CV system Flashcards
Name some examples of a-blockers?
Doxazoin, Tamsulosin, alfuzosin
Name some common indications for a-blockers?
- Treatment for BPH, when lifestyle changes are insufficient. 5a-reductase inhibitors may be added in selected cases.
- As an add-on treatment in resistant hypertension
How do a-blockers work?
a1-adrenoreceptors are found mainly in smooth muscle, including in blood vessels and the urinary tract. Stimulation induces contraction, blockade induces relaxation. a1 blockers therefore cause vasodilation and a fall in BP, and reduced resistance to bladder outflow
What are the important adverse effects of a-blockers?
They can cause postural hypotension, dizziness and syncope. This is particularly prominent after the first dose
When should a-blockers not be used?
In patients with existing postural hypotension
What are the important interactions of a-blockers?
When combined with anti-hypertensives, can result is a large BP drop
May be necessary to omit doses of anti-hypertensives on the day a-blockers are started. This is particularly the case for B blockers, which inhibit the reflex tachycardia that forms part of the compensatory response to vasodilatation
How are a-blockers prescribed?
Doxazosin is licensed both for BPH and hypertension; it is typically started at a dose of 1mg daily and increased at 1-2 week intervals according to response
Tamsulosin is licensed for BPH only. It is given at 400mcg daily
Men with BPH often have hypertension so it can be given earlier in the treatment pathway for hypertension ‘killing 2 birds with 1 stone’
What advice would you give to patients about taking a-blockers?
Advise them to start taking the medicine at bedtime to minimise the impact of dizziness
What is adenosine used for?
A first-line diagnostic and therapeutic agent in supraventricular tachycardia (SVT), usually evident on an ECG as a regular, narrow-complex tachycardia
How does adenosine work?
Increases atrioventricular node refractiveness which breaks the re-entry circuit causing SVT
“Resets heart rhythm”
What are important adverse effects of adenosine?
Bradycardia and asystole
Feels like a sinking feeling in the chest, accompanied by breathlessness and a sense of impending doom
Only lasts for a couple of seconds
What are the warnings for prescribing adenosine?
Don’t prescribe for patients with hypotension, coronary ischaemia, decompensated heart failure
It may also induce bronchospam so avoid is asthmatics and caution with COPD
Are there by important interactions for adenosine?
Dipyridamole (anti platelet agent) increases its effect so the dose should be halved
Theophylline and aminophylline reduce its effect so may need higher dose
How is adenosine prescribed?
6mg IV once only
If ineffective give 12mg dose
Needs large-bore cannula in the antecubital fossa
Give quickly then flush with 20ml of saline
Effect is evident on cardiac monitor in 10-15 seconds
What are the common indications of adrenaline?
- Cardiac arrest
- Anaphylaxis
- Local vasoconstriction e.g. To control mucosal bleeding in endoscopy
How does adrenaline work?
It is a potent agonist of a1,a2,B1 and B2 adrenoceptors so has have fight or flight effects
What are the effects of adrenaline acting on:
a1
B1
B2?
a1- vasoconstriction of vessels supplying skin, mucosa, and abdominal viscera
B1- increases HR, force of contraction and myocardial excitability
B2- vasodilatation of vessels supplying the heart and muscles. Also bronchodilatation and suppression of inflammatory mediator release from mast cells
What are important adverse effects of adrenaline?
Adrenaline-induced hypertension
Anxiety, tremor, headache an palpitations
Angina, MI, arrhythmias
Are there any warnings for use of adrenaline?
No CIs to use in anaphylaxis or cardiac arrest
When used to induce vasoconstriction, it should be used with caution in patients with heart disease
Are there any important interactions for adrenaline use?
B-blockers
As the a1 mediated vasoconstriction is not opposed by B2 mediated vasodilatation
How is adrenaline prescribed?
