Cardio Flashcards
(145 cards)
1
Q
What are arrythmias
A
Disorders of heart rate or rhythm caused by either abnormal generation or conduction of electrical impulses.
2
Q
What is atrial fibrillation caused by?
A
Rapidly firing ectopic foci located inside one or more pulmonary veins generates the arrythmia, and it is maintained by abnirmal atrial tissue substrate capable of maintaining the arrythmia.
3
Q
How is AF treated?
A
Rate control:
1. beta-blocker of rate-limiting CCB
2. digoxin
3. 2 of beta-blocker, diltiazem, and digoxin.
Rhythm control:
1. beta-blocker
2. dronedarone
Stroke prevention: DOAC or warfarin.
4
Q
How is AF diagnosed?
A
- Identify irregular pulse.
- Confirm with 12-lead ECG. Shows irregularly irregular ventricular rate with no distinguishable P-waves.
5
Q
How is ventricular tachycardia diagnosed?
A
12-lead ECG showing wide QRS complex (>120 ms) and a heart rate >100bpm.
6
Q
How is ventricular tachycardia treated?
A
Adenosine or Procainamide
7
Q
What is torsades de pointes?
A
A polymorphic ventricular tachycardia associated with QT interval prolongation, often due to electrolyte abnormalities.
8
Q
How is torsades de pointes treated?
A
IV magnesium sulfate
+ correct electrolyte abnormalities and withdraw causative agents.
9
Q
What are the 5 classes of anti-arrythmatic drugs?
A
Class I - membrane stabilising drugs e.g., lidocaine, felcainide. Block sodium channels to slow depolarisation. Can cause CNS toxicity & N &V.
Class II - beta-blockers. Act on the AV node to reduce rate of spontaneous depolarisation and decrease heart rate. Can cause postural hypotension, bradycardia, heart block, bronchoconstriction, hypoglycaemia.
Class III - e.g., amiodarone and sotalol. Block potassium channels responsible for completion of repolarisation in contractile cells leading to an extended refractory period. Can cause peripheral neuropathy and photosensitivity, and potentiate effects of digoxin and warfarin.
Class IV - non-dihydropyridine CCBs e.g., verapamil, diltiazem. Block L-type calcium channels in autorhythmic cells to prevent spontaneous depolarisation. Can cause bradycardia, heart block, flushing, peripheral oedema.
Class V - cardiac glycosides, adenosine, magnesium sulfate, atropine.
Class I (only affect 1 electrolyte).
Class 2 (b is 2nd letter)
Class 3 (2 drugs + 1 channel)
Class 4 (CCBs)
Class 5 (others)
10
Q
What does chronotropic refer to?
A
A positive or negative change in heart rate.
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11
Q
What does inotropic refer to?
A
A positive or negative change in the strength of contraction.
How hard it contracts in
12
Q
How does digoxin work?
A
Normally: Na+/K+ ATPase pump in cardiomyocytes pumps 3 Na+ out and 2 K+ into the cell, in order to drive calcium out of the cell via an exchanger.
Digoxin inhibits this pump to increase intracellular calcium, therefore causing an increased contractile force in the heart to improve left ventricular ejection fraction. It also stimulates the parasympathetic nervous system via the vagus nerve which leads to sinoatrial (SA) and atrioventricular (AV) node effects, which decreases the heart rate. Digoxin also helps to decrease noradrenaline levels through activation of the paraysmpathetic nervous system.
13
Q
Symptoms of digoxin toxicity
A
PR prolongation
N&V
Visual disturbances - xanthopsia (yellow halo around lights)
Insomnia
Bradycardia
Arrythmias
14
Q
What is the therapeutic range for serum digoxin concentration?
A
0.7 nanograms/mL - 2.0 nanograms/mL
15
Q
When does digoxin toxicity occur?
A
Digoxin toxicity can occur even within the therapeutic range, although:
- Levels less than 1.5 micrograms/L in the absence of hypokalaemia suggest digoxin toxicity is unlikely.
- Levels between 1.5–3 micrograms/L suggest digoxin toxicity is possible.
