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Health.2 > ZJ: cardiac clinical 🫀 > Flashcards

ZJ: cardiac clinical 🫀 Flashcards

1
Q

L: Arrhythmia and Anticoagulation

Whats an arrythmia? and 2 possible reasons for it

A

change in normal rate/rhythm of heart.

  • altered impulse gen e.g. changes in automaticity of pacemaker cells in SAN/ APs from elsewhehre
  • altered impulse conduction e.g. complete/ partial block of conduction pathways in myocardium
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2
Q

3 types of arrhythmias?

A
  • bradycardia: HR < 60bpm
  • tachycardia: HR > 100bpm
  • AF
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3
Q

whats sinus bradycardia?

and what might bradyc. also be caused by?

A

slowed HR but rhythm unchanged.

heart block

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4
Q

whats the differenc ebetween supra-ventricular tachycardia and ventricular tachycardia?

A

SVT: arise above level of ventricles wither within atria
VT: arise within ventricles themselves

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5
Q

how may sinus tachycardia occur?

A

HR increased but rhythm unchanged

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6
Q

affect of rapid atrial rate and disturbance of conduction pathways in atrial flutter?

A

increased risk of localised thrombus formation and secondary embolic events (i.e. thrombotic stroke)

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7
Q

most common type of arrythmias and who is it more prevalent in/risk factors?

A

atrial FIBRILLATION

  • older people
  • hypertensive
  • HF
  • coronary artery disease
  • valvular artery disease
  • obesity
  • DM
  • CKD
  • caffeine
  • alcohol
  • cardiac surgery
  • stress
  • pulmonary embolism
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8
Q

complications of AF?

A

stroke

congestive HF

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9
Q

AF symptoms

A
  • breathless
  • light headed
  • fatigue
  • palpitations- racing, pounding, thumping in chest
  • chest pain
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10
Q

how is AF diagnosed in prim care?

A

WatchBP: oscillometric BP monitor (microlife).

records BP and detects pulse irregularity that may be caused by symptomatic/asymptomatic AF.

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11
Q

whats AF often associated with?

A

other arrhythmias: atrial flutter/ supraventricular tachycardia

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12
Q

what may occur during treatment of AF with anti-arrhythmic drugs?

A

atrial flutter

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13
Q

6 classes of antiarrhythmic meds:

A

Na+ channel blockers (and affect phase 0)

  • IA
  • IB
  • IC

beta blocker
- II

K+ channel blocker
-III

Ca+ channel blcoker
- IV

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14
Q

why monitor for bradycardia when using II anti-arrhythmic drugs.

A

have beta blocker mechanism of action.

block symp activity; reduce rate! and conduction

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15
Q

AF diagnosis?

A
  • ECG
  • ECHO
  • TFTs
  • CXR.

also maybe thyoid function

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16
Q

3 types of AF?

A

paroxysmal: spontaneous within 7 days
persistent: > 7 days
permanent: over a year. needs management

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17
Q

how is AF managed?

A

arrhythmia control (by rhythm/rate control)

thromboprohylaxis: to prevent strokes
treat underlying caus

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18
Q

NICE: rate control is offered as first line strategy in AF patients EXCEPT?

A
  • if their AF has reversible cause
  • have HF primarily caused by AF
  • new onset AF
  • rhythm control strategy more suited (clinical judgement)
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19
Q

rate control guidelines: what is offered (2) as part of strategy? NICE

A

standard beta blcoker or
rate limiting calcium channel blocker as initial monotherapy

consider digoxin monotherapy for those with non-paroxysmal AF only if theyre sedentary.

if doesnt work, consider combination therapy with:

  • beta blcoker
  • diltiazem
  • digoxin
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20
Q

rate control guidelines: what must not be offered for long term rate control?

A

amiodarone

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21
Q

what must be considered (2) for patients with AF?

A

pharmacological and/or electrical rhythm control

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22
Q

what is offered as therapy for patients having cardioversion for AF, thats persisted longer than 48h?

A
  • offer electrical (instead of pharmacological) cardioversion.
  • consider: amiodarone starting 4wks before and contrinuing up to 12 months after: electrical cardioversion. maintaining sinus rhyhtm.
  • discuss benefits/risks of amiodarone.
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23
Q

long term treatment options for rhythm control

A
  • standard beta blocker first line unless contraindicated: then assess comorbidities:
  • dronedarone for maintenance of sinus rhythm after successful cardioversion in those with paroxysmal/persistent AF/
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24
Q

what drugs to avoid in tretment of rhythm control in patients with known ischaemic/structural heart disease?

