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Case 13 Flashcards

1
Q

What is the BP range for hypertension and when is it considered an emergency ?

A

Hypertension >140/90

Emergency >180/110

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2
Q

What sx may be present when px moves into emergency hypertension ?

A

Painful headaches and visual disturbances

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3
Q

What is primary hypertension and what are the risk factors?

A

Idiopathic (95% of all cases). Heterogenous risk fx, strong familial link. Epigentics

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4
Q

What is secondary hypertension and how would you treat it ?

A

Secondary to an identifiable underlying cause, target the cause and BP should decrease eg. renin artery stenosis.

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5
Q

Name the 3 common non invasive measurements of hypertension ?

A

Fundoscopy
Urinanalysis
NIBP - non invasive intermittent blood pressure monitor

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6
Q

What would urinalysis show if hypertensive and why?

A

Proteinuria. pressure on kidneys decreases filtering capacity.

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7
Q

What test would you do if you suspected a px with white coat hypertension ?

A

NIBP, records BP every hour for a 24 hour period to show trajectory of BP.

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8
Q

What is vascular rarefaction ?

A

Decreased density of capillary in tissue

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9
Q

What is the function of the vascular endothelium?

A

Generates NO (potent vasodilator) that blocks Ca entry into SM. This decreases vasoconstriction.

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10
Q

How is vasomotor tone controlled in SM cells ?

A

Post ganglion sympathetic innervation. NA from synapse binds to a1 + a2 adrenoreceptors to ^ Ca in VSMC.

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11
Q

Describe how the RAAS would incur a BP ^ ?

A

BP drop detected by juxtaglomerular cells, release Renin converts AT -> AT1. AT1 goes to lungs -> AT2 via ACE. AT2 binds to receptor ^ aldosterone + vasoconstriction BP ^

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12
Q

What should be altered in a hypertensive px before drug options are considered?

A

Px modifiable fx eg. salt, sat fat, obesity, smoking, alcohol consumption all decrease. Less sedentary lifestyle.

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13
Q

What is the MOA of an ACE inhibitor (kidney, cardiac, vascular) and name one ….

A

Ramipirl - inhibits ACE so no AT2, BP down.
Kidney - indirect block Na uptake
Cardiac - limits LV remodelling
Vascular - decreases vasomotor tone (block AT2 creation)

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14
Q

What is Lasartan?

A

Angiotensin receptor blocker

Antagonistically blocks AT2 receptor so no effects BP down.

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15
Q

Name a Ca channel blocker and describe MOA (cardiac, vascular)

A

Nifedipine. Inhibits VSMC contraction.
Cardiac - -ve ino/chronotrope stops Ca into contracting/conducting cells
Vascular - prevent SM contraction through Ca down.

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16
Q

What is the general MOA of diuretics, name 3 ?

A

Prevent H2O reabsorption by blocking ion transfer from fluid to blood
Furosemide , Bendoflumethiazide, Spironolactone

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17
Q

What is the specific MOA of Sprionolactone ?

A

Prevents H2O reabsorption by trapping electrolytes in the urine so fluid loss decreases. Acts in collecting duct as a weak K sparing diuretic. Blocks aldosterone receptors prevents Na reabsorption

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18
Q

What is the effect of blocking b1 receptors in cardiac tissue ?

A

cAMP down -> Ca down -> -ve chronolo/inotropy -> Co Down -> BP down.

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19
Q

What is the effect of Atenolol on the RAAS ?

A

Inhibits renin release

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20
Q

What drug (and type) stimulates sGC that leads to relaxation through what MOA ?

A

GTN - glyceryl trinitrate

GTN -> NO -> sGC -> cGMP -> (in VSMC) K efflux -> Ca down -> MLCP up -> vasodilation.

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21
Q

What is the order of the layers of the adrenal cortex from out to in ?

A

Zona ; Glomerulus
Fascicularis
Reticularis

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22
Q

What is the function of androgens produced in the zona reticular ?

A

Taken up by the ovaries/testis to produce Oestrogen/testosterone

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23
Q

What substances regulates androgen secretion ?

A

ACTH

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24
Q

What are the qualities of funny currents (3)

A

Mixed Na/K permeability
Activation on hyperpolarisation
Very slow continual kinetics

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25
Q

Why does warfarin target clotting fx 2,7,9,10 specifically?

A

they contains glutamic acid. Warfarin inhibits VKOR which is required for these clotting fx to be activated enough to form clots.

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26
Q

What is the ERP?

A

Effective refractory period

experimental period in which another AP won’t cause depolarisation

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27
Q

How are slow and fast waves compensated ?

A

The fast wave will extinguish the slow wave so they continue to ventricles as one

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28
Q

How is tachycardia induced through slow wave conduction ?

A

Fast in ERP so can’t be stimulated. Slow reaches apex and fast no longer in ERP so it loops back around in fast -> circular movement tachycardia

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29
Q

During circular movement tachycardia, how is HR calculated ?

A

Number of times the circuit goes round the loop, each loop stimulates atria/ventricles

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30
Q

What is the accessory pathway ?

A

Muscle strand between atria and ventricles, allows conduction bypassing the AVN and causing reentry (AVRT)

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31
Q

In terms of AVN dependant tachycardia, what are 10% of the population born with ?

A

Accessory pathway so they have dual input. Leads to AVRT due to macro reentry.

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32
Q

How does the orientation of fibres affect conduction speed ?

A

Conduct rapidly in the parallel direction but slowly when perpendicular

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33
Q

What are the 3 zones related to a scar related VT ?

A

Dense scar, peri infarct zone, unaffected area

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34
Q

How is VT initiated ?

A

ectopic across peri infarct zone; some signal blocked some gets through -> partial signal return -> ready to activate. Circuit overrides sinus rhythm and drives heart.

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35
Q

What is the consequence of VT ?

A

Too fast for ventricles to fill. Pulse decreases leads to cardiac death

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36
Q

What can occur if the QT interval prolongs too much during ^ ERP?