- Levels greater than 3 micrograms/L suggest digoxin toxicity is likely.
16
Q
How does adenosine work?
A
Acts on SA node to reduce heart rate (negative chronotrope) and on AV node to slow conduction.
17
Q
How does atropine work?
A
Muscarinic antagonist which inhibits vagal activity to alleviate parasympathetic depression of SA node activity to increase heart rate.
18
Q
How does amiodarone work?
A
Blocks K+ currents which cause repolarisation in cardiac muscle during the 3rd phase of the cardiac action potential, therefore increasing the duration of the action potential and the effective refractory period of the cardiomyocytes. This reduces cardiac muscle cell excitability
19
Q
What are some adverse effects of amiodarone?
A
miLungs - pulmonary toxicity. Report any respiratory symptoms.
Eyes - corneal microdeposits and visual disturbances (STOP - reversible).
Hepatic - increases PPARs leading to steatogenesiss (fat build up) in the liver.
Thryoid - due to high iodine content, amiodarone can bind to thyroid receptor and induce hypothyroidism and thyrotoxicosis.
Skin - photosensitivty (avoid sunlight).
Heart - arrythmias and bradycardia.
20
Q
Dose adjustments for digoxin.
A
- Half dose with concurrent use of amiodarone, dronedarone, and quinine.
- When switching from IV to po, increase dose by 20-33% to maintain plasma-digoxin concentration.
- eGFR < 30 – max 125mcg
- Elderly – consider reducing
21
Q
When should digoxin levels be taken?
A
6-12 hours post dose.
22
Q
Treatment of ischaemic stroke?
A
After ruling out haemorrhage:
300mg aspirin ASAP
+
Alteplase within 4.5h (bolus + infusion)
+
Thrombectomy with IV thrombolysis within 6h
23
Q
Secondary prevention following ischaemic stroke.
A
Antiplatelet therapy:
1. clopidogrel 75mg OD
2. aspirin 75mg OD + dipyridamole 200mg MR BD
3. aspirin 75mg OD OR dipyridamole 200mg MR BD
High risk: aspirin 75mg OD + clopidogrel 75mg OD OR aspirin + ticragelor
Lipids: 80mg atorvastatin or other high intensity statin.
Antihypertensives: according to guidlines
24
Q
Who requires primary prevention of CVD?
A
- QRISK3 >10%
- T1DM, CKD, or familial hyperhcolesterolemia.
- > 85y
25
What is primary prevention of CVD?
High intensity statin: atorvastatin 20mg.
Or ezetimibe if statin CI.
26
What are "low", "medium" and "high" intensity statins?
High intensity: LDL reduction >40%.
- Atorvastatin 20-80mg
- Rosuvastatin 10-40mg
- Simvastatin 80mg (risk of myopathy)
Medium intensity: LDL reduction 31-40%
- Atorvastatin 10mg
- Rosuvastatin 5mg
- Simvastatin 20 & 40mg
- Fluvastatin 80mg.
Medium intensity: LDL reduction 20-30%
- Simvastatin 10mg
- Pravastatin 10-40mg
- Fluvastatin 20 & 40mg.
27
What is the aim of primary prevention?
Non-HDL cholesterol reduced by >40% in 2-3 months.
28
What is the aim of secondary CVD prevention?
LDL cholesterol levels of <2.0mmol/L
or
non-HDL cholesterol levels of <2.6 mmol/L
29
What are the escalations in lipid-modification treatment if targets are not met?
1. High intensity statin.
2. Increase statin dose.
3. Add ezetimibe OR add icosapent ethyl OR use inclisiran, alirocumab, or evolucumab.
4. Ezetimibe + bempedoic acid OR use inclisiran, alirocumab, or evolucumab.
30
How do statins work?
Inhibit hepatic cholesterol synthesis via HMG CoA reductase, the rate-limiting enzyme in cholesterol synthesis.
Reduced intracellular cholesterol promotes increased LDL receptor expression on hepatocyte surfaces, resulting in increased uptake of LDL from the blood i.e., lower plasma LDL.
31
Cautions and contraindications of statins?