A

class 1c antiarrhythmic drugs e.g. flecainide/propafenone

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25
Q

what strategies should be considered in people with infrequent paroxysms and few symptoms/ where symptoms induced by known factors (alcohol/caffeine)?

A

‘no drug treatment’/’pill in the pocket’

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26
Q

what is amiodarone and what type of effects does it have?

whats its dominant effect?

A
  • iodine containing. struc similar to thyroxine.
  • complex effects.
  • Clas I, II, III, IV actions.
  • dominant effect = prolongation of AP and refractory period.
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27
Q

amiodarone pahrmacokinetics

A
  • incompletely absorbed after oral admin
  • unusual: prolonged half life of several wks and extensively distributed in adipose tissue
  • full clinical effects after months of treatment start
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28
Q

common side effects of amiodarone

A
  • interstitial pulmonary fibrosis
  • hyper/hypothyroidism
  • liver tox
  • photosensitivity: affect skin. wear big hats, sunscreen
  • blue skin discolour- iodine accumulation in skin
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29
Q

amiodarone counselling points

A
  • possible phototox: shield skin from light during treatment and months after.
  • use wide spectrum sunscreen
  • blurred vision- counsel on driving and skilled tasks
  • symptoms of bradycardia and heart block if taken with sofosbuvir- containing regiments.
  • compliance
  • dont drink grapefruit juice: higher chance of SE
  • Do not take if allergic to iodine.
  • Discuss with your pharmacist or doctor if you are intolerant to lactose
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30
Q

non drug treatment options (5)

A
  • ablation (pulmonary vein)
  • ablate and pace (AV node ablation)
  • atrial defibrillators
  • maze procedure
  • removal of left atrial appendage
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31
Q

antithrombotic therapy:

  • risk and benefits of anticoags
  • place of NOACs in AF management

due to rhythm abnormalities with AF, what is there a risk of to patient? how is this risk assessed?

A

risk of blood clotting.

using CHA2DS2-VASc scale

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32
Q

with CHA2DS2-VASc scale, which patients dont require antithrombotic therapy?

A

patients with AF who are clearly low risk. (age<65 and lone AF).
= males with score 0
= females with score 1 (point for F sex)

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33
Q

CHA2DS2-VASc scale: score 0-9 with 9 as highest annual stroke rate.
what are each points assigned for?

A

The acronym CHA2DS2-VASc stands for

Congestive heart failure, 
Hypertension, 
Age ≥75 (doubled), 
Diabetes, 
Stroke (doubled), 
Vascular disease, 
Age 65 to 74 and 
Sex category (female)
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34
Q

what scale/score is used to assess bleeding risk in patients started on anticoagulation

A

HAS-BLED:

Hypertension: Uncontrolled, >160 mmHg systolic
Absorbance renal/ liver function: 1/2
Stroke history
Bleeding 
Labile INR
Elderly >65
Drugs/alcohol use: 1/2

score= 3: increased 1 year bleed risk

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35
Q

whats the other clinical prediction calcluator for decisions on non-VKA oral anticoag (NOAC) and a vitK antagonist (VKA)?

A

the SAMe-TT2R2 score

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36
Q

role of anticoagulant?

A

preventing stroke and arrhythmias consequences

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37
Q

5 examples of anticoag?

A 
apixaban
dabigatran etexilate
rivaroxiban
edoxaban
vit K antag e.g. warfarin
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38
Q

warfarin is a well established VKA that requires…

A

regular blood tests and counselling as many interactions

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39
Q

what is warfarin indicated for and what 2 things done prior to starting therapy?

A

PE, DVT, AF, mechanical heart valves etc…

  • rule out contrainds e.g. active bleeding (main SE)
  • baseline international normalised ratio (INR) taken
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40
Q

effect of anticoagulant therapy e.g. warfarin on INR

A

normal INR = 1.
warfarin adjusts this to 2-4.
i.e. anti-coagulated blood taken 4x as long to clot

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41
Q

target INR for:

a) AF, DVT, PE
b) mechanic heart valve?

A

a) 2-3

b) 2.3-3.5

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42
Q

how to initiate warfarin therapy for: patients requiring rapid anticoag?

A
  • 5-10mg on 1st day (lower induction dose for elderly)- given with a heparin usually LMWH.
  • continue for min. 5 days and until INR=2 for 2 consec days.
  • subsequent doses depend on prothrombin time, reported as INR.
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43
Q

how to initiate warfarin therapy for: patients NOT requiring rapid anticoag?

