood stream.

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51
Q

What are the benefits of having different subtypes of receptors/in different tissues?

A

Allows for diversity of action

Enables selectivity of drug action

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52
Q

Name 2 co-transmitters which may be released with noradrenaline or adrenaline at then postganglionic synapse with effector cells

A 
Neuropeptide Y (NPY)
ATP
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53
Q

What type of ACh receptors are on effector cells?

A

Muscarinic

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54
Q

What type of ACh receptors are on postganglionic neurones (proximal/receiving end)?

A

Nicotinic

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55
Q

What does the ANS control in the cardiovascular system?

A

Heart rate (but does not initiate electrical activity)
Force of contraction of the heart
Peripheral resistance of blood vessels

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56
Q

What effect does sympathetic input to the heart have?

A

Positive chronotropic effect (increases heart rate)
Positive inotropic effect (increases force of contraction)
Acts mainly on beta1 adrenoreceptors, release noradrenaline

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57
Q

What happens to the If (funny current) if the heart rate speeds up?

A

Slope steepens

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58
Q

Which receptors of the heart mediate the sympathetic effect?

A

Beta1

G protein coupled receptors, increase cAMP, speeds up pacemaker potential

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59
Q

Which receptors of the heart mediate the parasympathetic effect?

A

M2 receptors

G protein coupled receptors, increase K+ conductance and decrease cAMP

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60
Q

What type of adrenoreceptors do most arteries and veins have?

A

Alpha1 (sympathetic)

Coronary and skeletal muscle vasculature also have beta2 receptors

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61
Q

Has circulating adrenaline got higher affinity for beta 2 or alpha 1 receptors?

A

Beta2, therefore will preferentially bind to such.

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62
Q

What do activated beta2 adrenoreceptors cause?

A

Vasodilation

Increases cAMP, produces PKA, opens K+ channels, inhibits MLCK, relaxation of smooth muscle

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63
Q

What do activated alpha1 adrenoreceptors cause?

A

Vasoconstriction
Stimulates IP3 production
Increase in [Ca2+]in from stores and via influx of Ca2+, contraction of smooth muscle

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64
Q

What are the name of the receptors for high pressure side of the system?

A

Baroreceptors

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65
Q

What are the name of the receptors for low pressure side of the system?

A

Atrial receptors

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66
Q

Define flow

A

The volume of fluid passing a given point over a unit time

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67
Q

Define velocity

A

The rate of movement of particles along the tube

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68
Q

Where does blood flow fastest?

A

Where the total cross sectional area is least

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69
Q

Describe laminar flow

A

Gradient of velocity from middle to edge of vessel (velocity is highest in the middle, fluid is stationary at the edge)

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70
Q

Describe turbulent flow

A

As mean velocity increases, flow eventually becomes turbulent. Velocity gradient breaks down, fluid tumbles over itself. Flow resistance greatly increased.

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71
Q

What does mean velocity depend on?

A

Viscosity of the fluid

Radius of the tube

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72
Q

Define velocity

A

The extent to which fluid layers resist sliding over one another. The higher the viscosity, the slower the central layers will flow, and the lower the average velocity.

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73
Q

Give 2 potential causes of hyperviscosity syndrome

A
  1. Abnormally high plasma protein levels (treatment: plasmapheresis)
  2. Abnormally high RBC or WBC count (treatment: phlebotomy)
    Note: underlying condition must be treated or HVS recurs.
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74
Q

How do you work out total resistance for resistances aligned in series?

A

Total resistance equals the sum of the individual resistances

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75
Q

How do you work out the total resistance for resistances aligned in parallel?

A

The reciprocal of the total resistance equals the sum of the reciprocal a of the individual resistance

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76
Q

Which vessels have the highest resistance?

A

Arterioles

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77
Q

When does blood flow become turbulent?

A

Flow velocity is high
Viscosity is low
Lumen of blood vessel is irregular (e.g. Athlerosclerosis)

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78
Q

What is a bruit?

A

Noise heard upon ausculation of turbulent bloodflow.

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79
Q

What happens to resistance in distensile vessels as blood pressure rises?

A

The vessel stretches, so resistance falls. The higher the pressure, the easier it is for blood to flow through.

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80
Q

Which vessels are the most distensible?

A

Veins

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81
Q

What is compliance?

A

The ability to distend and increase volume due to pressure increase

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82
Q

What is capacitance?

A

Measure of relative volume increase per unit increase in pressure C=V/P
Effectively the same as compliance

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83
Q

What is pressure?

A

Measure of mechanical energy gradient in blood that drives its flow round different parts of the system

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84
Q

What is total peripheral resistance (TPR)?

A

The sum of all arteriolar resistance

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85
Q

What is cardiac output?

A

Cardiac Output = Stroke Volume x Heart Rate

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86
Q

What is the ‘Windkessel’ effect?

A

Aortic compliance dampens pulsatile nature of systolic pressure wave. ‘Smooths out’ blood flow

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87
Q

What is the maximum arterial pressure called?

A

Systolic pressure (~120mmHg)

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88
Q

What is the minimum arterial pressure called?