CI:
- Liver disease (check transaminases before)
- Pregnancy and breastfeeding - wait 3 months after treatment before conception.
Caution:
- risk factors for muscle toxicity e.g., myopathy or rhabdomyolysis.
32
Statins Interactions
CYP3A4 inhibitors - mainly clarithromycin and erythromycin, also grapefruit juice.
Hepatotoxic drugs - monitor LFTs.
33
What is the MOA of ezetimibe?
Inhibits intestinal uptake of dietary and biliary cholesterol without affecting absorption of fat-soluble nutrients, thus decreasing the amount of cholesterol delivered to the liver.
Reduced intracellular cholesterol promotes increased LDL receptor expression on hepatocyte surfaces, resulting in increased uptake of LDL from the blood i.e., lower plasma LDL.
34
What blood test indicates rhabdomyolysis?
Creatine kinase >5x upper limit of normal.
35
How does bempedoic acid work?
Inhibits ACL to reduce cholesterol synthesis in the liver.
Reduced intracellular cholesterol promotes increased LDL receptor expression on hepatocyte surfaces, resulting in increased uptake of LDL from the blood i.e., lower plasma LDL.
36
Why should bempedoic acid not be given with statins?
No clinical contraindication.
Expensive so should be reserved for use in people who are not responding to statin treatment.
37
Adverse effects of bempedoic acid
- Hyperuricaemia and gout.
- hepatic impairment
- May cause reproductive toxicity so avoid in pregnancy (and breastfeeding).
38
What is inclisiran?
A small interfering RNA which inhibits production of PCSK9, an enzyme involved in down-regulation of LDL receptors. Inhibition of PCSK9 stops low-density lipoprotein (LDL) receptors in the liver from degrading.
Increased LDL receptor expression on hepatocyte surfaces, resulting in increased uptake of LDL from the blood i.e., lower plasma LDL.
39
What are alirocumab and evolucumab?
Monoclonal antibodies which inhibit production of PCSK9, an enzyme involved in down-regulation of LDL receptors. Inhibition of PCSK9 stops low-density lipoprotein (LDL) receptors in the liver from degrading.
Increased LDL receptor expression on hepatocyte surfaces, resulting in increased uptake of LDL from the blood i.e., lower plasma LDL.
40
What is icosapant ethyl?
An ethyl ester of the omega 3 fatty acid eicosapentaenoic acid which suppressing cholesterol-, fatty acid-, and triglyceride-synthesising enzymes, resulting in decreased hepatic triglyceride synthesis and release.
41
What is the difference between AF and ectopic beats?
Ectopic beats - spontaneous and rarely require treatment, sometimes may need beta-blockers.
AF - requires ventricular rate control and sinus rhtythm control, and can lead to complications such stroke, so requires OACs.
42
Treatment of life-threatening haemodynamic instability caused by acute AF.
Emergency electrical cardioversion to achieve anticoagulation.
43
Treatment of acute AF (non-life-threatening)
If onset <48h: rate or rhythm control
If onset >48h: rate control
44
What is cardioversion?
Rhythm control in acute AF
45
staWhat are the treatment options for cardioversion?
Pharmacological: flecainide or amiodarone
Electrical (start IV anticoagulation and tule out a left aitrial thrombus)
46
Maintenance AF treatment
1 - Rate control (monotherapy):
* A beta-blocker (not sotalol)
* Rate-limiting CCB
* Digoxin (usually in sedentaty patients with non-paroxysmal AF.
2 - Rate control dual therapy
- 2 of: beta-blocker (not sotalol), diltiazem, or digoxin.
3 -Rhythm control
* electrical/pharmacological cardioversion - electrical preferred in longterm AF
47
What drug treatment is required for a patient undergoing cardioversion?
Pre:
- anticoagulated for at least 3 weeks (electric only)
Post:
- oral anticoagulation for at least 4 weeks (electric only)
- may equire beta-blocker
- May also require sotalol, propafenone, amiodarone, or flecainide (SPAF).
- Amiodarone can be started 4 weeks before and continued for upto 12 months after electrical cardioversion to increase success of the procedure.
