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Medicine block (Y3) > Week 4: Cardiology (4) ( arrhythmia and anticoagulation) > Flashcards

Week 4: Cardiology (4) ( arrhythmia and anticoagulation) Flashcards

1
Q

Haemostasis

A
  • Limits bleeding following injury- adhesion and activation of platelets and fibrin formation
    • Haemostatic plug + fibrin mesh= stable bleeding control
  • Thrombosis= pathological haemostasis – in the absence of bleeding (things have gone wrong)
  • Thromboembolic disease is common
    • deep vein thrombosis (DVT) and pulmonary embolism (PE)
    • transient ischaemic attacks (TIA), ischaemic stroke - myocardial infarction (MI)
    • consequence of atrial fibrillation (AF)
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2
Q

Venous and intracardiac thrombosis driven largely by

A

by coagulation cascade

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3
Q

arterial thormbus mainly driven by

A

platelets

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4
Q

Anticoagulant drugs- prevent x

A

Anticoagulant drugs- prevent thrombus formation and thrombus growing

(whereas antiplatelets stop things like MI)

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5
Q

Anticoagulants

A
  • Heparins
  • Warfarin
  • Direct oral anticoagulants (DOACS)
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6
Q

types of heparin

A
  • Unfractionated heparins (UFH) are large ~7-30 kDa
  • Low molecular weight heparins (LMWH) ~1-6 kDa produced in 1980’s
  • Inhibit coagulation in vitro and in vivo
  • Enhance antithrombin III (AT-III) activity - ~ 1000-fold
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7
Q

Indications for use of heparins

A
  • Prevention of venous thromboembolism
    • perioperative prophylaxis with LMWH - duration and dose is dependant on risk
  • During pregnancy used as do not cross placenta – monitored with caution
  • Venous Thromboembolism (VTE)–DVT and PE
    • initial treatment prior to oral agents (see later slides)
    • Long term in some patient group
    • Cancer related VTE
  • Acute Coronary Syndromes (ACS)
    • short term - reducing recurrence and or extension of coronary artery thrombosis post STEMI- PCI and non PCI patients
    • NSTEMI
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8
Q

MOA of unfractionated heparin (UFH

A
  • Binding to antithrombin (ATIII) causing conformational change and increased activity of ATIII
  • To catalyse inhibition of thrombin (IIa), heparin needs to simultaneously bind ATIII AND IIa.
  • Xa inhibition only needs ATIII binding
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9
Q

name a LMWH

A
  • dalteparin, enoxaparin, fondaparinux
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10
Q

Pharmacokinetics of LMWH

A
  • Typically ~ 15 polysaccharides which are absorbed more uniformly (units/kg dosing)
  • Almost always s.c. (enoxaparin i.v. in ACS)
  • Bioavailability > 90%, longer t1/2 ~ 2+h
  • More predictable dose response as does not bind to endothelial cells, plasma proteins and macrophages – it isn’t long enough
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11
Q

Mode of action of LMWH

A
  • Do not inactivate thrombin (IIa) – not long enough
  • Inhibition of Xa specifically – by enhancing ATIII activity
  • Fondaparinux – synthetic pentasaccharide selectively inhibits Xa by binding to ATIII – s.c., t1/2 18h
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12
Q

compare UFH with LMWH

A

admin:

  • UFH: IV bolus then ivi
  • LMWH: SC not IM
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13
Q

Adverse drug reaction heparin

A
  • Bruising and bleeding (most common)
    • Intracranial
    • Site of injection
    • GI
    • Epistaxis
  • Heparin induce thrombocytopenia (HIT)
    • Autoimmune response 2-14 days after initiation of heparin
      • Antibodies to heparin platelet factor 4 complex produced
      • Depletion of platelets
      • but paradoxically can lead to thrombosis as more platelets activated by damaged endothelium
  • Hyperkalaemia- inhibition of aldosterone secretion
  • Osteoporosis- rare long-term use, higher risk with UFH and more prevalent in pregnancy (least common)
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14
Q

contraindication heparins

A
  • Clotting disorder
  • Renal impairment (LMWH and fondaparinux)
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15
Q