A

Diastolic pressure (~80mmHg)

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89
Q

List 3 factors effecting systolic and diastolic pressure

A
  1. Cardiac output SVxHR (how hard heart is pumping)
  2. Arterial compliance (‘stretchiness’ of elastic arteries ~1.5-2%/mmHg)
  3. Total Peripheral Resistance
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90
Q

What is pulse pressure?

A

The difference between systolic and diastolic pressure ~40mmHg

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91
Q

What is the average pressure?

A

Diastolic pressure + 1/3 pulse pressure

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92
Q

Does the cardiac system spend more time in systole of diastole?

A

Diastole (~0.55s)

Compared to ~0.3s in systole

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93
Q

What controls the flow to capillary beds?

A

Arterioles and pre-capillary sphincters - ‘resistance vessels’

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94
Q

What are the levels of vasomotor tone at rest?

A

High - tonic contraction of smooth muscle

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95
Q

How is contraction of vascular smooth muscle achieved?

A

Release of noradrenaline by sympathetic nervous system, acts on alpha-1 GPCRs causing Ca2+ influx, therefore contraction

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96
Q

How is vascular vasodilatation achieved?

A

Achieved by local vasodilator factors produced by metabolically active tissues e.g. H+, CO2, K+, lactate
These act to relax vascular smooth muscle

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97
Q

What is the difference between vasodilation and vasodilatation?

A

Vasodilation - vasodilation in absence of vasoconstrictive signal.
Vasodilatation - reduction/offset of active vasoconstriction in presence of ongoing vasoconstrictive signal.

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98
Q

What regulates right atrium filling, and therefore stroke volume?

A

Veins/great veins

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99
Q

What controls total peripheral resistance?

A

Arterioles

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100
Q

At rest, what is the approximate mean arterial blood pressure?

A

~95mmHg

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101
Q

Why is the mean arterial blood pressure ~95mmHg?

A

This value is ‘engineered to humans’ - provides adequate pressure to perfume and drive blood through whole vasculature, ensuring positive central venous pressure
Significant functional reserve still available - many capillary beds not perfused

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102
Q

If hypotensive, at what value would mean arterial blood pressure falling below would tissue perfusion become inadequate?

A

60mmHg

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103
Q

What is the acute effect on the whole CVS of standing up?

A

CVP falls directly -RA filling decreases
Stroke volume decreases (by starlings law)
Mean arterial pressure falls (by ~20-25mmHg)
Both arterial and venous pressure falling acutely
This is signalled via baroreceptors
HR then increased (by ~10-25bpm) in response

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104
Q

What is the effect on the CVS of massive haemorrhage?

A

Hypovolemic shock if residual blood volume

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105
Q

How does exercise aid circulation?

A

Contractile activity of skeletal muscle in exercise actively aids whole circulation of blood (up to 50% of energy required to drive blood in circulation can come from muscle activity in exercise)

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106
Q

What is the response of the CVS to eating a large meal?

A

Local GI vasodilation leads to decrease in TPR. Initial decrease in arterial pressure. Flow out liver increases, leading to rise in CVP - rise in RA filling, so cardiac output increases
Parasympathetic activity increases
Greater flow to GI

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107
Q

What determines arterial pressure?

A

Cardiac output

Total peripheral resistance

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108
Q

What determines venous pressure?

A

Rate blood enters veins

Rate heart pumps

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109
Q

What is stroke volume?

A

End Diastolic Volume - End Systolic Volume

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110
Q

What is the relationship between venous pressure and ventricular volume know as?

A

The ventricular compliance curve

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111
Q

What is starlings law of the heart?

A

The more the heart fills, the harder it contracts (up to a limit). The harder it contracts, the bigger the stroke volume.
Rises in venous pressure automatically lead to rises in stroke volume.

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112
Q

What is contractility?

A

The EFFICIENCY of contraction (not the force!)

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113
Q

What does how much the ventricle contracts depend upon?

A

How hard it contracts

How hard it is to eject blood

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114
Q

What is the force of contraction dependent upon?

A

End diastolic volume (starlings law)

Contractility

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115
Q

Why, in starlings law of the heart, does the stretch of ventricular muscle only increase force of contraction up to a limit?

A

Beyond said limit tissue is damaged

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116
Q

What determines the difficulty of ejecting blood?

A

Total peripheral resistance

The harder it is to eject blood, the higher pressure rises in the arteries

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117
Q

What determines the end systolic volume?

A

The easier it is to eject blood, the more comes out in systole. So if arterial pressure falls, end systolic volume will fall, stroke volume will rise.

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118
Q

What will happen to stroke volume if venous pressure rises?

A

Stroke volume will rise

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119
Q

What will happen to stroke volume if arterial pressure rises?

A

Stroke volume will fall

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120
Q

How is autonomic outflow of the heart controlled?

A

Signals from baroreceptors

Carotid sinus senses arterial pressure, sends signals to medulla which then controls the heart

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121
Q

How is heart rate increased?

A

Increased sympathetic activity

Decreased parasympathetic activity

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122
Q

How is contractility increased?

A

Increased sympathetic activity

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123
Q

Where are rises in venous pressure detected?

A

Right atrium
Leads to reduced parasympathetic activity (therefore rise in HR)
‘Bainbridge reflex’

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124
Q

What do rises in venous pressure cause?