48
Treatment of paroxysmal AF
1. beta-blocker
2. sotalol, propafenone, amiodarone, or flecainide (SPAF)
PRN flecainide or propafenone can be used to restore rhythm during paroxysmal episode.
49
What assess risk of stroke and need for thromboprophylaxis in AF?
CHA2DS2VASc:
- Congestive heart failure
- Hypertension
- Age 75+ (2 points)
- Daibetes
- Stroke/TIA (2 points)
- Vascular disease
- Age 65-74
- Sex = female
A score of 0 in men or 1 in women means thromboprophylaxis is not needed.
50
Treatment of atrial flutter
Rhythm or rate control (although responds less well to drug treatment).
Rate:
- beta-blockers
- rate-limiting CCBs
Rhythm:
- electric cardioversion
- pharmacological cardioversion
- catheter ablation (for recurrent attrial flutter)
51
Paroxysmal supraventricular tachycardua treatment pathway
Treatment usually not required as terminates spontaneously alone.
If required:
1. Reflex vagal stimulation using valsalva manouvre, carotid sinus massage, immerse face in cold water (ensure ECG monitoring).
2. IV adenosine
3. IV verapamil
4. Catheter ablation of recurrent sympytoms
5. Prevention: beta-blocker or rate-limiting CCB
52
Which arrythmias require resuscitation
Pulseless ventricular tachycardia
Ventricular fibrillation
53
Treatment of unstable ventricular tachycardia
1. Direct current cardioversion
2. IV amiodarone
3. Repeat current cardioversion
54
Treatment of stable ventricular tachycardia
1. IV amiodarone
2. Direct current cardioversion
55
Treatment of non-sustained ventricular tachycardia
Beta-blocker
56
When might maintenance therapy be required for ventricular tachycardia?
If at high risk of cardiac arrest, they may require an implantable cardioverter defibrillator. Can also add beta-blocker +/- amiodarone
57
What is torsades de pointes?
QT prolongation: a QTc >0.44 seconds
58
Causes of QT prolongation
* Drug-induced e.g., amiodarone, sotalol, macrolide abx, halopridol, SSRIs, TCAs, antifungals
* Hypokalaemia
* Severe bradycardia
59
Treatment of Torsades de pointes
Usually self-limiting, but can lead to impaired consciousness or ventricular fibrillatio (which can result in death).
Treated with IV magnesium sulphate.
60
What is important to remember about amiodarone adverse effects?
Amiodarone has a very long half life, so adverse effects and drug interactions can occur several weeks or months after stopping treatment.
61
Amiodarone interactions
* Drugs that cause hypokalaemia
* Drugs that cause QT prolongation
* Drugs that cause bradycardia
* CYP450 substrates (acts as inhibitor)
* CYP450 inhibitors and inducers (also a substrate)
* Digoxin - half digoxin dose.
62
Amiodarone monitoring
Before treatment:
* TFTs
* LFTs
* K+
* CXR
6 monthly:
* TFTs
* LFTs
Annually:
* Eye examination
With IV use: ECG and liver transaminases
63
Treatment of digoxin toxicity
Digoxin-specific antibody
64
Digoxin interactions
* Beta-blockers: increased risk of AV block and increases plasma concentration
* TCAs: can induce arrythmias
* Drugs causing hypokalaemia: increased risk of digoxin toxicity
* CYP450 inducers and inhibitors
65
Prevention of bleeding in surgeries/menoorhagia/dental extractions
Tranexamic acid
66
Common side effects of tranexamic acid
Nausea and vomiting
67
Treatment of haemophilia and von WIllebrand's disease
Desmopressin
68
Symptoms of HF
* SOB
* Persistent coughing/wheezing
* Oedema
* Reduced exercise tolerance
* Fatigue
69
Treatment of chronic HF
1. Beta-blocker + ACE inhibitor (or ARB) (or hydralazine + a nitrate if ACEi/ARB not tolerated)
2. Add a MRA: spironolactone or eplerenone
3. Add amiodarone, digoxin (for patients in sinus rhythm), ivabradine, SGLTi (empagliflozin or dapagliflozin). Can also swap ACEi/ARB to sacubitril + valsartan.