In a shockable rhythm in cardiac arrest (VF or pulseless ventricular tachycardia) , adrenaline is given 1mg IV after the 3rd shock and repeated every 3-5 mins
In a non-shockable rhythm, adrenaline 1mg IV is given instantly, and repeated every 3-5 mins
In anaphylaxis, give 500mcg IM and repeat after 5 mins if necessary
Can be mixed with LA if being used sub-cut to induce local vasoconstriction
What are some examples of aldosterone antagonists?
Spironolactone, eplerenone
What are the common indications for aldosterone antagonists?
- Ascites and oedema due to liver cirrhosis- spironolactone is 1st line diuretic
- Chronic heart failure- moderate severity, usually as an addition to BB, ACEi/ARB
- Primary hyperaldosteronism- for patients awaiting surgery or for whom surgery is not an option
How do aldosterone antagonists work?
They inhibit the effect of aldosterone by competitively binding to the aldosterone receptor- increasing sodium and water excretion and potassium retention
What are important adverse effects of aldosterone antagonists?
Hyperkalaemia- which can lead to muscle weakness, arrhythmias and cardiac arrest
Gynaecomastia from spironolactone
Liver impairment and jaundice which can cause Stevens-Johnson syndrome
Which patients are aldosterone antagonists contraindicated or warned in?
Those with severe renal impairment, hyperkalaemia and Addison’s disease
They can also cross the placenta during pregnancy so should be avoided in pregnant and lactating women
Are there any drugs that interact with aldosterone antagonists?
Those that elevate potassium- ACEi, ARBs
Could be beneficial in heart failure though
How are aldosterone antagonists prescribed?
Orally, should be taken with food
Usually a single daily dose, e.g. Spironolactone 100mg daily for ascites compared to 25mg daily for heart failure
How should be aldosterone antagonists be monitored?
Renal function and serum potassium
Monitor efficacy through clinical improvement e.g reduction of ascites
What is amiodarone used for?
Used in tachyarrhythmias (AF, atrial flutter, SVT, VT and VF)
It is used when other drugs haven’t worked
How does amiodarone work?
Blockades sodium, potassium and calcium channels, and antagonises a- and B-adrenergic receptors
These reduce spontaneous conduction, slow conduction velocity and increase resistance to depolarisation (refractoriness)
What are the adverse effects of amiodarone?
Causes relatively little myocardial depression
Can cause hypotension
When taken chronically it can cause pneumonitis, bradycardia, hepatitis, thyroid abnormalities (due to iodine content), photosensitivity and grey discolouration
What are the warnings surrounding amiodarone?
Should be avoided in patients with severe hypotension, heart block and active thyroid disease
What are the important interactions with amiodarone?
Reacts with many- notably digoxin, diltiazem and verapamil which can increase risk of bradycardia and AV block
How is amiodarone prescribed?
In cardiac arrest, it is given for VF or pulseless VT, 300mg IV, followed by 20ml of 0.9% saline or 5% glucose as a flush
How is amiodarone administered?
Given as a bolus injection in cardiac arrest
Outside ca, should be given via a central line if repeat infusions are administered
Should be continuous cardiac monitoring
Name some examples of angiotensin receptor blockers?
Losartan, candasartan, irbesartan
What are ARBs indicated for?
Generally used when ACEis are not tolerated due to cough
- Hypertension
- Chronic heart failure
- Ischaemic Heart Disease
- Diabetic nephropathy and CKD with proteinuria
How do ARBs work?
They block the action of angiotensin II on the angiotensin type 1 (AT) receptor
What are the adverse effects of ARBs?
They can cause hypotension, hyperkalaemia and renal failure
They don’t cause a cough as they don’t affect the bradykinin mechanism
Which patients are ARBs warned in?
Should be avoided in patients with renal artery stenosis or AKI, and cautioned in women who could be pregnant and those who are breastfeeding
What are the important interactions of ARBs?
Avoid potassium elevating drugs- K-sparing diuretics, potassium supplements
The combination of NSAIDs with ARBs increases the risk of nephrotoxicity
How are ARBs prescribed?