A

-lower LD over 3-4wks

daily maintence: 3-9mg. taken at same time each day. (-6pm)

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44
Q

in which situations is INR regularly/not reg monitored?

A

if patients on oral anticoags- monitor INR

NOACS/DOACS- dont need to monitor INR

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45
Q

how do the following NOACS/DOACS work?

a) dabigatran etexilate
b) rivaroxiban and apixaban
c) edoxaban

A

a) direct thrombin inhibitor
b) inhibit activated factor Xa
c) reversive and direct inhib of activated factor X (factor Xa)

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46
Q

whats recommended as an alternative to warfarin and what used for?

A

NOACS= alternative.

prevention of stroke, systemic embolism in patients with AF.

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47
Q

how do NOACS compare with warfarin in reduction of relative risk of stroke and systemic embolism in AF patients?

A

NOACS are as effective as warfarin :)

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48
Q

what patients is anticoagulation offered to?

A

people with CHA2DS2-VASc score of 2 or more.

taking bleeding risk into account

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49
Q

do not offer aspirin therapy solely for….

A

stroke prevention to people with AF

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50
Q

() when may idarucizumab (PRAXBIND) be used?

A

when rapid reversal of anticoag effects of DABIGATRAN is needed for emergency surgery/urgent procedures / in life threatening/uncontrolled bleeding

but studies of efficacy and safety are ongoing.

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51
Q

noacs side effects

A

bleeding,
minor (e.g., slight bruising/ occasional bleeding from the gums when bruising teeth) –> serious (e.g., vomiting blood, blood in stools/urine/ bleeding inside head).

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52
Q

2 types of heparin and the differences?

A

UFH- unfractioned: conventional heparin

  • large mucopolysacc mols
  • immediate anticoag properties

LMWH- low MW hep

  • smaller polysacc chains
  • longer and more predicatble half life than UFH
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53
Q

what does UFH do and how does it compare with LMWH?

A

UFH
prevents production of fibrin from fibrinogen
also has effects on inhibition of production of activated clotting factors.

LMWH
anticoag effect by inactivating factor Xa

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54
Q

which heparin more suitable for renal impairment?

A

UFH as short half life than LMWH- which also exreted renally.

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55
Q

how is UFH administered?

A

IV/ SC

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56
Q

adverse effects of the heparins?

A

UFH: major= haemorrhage
LMWH: potential= heparin induced thrombocytopenia. smaller risk

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57
Q

when is APTT coag monitoring required and when is it not?

A

req for high dose heparin

no need for LMWH

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58
Q

whats Fondaparinux and when used?

A

synthetic pentasacc - inhibits activated factor X.
use: prophylaxis of VTE and treatment of DVT, PE.
used in acute management of MI.

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59
Q

what has a greater risk of intracranial haemorrhage: warfarin/DOACS?

A

warfarin

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60
Q

time to get to peak effect (Tmax) for DOACS?

A

immediate anticoag effect: 1-4hrs

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61
Q

is effect of missed doses greater for warfarin or DOACs and why?

A

greater loss of anticoag from missed doses for DOACS and they have a shorter half life

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62
Q

3 points to do before prescribing doacs/ warfarin?

A
  • view patient holistically- comorbidities, indications for use of DOACS for appr treatment
  • review compliancee
  • review all meds, check inetractions.
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63
Q

clincially: whats checked before prescribing warfarin/doacs?

A
  • renal function and consider cautions and dose adjustments
    e. g. apixaban risk of bleeding if eGFR <15ml/min/1.73m2…
  • monitor renal func annually esp in elderly w age relaed decline in kidney func
  • review hepatic impairment, avoid in severe impairment
  • account for patient weight if needed.
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64
Q

L: cardiac clinical pharmacy

how can drugs affect heart function? 2

A

direct: force of contraction or rate/rhythm
indirect: vasculature or BV/composition- diuretics

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65
Q

whats CO? and eqn?

A

CO= HR x SV

vol of blood ejected for each vent contraction

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66
Q

2 things SV is determined by?

A

preload/ LV EDP

afterload: pressure in wall of LV during ejection
inotropy: contractility

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67
Q

What determines contractility?

A

the myocardial striated muscle, involving Ca2+

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68
Q

What do inotropic drugs affect?

A

the force of the heart contractions

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69
Q

What do positive inotropic drugs do and how?