Loop diuretics may be used to relieve breathlessness/oedema due to fluid retention.
70
Indications for lipid-lowering treatment
* QRISK3 >10%
* T1DM for >10 years or aged >40/
* CKD
* Familial hypercholesterolaemia
71
What should be checked before initiating statin?
* TFTs - hypothryoidism can cause elevated cholesterol and once treated may negate the need for statin.
* HbA1c or fasting blood glucose (if high risk of diabetes) - statins may cause hyperglycaemia and insulin resistance AND link between high cholesterol and diabetes. Repeat after 3 months.
* Full lipid profile - for monitoring
* Renal function
* Liver function
* Creatine kinase - if patient has history of persistent muscle aches. If measurement >5x upper limit, remeasure in 7 days. If still >5x UL - do not start. If raised but <5x UL - start at lower dose.
* Pregnancy (teratogenic)
72
Statins continuous monitoring
* HbA1c - before + 3 months
* LFTs - before + 3 months + 12 months. Discontinue of serum transaminases >3x upper limit.
* Lipid profile - monitor treatment effectiveness.
73
Statins adverse effects
* Muscle toxicity, myopathy, and rhabdomyolysis - report muscle aches and pains.
* Intersitial lung disease - report dysponea, cough, weight loss.
* Teratogenic - discontinue 3 months before conception.
74
Statins key interactions
* CYP inducers and inhibitors
* Oral fusidic acid - restart statin 7 days after last dose.
75
Maximum dose of statins (with interacting drugs)
Simvastatin with:
* amiodarone = 20mg
* amlodipine = 20mg
* diltiazem or verapamil = 20mg
* Ticagrelor = 40mg
Atorvastatin with:
* Ciclosporin = 10mg
* Tipranavir = 10mg
76
What are fibrates?
Lipid-lowering agents:
* Bezafibrate
* Ciprofibrate
* Fenofibrate
* Gemfibrozil
77
Fibrates considerations
Renal impairment + concurrent statin use: higher risk of rhabdomyolysis/mytoxicity.
If CrCl <15ml/min avoid IR preparations. If CrCl <60ml/min avoid MR preparations.
Monitor LFTs initially and at 3 months if used with statin.
HOWEVER, fibrates only recommended when patient cannot tolerate statin.
78
Hypertension stages
1. 140/90-149/99mmHg (clinic) or 135/85-149/94mmHg (ambulatory)
2. 160/100-180/120mmHg (clinic) or 150/95mmHg (ambulatory)
3. >180/120mmHg
79
When does hypertension require treatment?
Stage 1 -drug treatment if:
* Kidney disease
* Diabetes
* CVD
* QRISK3 >10%
* >80 + BP >150/90mmHg
Stage 2 - drug treatment
Stage 3 - medical emergency
80
Hypertension treatment pathway in individuals under 55 or with T2DM
1. ACEi/ARB
2. ACEi/ARB + CCB or thiazide-like diuretic
3. ACEi/ARB + CCB + thiazide-like diuretic
4. K+<4.5mmol/l = low dose spironolactone. K+>4.5 mmol/l = alpha or beta-blocker
81
Hypertension treatment pathway in patients >55 or of afro-caribbean origin.
1. CCB
2. CCB + ARB/ACEi or thiazide-like diuretic
3. CCB + ARB/ACEi + thiazide-like diuretic
4. K+<4.5mmol/l = low dose spironolactone. K+>4.5 mmol/l = alpha or beta-blocker
82
ACE inhibitor side effects
CCHARED
* Cough
* Hyperkalaemia
* Hepatic failure
* ANgioedema (face swelling)
* Renal impairment
* Dizziness and headaches.
83
ARBs side effects
* Hyperkalaemia
* Hepatic failure
* Renal impairment
* Dizziness and headaches
84
Interactions of ACE inhibitors
* Nephrotoxic drugs e.g., ARBs, NSAIDs, diuretics
* Hyperkalaemia e.g., heparins, NSAIDs, MRAs, ARBs, beta-blockers
* Volume depletion e.g., diuretucs
* Lithium - increased levels
85
Which beta-blockers are cardioselective? What does this suggest?