Orally
E.g losartan 12.5mg daily in HF or 50mg daily in other indications
Start low and titrate up
How are ARBs taken?
Can be taken with or without food, it is best to take the first dose before bed to avoid reduce symptomatic hypotension
What tests need to be done before and during ARB treatment?
U&Es, renal function before and 1-2 weeks into treatment and after increasing the dose
When should ARBs be stopped?
When serum creatinine rises more than 30% or the eGFR falls more that 25%
If serum potassium goes above 5, firstly stop nephrotoxic drugs and if it continues to be high, reduce the dose of the ARB
What are examples of ACE inhibitors?
Ramipril, lisinopril, perindopril
What are the clinical indications for ACE inhibitors?
- Hypertension
- Chronic heart failure
- Ischaemic heart disease
- Diabetic nephropathy and CKD
How do ACE inhibitors work?
Prevent the conversion of angiotensin I to II.
In turn it lowers BP, slows progression of CKD and reduces venous return (has benefits in HF)
What are the important adverse effects of ACEi?`
Hypotension, persistent dry cough and hyperkalaemia
They can cause or worsen renal failure
Rare side effects include angioedema and anaphylactoid reactions
What are the warnings for taking ACEi?
Should be avoided in patients with renal artery stenosis or AKI, in women who could be pregnant or are breastfeeding
What are the important interactions for ACE inhibitors?
Avoid potassium-elevating drugs including potassium sparing diuretics and K supplements
The combination of an NSAID and ACEi increases the dose of nephrotoxicity
How are ACE inhibitors prescribed?
Orally
A common choice is Ramipril 1.25mg daily in heart failure or nephropathy, or 2.5mg daily in most other indications
This is titrated up to a max of 10mg daily over a period of weeks
How are ACE inhibitors taken?
With or without food
It is best to take the first dose before bed to reduce symptomatic hypotension
How are ACE inhibitors monitored?
Monitor efficacy clinically
For safety, check U&Es and renal function before starting treatment. Repeat these 1-2 weeks into treatment and after increasing the dose
When should ACE inhibitors be stopped/ changed?
Stop ACEi if the serum creatinine conc rises more than 30% or the eGFR falls more than 25%
If serum potassium rises above 5, stop any nephrotoxic drugs. If it continues to remain high, reduce the dose of the ACEi
Name some examples of antimuscarinics used for CV and GI causes?
Atropine, hycosine bromide, glycopyrronium
What are the indications for antimuscarinics for CV and GI causes?
- Atropine is used as a first-line treatment in the management of severe or symptomatic bradycardia to increase heart rate
- Treatment for IBS (particularly hycosine bromide) due to their anti-spasmodic effect
- Reducing copious respiratory secretions in the dying patient (hycosine bromide)
How do antimuscarinics work?
The are a competitive inhibitor of acetylcholine at the muscarinic receptor
As a result, they increase HR and conduction, reduce smooth muscle tone and peristaltic contraction, including the gut and urinary tract, and reduce secretions from glands in the resp tract and gut
In the eye they cause relaxation of the pupillary constrictor and ciliary muscles
What are the important adverse effects of antimuscarinics?
Tachycardia, dry mouth, constipation, urinary retention (in patients with BPH), blurred vision
‘Can’t see, can’t wee, can’t shit, can’t spit’
Some antimuscarinics have central effects, which may precipitate drowsiness and confusion, particularly in the elderly
What are the warnings for taking anti-muscarinics?
Should be used in caution in patients susceptible to acute-closure glaucoma, in whom they can precipitate a dangerous rise in intraocular pressure
Cautioned in patients with increased risk of arrhythmias
What are the important interactions with antimuscarinics?
Others with anti-muscarinic effects, such as tricyclic antidepressants
How are anti-muscarinics prescribed?