A

Increase force of heart’s contraction by increasing calcium, therefore increase heart rate

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70
Q

What do negative inotropic drugs do? give example drug

A

decrease the force of the heart’s contraction and therefore decrease heart rate
Verapamil

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71
Q

What are 3 inotropic drug classes?

A
  • Cardiac glycosides
  • Sympathomimetics
  • Phosphodiesterase inhibitors
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72
Q

How does digoxin work?

image p46 s1 w9

A
  • inhibits cell memb Na+/K+ATPase -> reversal of usual Na/Ca exchange
  • normally, ⬆ intracellular Ca -> enhanced strength of contraction (+ inotropism)
  • also affects elec physiology of heart, blocking (AV) conduction and ⬇ HR by enhancing vagal nerve activity

⬆Ca, contraction, HR

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73
Q

What is the principal indication of digoxin?

A

permanent/persistent Atrial Fibrillation (AF) with a fast ventricular rate - but not preferred first-line

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74
Q

What does NICE guidance suggest digoxin should be used as first-line in?

A

patients with AF who also have co-existing HF

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75
Q

Digoxin is reserved for patients where the heart failure is due to… and has worsened despite the use of…

A
  • due to left ventricular dysfunction
  • despite the use of angiotensin-converting enzyme (ACE) inhibitors, beta-blockers and diuretic therapy (No impact on mortality).
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76
Q

Is the therapeutic index of digoxin low or high? What action should be taken?

A

low, so patients should be reviewed for clinical signs

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77
Q

What are the signs and symptoms of digoxin toxicity?

A
  • Bradycardia
  • Arrhythmia
  • Nausea, vomiting
  • Confusion
  • Visual disturbances, blurred or yellow vision
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78
Q

Digoxin toxicity is more pronounced with what types of disturbances? What action should be taken consequently?

A

with metabolic or electrolyte disturbance (potassium levels?) - electrolyte monitoring is important

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79
Q

What might be required when treating digoxin-toxicity in an emergency?

A

Digoxin-specific antibody fragments

80
Q

What is the inital dosing of digoxin for patients with AF and atrial flutter?

A

high dose as initial LD (rapid digitalisation)
15mcg/kg lean body weight

LBW= total body mass-fat mass

81
Q

The maintainance dose of digoxin is calculated as a fraction of the XX and is adjusted for renal function based on XX

A

fraction of the effective loading dose..

..based on creatinine clearance (mL/min)

82
Q

Monitoring for digoxin is important to prevent factors that can provoke toxicity. Name two of these factors?

A

renal dysfunction and hypokalaemia

83
Q

How often should urea and electrolytes be measured in patients taking digoxin?

A

anually but more regularly if change in dose or clinical status

84
Q

inotropic drug receptors position and action.

Where are alpha receptors expressed?

A

vasculature

85
Q

Do alpha receptor agonists cause vasoconstriction or vasodilation?

A

vasoconstriction

86
Q

Where are beta 1 receptors expressed?

A

in the heart

87
Q

Are beta 1 agonists positively or negatively chronotropic?

A

positively

88
Q

Where are beta 2 receptors predominantly expressed?

A

vasculature

89
Q

Do beta 2 receptor agonists cause vasodilation or vasoconstriction?

A

vasodilation

90
Q

Sympathomimetics are mostly limited to hospital use. What is the route of admin of them?

A

IV

91
Q

medium dose of dopamine is associated with what?

A

b1 tachycardia and increased force of contraction

92
Q

whats large dose dopamine predominanty assoc with?

A

alpha effects causing peripheral vasoconstriction

93
Q

Which receptors does dobutamine act on?

A

predominatly b1 and some b2

94
Q

Does dobutamine cause more or less tachycardia than dopamine?

A

less

95
Q

Why is dobutamine used in cardiogenic shock?

A

b2 action offloads heart and b1 action increases force of contraction

96
Q

which receptors does adrenaline act on?

A

b1 and b2

97
Q

What is the rationale behind using adrenaline for cardiac arrest?

A

attempts to save brain and myocardium from ischaemia by causing mass peripheral vasoconstriction (alpha effects) and strong positive chronotropia (B1 effects)

98
Q

Noradrenaline is an alpha adrenoceptor.

Does it cause vasoconstrictor or vasodilator action?

A

vasoconstrictor

99
Q

Why are phosphodiesterase inhibitors rarely used now and only in severe heart failure as adjunctive therapy?

A

risk of mortality

100
Q

Give two adverse effects of phosphodiesterase inhibitors associated with chronic use?