BAtMAN
* Bisoprolol
* Atenolol
* Metoprolol
* Acebutolol
* Nebivolol
Less likely to cause bronchospasm
86
Which beta-blockers are water soluble? What does this suggest?
CANS
* Celiprolol
* Atenolol
* Nadolol
* Sotalol
Less likely to cross BBB and cause nightmares.
| Think of cans of water
87
Which beta-blockers are intrinsic sympathomimetics? What does this suggest?
PACO
* Pindolol
* Acebutolol
* Celiprolol
* Oxprenolol
Less likely to cause cold extremities.
| Think of an ICE PAC-O
88
Beta-blockers side effects
* Bradycardia
* Hyperglycaemia
* Bronchospasms - contraindicated in asthma
* Can mask symptoms of hypoglycaemia
89
2 classes of CCBs
Dihydropyridine: Amlodipine, Felodipine, Lacidipine, Lercanidipine, Nifedipine.
Rate-limiting: Diltiazem, Verapamil.
90
CCB side effects
* GI discomfort
* Gingival hyperlasia (enlarged gums)
* Peripheral oedema
* Vasodilatory effects e.g., dizziness, headache (more Dihydropyridines)
* Complete atrioventricular block (more rate-limiting)
91
Risk factors for pre-eclampsia
* Kidney disease
* Diabetes
* Autoimmune diseases
* Hypertension
92
Treatment of hypertension in pregnancy
If BP >140/90mmHg
1. Labetalol
2. Nifedipine or Methyldopa
93
Target BP in pregnancy
135/85mmHg
94
Target BP aged <80
* Clinical: 140/90mmHg
* Ambulatory: 135/85mmHg
95
Target BP aged >80
* Clinical: 150/90mmHg
* Ambulatory: 145/85mmHg
96
Target BP in CKD (with/without T1DM)
| (Clinical)
- ACR 70+: 130/80mmHg
- ACR <70: 140/90mmHg
| If >80: 150/90mmHg as normal.
97
What is ACS/IHD?
A build up of atherosclerotic plaques which restrict arteries, reducing the supply of blood and oxygen to the heart.
98
Stable angina long-term prevention/treatment pathway
1. Beta-blocker (or RL-CCB)
2. Beta-blocker (or RL-CCB) (other one)
3. Beta-blocker + dihyd CCB
4. ISMN, nicorandil, ivabradune or ranolazine
99
Key side effect of nicorandil
GI and mucosal ulceration
100
Side effects of nitrates
Dizziness
Flushing
Headaches
Risk of falls
Oedema
101
How to achieve nitrate-free period using patches?
Remove patch for 8-12h a day.
102
When should GTN SL tabs be discarded?
8 weeks after opening bottle
103
Initial management of ACS
| Unstable angina/NSTEMI/STEMI
* Loading dose aspirin 300mg
* Pain relief: GTN +/- IV morphine
* Oxygen if required
* PCI (Stent) within 2 hours for **STEMI** (may be done later on for NSTEMI)
104
Unstable angina vs NSTEMI vs STEMI
* Unstable angina: partial blockage of artery leading to myocardial ischaemia.
* NSTEMI: partial blockage of artery leading to myocardial necrosis. Tests: elevated Troponin.
* STEMI: complete blockage of artery leading to myocardial necrosis. Tests: elevated troponin and ST zone on EG.
105
Long-term ACS management/secondary prevention
* DAPT: lifelong aspirin + 12 months of either clopidogrel, prasugrel, or ticagrelor (prasugrel if PCI).
* ACE inhibitor or ARB
* Beta-blocker for 12 months (lifelong in LVSD)
* High strength statin - usually atorvastatin 80mg.
106
Types of diuretics MOA and examples
* Thiazide: Inhibit sodium reabsorption in distal convoluted tubule e.g., Bendroflumethiazide and Indapamide
* Loop: Inhibit sodium reabsorption from ascending limb of the loop of Henle e.g., Furosemide, Bumetanide, Torasemide.
* Potassium-sparing diuretics: prevent sodium reabsorption in the distal tubule collecting duct e.g., amiloride, triamterene.