A

afterdepolarisations -> tachycardia

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37
Q

What condition shows palpitations, syncope, transient loss of consciousness, loss postural tone, pale, motionless but then leads to a quick recovery ?

A

Torsade de pointes (TdP)

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38
Q

What are the implications for TdP?

A

Torsade de pointes
V high risk for cardiac arrest. if episode doesn’t terminate -> V fibrillation.
Admit px for constant monitoring and tx.

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39
Q

What drugs can prolong the QT interval ?

A 
Antiarryhthmic VM class 3 lengthen refractory period and can be overdone -> long QT. 
Antidepressatns/antipsychotics can prolong.
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40
Q

What electrolyte imbalance can result in a depolarisation abnormality and what is it common in ?

A

Hypokalaemia

Chronic renal failure, K losing diuretics (esp in elderly) , vomiting/diarrhoea.

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41
Q

What are the two types of tachycardia and how are they defined ?

A

Broad complex >120 ms
Narrow complex <120 ms
Based on broadest QRS on whole ECG

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42
Q

What are some common NCTs that show a distinctive pattern ?

A

Narrow complex tachycardias

AF, atrial flutter, multifocal atrial tachycardia (definite P waves but 3 different paths)

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43
Q

List some BCTs ?

A 
Broad complex tachycardias 
Ventricular tachycardia (most common) , SVT and bundle branch block, accessory pathway related tachycardias
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44
Q

What are the pros/cons of 24 hour tape monitoring using portable ECG ?

A

non invasive, useful for particular day episodes. Doc can apply so readings will be accurate.
Unlikely to pick up problems if they have weekly episodes for example.

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45
Q

How long will an injectable loop recorder last ?

A

Up to 3 years. Uses a base unit to upload information to Docs using wifi.

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46
Q

What is and how long is the PR interval ?

A

duration of atrial depolarisation and the delay during conduction through AVN. Normal is 120-200 ms

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47
Q

Where is there a difference in height in the P and R waves ?

A

Atria have thin walls so have reduced conduction compared to the thicker ventricular walls

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48
Q

When can sinus arrhythmia be considered normal ?

A

Youths

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49
Q

How can conduction velocities be varied ?

A

Drugs, para/sympa stimulation, ischemia

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50
Q

What do the P, QRS and T wave correspond to ?

A 
P = atrial depolarisation 
QRS = Ventricular depolarisation (atrial repolarisation masked)
T = Ventricular repolarisation
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51
Q

What are the possible sx of arrhythmias ?

A

nothing at all, palpitations, breathlessness (dyspnoea) , chest pain, dizziness, lightheadedness (pre-syncope) , T-LOC, syncope, sudden death

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52
Q

Palpatations; what exacerbates them?

More common in what? (3 each)

A

caffeine , stress, alcohol

Puberty, pregnancy, menapause

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53
Q

What is the cause of breathlessness ? (in tachycardia and Brady)

A

due to decreased CO
Tachy = decreased SV as insufficient time to fill and empty
Brady = decreased HR

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54
Q

What is the consequence if PQRST is disturbed during breathlessness ?

A

Loss of active atrial filling

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55
Q

Why does dizziness/lightheadness occur during chest pain ?

A

less blood to the brain, Co Down leads to BP down which leads to less cerebral diffusion -> T-LOC (in extreme)

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56
Q

What happens If PMVT is not tolerated ?

A

polymorphic ventricular tachycardia , cardiac arrest.

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57
Q

What is cardiomyopathy ?

A

Group term for conditions in which heart muscle problem is acquired or inherited

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58
Q

When are ILRs used ?

A

Injectable loop recorders , only used after T-LOC due to price

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59
Q

How would you tell the origin of an ectopic beat ?

A 
Broader = ventricles 
Atria = narrower
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60
Q

What normally follows an ectopic beat ?

A

Compensatory phase, inverted P wave not from sinus node

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61
Q

How does Starling’s law effect emptying ?

A

If heart takes longer to fill then the emptying will be more vigorous

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62
Q

What lifestyle management can be put in place to limit ectopic beats ?

A

Smoking, alcohol, caffeine, Chinese food (monosodium phosphate)

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63
Q

What is atrial fibrillation ?

A

Irregular uncoordinated rhythm arising from atria. Irregularly irregular without P waves.

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64
Q

What are the 3 classes of AF ?

A

paroxysmal, episode lasts <48 hrs
Persistent, episode >48 hrs - 1 week
Permanent

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65
Q

What is the ventricular response to AF if px is born with an accessory pathway ?

A

Conduction bypasses AVN (not slowed) so ventricular rate = atrial rate

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66
Q

What cerebral thromboembolic events may be the first presentation of AF ?

A

Stroke, TIAs

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67
Q

Why does Athletes heart syndrome ^ risk of AF?

A

Enlarged LV

Anything that enlarges the atria ^ risk of AF

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68
Q

How would you assess wether to control rate or rhythm during AF tx ? (3 tests)

A

Rhythm - AFFIRM study
Assessment of stroke - CHADS2VASC score
Anti coagulation - HASBLED score

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69
Q

How do beta blockers affect AF ?

A

target AVN to decrease conduction, still in AF but slower. Help decrease the rate

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70
Q

What is the advantage of the ‘ablate and pace’ method of tx ?

A

destroy AVN insert pacemaker. The heart beats and controlled and slower so more comfy for px.

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71
Q

What drugs can be used in rhythm control tx of AF ?

A 
VW class 1c (flecainide, propapenone) 
VW class 3 (amiodorone, dronedarone, sotalol)
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72
Q

What is the disadvantage of DC cardioversion ?

A

Shock to return to sinus rhythm. Px may slip back into AF over next few weeks

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73
Q

What is TOE and why is it used ?

A

Transosophageal echo, US

goes just behind the heart shows area of heart contractions.