A

arrhythmias and increased mortality

101
Q

give two examples of phospdiesterase inhibitors?

A

enoximone and milrinone

102
Q

affect of phosphodiesterase inhibs?

A

⬆ contractility + ⬆ HR

103
Q

What is the mechanism of action of phosphodiesterase inhibitors?

A
  • ⬆ CAMP via coupling with other intracellular messengers
  • ⬆ inotropy and chronotropy
    (contractility and HR)
  • cyclic AMP broken down by cAMP dependant PDE enz
  • so inhibitors inhibit degradation of intracellular conc of cAMP
104
Q

What is the difference between inotropy and chronotropy?

A

inotropy is contractility and chronotropy is heart rate

105
Q

What are the 3 different types of HF?

A

LVSD
HFPEF
HF caused by diseased/damaged heart valves

106
Q

Which type of heart failure is due to the left ventricle which pumps blood around the body becoming weak?

A

LVSD

107
Q

which type of HF is due to the left ventricle becoming stiff and therefore it becomes difficult for the heart chamber to fill with blood?

A

HFPEF

108
Q

Give 6 signs of heart failure?

A

rapid weight gain, shortness of breath, increased swelling in lower body, trouble sleeping, frequent dry hackign cough and loss of appetite

109
Q

What thought should be given to medicines adherence in the general principles of management of HF?

A

keep dosing regimens as simple as possible and fully inform patients and carers

110
Q

What are the 3 components of the general principles for the treatment of HF?

A

medicines adhrenece, multidisciplinary approach to care and comorbidities

111
Q

first thing given to HF patients diagnosed (before checked for hefref/ hefpef)?

A

offer diuetics- relief of congestive symptoms + fluid retention

112
Q

What is the first line treatment offered to patients with HF with reduced ejection fraction?
HFrEF

A

ACEi and BB

MRA if symptoms continue

113
Q

How should acei be introduced in the first line treatment of HF?

A

start at low dose and titrate upwards at short intervals until target or max tolerated dose is achieved

114
Q

Give two counselling points that it would be important to tell patients who are about to start ACEi therapy?

A

take first dose at night to avoid dizziness caused by low blood pressure
report a persistent/ troublesome dry cough

115
Q

what to monitor- first line ACEi for HF?

A

serum Na, K and renal function before and 1/2 wks after starting
and after each dose increment

116
Q 
What is the first line drug class that should be offered to all HF patients due to left ventricular systolic dysfunction?
LVSD
A

beta blockers

117
Q

How should beta blockers be introduced in the first line treatment of LVSD?

A

start low go slow

118
Q

What should be assessed after each titration of beta blockers in the treatment of LVSD?

A

HR, BP and clinical status

119
Q

What counselling would you give to someone who has just started beta blockers for LVSD? 3

A

do not stop taking unless doctor advises
may experience SE: fatigue, cold hands and feet and dizziness.
Doctor will gradually increase dose so regular check ups required

120
Q

What is the first line drug class that should be considered in HF patients due to LVSD who have intolerable effects such as a dry cough?

A

ARB

121
Q

If a patient is intolerant to both an ACEi and an ARB, would would be the next step in the treatment plan?

A

seek specialist advice and consider hydralazine with a nitrate

122
Q

What two drugs classes are usually the first line used together for HF patients?

A

acei and bb

123
Q

What should be offered to patients who have heart failure with reduced ejection fraction who continue to have symptoms after using ACE/ARB and BB?

A

MRA:

mineralocoricoid recp antagonist

124
Q

What should be measured and when in relation to MRAs?

A

serum K and Na and renal function before and after starting MRA and after each dose increment

125
Q

which ethnic group of patients may benefit from hydralazine in combination with a nirate for second line treatment of uncontrolled HF with moderate to severe HF?

A

afro caribbean

126
Q

specialist treatment of HF:

Sacubitril valsartan is used for treating symptomatic chronic HF with REF only in which groups of patients?

A

NYHA 2 to 4 symptoms, and w
LV ejection fraction 35% or below and
taking a stable dose of ACEi/ARB

should be started by HF specialist w access to multidisciplianry HF team

127
Q

Where digoxin tox/ non adherence is suspected, serum levels should not be monitored routinely. How should they be monitored?

A

within 8-12 hrs of last dose

128
Q

whens digoxin recommended for use in HF?

A

worsening/ severe HF due to :VSD despite first and second line treatment for HF/

129
Q

whats a big problem w digoxin and what does this mean for monitoring?