A

Increased stroke volume (starlings law)

Increased heart rate

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125
Q

What do falls in arterial pressure cause?

A

Increased stroke volume (sympathetic activity as well as direct effect)
Increased heart rate

126
Q

What is the typical cardiac output range?

A

5-15 l/min

127
Q

What’s the typical heart rate range?

A

60-180 bpm

128
Q

What’s the typical stroke volume range?

A

60-150 ml

129
Q

What is hyperemia?

A

The increase of blood flow to different tissues of the body

130
Q

Describe the response of the CVS to eating a large meal

A

Increased activity of the gut leads to release of metabolites and local vasodilation.
TPR falls, so arterial pressure falls, venous pressure rises
Cardiac output rises (increased HR and CO)
Extra pumping of the heart reduces venous pressure and raises arterial pressure
Demand met, system stable

131
Q

Describe the response of the CVS to standing up

A

On standing, blood pools in superficial veins of the legs due to gravity
Central venous pressure falls, therefore cardiac output falls also (due to starlings law)
Arterial pressure falls, baroreceptors detect fall in arterial pressure
HR raised, TPR increased

132
Q

What is postural hypotension?

A

Failure of the CVS to cope with changes in bloodflow upon standing up

133
Q

Describe the response of the CVS to haemorrhage

A

Reduced blood volume lowers venous pressure
Cardiac output falls due to starlings law
Arterial pressure falls
Baroreceptors detect fall in arterial pressure, increase HR, increase TPR
Rise in HR lowers venous pressure further (MAKING PROBLEM WORSE)
Venous pressure needs to be increased to fix problem, but HR can become very high
Veno-constriction occurs
Treatment is blood transfusion to replace lost volume

134
Q

Describe the response of the CVS to exercise

A

Enormous increase in demand
‘Muscle pumping’ forces extra blood back to the heart
Increased venous pressure, decreased arterial pressure. If heart cannot cope risk of pulmonary oedema
Overfilling of ventricles prevented by a rise in heart rate - when venous pressure starts to rise HR is already high
Stroke volume kept down, but CO increased
Demand met - system stable

135
Q

What deflection will depolorisation moving towards an electrode show?

A

Positive deflection from baseline

136
Q

What deflection will depolarisation moving away from an electrode show?

A

Negative defection from baseline

137
Q

After how long will cardiac cells start to repolorise?

A

~280ms

138
Q

Which surface of the heart repolarises first?

A 
Epicardial surface
(Endocardial surface repolarises last)
139
Q

What deflection will repolorisation moving towards an electrode show?

A

Negative deflection from the baseline

140
Q

What deflection will repolorisation moving away from an electrode show?

A

Positive deflection from the baseline

141
Q

What does the amplitude of an ECG signal depend upon?

A

How much muscle is depolarising

How directly towards the electrode the excitation is moving

142
Q

What does the P wave show?

A

Atrial depolarisation

143
Q

What does the Q wave show?

A

Septal depolarisation spreading to ventricle

144
Q

What does the R wave show?

A

Main ventricular depolarisation

145
Q

What does the S wave show?

A

End ventricular depolarisation

146
Q

What does the T wave show?

A

Ventricular repolarisation

147
Q

List possible confounders for ECG readings

A

Lead misplacement
Muscle contractions (e.g. Movement, shivering, talking, coughing)
Interference (e.g. Alternating current)
Poor electrical contact (e.g. sweat, cable pull, hair)

148
Q

How many squares is one second on an ECG?

A

5 large

149
Q

How do you calculate the rate of a regular rhythm from an ECG?

A

Divide 300 by no. of large squares of R-R interval

150
Q

How do you calculate the rate of an irregular rhythm from an ECG?

A

Count the no. of QRS complexes in 6s, then multiply by 10

151
Q

Approximately how long should the PR interval be?

A

0.12-0.20s

3-5 small boxes

152
Q

Approximately how long should the QT interval be?

A

Male: less than 0.45

Female : less than 0.47

153
Q

What do you look at to assess the rhythm of an ECG?

A

The rhythm strip

154
Q

What is the average no. bpm for normal sinus rhythm?

A

60-100 bpm

155
Q

On an ECG, how much time is represented by 1 large square (5mm)?

A

0.2s

156
Q

On an ECG, how much time is represented by 1 small square (1mm)?

A

0.04s

157
Q

List some points to assess when interpreting the rhythm of an ECG

A

Assess P waves (indicates atrial depolarisation)
Calculate PR interval (estimates conduction in AV node & bundle of his)
Assess the relationship between P waves and QRS complex (is every P wave followed by QRS/vice versa?)
Assess QRS complex (narrow? - rhythm originating in atria/AVN. Broad? - rhythm originating in ventricles)

158
Q

What is a normal QRS complex width?

A

Less than or equal to 3 small boxes (0.12s)

159
Q

What is the normal PR interval?

A

3-5 small boxes

0.12-0.20s

160
Q

Describe atrial fibrillation

A

Atrial depolarisation chaotic - leads to loss of normal atrial contraction (atria quivering not contracting)
Impulses conducted irregularly to ventricles
Due to multiple abnormal atrial pacemakers discharging randomly
Ventricular depolarisation normal via his-purkinje system, hence narrow QRS complexes
Pulse and heart rate irregularly irregular

161
Q

Are P waves present in atrial fibrillation?