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74
Q

How would you imagine orientation on an US ?

A

imagine toes coming out toward you with the px lying down.

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75
Q

What would an ECG show during accessory pathways ?

A

short PR interval plus ‘delta waves’.

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76
Q

What is the name for a slurred QRS upstroke ?

A

Delta wave.

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77
Q

What is 1st degree heart block?

A

Long PR (>200ms) no sx or tx. Often caused by AVN blocking drugs

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78
Q

Which heart block presents with; intermittent P waves, breathless, T-LOC ?

A

2nd degree

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79
Q

How can the heart still beat during 3rd degree heart block ?

A

Escape rhythms, from BoH (30-40 bpm) and ventricular myocytes (20-30)

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80
Q

How would you differentiate 2nd and 3rd degree heart block on an ECG ?

A

3rd has superimposed P waves. They can appear either side of QRS with no relation

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81
Q

Why can dementia tx lead to heart block and how would you rectify it ?

A

Uses drug Donepezil which commonly causes heart block. Better to stay on tx and put in a pacemaker rather than switch medication.

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82
Q

What are some common causes of heart block ?

A

age related degeneration , acute ischemia, drugs, hypokalaemia, hypothyroid, ^ intracranial pressure (Cushing’s reflex)

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83
Q

Where would the scar be if px has a PPM inserted ?

A

Permanent pacemaker

5cm just below clavicle, inserted under x ray

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84
Q

How often do px with PPMs need to be seen and when are they replaced ?

A

at least yearly checks.

Generator every 5 years and leads every 10

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85
Q

What would you do during ventricular tachycardia ?

A
  1. return px to safe rhythm

Then do an echocardiogram and a coronary angiogram.

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86
Q

What is the purpose of EPS ?

A

Electrophysical studies

Put px in VT, then locate pathology area. Scarring causes non conduction

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87
Q

How do you differentiate between ICDs and pacemakers ?

A

ICDs appear bright white on X-ray , if not white then its a pacemaker. The shock coils are the bit that deliver the impulse.

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88
Q

What groups of inherited heart disease can pre dispose to arrhythmias ?

A

Cardiomyopathies

Primary arrhythmias

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89
Q

How does parasympathetic stimulation affect heart rate ?

A

Increased ACh decreases HR

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90
Q

What does lusitrophy mean ?

A

^ rate of relaxation, heart recovers faster in diastole

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91
Q

What is the term used to refer to the rate of delay at the AVN ?

A

Dromotropy

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92
Q

In ionic channels, what governs the rate of flow ? (4)

A

Selectivity to the specific ion, which part of the heart (expression) , activation (of cAMP etc) and inactivation (relative period to how long active for)

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93
Q

What is significant about the IK1 channel ?

A

underlies resting potential not voltage potential. Not voltage dependant, can be phosphorylated

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94
Q

Which channels help maintain the plateau during phase 2 ?

A

balance between ICaL (long) in and K out (IKr+IKs)

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95
Q

What are ionic channels ?

A

Large complexes, contain repeats of 6 transmembrane segments each with a P loop (domain).

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96
Q

What is significant about the P loop ?

A

Forms the core of the segments for the ions to flow through

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97
Q

What domains are thought to influence Na inactivity ?

A

Na channels rapidly inactivate, thought to be linked between domains 3 and 4

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98
Q

Which Na channels can cause long QT syndrome ?

A

Type 3, activate for longer -> longer AP -> long QT

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99
Q

What is the difference between cardiac and neuronal channels in terms of sensitivity ?

A

Neuronal sensitive to TTX (tetrodotoxin) which blocks Na channels hindering conduction. Cardiac insensitive

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100
Q

What are the general properties of L type Ca channels ?

A

In the ventricles, powerhouse of inotropy.

L activate rapidly and deactivate slowly allowing more time for Ca to enter.

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101
Q

How is inotropy stimulated ?

A

Sympathetic activation -> b1 stimulation -> protein kinase C -> Ca ^ into myocytes -> ^ inotropy

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102
Q

What is verampil ?

A

Phenylalkamine drug that blocks Ca entry in cardiac cells

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103
Q

What is different about the dihydropyridine class of drugs and give an example ?

A

More selective for SM

Methanamine

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104
Q

What feature do the Ito channels contribute to in the ventricular action potential diagram ?

A

Cardiac notch in phase 1. ‘current transient outward’. Flow out of myocyte channels inactive rapidly causing transient repolarisation.

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105
Q

Which channels in cardiac ventricules are voltage dependant ?

A

Ito , Ikr, Iks

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106
Q

Which channel is associated with long QT type 2 syndrome ?

A

Ikr, this is the rapid of the slow channels. No K channel function so longer depolarisation if abnormal in long QT.

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107
Q

Which channel has a slow switch on time during plateau that can lead to long QT type 1

A

Iks, slow channel

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108
Q

How does b stimulation favour different channels ?

A

stimulates the out currents (Iks, Ik1) more than the in currents (IcaL) so that repolarisation happens earlier in AP.

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109
Q

During CICR, Ca triggers the opening of which channel in what region ?

A

Opening of the RyR channel in the dyadic cleft (proximal to the T-tubule connection to cytoplasm)
Calcium induced Calcium release

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110
Q

What two substances inhibit RyR ?

A

Calsequestrin and FKBP (calstabin)

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111
Q

When does Calsequestrin stop inhibiting RyR ?

A

In diastole Ca ^ in SR -> Ca binds to Calsequestrin (relieves inhibition) -> Ca then released into cytoplasm

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112
Q

What are the two methods of Ca movement during diastole ?

A

Taken back into SR (Ca ATPase)

Or taken across sarcolemma (Na/Ca exchange)

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113
Q

Why does Ca usage in systole have to equal Ca in diastole ?

A

If it doesn’t equal then arrhythmias arise leading to sudden cardiac death

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114
Q

What is the function of the Na/Ca exchange at rest ?