A

toxicity can occur in therapeutic range, so interpret in cinical context and monitor

130
Q

Name a drug that inhibits the If channel in the sinus node?

A

ivabradine

131
Q

What is the only known pharmacological effect of ivabradine?

A

slow heart rate in patients sinus rhythm

132
Q

Who should initiate ivabradine?

A

HF specialist

133
Q

What are some of the benfits of Ivabradine?

A

shown to reduce CV death or hospitalisation for HF. Improved left ventricular function and quality of life

134
Q

What food product should be avoided by patients that are taking ivabradine?

A

grapefruit juice

135
Q

Why should people taking ivabradine be careful driving or using machines at times where there could be a sudden change in light intensity especially driving at night?

A

may cause temporary luminous visual phenomena

temp brightness in field of vision

136
Q

Give 3 side effects that patients taking Ivabradine may experience?

A

breathlessness, fatigue and irregular heartbeat

137
Q

Why are loop diuretics such as furosemide commonyl used in HF patients?

A

treat fluid that accumulates in the body due to heart not pumping blood around the body as well as it should

138
Q

Apart from furosemide name two other loop diuretics?

A

bumetanide and torasemide

139
Q

who to avoid CCBs in and why?

verapamil, diltiazem, short acting digydropyridine agents

A

ppl w HF and reduced ejection fraction as they reduce cardiac contractility

140
Q

L: Acute Coronary Syndromes and Stable Angina

Define Acute Coronary Syndrome

A

any group of syndromes attributed to obstruction of coronary arteries

inc:
NSTEMI
STEMI
unstable angina

141
Q

common cause of MI (heart attack)?

A

blood clot- stops blood flowing to part of heart muscle
, commonly clot formed inside coronary artery/ branch

may form if theres atheroma (plaques) that develop inside lining of arteries

142
Q

in MI, a rise in what can be seen? and whne do levels become detectable?

A

cardiac enzyme troponin
- inc when cells are damaged

Toponin I and T: detectable in serum 3-6hrs after infarction.
peak: 12-24hrs
remain raised for up to 14 days

143
Q

with MI, when are troponins (enz) testsed?

A

5-12 hrs after onset of pain as thats when become detectable and reaching peaks

144
Q

2 types of MI?

A 
ST elevated (STEMI)
- elevation on ST segment - after peak- of 12 lead ECG

Non ST elevated (NSTEMI)
- no change in 12 lead ECG

145
Q

why are death rates higher in first few hours of cardiac event?

A

heart muscle starts to die within 80-90 minutes after it stops getting blood, and within six hours, almost all the affected parts of the heart could be irreversibly damaged.

get abnormal heart rhythms called arrhythmias!!!

146
Q

MI caused by atherosclerotic plaque formation- what does this do?

  • stable plaque
  • unstable
A

stable plaques: can obstruct arterial blood flow and = symptoms of angina

unstable plaques: prone to rupture and can form thrombus

147
Q

modifiable risk factors for MI?

A 
tobacco smoke
high cholesterol
high BP
physical inactivity
obese
diabetes
148
Q

non-modifiable risk factors for MI?

A

age: over 65
male
family history
race

149
Q

symptoms of MI?

A

suddent onset crushing chest pain
starts in centre chest, radiates to arms, neck, jaw
sweating +shortness breath

150
Q

MI symptoms often similar to..?

A

sometimes diff to distinguish: heart related chest pain and GORD

151
Q

STEMI treatment?

aspirin 300mg + ….. (4)

A

coronary reperfusion therapy

  • prim percutaneous coronary intervention (PCI) with antiplatelet (ticagrelor/ prasugrel)
  • or fibrinolysis (reteplase/ tenecteplase)

coronary angiography- find blockage w dye

med management and sec prevention

pain relief, anti-emetics, glycaemic control

152
Q

3 antiplatelet examples used in STEMI treatment?

A

Prasugrel
Ticagrelor
Cangrelor

153
Q

how does prasugrel anti-platelet inhibit platelet activation and aggregation?

A

through irreversible binding of its metabolite to P2Y12 class of ADP receptors on platelets

154
Q

when prasugrel prescribed in MI?

A

with aspirin- prevntion of atherothrombotic events in STEMI having primary/ delayed PCI

155
Q

whens ticagrelor (antiplatelet) used in MI treatment and what is it?

A

STEMI: PCI,med management

  • ADP rec antagonist
156
Q

Ticagrelor: SE?

A

dyspnoea, haemorrhage
PLATO-trial
advantage may lie in faster onset of action

157
Q

when/hows cangrelor given in STEMI treatment?

