ACC Cardiac/ arrythmia drugs Flashcards
Clinical indications for O2? x3
- Hypoxaemia
- PTX: To accelerate resorption of pleural gas
- CO poisoning: to reduce half life of carboxyhaemoglobin
O2 MOA?
Increases the PO2 in alveolar gas.
In PTX: it reduces the fraction of nitrogen in alveolar gas
In CO poisoning, it competes with CO to bind with hb and shortens half life of carboxyhaemoglobin
O2 side effects/ warnings?
Lack of water vapour: dry throat
In T2RF/ COPD pts it results in high CO2 concentration causing resp acidosis, depressed consciousness and worsened tissue hypoxia
O2 Doses?
Acute setting: 15L/ min via non-rebreathe mask (60-80%)
28% for T2RF patients
Nasal cannulae (24-50%) flow rate 1-4L/min)
Nitrates clinical indication? X3
Short acting (GTN): Acute angina and ACS Long acting (Isosorbide mononitrate): angina prophylaxis where Bblockers and or CCB don't work IV nitrates: Pulmonary oedema- used in combo with furosemide and O2
Nitrates MOA?
Nitrates elimination?
Nitrates are converted to NO
NO increases cGMP synthesis and reduces intracellular Ca2+ in SM cells= relaxation
This causes venous and a little arterial vasodilation
This reduces cardiac work and myocardial O2 demand relieving angina and cardiac failure
Eliminated by liver and partly passed unchanged in the urine
SE of nitrates?
Headaches/ lightheadedness
Flushing
Hypotension
Sustained use= tolerance
Cautions/ contraindications of Nitrates
CI: severe AS pts= cv collapse bc the heart can’t increase CO sufficiently to maintain pressure in dilated vasculature
CI: Pts with haemodynamic instability and HTN
Nitrates interactions
Phosphodiesterase inhibitors e.g. sildenafil: enhance and prolong hypertensive effect of nitrates
Caution in pts already taking hypertensive medication= precipitate hypotension
GTN and Isosorbide dose?
Spray GTN for angina prophylaxis: 400-800mg under tongue prn
Spray GTN for angina treatment: 400-800mg under tongue- 5 min intervals- after 3 seek medical attention
IV GTN= solution containing 50mg in 50ml= 1mg/ml
ISMN: angina prophylaxis and adjunct in CHF = 20mg BID-TID, increase if necessary to 120mg in divided daily dose
How would you explain to the pt what the nitrates are for?
This medication is being prescribed to help you with your chest pain and or breathless.
You might develop a headache but this usually doesn’t last for long.
We normally advise patients to use GTN before an activity that might bring on your angina
As your BP can drop, it’s a good idea to sit down and rest for about 5 mins while taking them
How do you monitor nitrate efficacy?
Do symptoms resolve
When using IV infusion measure blood pressure frequently
Aspirin drug class and clinical indications x 3
Salicylates
ACS/ Acute Ischaemic stroke: rapid inhibition of platelet aggregation
Long term secondary prevention of thrombotic arterial events in patients with CV, cerebrovascular and PAD
To reduce risk of intracardiac thrombus and embolic stroke in AF
Aspirin MOA?
Aspirin elimination?
Irreversibly inhibits COX to reduce production of arachidonic acid
This reduces platelets aggregation and the risk of arterial occlusion
Antiplatelet effects of aspirin occur at low doses and last for a lifetime
Elimination: Effects of aspirin last for the lifetime of the platelet, urinated out
SE aspirin?
Gastrointestinal irritation
GI ulceration and haemorrhage
Hypersensitivity reactions= bronchospasm
Regular high-dose therapy will cause tinnitus
Life threatening in overdose: will cause hyperventilation, hearing changes, metabolic acidosis and confusion
Aspirin contraindications/ caution?
Children <16 due to risk of reye’s syndrome
Pt’s with aspirin hypersensitivity
Should be avoided in the 3rd trimester of pregnancy where prostaglandin inhibition may lead to premature closure of the ductus arteriosus
Caution: people with peptic ulcers, provide gastric protection
Gout pts: can trigger an acute attack
Aspirin interactions?
Interacts with other antiplatelet agents and increases risk of bleeding
Aspirin dose and route?