A

No, as no atrial depolarisation occurs

162
Q

What does the P-R interval show?

A

The time taken for conduction of impulse to ventricles

Should be 3-5 small squares (0.12-0.2s)

163
Q

Where do you measure a P-R interval from?

A

The start of the P wave to the start of the QRS complex

164
Q

Describe a 1st degree heart block

A

Slow conduction in AV node and His bundle due to ischaemia or degenerative change
PR interval prolonged (>5 small squares/0.2s)
QRS/P wave both normal

165
Q

Describe a type 1 second degree heart block (AKA Mobitz type 1 HB / Wenkebach phenomenon)

A

Progressive lengthening of PR interval till one P is not conducted (enabling AVN to recover). Cycle then repeats

166
Q

Describe type 2 second degree heart block

A

Sudden lack of conduction of a beat (dropped QRS)
High risk of progression to complete heart block, requires insertion of a pacemaker
PR interval normal

167
Q

Describe a third degree heart block

A

P waves normal, but not conducted to ventricle. Ventricular pacemaker takes over ‘ventricular escape rhythm’, rate is very slow (~30-40bpm). Usually wide QRS complexes.
Heart rate is too slow to maintain blood pressure and perfusion - urgent pacemaker insertion required

168
Q

What are ectopic foci?

A

Abnormal pacemaker sites within the heart muscle that display automaticity. They are normally suppressed by the higher rate of the SA node (overdrive suppression). Can occur within the atria (atrial ectopics) or ventricles (ventricular ectopics)

169
Q

Describe the characteristics of ventricular ectopic beats

A

Ectopic focus is in ventricle; depolarisation spreads through muscle, not via the Purkinje system. Therefore much slower depolarisation of ventricle. Wide QRS complex, different in shape to usual QRS.

170
Q

A run of 3 or more consecutive ventricular ectopics is defined as….

A

Ventricular Tachycardia (VT)

171
Q

Describe ventricular fibrillation

A

Abnormal, chaotic, fast, ventricular depolarisation from impulses arising in numerous ectopic sites in ventricular muscle. No co-ordinated contraction. No cardiac output, no pulse or heart beat. Cardiac arrest.

172
Q

What do you look at on an ECG to assess ‘structural’ abnormalities

A

P-QRST in all 12 leads to identify problem/affected part of the heart.

173
Q

What is a ‘lead’ in an ECG?

A

An electrical view of the heart

174
Q

In what plane do the limb leads view the heart?

A

Vertical plane

175
Q

In what plane do the chest leads view the heart?

A

Horizontal plane

176
Q

Describe how partial occlusion of coronary arteries may present

A

Poor myocardial perfusion particularly on exercise - pain on exercise (angina)
ECG often normal at rest, but changes seen on exercise

177
Q

Name 3 ECG features of a fully evolved myocardial infarction, in ECG leads facing the infarct end area.

A
  1. Q waves, due to myocardial necrosis
  2. ST segment elevation, due to subepicardial injury
  3. T wave inversion
178
Q

Describe the exercise ECG of a patient with angina

A

Sub-endocardial ischaemia causing ST depression in ECG leads facing the affected area/s

179
Q

What are pathological Q waves?

A

Q waves of more than 0.04s (1small square) / >2mm deep. Present in full thickness myocardial infarction. Remain after other changes have been resolved.

180
Q

What is the cardiac axis?

A

The average (overall) direction of spread of the ventricular depolarisation

181
Q

In which direction is the cardiac axis usually?

A

Downward and to the left, between -30 and +90 degrees

182
Q

What is left axis deviation associated with?

A

Left ventricular hypertrophy (LVH)

Conduction blocks in anterior part of the left bundle branch

183
Q

What is right axis deviation associated with?

A

Right ventricle hypertrophy

184
Q

What would axis deviation of >+90 degrees be?

A

To the right

‘Reaching’

185
Q

Give the 8 points to give when reporting an ECG

A 
Rate
Rhythm 
Conduction intervals (PR, QRS, QT)
Axis (several methods of calculating this)
P wave (LA or RA enlargement)
Description of QRS complex
ST segment
T wave
186
Q

In which direction is the shunt in a cyanotic heart defect?

A

Right to left

Generally complex issues!

187
Q

In which direction is the shunt in an acyanotic heart defect?

A

Left to right

188
Q

Give some examples of what drugs might be used to treat, with regards to cardiovascular diseases

A 
Arrhythmias
Heart failure
Angina
Hypertension
Risk of thrombus formation
189
Q

Give examples of what drugs can alter, with regards to the cardiovascular system

A

The rate a rhythm of the heart
Force of myocardial contraction
Peripheral resistance and blood flow
Blood volume (via kidneys)

190
Q

Give 3 possible causes of arrhythmias

A

Ectopic pacemaker activity
Afterdepolarisations
Re-entry loop

191
Q

What are the 4 basic classes of anti-arrhythmic drugs?