A

with aspirin, to reduce thrombotic CV events in patients w coronary artery disease undergoing perc coronary intervention (PCI).. whove not had treatment w oral clopidogrel, prasugrel, ticagrelor prior… and cant take oral drugs.

give under expert supervision only

158
Q

secondary prevention of STEMI?

aspirin low dose (75mg) lifelong +….

A

+ dual antiplatelet therapy (clopidogrel) if had stent
+ ticagrelor with aspirin for up to 12 months
- PPI to reduce GI SE
- BB to reduce mortality after MI
- lipid lowering treatment
- ACEi
- aldosterone antogonist (epleronone) w HF post MI
-low dose rivaroxaban w aspirin/ aspirin + clopidogrel- preventn of atherothrombotic events after STEMI. anticoag

159
Q

rational for using factor Xa inhibitor: rivaroxaban as sec prevtnion of STEMI?

A

low dose rivaroxaban w aspirin/ aspirin + clopidogrel

prevention of atherothrombotic events after STEMI.

160
Q

whats Unstable Angina?

A

patient has symptoms of MI but not sufficient/no troponin rise

may/ may not have changes on ECG

161
Q

treatment of STEMI and Unstable Angina?

Aspirin LD 300mg +….? (5)

A
  • Ticagrelor (180mg LD)
  • eptifibatide/tirofiban (diff antiplatelet mechs) for patients undergoing coronary angioplasty/ abciximab as ajunct to PCI
  • antithrombin therpay w fondaparinux/ unfractioned heparin
  • coronary angiography w/wout PCI/ CABG
  • pain relief and anti-emetics
162
Q

treating NSTEMI, unstable angina: consider eptifibatide/tirofiban (diff antiplatelet mechs) for what patients?

A

undergoing coronary angioplasty/ abciximab as adjunct to PCI

163
Q

individual risk of future adverse CVE after NSTEMI/ unstable angina?

A

low: up to 3%
inter: 3-6%
high: <6%

164
Q

secondary prevention of NSTEMI and unstable angina? (4)

A
  • dual antiplatelet therpay
  • lipid lowering med statins
  • ACEi
  • beta blockers
165
Q

lifestyle changes - cardiac rehab services for sec prevention?

A

stress management
physical activity

  • healthy eating: meditt diet: more bread, fruit, veg
  • less alcohol (14 units wk max)
  • 20/30min activity a day
  • stop smoking
  • BMI
166
Q

cardiac rehabilitation- when offered to patients?

A

to px soon after cardiac event

highlight benefits of program

start within 10 days of hospital discharge

diet, meds, exercise, therapy

167
Q

Understand what stable angina is

- what does it result from?

A

chest pain/ discomfort caused when heart muscle doesnt get enough blood

  • demands of myocardum being unstable to be met by blood supply
168
Q

what happens to coronary arteries in stable angina? and when?

A

narrowing of one/more

occur when heart has to do work- exercise/ emotional stress

169
Q

stable angina= imbalance in what?

A

myocardial O2 sypply… and O2 demand.

need more O2!!

170
Q

when does stable angina pain occur and what should it be managed as form of?

A

precipitated by predicatable factors- exercice
any time,
consider as acute coronary syndrome

171
Q

aim of management of stable angina?

A

manage as acute coronary syndrome…

  • stop/minimise symptoms
  • imporve quality of life + long term morbidity + mortality
172
Q

where does anginal pain occur and how is it relieved?

A

constricting discomfort in fron of chest, neck, shoulders, jaw, arms
precip by physical exertion

relief by rest/ GTN in about 5 mins

173
Q

Describe the management of stable angina

A
  • GTN for rapid symptom relief
  • bb/ CCB as first line

symptoms not adequately controlled/ tolerated… switch to other/ use combo of both

174
Q

Describe the monotherapy management of stable angina

IF bb/CCB not adeq controlled symptoms/ contraindicated/ not tolerated (3)

A
  • long acting nitrate
  • Ivabradine (selective inhib of sinus node pacemaker activity)
  • Ranolazine (⬇ MIscaemia by acting on intracellular Na+ currents)
175
Q

management of stable angina: what to use if using ccb with bb/ ivabradine?

A

slow release nifedipine, amlodipine, or felopdipine

176
Q

management of stable angina: when can third anti-angina drug be added?

A

px symptoms inadequately controlled w 2 drugs

px waiting for revascularisation/ not appropriate/ not acceptable

177
Q

management of stable angina: when only to consider nicorandil?