Drug-drug interactions heparins

A
  • Antithrombotic drugs
  • ACEi/ARB
  • Spironolactone
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16
Q

Heparin monitoring

A
  • (activated) partial thomboplastin time (aPTT) when using therapeutic i.v. doses of UFH required – dose titrated/adjusted against this value
  • LMWH much more predictable in its action so normally requires little monitoring
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17
Q

heparin reversal

A
  • Protamine sulphate forms inactive complex with heparin – given i.v. dissociates heparin from ATIII, irreversible binding amount given guided by heparin dose
    • Paradoxically can cause bleeding!?
    • Much greater effect with UFH than LMWH, no affect on fondaparinux
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18
Q

vitamin K antagonist

A

warfarin

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19
Q

warfarin used

A
  • PE
  • DVT (and secondary prevention Superficial vein thrombosis)
  • Atrial fibrillation with high risk of stroke (use CHA2DS2Vasc)
  • Patients who need cardioversion
  • Heart valve replacement bio prosthetic and some mechanical
  • Generally used in longer term anticoagulation compared to heparins
  • Slow onset of action likely to require heparin cover (see later slides) if anticoagulation needed immediately
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20
Q

warfarin pharmacokinetics

A
  • Good GI absorption and taken orally ~95+% bioavailability
  • Functional CYP2C9 polymorphisms contribute to significant inter individual variability
  • [Plasma] does not correlate directly with clinical effect
  • Warfarin is a racemic mixture of two enantiomers – R and S which have different potency and metabolised differently
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21
Q

how is warfarin diff to heparin

A
  • Delay in onset of action as circulating active clotting factors present for several days
  • Must be cleared and replaced with non-carboxylated forms (inactive clotting factors)
  • Half life= 36-48h (some variation)
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22
Q

MOA of warfarin

A
  • Inhibit activation of vitamin K dependant clotting factors (coagulation vitamin)
  • Inhibits conversion of vitamin K to active reduced form – competitive inhibition of VKOR
  • Hepatic synthesis of clotting factors II, VII, IX and X requires vitamin K as cofactor for activation
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23
Q

ADR warfarin

A
  • Bleeding- any pt taking warfarin are of clinical interest
    • Epistaxis and spontaneous retroperitoneal bleeding
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24
Q

antidote of warfarin

A
  • Most effective antidote is vitamin K1
    • addition of prothrombin complex concentrate i.v. Stop warfarin!
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25
Q

warfarin contraindications

A
  • Pregnancy
    • Crosses the placenta
    • Avoided at least in 1st 9teratoegnic) and 3rd (haemorrhage) trimesters
  • Hepatic disease
  • Response affected by CYP2C9
  • Perioperative anticoagulation needs to be considered – need to consider if and when to pause warfarin specific patient group and local guidelines will dictate
    • Bridging therapy with LMWH often required when initiating or temporarily stopping warfarin (surgery, sickness…)
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26
Q

warfarin use and INE

A
  • Monitoring required due to huge variation in patient response
  • Keeping diet and lifestyle/medications stable is important
  • Factor VII most sensitive to vitamin K deficiency so used in prothrombin time - standardised against control plasma
  • Referred to as international normalised ratio – INR - clotting time against a standard
    • Allows for standard corrected value comparable across all laboratories
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27
Q

INR 2.5

A
  • DVT
  • PE
  • AF (risk
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28
Q
  • INR 2.5
    • DVT
    • PE
    • AF (risk
A
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29
Q

INR 3.0 - 3.5

A

Recurrent DVT or PE in patients currently receiving anticoagulation

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30
Q

people on warfarin carry

A

YELLOW anticoagulant card

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31
Q

DOACS act on

A

Xa or IIa

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32
Q

which doacs act on Xa

A
  • Apixaban
  • Edoxaban
  • Rivaroxaban
    • Inhibit both free Xa and that bound with ATIII, do not directly effect thrombin (IIa) - hepatic metabolism and excreted partly by kidneys
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33
Q

which DOAC acts on IIa

A
  • Dabigatran
    • Selective direct competitive thrombin inhibitor, both circulating and thrombus bound IIa
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34
Q

why are DOACs great

A
  • Oral administration, standard dosing and little to no direct monitoring required
    • When would monitoring be beneficial? E.g. where adherence isn’t good
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35
Q