* Potassium-sparing diuretics + aldosterone antagonists: inhibit potassium secretion in the fistal tubule collecting duct e.g., spironolactone and eplerenone.
107
Difference in administration of different diuretics
Thiazide diuretics: Long-acting (last up ot 24h) so should be given early in the day to avoid sleep disruption.
Loop diuretics: last around 6 hours so can be given twice a day without interfering with sleep.
108
Key side effect of triamterene
Blue urine
109
Diuretics side effects
* Hyponatraemia
* Hypomagnesaemia
Loop + thiazide:
* Hypokalaemia
* Exacerbate diabetes
* Exacerbate gout
* Hypotension
Potassium-sparing:
* Hyperkalaemia
* Breast pain/tenderness and change in libido
110
Types of peripheral vascular disease
Occlusive peripheral vascular disease: caused by atherosclerosis and reduced by lifestyle changes, statins, and anti-platelets.
Vasospastic peripheral vascular disease (aka Raynaud's): avoid exposure to cold and stop smoking. May use nifedipine.
111
Initial management of ischaemic stroke
Once haemorrhagic stroke excluded:
* Aspirin 300mg OD for 2 weeks
* Alteplase - within 4.5h of onset of symtoms.
112
Long-term management/secondary prevention of ischaemic stroke.
* Antiplatelet therapy: Clopidogrel 75mg OD lifelong (or aspirin 75mg OD)
* PPI if necessary - NOT omeprazole with clopidogrel
* High-intensity statin
* Manage comorbidities e.g., DM, HTN, AF.
113
Initial management of haemorrhagic stroke
* Surgery to remove haematoma or relieve intracranial pressure.
* Stop/reverse any blood thinners
* Rapid blood lowering treatment for acute intracerebral haemorrhage within 6h if they have SBP of 150-220mmHg. This should NOT be used for structural causes, GCS score <6, neurosurgery to evacuate haematoma, or very large haematoma with poor prognosis.
114
When should pharmacological VTE prophylaxis be started in hospital if required?
Within 14 hours of admission
115
VTE prophylaxis in surgial patients
TED stockings - until patient is sufficiently mobile or discharged from hospital.
Pharmacological: generally 7 days post-surgery and/or mobilising sufficiently with:
- LMWH: usually
- * Unfractioned heparin: renal impairment
* Fondaparinux: lower limb immbolisation or pelvic fragility fractures.
116
Length of VTE prophylaxis after majot cancer surgery of the abdomen
28 days
117
Length of VTE prophylaxis after spinal surgery
30 days
118
VTE prophylaxis following elective hip replacement
One of:
* LMWH 10 days then 75mg aspirin 28 days
* LMWH for 28 days and stockings until discharge
* Rivaroxaban
119
VTE prophylaxis following elective knee replacement
One of:
* 75mg aspirin 214 days
* LMWH for 14 days and stockings until discharge
* Rivaroxaban
120
General medical patients VTE prophylaxis duration
If high risk, at least 7 days, or TEDS until mobile.
121
VTE prophylaxis in pregnancy
LMWH until discharge or there is no longer a risk of VTE, + if immobilised, use TEDS until mobile or discharged.
122
VTE prophylaxis for women who have given birth, had a miscarriage, or abortion in the past 6 weeks.
Start LMWH 4-8h after the event and continue for minimum 7 days
+ if immobilised, use TEDS until mobile or discharged.
123
Why is unfractioned heparin better than a LMWH in patients at high risk of haemorrhage?
Shorter half-life, so anticoagulant effect doesn't last as long.
124
VTE treatment pathway.
First choice: Apixaban or Rivaroxaban.
If unsuitable, either:
* LMWH for at least 5 days, followed by dabigatran or edoxaban.
* LMWH + warfarin for at least 5 days or until INR 2.0+ for 2 consecutive readings, followed by warfarin alone.
125
Duration of VTE treatment
* Distal (calf) DVT: 6 weeks
* Proximal DVT/PE: 3+ months (3-6 months in active cancer)
* Provoked DVT/PE: 3 months then stop if proviking factor resolved.