A

other meds unsuitable bc risk of ulceration.

178
Q

management of stable angina: whats nicorandil- MoA?

A

properties of nitrate but also activates ATP-dpeendant K+ channels.
opens them -> muscle cells in blood vessel walls relax -> widen -> more blood flow ☺

179
Q

whens coronary revascularisation required?

A

in px at high risk

those who have failure to be controlled by medical therapy

180
Q

coronary revascularisation: nitrates- types and what do they protect against?

problem with them?

A

short vs long acting

  • protect against exercise induced ischaemia

can get tolerance after certain timings in day

181
Q

what to remember when how to prescribe nitrates?

SE?

A

adjunctive therapy not monotherapy

headache and cutaneous flushing…
also maybe post hypotension and reflex tachycardia

182
Q

how do nitrates work? to cause vasodilation and relax vasc SM?

A
  • mimic endogenous NO (release it)-> vasodil by relaxing smooth muscle
  • improve coronary blood flow,
    ⬇ pre load- dilate veins and afterload- dilate arteries
183
Q

main limitation of nitrates?

how to resolve/help

A

tolerance!
develops rapidly

nitrate free period of few hrs each 24hrs
should coincide w period of lowest risk- usually night time

184
Q

DDI between nitrates and phosphodiesterase-5 (PDE5) inhibitor sildenafil?

A

dont combine… can -> severe hypotension and death

185
Q

patient care after MI?

A
  • diet, exercise, smoking cessation
  • cardiac rehab
  • med adherance
  • divide med:
  • presc to ⬇ reinfaction and mortality
  • presc for symtpom control
  • what to do if SE happen
  • identify concerns openly-encourage
186
Q

common problems to dicuss w patients after MI. patient care

A
  • use of nitrates
  • use of NSAID, ACEi
  • SPEED! if fibrinolytic drugs needed after MI
  • aspirin and GIT bleeding. take w food and water
  • unpleasant bb SEs
187
Q

whats are some unpleasant beta blocker SEs

common

A

feeling tired, dizzy or lightheaded (slow heart rate)
cold fingers or toes (blood supply affected)
difficulties sleeping or nightmares
feeling sick

188
Q

how are stents placed into artery?

Coronary angioplasty and stent insertion

A
  • coronary artery on surface on heart.
  • balloon catheter put in with a closed stent around it
  • balloon is inflated and stent expands and plaque around it is compressed= widened artery, inc blood flow

When the operation is finished, the cardiologist will check that your artery is wide enough to allow blood to flow through more easily. This is done by monitoring a small amount of contrast dye as it flows through the artery.

The balloon, wire, catheter and sheath are then removed and any bleeding is stopped with a dissolvable plug or firm pressure. In some cases, the sheath is left in place for a few hours or overnight before being removed.

189
Q

meds usually taken with a stent (NHS site)

A

aspirin – taken every morning for life

clopidogrel – taken for 1 to 12 months depending on whether you have had a bare metal or drug-eluting stent, or whether you have had a heart attack

prasugrel or ticagrelor – used as alternatives to clopidogrel in people who have been treated for a heart attack

190
Q

4 types of antiplatelet drugs

A

cox inhib: aspirin
P2Y12 receptor blockers: irreversible/reversible
GP IIb IIIa inhibitors
phosphodiesterase inhibitors

191
Q

examples of:

  • irreversible P2Y12 receptor blocker antiplatelets
  • reversible P2Y12 receptor blocker antiplatelets
A
  • ticlopidine, clopidogrel, prasugrel

- ticagrelor, cangrelor

192
Q

examples of: GP IIb IIIa inhibitors antiplatelets

  • monoclonal antibody ones
  • synthetic molecules
A
  • abciximab
  • eptifibatide, tirofiban

… prevent platelet aggregation

193
Q

2 examples of antiplatelet: phosphodiesterase inhibitors?

A

dipyridamole, cilostazol

194
Q

how does aspirin (cox inhib) prevent platelet recruitment and activation?

A

inhib cox, key enzyme in TXA2 generation

potent antiplatelet for inhibiting TXA2

195
Q

how do P2Y12 receptor inhibitors inhib platelet recruitment + activation?

A

through irreversible binding of its active metabolite to P2Y12 class of ADP rec on platelets

196
Q

how do GPIIb/IIIa inhibitors prevent platelet aggregation?

A

block GP… receptors on platelet surface

- most abundant rec on surface, and are final common pathway of platelet aggregation

Health.2 (19 decks)

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