ACS: Should be prescribed as a once only loading dose of 300mg followed by a regular dose of 75mg daily
Acute ischaemic stroke: 300mg QD for 2 weeks before switching to 75mg
Long term prevention of thrombosis: Useful after an acute event or in people with AF, 75mg QD
Pregnant women at mod-high risk of pre-eclampsia: 75–150 mg once daily from 12 weeks gestation until the birth of the baby.
Max daily dose of 4g: take with food to minimise gastric irritation
What would you tell the pt when prescribing Aspirin?
Safety net: This drug aims to prevent heart attacks, stroke and to prolong life.
Watch out for indigestion of bleeding symptoms- seek medical advice if these occur
Atropine clinical indications X 4/ drug class?
Muscarinic antagonist- emergency drug
Intraoperative bradycardia
Symptomatic bradycardia due to acute overdose of bblockers
Treatment of poisoning caused by organophosphorous insecticide/ nerve agent
GI disorder caused by SM spasms
Atropine MOA?
Atropine metabolism/ elimination?
It binds to and inhibits muscarinic acetylcholine receptors producing a wide range of ACh effects- M1-M5 receptors
By the liver. 13-50% excreted unchanged in the liver
Atropine SEs? x6
Constipation, urinary retention and anhidrosis (elderly) Dizziness Photophobia (eye) Drowsiness Dry mouth Flushing
Atropine contraindications/ cautions?
Pts with: Acute closure glaucoma GI obstruction Paralytic ileus Pyloric stenosis Severe UC
Caution: adults: acute MI, arrhythmias, autonomic neuropathy and elderly with polypharmacy: 2 or more antimuscarinics= toxicity
Atropine interactions
add
Atropine dose and route
add
Indications for morphine (X4) and drug class
Rapid relief for acute severe pain e.g post op pain and MI
Relief of chronic pain where other 2 rungs of ladder failed
For relief of breathlessness in end of life care
To relieve breathlessness and anxiety in acute pulmonary oedema (used with oxygen, nitrates and furosemide)
It’s an opioid analgesic
Morphine MOA
Works mainly by binding to mu-opioid receptor: activation of descending inhibitory pathways of the CNS AND inhibition of the nociceptive afferent neurons of the PNS
Morphine SEs
Constipation: Mu receptor activation increases SM tone and reduces motility
N+V: from activated chemoreceptive trigger zone
Drowsiness
Respiratory depression: reduces respiratory drive
Confusion
Pupillary constriction: due to activation of Edinger-westphal nucleus
Neurological depression in higher doses
Itchy skin due to histamine release
Morphine interactions
Should not be used with other sedating drugs:
Antipsychotics
Benzodiazepines
TCAs
Morphine contra-indications/ cautions x3
Morphine relies on liver and kidneys for elimination. Dose should be reduced in hepatic failure and renal impairment
Morphine should not be given in resp failure unless for palliative purposes under senior guidance
AVOID in biliary colic patients as it may cause spasm of the sphincter of oddi
Morphine dose and route
Acute severe pain: IV 2-10mg- tailor to pain
Chronic pain: Oral immediate release morphine: 5mg every 4 hours
Breakthrough analgesia should be prescribed alongside regular treatment
Immediate release should be 1/6 the total regular daily dose
Ticagrelor drug class and indications?
p2y12 inhibitor/ antiplatelet drug
Prevention of Atherothombotic events in patients with ACS or history of MI (used with aspirin)
Ticagrelor MOA
Ticagrelor elimination?
Prevents platelet activation and aggregation by inhibiting P2Y12 Receptor antagonist
Eliminated by the liver
Ticagrelor SEs?
Constipation/ diarrhoea/ dyspepsia Haemorrhage Headache/ dizziness Hyperuricaemia/ gout/ gouty arthritis Skin reactions
Ticagrelor interactions
Interacts with many drugs and increases risk of bleeding (tyrosine kinase inhibitors/ anticoag meds) , bradycardia (beta blockers/ ccbs/ strong opioids) or ticagrelor toxicity
Ticagrelor contraindications/ cautions
Contraindicated in patients with:
active bleeding
history of intracranial haemorrhage
Use with cautions in patients with:
Asthma, bradycadia, COPD (DISCONTINUE 5 days before surgery), history of hyperuricaemia and second or 3rd degree block
Ticagrelor dose and route
ACS patients: Initially 180mg for 1 dose. Then twice daily 90mg for up to 12 months
Patients with history of MI: 60mg twice daily
What should be monitored in patients who have just started ticagelor?