A

Maintains low Ca in sarcoplasm. 3Na in for 1Ca out so net +ve charge movement causing depolarisation of myocytes.

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115
Q

Name the two Ca ATPases and their brief function ?

A

PMCA, transports 2Ca/atp out of sarcolemma

SERCA, transports 1Ca/atp into SR

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116
Q

What regulates the ATP pump ?

A

Calmodulin, Ca dependant

117
Q

How are PMCA2 and SERCA2a regulated ?

A

PMCA, calmodulin regulation ^ Ca removal from sarcolemma

SERCA2a, phospholamban regulation inhibits Ca uptake into SR

118
Q

What is the function of TnC relative to Ca ?

A

Binds to Ca removing inhibition of tropomyosin on actin and myosin

119
Q

What happens when TnI becomes phosphorylated and when does it happen?

A

moves tropomyosin away allows actin to bind to myosin -> contraction. Occurs during b stimulation.

120
Q

What causes a decrease in TnC sensitivity for Ca?

A

Phosphorylation of TnI , Ca released faster -> contraction shorter, lucitropy ^

121
Q

Which membrane currents does b-adrenergic stimulation stimulate ?

A

IcaL , Iks, Ik1

122
Q

What effect does b-adrenergic stimulation have on TnI ?

A

Decrease sensitivity for Ca.

123
Q

How are funny currents generated ?

A

Flow through If channels, HCN (hyper polarisation activated cyclic nucleotide gated). phase 4 dominant.

124
Q

When is IcaT active ?

A

Later end of phase 4, brings in Ca for Na/Ca exchange

125
Q

What effects does the IkACh channel have ?

A

-ve inotropic effect. paired to muscarinic receptors. ACh activates it -> hyperpolarise -> -ve inotropy.

126
Q

What process is induced through ^ cAMP binding to HCN4 allowing ^ Na into pacemaker cells -> depolarisation ?

A

Tachycardia

127
Q

How is bradycardia stimulated ?

A

Decreased cAMP bind to HCN4 -> ^ IkACH -> depolarisation decreases

128
Q

What is the action of Ivabradine?

A

selectively blocks HCN channels. Pacemaker works but slower (failsafe)

129
Q

What is the function of connexins ?

A

Form connexons, facilitate current spread to adjoining myocytes.

130
Q

Which connexons are associated with the AVN ?

A

30 and 45 , have ^ R so less conductivity (delay feature)

131
Q

Where are connexons cx 40 + 43 found ?

A

In the purkinje fibres, ^ conduction force.

132
Q

What are the 3 main reasons for treating somebody with an arrhythmia ?

A

Relieve sx/improve QoL
Prevent complications (stroke, worsening heart failure)
Prevent sudden cardiac death

133
Q

What is the valsalva manoeuvre ?

A

Deep breath in hold nose and pop eardrums to ^ intrathoracic pressure. Can ^ vagal drive to transiently block AVN (terminates AVN tachys)

134
Q

What is the approach to alcohol and caffeine during arrhythmia treatment ?

A

Only limit if drinking excessive amounts. No point if normal

135
Q

What is an SVT ablation ?

A

burn myocardium to modify AVN input using radio frequency ablation. 1st line for AVNRT.

136
Q

What is PVI ?

A

Segmental pulmonary isolation, used when v. symptomatic and has failed 1+ drug tx. Ablation strategy, day procedure LA for 2-3 hrs.

137
Q

What is the ‘ablate and pace’ strategy ? Why is it limited ?

A

Destroy AVN, ventricles then paced whilst atria remains fibrillating. Still needDOACs but still need rate limiter (b blocker)

138
Q

What is the scoring system used for stroke risk ?

A 
Congestive heart failure 
Hypertension 
Age >75 (2)
Diabetes mellitus 
Stroke/TIA/TE (2) 
Vascular disease (prior MI, aortic plaque)
Age >65 
Sex (female = 1)
139
Q

What tx should be offered to a male with recurrent AF and a CHADSVAS score >1 ?

A

Lifeling anticoagulants.

140
Q

Why might someone not be put on DOACs even when their CHADSVAS score is 1 ?

A

Risk of major bleeding on DOACs is similar to risk of stroke so px may not feel it’s necessary.

141
Q

How should AV synchrony change with rhythm tx?

A

Should improve. During AF you loose atrial contribution to ventricular filling so ventricles can’t relax properly. Tx should allow more unified contraction.

142
Q

What method of tx puts the px back into sinus rhythm and then uses drugs to maintain it ?

A

DCCV (DC cardioversion). Px may relapse in which case PVI can be used.

143
Q

How does out of hospital cardiac arrest survival rates differ with time ?

A

For every 1 minute your chance of survival decreases by 10%

144
Q

What method of tx can be used for px who may suffer cardiac arrests ?

A

ICD (implantable cardiac defibrillator) delivers 700v shock within 15 seconds of arrest. Success rate 99.9%

145
Q

How does the SAN rate change during ^ sympathetic innervation ?

A

^ HR due to activation of b1-adrenergic receptors by NA/A.

146
Q

Which type of Ca channel are key for stimulus of an action potential ?

A

L type channels

T type only involved during later end of phase 4 but have lesser effect.

147
Q

Which channels react to hyper polarisation?

A

If ‘funny currents’. They cause gradual depolarisation during phase 4 as part of the ‘pacemaker potential’.

148
Q

What structures do rate and rhythm control drugs target respectively ?

A 
Rate = b-1 and phase 4. 
Rhythm = Ca channel blockers
149
Q

When is a gate said to be in refractive state and what significance does this have ?

A

When it’s inactive/v. depolarised. They can’t be stimulated at all so no contribution to impulse propagation

150
Q

What are the general causes of arrhythmias ? (5)

A

damage to cardiac tissue/nodes (eg. CAD) , automaticity/spontaneous generation , congenital abnormalities (having extra conducting pathway) , drug effects, electrolyte imbalance (hypokalaemia)

151
Q

What are the key characteristics of AF ?