A
  1. Drugs that block voltage-sensitive sodium channels
  2. Antagonists of beta-adrenoreceptors
  3. Drugs that block potassium channels
  4. Drugs that block calcium channels
192
Q

Give an example of a a drug with blocks voltage-gated Na+ channels (class 1)

A

Lidocaine

193
Q

How does lidocaine work, and when would it be used?

A

Blocks open/inactive Na+ channels, dissociates rapidly in time for new AP. Prevents automatic firing of depolarised ventricular tissue, little effect on normal cardiac tissue. Used if patient shows signs of ventricular tachycardia, given intravenously.

194
Q

Give example(s) of beta adrenoreceptor antagonist drugs (class 2)

A

Propranolol

Atenolol (beta blockers)

195
Q

How do beta adrenoreceptor antagonist drugs (class 2) work?

A

Block sympathetic action (noradrenaline binding to beta adrenoreceptors in the heart). Decrease slope of pacemaker potential in SA. Reduces O2 demand. Can prevent supraventricular tachycardias

196
Q

How do drugs that block K+ channels work?

A

Prolongs the AP, lengthening ARP, preventing new AP occurring too soon

197
Q

Why aren’t drugs that block K+ channels used all that much?

A

Can be pro-arrhythmic

198
Q

What is the exception for drugs that block K+ channels, and what is it used for?

A

Amiodarone
Has other actions in addition to blocking K+ channels
Used to treat tachycardia associated with Wolff-Parkinson-White syndrome

199
Q

Give an example of a drug which blocks Ca2+ channels

A

Verapamil

200
Q

How do drugs which blocks Ca2+ channels work?

A

Decrease slope of AP at SA node, decreases AV nodal conduction, decrease force of contraction
Also some coronary and peripheral vasodilation

201
Q

What effect do dihydropyridine Ca2+ channel blockers have on the CVS?

A

They are not effective in preventing arrhythmias, however do act on vascular smooth muscle (different types of L-type Ca2+ channels)
E.g. Amlopidine, felopidine, nicardipine

202
Q

What does Adenosine act upon?

A

Produced endogenously but can also be administered intravenously. Acts on alpha 1 receptors at AV node

203
Q

What is the effect of adenosine on the CVS?

A

Enhances K+ conductance (hyper polarises cells of conducting tissue)
Anti-arrhythmic drug, but doesn’t fit into any of the 4 basic categories

204
Q

Define heart failure

A

Chronic failure of the heart of provide sufficient output to meet the bodies requirements

205
Q

What can drugs used to treat heart failure target?

A

Positive inotropic increase cardiac output (improves symptoms, but not long term outcome)
Drugs which reduce work load of the heart

206
Q

Give two types of drug which are used in heart failure which have a positive inotropic effect so increase cardiac output

A

Cardiac glycosides

Beta-adrenergic agonists

207
Q

How do cardiac glycosides work?

A

Block Na+/K+ ATPase, resulting in a rise in intracellular Na+. Therefore less Ca2+ extrusion occurs via Na+/Ca2+ exchanger. Rise in intracellular Ca2+, so increased force of contraction.

Also cause increased vagal activity (slows AV conduction, slows heart rate).

208
Q

What drugs increase myocardial contractility, and give an example

A

Beta-adrenoreceptor agonists

E.g. Dobutamine (acts on beta 1 receptors)

209
Q

What is dobutamine used for? What does it do?

A

Cardio genie shock
Acute but reversible heart failure, e.g. Following cardiac surgery

Increases myocardial contractility by acting as an agonist to beta 1 receptors

210
Q

What do ACE inhibitors do? How?

A

Reduce the workload of the heart by inhibiting the action of angiotensin converting enzyme (thus preventing the conversion of angiotensin 1 to angiotensin 2, which increases Na+ and H2O retention by kidneys and is a vasoconstrictor)
Therefore decreases vasomotor tone, and blood volume, reducing after load and preload of heart,

211
Q

What drugs reduce the workload of the heart?

A 
ACE inhibitors
Beta adrenoreceptor antagonists (beta blockers)
Diuretics
Ca2+ channel antagonists
Organic nitrates
212
Q

What two mechanisms are used for treating angina?

A

Reduce workload of the heart

Improve the blood supply to the heart

213
Q

What type of drugs are used to improve the blood supply to the heart?

A

Organic nitrates

Ca2+ channel antagonists

214
Q

How do organic nitrates work?

A

In the body, react with thiols (-SH group) in vascular smooth muscl, causing NO2- to be released. NO2- is reduced to NO (nitric oxide, powerful vasodilator)

215
Q

How does NO (nitric oxide) cause vasodilation?

A

NO activates guanylate cyclase
Increases cGMP
Lowers intracellular Ca2+ conc.
Causes relaxation of vascular smooth muscle

216
Q

How does vasodilation relieve symptoms of angina?

A

Primary action - venodilation lowers preload, reducing work load of heart, heart fills less therefore force of contraction reduced (starlings law), lowering O2 demand
Secondary action - action on coronary arteries improves O2 delivery to ischaemic myocardium (acts on collateral arteries rather than arterioles)

217
Q

What parts of the vascular system does NO dilate?

A

Dilate collaterals

218
Q

What heart conditions are at a particular risk of thrombus formation?