* Unprovoked DVT/PE: 3+ months
* Recurrent DVT/PE: longterm
126
Target INR
* 2-3 (2.5): VTEs, AF, cardioversion, MI, cardiopathy.
* 3-4 (3.5): mechanical heart valve or recurrent VTE.
127
What to do if INR is too high?
* INR 5-8 + no bleeding: withhold 1-2 doses.
* INR 5-8 + minor bleeding: stop warfarin + give IV phytomenadione
* INR >8 + no bleeding: stop warfarin + give oral phytomenadione
* INR >8 + minor bleeding: stop warfarin + give IV phytomenadione
* Major bleeding: stop warfarin + give IV phytomenadione and dried prothrombin.
Restart warfarin when INR <5
128
How often should INR be monitored
Every 1-2 days at initiation until stable, then every 12 weeks.
129
Warfarin side effects
* MHRA warning: skin necrosis and calciphylaxis - report painful skin rashes.
* Bruising
* Bleeding
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Warfarin antidote
Phytomenadione (Vitamin K1)
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Can warfarin be used in pregnancy?
No - teratogenic. Use contraception.
Especially avoid in 1st and 3rd trimester.
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Warfarin key interactions
* Vitamin K rich foods e.g., leafy greens: reduced warfarin efficacy i.e., decreased INR.
* Pomegranite & cranberry juice: increased INR.
* Miconazole (Daktarin oral gel): increased INR
* Tramadol: increased INR.
* CYP inhibitors (increased warfarin) and inducers (decreased warfarin).
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Warfarin tablet colours
* 0.5mg = white
* 1mg = brown
* 3mg = blue
* 5mg = pink
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How should warfarin be handled with minor surgery with low bleed risk?
Ensure INR <2.5 + restart within 24h.
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How should warfarin be handled with major surgery and high bleed risk?
Stop 3-5 days prior and give vitamin K of INR 1.5+ the day befor surgery.
If high VTE risk bridge with LMWH - stop 24h before and restart 48h after.
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How should warfarin be handled with emergency surgery?
- If can be delayed 6-12h give IV vitamin K
- If can't be delayed 6-12h give IV Vitamin K + dried prothrombin complex.
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DOAC dosing for VTE treatment
* Apixaban: 10mg BD 7 days then 5mg BD
* Rivaroxaban: 15mg BD 3 weeks then 20mg OD.
* Dabigatran (after 5 days LMWH): 150mg BD
* Edoxaban: 60mg OD
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Why are DOACs time sensitive?
Anticoagulant effects diminish within 12-24h so omitted or delayed doses can increase clotting risk.
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DOAC reversal agents
* Andexanet alfa - apixaban, rivaroxaban
* Idarucicizumab - dabigatran
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Pros and cons of unfractioned heparin vs LMWH:
Unfractioned heparin:
* Quick initiation and eliminiation which is ideal in patients with a high bleeding risk.
* Preferred in renal impairment
* Higher risk of heparin-induced thrombocytopenia
LMWHs:
* Preferred in pregnancy
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Unfractioned heparin antidote
Protamine sulphate
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Dose adjustments for edoxaban
* <61kg: 30mg OD
* Concurrent use of ciclosporin, dronedarone, erythromycin, ketoconazole: 30mg OD
* CrCl 15-50ml/min: 30mg OD
* CrCl <15ml/min is contraindicated.
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Dose adjustments for apixaban
* 2 of: age 80+, weight <61, Cr 133+: 2.5mg BD
* CrCl 15-29ml/min: 2.5mg BD
* CrCl <15: contraindicated
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Dabigatran dose adjustments
| For VTE treatment
* Normally: 150mt BD
* 75-79y: 110-150mg BD
* 80+: 110mg BD
* CrCl 30-50ml/min: 110-150mg BD
* CrCl <30ml/min: contraindicated
* Severe hepatic impairment/liver enzymes >2x ULN: avoid.
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Rivaroxaban dose adjustment
| For VTE prophylaxis
* CrCl 15-49ml/min: 15mg OD
* CrCl <15ml/min: contraindicated