A

Irregularly irregular rhythm with absent P waves.

152
Q

What are the 3 types of AF ?

A

Paroxysmal, self terminate within 24 hours
Persistent, sx >24 hours
Permanent, sx resistant to tx

153
Q

What 3 major things might predispose somebody to AF ?

A

Hypertension (fluid overload distends pulmonary veins)
CAD (leads to ischemia)
Valvular disease eg. mitral stenosis

154
Q

What Ca channel blocker can be used as a rate and rhythm control drug in tx of AF ?

A

Verapamil (IV) decreases CICR to slow nodal output. Limited ADRs

155
Q

What is the action of Flecainide in rhythm control ?

A

Type 1 blocker, decreases electrical activity to extinguish tachycardia. No effect on the nodes

156
Q

Which R+R drug has a side effect that can lead to Torsade de Pointes ?

A

Amiodarone. acts as b blocker (rate) and type 3 (rhythm) to ^ refractory period and QT interval. ^ QT interval too much -> TdP

157
Q

Warfarin; what are it’s actions , antidote, how would you monitor, how is it administered ?

A

Vit K epoxide reductase inhibitor blocks synthesis of fx 2,7,9,10.
Vit K
monitor INR for prothrombin time
Px can take orally at home, unpredictable pharmacodynamics.

158
Q

What is the dual action of heparin ?

A 
Activates prothrombin 2. 
Inhibits thrombin (generates fibrin clot) and Fx Xa.
159
Q

Px ODs on heparin, what would your tx plan be ?

A

Give them protamine sulphate. Monitor via APTT (activated partial thromboplastin time)

160
Q

What are the pros/cons of DOACs ? give two examples …

A

More predictable pharmacodynamics
Fewer antidotes so bleeding has ^ risk.
Dabigatran (thrombin) and Rivaroxaban (Fx Xa)

161
Q

What are the key features of SVT and what is is caused by ?

A

Supraventricular tachycardia
Regular rate 140-280 ppm, narrow QRS with ‘buried’ P waves.
Normal variants in fast/slow conducting fibres around AVN.

162
Q

What are the 3 main predisposing fx for SVT ?

A

Caffeine (stimulants) , psychological stress, hyperthyroidism

163
Q

How is adenosine used as a rhythm drug?

A

Binds to adenosine receptors to hyperpolarise AVN to decrease nodal excitability to decrease SVT. V short half life.

164
Q

What is the characteristic appearance of atrial flutter on ECG ?

A

Sawtooth flutter waves with atrial rate 300bpm. Narrow QRS.

165
Q

What are the 3 predisposing fx for AFl?

A

Hypertension, cardiomyopathy, valvular dysfunction/disease

166
Q

What rate control drugs can be used for treating AFl ?

A

beta blockers eg. metoprolol , decreases ventricular rate that blocks b1. decreases automaticity in nodes to slow HR

167
Q

What is the MOA of digoxin ?

A

blocks Na/K ATPase in brainstem cardiac centre to ^ vagal stimulation of AVN -> refractory + limits AVN output. Stops impulses reaching ventricles

168
Q

What are the key features of BCT on X-ray ?

A

regular monomorphic rhythm, QRS >120ms , HR >100 bpm.

169
Q

What is Alteplase ?

A

Fibrinolytic drug used during MI , analogue of tissue plasminogen activating fx.
Plasmin release -> dissolves clot that was causing infarct.

170
Q

What tx would you give for post MI anti platelet ?

A

Aspirin, blocks thromboaxane A2 mediated platelet aggregation
Clopidogrel, inhibits ADP receptor mediated platelet aggregation (clot formation).
Overall platelets can’t trigger intravascular clot

171
Q

What are the types of Na channel blocker?

A 
All class 1; 
a = moderate eg. procainamide 
b = weak eg. lidocaine
c = strong eg. flecainade
172
Q

What is voltage conduction defined as ?

A

How rapid the voltage channels cycle through their states and refractory periods

173
Q

How does conduction speed and time spent in ERP vary between fast and slow channels?

A

Slow; slow conduction speed but short ERP

Fast; fast conduction speed but long ERP

174
Q

How does giving Flecainade as tx alter reentry arrhythmias ?

A

semi selective for the fast pathway. stays bound longer than other class 1 to remove reentrant potential because fast pathway isn’t available.

175
Q

Apart from accessory pathway defects, why does is the AVN the only pathway to the ventricles ?

A

atria and ventricles divided by cartilage. Creates area of CT separates A and V.

176
Q

What other areas of the heart can control rhythm if an SAN pathology is present ?

A

AVN ‘junctional rhythm’ 50 bpm

Purkinje fibres ‘escape rhythm’ 30 bpm

177
Q

What differences would be seen on ECG for a LBBB and why ?

A

Wide QRS with normal HR. Slow depolarisation of the ventricles due to APs moving from R -L as only conduction.

178
Q

What is the ‘R on T’ phenomenon ?

A

Prolonged QT , refractory period over but cells remain hyper polarised so easily repolarised. leads to tachycardia -> VF.

179
Q

What is WPWS?

A

Wolff Parkinson White syndrome. deformity in ring of valve of AVN so alternate pathway between atria and ventricles. Wave forms return and depolarise atria too quickly.

180
Q

What condition is indicated by a sloped Q wave and a shorter PR interval ?

A

WPWS, shows premature atrial contraction. PR (0.04-0.08) starts slow because ventricles only partially depolarised.

181
Q

Where do the left and right bundle branches arise from ?

A

Originate in the bundle of his, branch off like a tuning fork

182
Q

In what tissue does phase 4 occur and through which channels ?

A

Only in nodal tissue. Uses If (funny current) pacemaker channels. Gradual depolarisation until threshold for phase 0 reached.

183
Q

How does the type of cardiac tissue affect which channels are involved in phase 0?