A

Atrial fibrillation
Acute MI
Mechanical prosthetic heart valves

219
Q

Name some anticoagulant drugs

A

Heparin
Fractionated heparin
Warfarin

220
Q

How does heparin work?

A

Given intravenously
Inhibits thrombin
Used acutely for short term action

(Fractionated heparin given subcutaneously)

221
Q

How does warfarin work?

A

Agonises action of vitamin K, can be used long term

222
Q

Name an antiplatelet drug, and suggest when it may be used

A

Aspirin

Used following acute MI of high risk of MI

223
Q

How may blood pressure be calculated?

A

Flow X resistance

CO X TPR

224
Q

What possible targets are there for treating high blood pressure

A

Lower blood volume (decreases CO via starlings law)
Lower cardiac output directly
Lower peripheral resistance

225
Q

How long should the QRS interval be?

A

0.08 - 0.10 s

226
Q

How is the progression of heart failure classified?

A

Class 1: No symptomatic limitation of physical activity
Class 2: Slight limitation of physical activity (ordinary physical activity results in symptoms). No symptoms on rest
Class 3: Marked limitation of physical activity (less than ordinary physical activity results in symptoms). No symptoms at rest
Class 4: inability to carry out any physical activity without symptoms. Discomfort increases with any degree of physical activity. May have symptoms at rest

227
Q

What should cardiac output be?

A

~5 l/min

228
Q

What should strove volume be?

A

~75 ml

229
Q

What should left ventricle end systolic volume be?

A

~75 ml

230
Q

What should left ventricle end diasystolic volume be?

A

~150 ml

231
Q

What should the ejection fraction be?

A

50% +

Less than 40% = bad

232
Q

What structural heart changes may occur in heart failure?

A

Loss of muscle
Uncoordinated or abnormal myocardial contraction (ECG changes)
Changes to the extracellular matrix (increase in collagen 5–>25%, slippage of myocardial fibre orientation)
Change of cellular structure and function (myocyte hypertrophy, Sarcoplasmic reticulum dysfunction, changes to Ca2+ availability, myocytolysis and vacuolation of cells)

233
Q

What does elevated angiotensin 2 do?

A

Potent vasoconstrictor
Promotes LVH and myocyte dysfunction
Promotes Na+/H2O retention
Stimulates thirst by central action

234
Q

What is RAAS?

A

Renin-Angiotensin-Aldosterone System

235
Q

What are the long term effects of having the sympathetic nervous system compensate for poor CO?

A

Beta-adrenergic receptors are down-regulated/uncoupled
Noradrenaline induces cardiac hypertrophy/myocyte apoptosis via alpha receptors.
Induces up-regulation of RAAS
Reduction in heart rate variability

236
Q

What are released upon atrial stretching?

A

Natriuretic hormones

237
Q

What do Natriuretic hormones do?

A

Decrease Na+ reabsorption in the collecting duct
Inhibits secretion of renin and aldosterone
Systemic arterial and venous vasodilatation
Predominate renal action, constricts afferent and vasodilate a efferent arteries

238
Q

Why is ADH increased in heart failure?

A

Increased H2O retention, tachycardia, reduced systemic resistance, resulting in increased CO

239
Q

What secretes endothelin?

A

Vascular endothelial cells

240
Q

What does endothelin do?

A

Potent systemic and renal vasoconstrictor acting via autocrine (local) activity, thus activating RAAS. Poor prognosis sign

241
Q

What do prostaglandins E2 and I2 do?

A

Act as vasodilators on afferent renal arterioles to attenuate effects of NA/RAAS.
Stimulated by NA and RAAS

242
Q

Why is endothelial cell production of NO reduced in HF?

A

NO synthase may be blunted. Resulting loss of vasodilatation balance

243
Q

What does bradykinin do?

A

Promotes natriuresis and vasodilatation. Stimulates production of prostaglandins.
Gets broken down in the body, this is prevented by ACE inhibitors.

244
Q

What is tumour necrosis factor (alpha-TNF)?

A

Increased levels in HF. Depresses myocardial function. Stimulates NO synthase

245
Q

Describe changes that may occur to skeletal muscle as a result of HF

A

Decrease in skeletal muscle blood flow results in decreased skeletal muscle mass (cachexia), affecting all muscles including limbs and respiratory.
Abnormalities of structure and function
Contributes to fatigue and exercise intolerance

246
Q

Describe the renal effects that may occur in HF

A

Initially GFR is maintained by haemodynamic changes at the glomerulus
Increased Na+/H2O retention due to neuro-hormonal activation
In severe HF, renal blood flow falls, leading to reduced GFR and a subsequent rise in serum urea and creatinine
This can be exacerberated by treatment inhibiting the actions of angiotensin 2.

247
Q

How may chronic HF cause anaemia?

A

In unhealthy kidneys - produce less erythropoietin

248
Q

Describe the signs and symptoms of left heart failure

A
  • Fatigue, exertional dyspnoear (breathlessness)
  • Tachycardia
  • Cardiomegaly (displaced apex beat, may be sustained)
  • 3rd or 4th heart sound (‘gallop rhythm’)
  • Functional murmur of mitral regurgitation
  • Basal pulmonary crackles
  • Peripheral oedema
249
Q

What is the most common cause of right heart failure?