Indications of DOAC

A
  • Different DOACs are indicated in many presentations where vitamin K antagonists (warfarin) used to be the only option
  • Antidotes now available
    • Andexanet and idarucizumab
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36
Q

ADR DOAC

A
  • Bleeding (lower intracranial bleed risk compared to warfarin)
  • Caution and dose adjustment separately in GI bleed risk groups
37
Q

Contraindications DOAC

A
  • Metabolism and elimination by several routes
  • X dabigatran contraindicated in low creatinine clearance (<30 mL/min)
  • others are at very low creatinine clearance (<15 mL/min)
  • Little information on use in pregnancy and breastfeeding – avoid
38
Q

Drug drug interaction : DOAC

A
  • Less frequent interactions than warfarin but affected by CYP inhibitors and inducers
    • [plasma] reduced by carbamazepine, phenytoin and barbiturates
    • [plasma] increased by macrolides
39
Q

basic ECG algorithm

A
  1. rate
  2. rhythm
  3. axis
  4. intervals
  5. ST/T wave changes
40
Q

calculating rate

A

QRS x 6

brady <50BPM

tachy >120 BPM

41
Q

classification of bradycardia

A

Classification

According to the pacemaker: sinus node or AV node

42
Q

rhythm can be

A

regular

sinus arrhythmia e.g. sinus tachy

irregular

43
Q

sinus rhythm

A

p wave before every QRS complex

44
Q

AXIS

A
  • Normal- I and II most positive
  • Left axis deviation (i.e. left ventricular hypertrophy)- aVL most positive
  • Right axis deviation- III most positive
45
Q

normal PR intervals

A

120-200ms

if short look for delta wave and therefore Wolf-parkinson-white

46
Q

QRS interval

A

up to 120 ms

-→ if tall consider left ventricular hypertrophy

47
Q

QTc interval

A

400-440ms or 2 large squares

48
Q

ST/T wave changes

A

look for elevation, depression, inversion

49
Q

bradycardia

A
  • <60bmp
  • Absolute <40bpm
  • Relative- inappropriate slow for haemodynamic state of patient
    • E.g. <90mmHg, HR,40bpm, poor perfusion and poor urine output, ventricular arrhythmias, heart failure
50
Q

bradycardia

A
  • <60bmp
  • Absolute <40bpm
  • Relative- inappropriate slow for haemodynamic state of patient
    • E.g. <90mmHg, HR,40bpm, poor perfusion and poor urine output, ventricular arrhythmias, heart failure
51
Q

sinus node bradycardia types

A

sinus bradycardia, sick sinus syndrome (tachy-brady), sinus arrest alone or as part of vasovagal syncope

52
Q

sinus node tachycardia caused by

A
  • Medications
  • Hypothyroidism
  • Hypothermia
  • Sleep apnoea
  • Less commonly: rheumatic fever, viral myocarditis, amyloidosis, haemochromatosis and pericarditis
53
Q

treatment of sinus node arrhythmia

A
  • Pacing rarely required in acute settings
  • Symptomatic patients may require a pacemaker
54
Q

sinus node brady on ECG

A
  • On the ECG: slow rate but every QRS is preceded by a p wave
55
Q

AV node brady cardia is classified accoding to degree of nodal dysfunction e.g.

A

first degree, second degree, third degree AV block

56
Q

first degree AV block

A
  • PR interval >0.2 seconds
  • Treatment- none
    • Take care with rate limiting drugs
    • If symptoms of syncope cardiac monitoring should be considered to identify higher degree of block
    • If patient on digoxin check for toxicity
57
Q

second degree AV block can be divided into

A

mobitz type 1 and type 2

58
Q

mobitz type I (wenckebach)