A

Nodal tissue = Slow Ca (CaL)
Other tissue = fast Na
The CaL produce a longer/slurred depolarisation that causes rate limitation in the AVN.

184
Q

What counteracts phase 1 in non nodal tissue ?

A

Activation of Ca channels. Repolarisation causes the plateau that extends AP.

185
Q

Why is there no phase 2 in non nodal tissue?

A

Slow Ca channels are active during phase 0 not phase 2. Ca must inactivate before repolarisation can commence.

186
Q

What is the significance of the ARP and when does it occur ?

A

Absolute refractory period, between phase 1 and end of 2.

187
Q

What is the period called when the majority of channels are inactive. Some may be activated in presence of depolarising impulse ‘afterdepolarisations’.

A

ERP , occurs during phase 1 and the start of repolarisation in phase 3.

188
Q

What is the RRP ?

A

Relative refractory period. Small no channels inactive, enough to propagate impulse. If impulse of sufficient strength then full depolarisation can occur. Between end of phase 3 and start of 4.

189
Q

What is the supernormal period ?

A

all channels available. Hyperexcitable period even small impulse can trigger new/mistimed cAP.

190
Q

What happens during an early AD in phase 2?

A

Afterdepolarisation. small bump but not enough Na to trigger new AP so QT interval ^.

191
Q

How would a full new cAP be caused during AD?

A

early phase 3 afterdepolarisation with enough Na -> QT ^.

192
Q

What are delayed ADs ?

A

^ Ca in phase 4, enough to reach Na threshold causing extrasystole. Fuels arrhythmia trains until Ca runs out.

193
Q

What effect can Digoxin and adrenaline have on ectopic activity ?

A

^ slope and decrease phase 4 time through ^ Ca causing a new mistimed AP.

194
Q

What does the valsalva manoeuvre cause ?

A

^ Vagal stimulation to the heart. HR decreases makes baroreceptors in aortic/carotid think there’s sharp ^ BP so HR and BP down. Hyperpolarisation in AVN so decrease impulse to ventricles.

195
Q

What does an upward trace show on an ECG?

A

Depolarisation toward the lead or

Repolarisation away from the lead.

196
Q

What is the antidote to the DOAC Dabigatran ?

A

Idarucizumab

197
Q

A px overdoses on an anti arrhythmic drug and are given Magnesium sulphate. Which drug was the original cause?

A

Amiodarone

198
Q

How does a lack of oxygen affect an ECG ?

A

causes ischemia, lack of ATP pump so more Na in cells and a higher +ve charge (stays depolarised).

199
Q

How is the ST segment flat on an ECG even though some ventricular cells are depolarising?

A

ECG measures overall so an equal (or similar) amount are repolarising causing flatline.

200
Q

What is the significance of the sub epicardial tissue ?

A

Last part of ventricle to depolarise so shorter AP and depolarises before the rest giving T waves +ve nature.

201
Q

What are the two types of ischemia ?

A

Transient (demand driven) eg. stable angina

Blockage (supply driven) eg. major coronary vessel blocked during an infarct.

202
Q

How would transient ischemia been shown on ECG ?

A

+ve baseline shows ST depression on exertion eg. stress test.

203
Q

Why does the ST depression occur during ischemia?

A

Ventricles repolarise faster than non ischemic tissue, ST more -ve. Sub endo stays ischemic so segment depressed compared to base.

204
Q

How does blockage ischemia respond to stress ?

A

Not triggered so no change

205
Q

The baseline on an ECG is more negative during blockage ischemia. What is this caused by?

A

Depolarisation waves are too large/too many so travel all directions including away from ECG -> more -ve.

206
Q

What is the result of ventricular repolarisation during blockage ischemia ?

A

Ischemic part still depolarised so impulses travel away from electrode. Lowered base so ST elevation compared to baseline.

207
Q

What is phase 4 and where does it occur ?

A

Gradual depolarisation (If) until threshold for phase 0 reached. ‘Pacemaker’ activity accounts for nodal automaticity + cAPs

208
Q

How does phase 0 vary between tissue types ?

A

Nodal tissue - slow Ca , longer slurred depolarisation with AVN rate limiting.
non nodal tissue - Fast Na open once threshold reached

209
Q

What is phase 2 and where does it occur ?

A

activation of Ca channels counteracting phase 1, repolarisation ‘plateau’ extends AP. Non nodal tissue (Ca are active during phase 0)

210
Q

What phase is caused by K efflux ?

A

3, depolarisation. Resets in advance of next cycle

211
Q

What happens if Na channels are stuck in refractory period ?

A

No AP will be generated so ventricles won’t be able to empty and refill effectively

212
Q

What is the supranormal period ?

A

All channels available, ‘hyper excitable’ period where even small impulse can trigger new/mistimed cAP.

213
Q

Which phases involve the RRP ?

A

Relative refractory period

End of phase 3

214
Q

What will happen if an after depolarisation is stimulated in phase 2 but with not enough force ?

A

Small bump but not enough Na to trigger new AP so QT interval ^

215
Q

What is an arrhythmia train and when does it stop ?

A

Delayed AD shows ^ Ca in phase 4 that is sufficient enough to trigger extrasystole. The train will run out when Ca runs out.

216
Q

What are 3 main causes for ectopic activity ?

A

Damage to heart
Some drugs eg. Digoxin, ^ slope and decrease phase 4 time by ^ Ca so new AP
Valsalva manœuvre

217
Q

How does damage to the heart cause ectopic activity ?

A

Causes sustained partial depolarisations which decrease the threshold for new APs (tissue like mini pacemaker)

218
Q

Which electrolyte is responsible for depolarisation of cardiac myocytes ?

A

Sodium, causes a rapid influx.

Slow influx Ca causes the plateau

219
Q

Px with SVT has a carotid sinus massage but they tachycardia persists. What is the next step?

A

IV adenosine, rapid onset and offset.

220
Q

Which part of the ECG corresponds to closure of the mitral valve ?