A

Secondary to left heart failure

250
Q

What are some possible causes of right heart failure?

A

Chronic lung disease
Pulmonary embolism/pulmonary hypertension
Pulmonary/tricuspid valvular disease
Left-right shunts (ASD/VSD)
Isolated right ventricular cardiomyopathy (disease of the heart)

251
Q

What are the signs and symptoms of right heart failure?

A
  • Relate to distension and fluid accumulation in areas drained by systemic veins
  • fatigue, dyspnoear, anorexia, nausea
  • increased jugular venous pressure
  • tender, smooth hepatic enlargement
  • dependent pitting oedema
  • ascites
  • pleural effusion
252
Q

What are the principles of managing heart failure?

A

Correct the underlying cause
Use non-pharmacological measures (reduce salt, alcohol, BP, increase aerobic exercise)
Pharmacological measures (symptomatic improvement, delay progression of HF, reduce mortality)
Treat complications/associated conditions/cardiovascular risk,me.g. Arrhythmias

253
Q

How do you calculate mean arterial blood pressure?

A

maBP = HR X SV X TPR

254
Q

50% reduction in diameter of a vessel resets in what fraction of the original flow?

A

1/16

255
Q

What % occlusion of coronary artery flow is required to result in compromised blood flow only when O2 demand increases?

A

Over 70% occlusion

256
Q

What % occlusion of coronary artery flow is required to result in ischaemia at rest?

A

90% occlusion

257
Q

When HR increases, what shortens?

A

Diastole

258
Q

What ECG change may be seen with ischaemic heart disease?

A

ST depression in effected leads of the heart

259
Q

Describe stable angina

A

Brought on by exercise, relieved by rest

260
Q

Describe unstable angina

A

Rapid onset of pain at rest
ST depression/T wave inversion
No detectable necrosis

261
Q

What is a STEMI MI?

A

Necrosis of full thickness of myocardial wall

262
Q

What ECG changes might be seen in a STEMI MI?

A

ST segment elevation, Q waves, T wave inversion

263
Q

What ECG changes might be seen in an NSTEMI MI?

A

More limited damage to myocoardium
ST depression
Inverted T waves

264
Q

What do you look for in the blood to confirm an MI?

A

Creatinine kinase

Specific isoforms of troponin (I and T)

265
Q

Define cardiac arrest

A

Unresponsiveness associated with a lack of pulse

266
Q

What is cardiac arrest due to asystole?

A

Loss of electrical and mechanical activity

267
Q

What is cardiac arrest due to (PEA)?

A

Pulseless Electrical Activity

268
Q

What is cardiac arrest due to ventricular fibrillation?

A

Uncoordinated electrical activity
Most common form of cardiac arrest, often following MI, electrical imbalance or some arrhythmias (e.g. Long QT/Torsades de pointes)

269
Q

What is the treatment for cardiac arrest?

A

Basic life support (chest compressions/external ventilation)
Advanced life support (defibrillation, depolarises cells putting the in refractory period, enabling coordinated electrical activity to restart)
Adrenaline (enhances myocardial function, increases peripheral resistance)

270
Q

What is haemodynamic shock?

A

An acute condition of inadequate bloodflow throughout the body. Catastrophic fall in arterial blood pressure leads to circulatory shock

271
Q

What things might haemodynamic shock result from?

A

Fall in CO (pump failure, mechanical - pump can’t fill, or loss of blood volume), or fall in TPR (massive vasodilation)

272
Q

What is cardiogenic shock?

A

Pump failure - ventricle cannot empty properly

273
Q

What is mechanical shock?

A

Obstructive - ventricle cannot fill properly

274
Q

What is hypovolaemic shock?

A

Reduced blood volume leads to poor venous return

275
Q

What are some potential causes of cardiogenic shock?

A

Post MI
Due to serious arrhythmias
Acute worsening of heart failure

276
Q

What are the characteristics of cardiogenic shock?

A

Dramatic drop in arterial BP
Central venous pressure may be normal or raised
Tissues poorly perfused (including coronary arteries, excuberating problem. Kidneys, resulting in oliguria)

277
Q

What is mechanical shock, cardiac tamponade?

A

Fluid build up in pericardial space, restricts filling of the heart, limits end diastolic volume. Effects both left and right heart.

278
Q

What are the characteristics of mechanical shock, cardiac tamponade?

A

High central venous pressure
Low arterial blood pressure
Continued electrical activity, heart attempts to beat

279
Q

What is mechanical shock, pulmonary embolism?

A

Embolus occludes a large pulmonary artery

280
Q

What are the characteristics of mechanical shock, pulmonary embolism?

A 
Pulmonary artery pressure is high
Right ventricle cannot empty
Central venous pressure is high
Reduced return of blood to left heart
Limits filling of left heart
Left atrial pressure is low
Arterial blood pressure is low
Results in shock (also chest pain, dyspnoea)
281
Q

What are possible causes of hypovolaemic shock?

A

Haemorrhage
Severe burns
Severe diarrhoea/vomiting
Loss of Na+

282
Q

What are the stages of hypovolaemic shock?