A
  • Progressive lengthening of PR, followed by dropped QRS (failure of atrial impulse to conduct to the ventricle)
  • Treatment- no specific therapy
    • Higher degrees of AV block should be looked for in patients with syncope or dizziness
    • When?
      • Can occur in young fit patients with high vagal tone so can be seen during night if monitored
      • After inferior MI- rarely proceeds to complete heart block
59
Q

mobitz type II

A
  1. Second degree AV block (Mobitz Type II)
    • Constant PR interval followed by sudden failure of p wave to be conducted to the ventricles (e.g. sudden droppage of QRS)
    • Treatment : in absence of recent acute coronary event, permanent pacing should be arrange (if drugs have been excluded)
60
Q

complete (third degree) AV block

A
  • No conduction from atria to the ventricles and therefore AV dissociation- no relationship between the P waves and QRS complexes
  • Block can occur above the AV node at the His region (narrow complex escape are usually well tolerated such as congenital complete heart block) or beneath the AV node with broad complex escape (not well tolerated)
  • ECG: can be intermittent therefore look for ECFs with trifasacular or bifascular block (RBBB, left axis deviation with or without prolonged PR interval) and alternating LBBB and RBBB
  • Treatment: urgent pacing
  • Causes
    • Antiarrhythmic drugs e.g. digoxin toxicity
    • Inferior STEMI- should resolve within hours to days
    • More ominous finding following anterior MI
    • Severe hyperkalaemia
    • Atropine (in haemodynamically unstable patient)- Isoprenaline administered at a rate of 5 μg/min can be tried.
61
Q

types of tachy cardia (>100bmp)

A

atrial fibrillation

supraventricular tachcardia

ventricular tachycardia

62
Q

risk factors for AF

A
  • High BP
  • Atherosclerosis
  • Heart valve disease
  • Congenital heart disease
  • COPD
  • PE
63
Q

triggers of AF

A
  • Binge drinking
  • Obesity
  • Cocaine ad amphetamines
64
Q

people with AF are at risk of

A
  • Cardioembolic stroke- due to statis of blood in the atria
  • Cardiac instability
  • And higher risk of death
  • Increased healthcare cost
65
Q

diagnosis of AF

A
  • Pulse- irregularly irregular
  • Symptoms
    • Breathlessness
    • Palpitations
    • Syncope/dizziness
    • Chest discomfort
    • Stroke or TIA
  • ECG
  • Echocardiogram
66
Q

cardiac monitoring of AF

A
  • If paroxysmal AF further monitoring recommended
    • 24h hour cardiac monitor- may not capture the arrhthmia if intermittent
  • Where suspicion remains high (in pt you would like to anticoagulated) or unexplained syncope  prolonged cardiac monitoring should be considered e.g. holter monitor of implantable loop recorder
67
Q

AF on ECG

A
  • Tachycardic
  • Absent P waves
  • Wavy baseline
  • Irregularly irregular
68
Q

Echocardiography in AF

When?

A
  • Performed if suspected structural heart disease (on basis of symptoms or examination finding of a murmur or signs of heart failure)
  • Where a rhythm control strategy (cardioversion) is being considered
  • Baseline echocardiogram required to inform long term management.
69
Q

natural history of AF

A
  • Initial manifests as brief paroxysms of increasing duration (transient) going on to become persistent and permanent AF
    • Many have no symptoms
  • Easily recognised when associated with complications, including haemodynamic instability due to tachyarrhythmia or bradyarrhythmia, ACS, congestive cardiac failure or cardioembolic stroke
70
Q

management of AF

A
  1. Anticoagulation to prevent stroke
  2. Rate control
  3. Rhythm control
71
Q

which scoring system is used to predict risk of stroke or embolism

A

CHA2DS2VaSc

72
Q

CHA2DS2VaSc

A
  • Quantifies risk of stroke or systemic embolism
  • Based on medical diagnoses and risk
  • Estimates adjusted stroke rate per year
  1. A score of 2 or more is associated with significant risk, where risk of embolic stroke is considered high enough to offer anticoagulation.
  2. A score of 1 in men is considered intermediate risk, where anticoagulation should be considered, and a careful decision has to be made keeping in mind the bleeding risk.
  3. A score of 0 indicates a truly low risk of stroke and anticoagulation is not offered.
  4. A score of 1 in women (due to gender) and a score of 0 are considered low risk, with anticoagulation not advised.
73
Q