A

QRS = ventricular depolarisation (contraction). This means P is higher in ventricles to mitral valve is closed to prevent back flow

221
Q

What is the normal resting potential of hearts ventricular and atrial contractile fibres resting potential ?

A 
Ventricular = -90mV
Atrial = - 80mV
222
Q

Px has persistent dry cough that isn’t improving on abx. What type of antihypertensive meds are responsible and give an example ?

A

ACE inhibitors eg. Lisinopril

223
Q

Px has 30 mins of central crushing chest pain, what feature will show MI at this stage ?

A

ST elevation or non ST elevation used at this stage.

Q waves haven’t had time to develop. Troponin tests used after 12 hours to indicate myocardial damage.

224
Q

What is the sign of ischemia on an ECG ?

A

Inverted T waves and ST depression

225
Q

What are the indications of first degree heart block ?

A

PR interval >200ms. (normal range 120-200). P wave may be ‘buried’ in end of T.

226
Q

81 yo female with palpitations in AF. She’s hypertensive and hypercholesterolaemic, what is the appropriate tx to reduce cardiac risk ?

A

CHADSVAS of 5 so high risk. Needs to be on antihypertensives (B blocker +statin). High risk = warfarin unless contraindicated.

227
Q

What is the normal range of cholesterol for a healthy and at risk adult ?

A

Healthy <5 mmol/L

Target <4 mmol/L

228
Q

What are the indications of hypokalaemia and hyperkalaemia on an ECG ?

A

Hypo; U waves , ST depression, absent T waves, prolonged PR, long QT
Hyper; tall sometimes prolonged pointy P waves

229
Q

What conditions are indicated for J and delta waves ?

A

Delta - WPWS

J - hypothermia

230
Q

What is the indication on an ECG for left atrial hypertrophy?

A

P wave shows twin peaks, with the second being higher.

231
Q

What condition is indicated on ECG by a tall P wave with a singular point ?

A

P pulmonalae

232
Q

Which inhibitory protein in cardiac muscle regulates the Ca ATPase pumps of the SR ?

A

Phospholambin

233
Q

What are the positions of the 6 chest leads ?

A 
V1; R of sternum 4th intercostal 
V2; L of sternum 4th intercostal 
V3; Midway between V2/V4
V4; L midclavicular line 5th intercostal 
V5; L anterior axillary 
V6; L mid axillary
234
Q

What territories do the 6 chest leads cover ?

A 
V1+2 = septal 
V3+4 = anterior 
V5+6 = lateral
235
Q

What territories do leads 1,2 and 3 cover and where are they positioned on the body?

A

1; L hand to R hand gives lateral view
2; L leg to R hand gives inf view.
3; L leg to L arm gives inf view.

236
Q

Which lead is used as the rhythm strip and why ?

A

Lead 2; P waves most visible

237
Q

How are the augmented leads calculated and what view do they give ?

A

aVL; LA-(LL+RA) shows L shoulder to R hip giving Lat view
avR; RA-(LL+LA) shows R shoulder to left hip gives Lat view
aVF; LL-(LA+RA) shows umbilicus to neck gives inf view.

238
Q

On an ECG, which leads give the views; septal, ant, lateral, inferior ?

A

Septal; V1, V2
Anterior; V3, V4
Iateral; V5, V6, aVL, aVR, 1
Inferior; aVF, 2, 3

239
Q

What are the orientation steps during an ECG for exam purposes ?

A 
Name+DOB of px 
Time and reason for ECG taken 
Checks stats top right, often give info/calculations 
Identify rhythm strip at the bottom 
Look at paper speed at bottom
240
Q

What should the paper speed by on a normal ECG ?

A

25m/s and mV =10

241
Q

How would you calculate HR for an irregular rhythm ?

A

Count no of QRS across 30 squares then x10

242
Q

What is the normal duration of the QRS complex ?

A

<120ms (3 small squares)

243
Q

What are the pathologies associated with abnormal QRS complexes ?

A 
Broad QRS (>120ms) , seen in BBB forcing longer, slower conduction route. Ventricular origin common 
Narrow QRS (much smaller than <120ms) , extra impulse in atria. Atrial or supraventricular tachycardia.
244
Q

What are the two possible causes of ST elevation ?

A

Infarct; 2+ chest leads shows acute MI (specific leads indicate location)
Inflammation e.g. pericarditis

245
Q

Which leads show T wave inversion? What is the indication if T waves are tall ?

A

aVR and V1

Tall T waves = hyperkalaemia

246
Q

What is the normal range for QT interval?

A

360-440 ms (9-11 small squares)

247
Q

What are the indications on an ECG and the px sx for AF ?

A

Atrial fibrillation. ECG; irregularly irregular rhythm with absent P waves.
Sx; irregular pulse (BP around 180/100), breathless, paroxysmal palpitations

248
Q

What course of tx would you advise for px in AF ?

A

Drugs; anticaogulants (warfarin in emergency) R+R (verapamil, amiodarone)
Procedures; DCCV, catheter ablation

249
Q

What condition shows regularly irregular rhythm with abscent/hidden P waves?

A

Supraventricular tachycardia

HR v ^ (140-280bpm) narrow QRS

250
Q

What are the causes of SVT, what px sx will be experienced ?

A

Causes; caffeine/stimulants , hyperthyroidism, stress

Px sx; sudden onset ‘racing heart’ , syncope, chest pain (if assoc CAD), light headed

251
Q

What tx can be used for SVT ?

A

acute use of adenosine , Ca blocker, vagal manoeuvres (first) eg. valsalva

252
Q

What are the features of WPWS on an ECG?

A

Long QRS, long QT, short PR, Slurred Q (delta waves).

253
Q

Why is AF in WPWS dangerous ?

A

WPWS is congenital and often asymptomatic. AF can be life threatening as impulse propagates to ventricles directly through accessory pathway causing ventricular fibrillation.