A

Less than 20% blood - unlikely to cause shock
20-30% - some signs of shock response
30-40% - substantial decrease in mean arterial BP and serious shock response

283
Q

What does the severity of hypovolaemic shock depend upon?

A

Volume of blood lost

Speed of blood loss

284
Q

Describe the sequence of events resulting in hypovolaemic shock?

A 
Venous pressure falls
Cardiac output falls (starlings law)
Arterial pressure falls
Detected by baroreceptors - causing sympathetic stimulation and compensatory response
Tachycardia
Increased force of contraction
Peripheral vasoconstriction 
Venoconstriction
285
Q

What is internal transfusion? (In hypovolaemic shock)

A

Increased peripheral resistance reduces the capillary hydrostatic pressure, net movement of fluid into capillaries

286
Q

What are the characteristics of hypovolaemic shock?

A

Tachycardia
Weak pulse
Pale skin
Cold, clammy extremities

287
Q

What is the decompensation response in shock?

A 
Tissue damage due to hypoxia
Release of chemical mediators (vasodilators)
TPR falls
Blood pressure falls dramatically
Vital organs can no longer be perfused
Multi organ failure
Death
288
Q

What is distributive shock?

A

Low resistance shock (normovolaemic). Profound peripheral vasodilation decreases TPR. Blood volume is constant, but volume of circulation has increased.

289
Q

Describe how toxic (septic) shock (septicaemia) occurs

A

Endotoxins released by circulating bacteria cause profound vasodilation - dramatic fall in TPR
Fall in arterial pressure
Impaired perfusion of vital organs
Also capillaries become leaky (reduction in blood volume)
Decreased arterial pressure is detected by baroreceptors, which increase sympathetic output, however vasoconstrictor effect is overridden by mediators of vasodilation (no vasoconstriction)

290
Q

Describe the characteristics of toxic (septic) shock (septicaemia)

A

Tachycardia

Warm, red extremities (although in the very later stages of toxic shock, vasoconstriction)

291
Q

What causes anaphylactic shock?

A

Severe allergic reactions

292
Q

Describe the process of anaphylactic shock

A

Release of histamine from mast calls (+ other mediators)
Powerful vasodilator effect (fall in TPR)
Dramatic drop in arterial pressure (increased sympathetic response. CO increased, but can’t overcome vasodilation)
Impaired perfusion of vital organs
Mediators also cause bronchoconstriction and laryngeal oedema (causing difficulty breathing)

293
Q

What are the characteristics of anaphylactic shock?

A

Difficulty breathing
Collapsed
Tachycardia
Red, warm extremities

294
Q

What is the treatment of anaphylactic shock?

A

Adrenaline, in high enough dose to cause vasoconstriction via alpha1-adrenoceptors

295
Q

What are the 3 places in the body which regulate BP?

A

Kidneys (regulation of blood volume, effects SV)
Heart (regulates CO via rate and force)
Vasculature (regulate TPR)

296
Q

What are the names of the major coronary veins?

A

Great, middle, small. Drain into the coronary sinus

297
Q

What is a hypoplastic left heart?

A

Congenital underdevelopment of the left heart. Ascending aorta is very small, right ventricle supports systemic circulation - obligatory right to left shunt.

298
Q

When is If activated?

A

At membrane potentials less than -50mV (the more negative, the more activated)

299
Q

What channels cause the If?

A

Hyperpolarisation-activated cyclic nucleotide-gated channels (HCN channels)

300
Q

What do gap junctions permit?

A

The movement of ions and electrically couple cells

301
Q

Parasympathetic nervous input to the heart is via which nerve?

A

The 10th cranial (vagus) nerve. Preganglionic fibres synapse with postganglionic fibres on epicardial surface/within walls of heart at the SA/AV nodes. Release ACh which acts upon M2 receptors

302
Q

How is the sympathetic effect upon the heart carried out?

A

NA is released at beta1 adrenoreceptors. Increases CO via increasing cAMP, which activates PKA. Phosphorylation of Ca2+ channels, so increased Ca2+ entry during plateau of AP. Increased Ca2+ uptake in SR, increased sensitivity to Ca2+

303
Q

What is the most important factor for ensuring adequate perfusion?

A

Local metabolites

304
Q

How do beta2 receptors exert their effect upon vasculature?

A

Cause vasodilation by increasing cAMP, which activates PKA. This causes K+ channels to open, and MLCK inhibition

305
Q

How do alpha1 receptors exert their effect upon vasculature?

A

Cause vasoconstriction. Increase IP3 production, so increases concentration of Ca2+ in cells, increasing the force of contraction

306
Q

What is the normal range for the cardiac axis?

A

-30 to +90

307
Q

What molecules can freely diffuse the blood brain barrier?

A

Lipid soluble molecules e.g. O2/CO2. Lipid insoluble molecules cannot

308
Q

What forms the blood brain barrier?

A

Cerebral capillaries

309
Q

What happens to the amount of ADH during heart failure

A

Increases (increased H2O retention, increasing CO)

310
Q

What are the long term responses to restore blood volume?

A

RAAS/ADH

20% blood loss can be restored within 3 days with adequate salts and H2O

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