Renal function- measured by U&Es
Enoxaparin (Dalta, Tinz and Fondaparinux) drug class and clinical indications
LMWH
VTE: LMWH- first choice drug for VTE prophylaxis in hospital inpatients.
DVT and PE
ACS: LMWH/ fonadaparinux are part of the first line therapy to improve revascularisation and prevent intracoronary thrombus progression
Enoxaparin and co MOA?
Elimination?
Generally heparins prevent the formation and propagation of blood clots
Unfractionated heparin activates antithrombin> inactivates clotting factor XA and thrombin
Enoxaparin preferentially inhibits factor XA
Fondaparinux is a synthetic compound that is similar to heparin
Elimination via kidneys half life 4.5 hours
LMWHs SEs?
Bleeding
Injection site reaction
Heparin induced thrombocytopenia (rare)
LMWH interactions?
Combining antithrombotic drugs increases risk of bleeding
Regarding bleeding caused by heparin therapy what’s the use of protamine?
Protamine can be given to reverse anticoagulation- this is only effective for unfractionated heparins
LMWH contraindications and cautions?
Should be used in caution with patients at increased risk of bleeding including those with
Clotting disorders , Severe uncontrolled hypertension,
Recent surgery or trauma
Heparins should be avoided around invasive procedures esp lumbar puncture and spinal anaesthesia
Should be used with caution in patients with renal impairment: use lower dose or unfractionated heparin instead
LMWH dose and route?
Usually given via subcut injection into abdominal wall. Don’t use the arm as there’s not enough flesh here
Prophylaxis of VTE: 40MG sc QD or Dalteparin 5000UNITS SC daily
VTE and ACS treatment: Unfractionated heparin may be given by IV infusion
What should you monitor while patient is on treatment of LMWH
FBC and renal profile should be checked
In prolonged therapy monitor platelet count
Adrenaline drug class and clinical indications? x3
It’s a sympathomimetic agent: a vasoconstrictor
Indications are
- In cardiac arrest
- Anaphylaxis
- To induce local vasoconstriction e.g. in endoscopy to control mucosal bleeding
Adrenaline MOA?
Potent agonist of the α1, α2, β1 and β2
adrenoceptors
α1-mediated: vasoconstriction of skin, mucosa and abdominal vessels
β1 mediated: increases chronotropy (HR), force of contraction (inotropy) and dromotropy (myocardial excitability)
β2 mediated: Vasodilation of vessels supplying heart and muscles. Also causes bronchodilation and suppression of inflammatory mediator release from mast cells
What do the following mean?
Positive chronotropy
Positive dromotropy
Positive inotropy
Positive lusitropy
Positive chronotropy (SA node) – increase heart rate
Positive dromotropy – faster conduction in AV node
Positive inotropy – stronger atrial and ventricular contractions
Positive lusitropy – greater relaxation to allow more blood in
Adrenaline onset time elimination?
3-5 mins. Excreted in the urine via the kidneys.
Adrenaline SEs
Think high speed!
Anxiety/ headache
Tremor/ anxiety palpitations
Can cause angina, MI and arrythmias esp in patients with existing heart disease
Adrenaline cautions/ contraindications
Should be given with caution in patients with existing heart disease
Combination adrenaline anaesthetic peps should not be used in areas supplied by an end artery (poor collateral supply)- vasoconstriction will cause necrosis
Adrenaline interactions?
Adrenaline + Bblockers= widespread vasoconstriction
Adrenaline dose and route?
CPR: 1 mg every 3–5 minutes as required, a 1 in 10 000 (100 micrograms/mL) solution is recommended
Acute hypotension in child: Initially 100 nanograms/kg/minute, adjusted according to response
Anaphylaxis adult: 500 micrograms, using adrenaline 1 in 1000 (1 mg/mL) injection, repeat dose after 5 minutes if no response
Anaphylaxis child 6months-5yrs/ 6-11ys/ 12-17yrs: 150mcg / 300mcg/ 500mcg: for all use 1mg/ml injection
Adenosine drug class and clinical indications?