254
Q

How would a STEMI show on an ECG ?

A

ST elevation in 3 adjacent leads . Irregularly irregular R+R. May show reciprocal depression in leads 3+aVF.

255
Q

What course of tx would you advise for a px with a STEMI?

A

PCI is gold standard. Maybe thrombosis if required. Can give pain relief eg. morphine

256
Q

If a px’s ECG shows; notched R waves, long QRS and large Q downstroke, what condition are they likely to have ?

A

Left bundle branch block.

V1 shows W and V6 shows M pattern

257
Q

What investigations would you do for a LBBB?

A

Cardiography and coronary angiography (catheter insertion)

258
Q

What is the normal PR interval ? What condition makes it longer ?

A

120-200ms
1st degree heart block is >200ms.
P wave may be ‘buried’ in T wave.

259
Q

What are the causes of 1st degree heart block?

A

AVN blocking drugs, hyperkalaemia, may be normal in athletes

260
Q

What are the px sx associated with 1st degree heart block and what tx plan would you advise for them ?

A

sx; may be asymptomatic, dyspnoea/fatigue on exertion

Tx; none if asymptomatic, if serious issue a dual pacemaker.

261
Q

What is LAD syndrome and what can it cause ?

A

Left anterior descending syndrome from severe stenosis/occlusion of LAD.
Can cause NSTEMIs

262
Q

What are px sx with NSTEMIs and what tx plan would you advise ?

A

Sx; Chest pain (at rest) breathless, sweating, syncope
Tx; Antiplatelets (aspirin+clopidogrel) , B blockers , pain (morphine) , check troponin for myocardial damage, coronary angiogram for PCI if needed.

263
Q

What condition shows a fixed PR interval with an intermittent QRS on an ECG ? What are the causes ?

A

2nd degree heart block (type 2).

Causes; age related conduction degeneration, MI, electrolyte imbalance

264
Q

What are the px sx for 2nd degree heart block and how would you advise tx?

A

Sx; bradycardia, syncope, haemodynamic instability

Tx; correct underlying cause, cardiac monitoring, permanent pacemaker insertion

265
Q

How would a 3rd degree heart block be displayed on ECG ?

A

Ventricular rate <40bpm , atrial rate uncoupled from ventricular. Looks like random squiggles.

266
Q

What are the cause of 3rd degree heart block?

A

Degeneration of AVN, inf MI, AVN blocking drugs, hyperkalaemia

267
Q

What are the key features of BCT?

A

broad complex tachycardia

assume VT until proven otherwise. Regular monomorphic rhythm. QRS >120ms , HR>100.

268
Q

What are the px sx of BCT?

A

Hypotension, pulmonary oedema, palpitations, syncope, chest pain, cardiac arrest

269
Q

What investigations would you do for BCT?

A

DCCV if unstable, anti arrhythmic drugs, echocardiography/angiography to determine cause.

270
Q

How is pulse pressure defined ? (2)

A

Systolic bp - diastolic bp

Delta V / Compliance

271
Q

What are the systolic and diastolic pressures ?

A

Systolic, max pressure in aorta when heart contracts and ejects blood into aorta from LV
Diastolic, min pressure in aorta when heart relaxes before ejecting blood into LV

272
Q

How does compliance vary through the human arterial system ?

A

Aorta is most compliant (so Pp is low) , compliance gradually down until min in saphenous and femoral arteries

273
Q

What are the parameters for narrow and wide Pp ?

A 
Narrow = <25% of systolic 
Wide = Pp of >100
274
Q

What are the 3 layers to a typical artery ?

A

Tunia intima, tunic media, tunica adventitia (externa)

275
Q

What are the components of the tunica intima ?

A

endothelial layer, subendo layer, internal elastic lamina

276
Q

Which layer of an artery has longitudinally orientated type 1 collagen ?

A

Tunica adventitia

277
Q

What is the tunic media made up of ?

A

concentric layers of helical SM cells, elastic and reticular fibres, proteoglycans.

278
Q

What type of artery regulates blood flow and how is it adapted?

A

Muscular artery, thin intimal layer with well developed internal elastic lamina. Regulates blood flow through adjustment of caliber.

279
Q

Apart from muscular, name another type of artery and state how it’s adapted for its function?

A

Elastic artery. Tunica media shows elastic fibres between SM cells. They store kinetic energy to smooth out surge in BP during systole

280
Q

What are 3 main ways in which pulse pressure can be ^ ?

A 
Endurance athletes (total peripheral resistance down, SV/CO ^) 
^ Age (compliance low, less elastin, ^ type 1 collagen , ^ calcification (stiff wall)) 
Valvular disease (aortic; stenosis, regurgitation)
281
Q

What is the action of class 1 drugs ?

A

Inhibit fast Na channels during depolarisation (phase 0) decreases conduction velocity and depolarisation.

282
Q

What is the difference between 1A, B and C drugs ?

A

a, prolonged AP duration
b, decrease AP duration
c, no effect on AP

283
Q

Give examples of 1 a, b and c drugs ?

A

A; Quinidine, Procainamide
B; Lignocaine, pheytoin
C; Flecainide, Encainide

284
Q

What is propranolol and what effect does it have ?

A

Class 2 b-adrenoreceptor antagonist. ^AVN ERP (phase 4) to decrease HR and O2 consumption.

285
Q

Which class of VW drug effect phase 3 of AP ?

A

Class 3 (inhibit K channels) to prolong cardiac depolarisation, AP duration and ERP.

286
Q

Give two examples of Class 3 drugs …

A

Amiodarone, Bretylium

287
Q

What is Diltiazem, give two more examples of its class ?

A

Class 4 VW drug

Verapamil, Nifedipine

288
Q

What are class 4 drugs ?

A

Inhibit inward slow Ca (L type) current that would contribute to VT. Impairs pacemaker activity (phase 0/4 in pacemaker). Phase 2 in cardiac AP.

test (14 decks)

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