scoring system used to quantify risk of major bleed

A

HAS-BLED

  • Quantifies risk of major bleeding
  • Rate of major bleeds per 100 patient years
  • Intended to enable identification and optimisation of reversible risk factors for bleeding including:
    • a) Uncontrolled hypertension (SBP>160mmHg)
    • b) Poor INR control (“labile INR”), as measured by time-in-therapeutic range (TTR)
    • c) Concurrent medication (aspirin, NSAIDs)
    • d) Harmful alcohol consumption (>14 units per week)
74
Q

recent onset of AF management

A
75
Q

long term heart rate control AF

A

first line - B- blockers if not asthmatic

76
Q

Anticoagulation options in AF

A

DOACs now drug of choice over other blood thinners such as warfarin

77
Q

DOACs

A
  • Inhibits factor Xa (apixaban, rivaroxaban and edoxaban) or direct thrombin inhibition (dabigatran)
  • Don’t need regular testing of levels compared to the INR monitoring of warfarin
  • No restrictions on food or alcohol
  • Excreted by the kidney so renal function is monitored yearly
  • Lower rate fo bleeding to warfarin and slightly better reduction in strokes
78
Q

supraventricular tachycardia

A
  • Most common: AVNRT (AV nodal re-entry tachycardia, 60% of SVT) or AVRT (atrio-ventricular re-entry tachycardia, 30% of SVT)
  • Can be terminated by transiently blocking AV nodal conduction
79
Q

first-line management of supraventricular tachycardia

A

vagal manouvres and carotid massage

80
Q

Vagal manoeuvres =

A
  • first lined in haemodynamically stable patients
    • Valsava manoeuvre ( i.e. having patient bear down as though having a bowel movement or blowing hard into a syringe to move the plunger
      • These all slow conduction in the AV node and can potentially interrupt the re-entrant circuit
81
Q

Carotid massage

A
  • Slows AV nodal conduction
  • Massage the carotid for several second on the non-dominant cerebral hemisphere side
  • For young patients- due to risk of stroke from emboli
    • Auscultate for bruits before attempting this manoeuvre
    • Do not perform carotid massage on both sides at the same time
82
Q

if vagal and carotid massage do not work in supraventiruclar tachycardia

A

adenosine or calcium channel blockers or synchronised cardioversion

83
Q

adenosine and supraventricular tachycardia

A
  • Short-acting drug that blocks AV node conduction
  • Rapid bolus IV by saline (0.9%)flush in the antecubital fossa
  • 3 way stopcock (6 mg stat followed by 12 mg if unsuccessful and then a further 12 mg if still unsuccessful)
  • Very short half life and may cause chest discomfort, transient hypotension and flushing
  • Should be avoided in patients with signif reversible airways disease
  • Crash trolley should be next to patient- risk of bradyarrhythmia or tachyarrhythmia
84
Q

calcium channel blockers and supraventricular tachycardia

A
  • (5 - 10 mg slowly IV) is an alternative but is dangerous and contraindicated in patients already on β-blockers or in patients with known significant LV dysfunction.
85
Q

if adenosine and verapamil are inefective

A
  • electrical cardioversion under general anaesthetic
    • Intravenous flecainide probably the best but should be avoided in patients with MI
86
Q

Synchronised cardioversion

A

Following sedation starting at 150J can be use immediately in pts who are hypotensive, have pulmonary oedema, have chest pain with ischaemia or are otherwise unstable

87
Q

second line drugs to prevent SVT

A

flecainide, sotalol or amiodarone.

88
Q

Ventricular tachycardia (VT)

A
  • Rapid broad complex tachycardia shortly after STEMI is nearly always VT
  • In patients with sustained VT who are haemodynamically compromised cardioversion is indicated (synchronised 140-2000j shock with biphasic def)
  • Suppression can be achieved with B blockers
  • Amiodarone (300mg IV ove r afew minutes, followed by 900mg over 24hours)
  • Lidocaine (50-100mg over 3-5 minutes), is an alterantive, which may be repeted after 5 minutes

Medicine block (Y3) (38 decks)

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