Adenosine receptor agonist
First line drug for supraventricular tachycardia (e.g. WPW)
Adenosine MOA
Adenosine elimination
Acts on the G-protein coupled receptors and produces the following actions:
- Reduces frequency of spontaneous depolarisation which slows sinus rate and conduction velocity
- This all increases AV node refractoriness
Elimination: cleared from the plasma by cellular uptake
Adenosine SEs
Bradycardia
Asystole
Breathlessness and sometime sense of impending doom
Adenosine contraindications/ cautions?
Contraindicated in patients who won’t tolerate transient Bradycardic effects e.g. patients with
a. Hypotension
b. coronary ischaemia
c. decompensated heart failure
Can induce bronchospasm, avoid in patients with
a. Asthma
b. Copd
Use with caution in patients with recent myocardial infarction, heart transplant and bundle branch block
Adenosine interactions
Dipyridamole blocks cellular uptake of adenosine- effects last for longer
Theophylline, aminophylline and caffeine are competitive antagonists and reduce its effects
Adenosine dose and route?
Initially 6 mg, administer into central or large peripheral vein and give over 2 seconds
Cardiac monitoring required
Followed by 12 mg after 1–2 minutes and another 12 mg after 1-2 mins if no response
Amiodarone drug class and clinical indications?
Anti-arrhythmics
AF, Atrial Flutter, SVT
VT, Refractory VF and shock resistant VF
Amiodarone MOA
Amiodarone elimination
Effects are on myocardial cells
Blockade of sodium, calcium and potassium channels
Antagonism of alpha and B-adrenergic receptors: these effects reduce spontaneous depolarisation (automaticity), slow conduction velocity and increase resistance to depolarisation (refractoriness)
By interfering with AV node conduction, amiodarone reduces the ventricular rate in AF and atrial flutter
Elim: Hepatic metabolism and biliary excretion
Amiodarone SEs
Can cause hypotension during IV infusion
Lungs: Pneumonitis
Heart: Bradycardia and AV block
Liver: Hepatitis
Skin: Photosensitivity and grey discolouration
Thyroid abnormalities: due to it’s iodine content (amiodarone) : hypo and hyperthyroidism
Compared to the other drugs it causes little myocardial depression
Amiodarone contraindications and cautions
Severe HTN
Heart block
Active thyroid disease
Amiodarone interactions
Increases the plasma concentration of
- Digoxin
- Diltiazem
- Verapamil
This may increase the risk of bradycardia, AV block and HF. Doses of the drugs should be halved if amiodarone is started
Amiodarone dose and route
For arrhythmias, when nothing else works: 200 mg TID for 1 week, then reduced to 200 mg BID for a further week, followed by maintenance dose, usually 200 mg daily
Initially 5 mg/kg, to be given over 20–120 minutes with ECG monitoring
CPR: Initially 300 mg, dose to be given over at least 3 minutes
Metoprolol drug class and clinical indications
Beta blocker
Angina and HTN
Prophylaxis for HF
Arrhythmias
Migraine prophylaxis
Metoprolol MOA
Elimination
Beta 1 adrenergic receptor inhibitor
This decreases CO by producing negative chronotropic and inotropic effects
Elim: Absorbed in GIT. Metabolised by CYP2D6 and to a lesser extent CYP3A4
Excreted by the kidneys
Metoprolol SEs
As with all beta blockers:
Abdo discomfort Bradycardia Confusion Depression Diarrhoea Dizziness Dry eye
Metoprolol contraindications and cautions
Portal HTN (risk of deterioration in liver function) Psoriasis
Caution in combo with diltiazem or verapamil: risk of heart block
With bradycardia (<50bpm)
In diabetic pts with hypos: risk of suppressing hypoglycaemic symptoms
Metoprolol interactions
NSAIDS may reduce the ability of metoprolol to lower the patient’s blood pressure
Catecholamine-depleting medications, such as guanethidine or reserpine, can have an additive effect when taken with beta-blocking agents like metoprolol.
Metoprolol dose
HTN: 100mg QD (IR) 200mg (MR)
Angina: 50-100mg (B-TID). 200-400mg (MR)
FILL IN arrythmias and migraine prophylaxis bnf
https://bnf.nice.org.uk/drug/metoprolol-tartrate.html#cautions