For bradycardia, atropine is usually preferred and given IV with incremental doses (e.g. 500mcg every 1-2 mins) until an acceptable HR is reached (some practitioners recommend no less than 600mcg as any less can SLOW the HR)
For IBS, taken orally e.g HB (Buscopan) 10MG 8-hourly- available w/o a prescription
For resp secretions, hycosine butylbromide or hycosine hydrobromide is given subcut
Name some examples of anti-platelets/ ADP-receptor antagonists?
Clopidogrel, icagrelor, prasugrel
What are anti-platelets indicated for?
MORE CARDS + ASPIRIN CARDSN IN BLOODS DECK
- Treatment of ACS (with aspirin)
- To precvent occlusion of coronary artery stents (with aspirin)
- Long term CV secondary prevention of thrombotic arterial events
Name some examples of B-blockers?
Bisoprolol, atenolol, propranolol, metoprolol, carvedilol
What are B-blockers used for?
- Ischaemic heart disease- improve symptoms and prognosis associated with angina and ACS
- Chronic heart failure
- AF- reduce ventricular rate and maintain sinus rhythm
- SVT- to restore sinus rhythm
- Hypertension- may be used with other therapies are insufficient or inappropriate
How do B blockers work?
They reduce the force of contraction and speed of conduction in the heart
They also prolong the refractory period of the AV node to slow the ventricular rate in AF
They also reduce BP by reducing renin secretion in the kidney
What are the adverse effects of B-blockers?
They commonly cause fatigue, cold extremities, headaches and GI disturbances e.g. nausea
They can cause sleep disturbances and nightmares
They may cause impotence in men
What are the warnings surrounding B-blockers?
Avoid in patients with asthma as they can cause bronchospasm
They should be avoided in patients who are haemodynamically unstable and are contraindicated in heart block
B blockers generally require dose reduction in hepatic failure
How are beta blockers prescribed?
Orally
Dose varies according to indication
When starting, you should chose a drug with a short half-life so it will be more responsive to dose adjustments quicker
e.g. Metoprolol 12.5mg 8-hourly initially, later increased to 25mg 8-hourly
Should be taken at roughly the same time each day
Name some examples of calcium channel blockers?
amlodipine, nifedipine, diltiazem, verapamil
Name some common indications for CCBs?
- Amlodipine and nifedipine are used for the 1st and 2nd line treatment of hypertension, to reduce the risk of stroke and MI
- Control stable angina
- Diltiazem and verapamil are used to control cardiac rate in people with SVT, atrial flutter and AF
How do CCBs work?
They decrease calcium ion entry into vascular and cardiac cells, reducing intracellular calcium conc. This causes relaxation and vasodilation in arterial smooth muscle, lowering arterial pressure
In the heart, the reduce myocardial contractility. They suppress cardiac conduction, particularly across the AV node, slowing ventricular rate and myocardial O2 demand- preventing angina
What are the different classes of CCBs?
Dihydropyridines- amlodipine and nifedipine, relatively selective for vasculature
Non-dihydropyridines- more selective for the heart, verapamil being the most cardioselective. Diltiazem also has some effect on blood vessels
What are the important adverse effects of CCBs?`
Amlodipine and nifedipine- ankle swelling, flushing, headache, palpitations
Verapamil- most commonly causes constipation, and less commonly bradycardia, heart block and cardiac failure
Diltiazem- can cause any of the above SEs
What are the warnings surrounding CCBs?
Verapamil and diltiazem should be used in caution in patients with poor left ventricular function as they can precipitate or worsen heart failure. Should be avoided in people with AV nodal conduction delay
Amlodipine and nifedipine should be avoided in patients with unstable angina as vasodilation causes a reflex increase in contractility and tachycardia, which increases myocardial O2 demand
In patients with severe aortic stenosis, amlodipine and nifedipine should be avoided as they can provoke collapse
What do CCBs interact with?
Non-dihydropyridine CCBs should not be prescribed with beta-blockers except under close supervision, as they are both negatively inotropic and can cause HF, bradycardia and even asystole
How are CCBs prescribed?
Usually taken orally
Amlodipine has a plasma half-life of 35-50 hours and is suitable for once-daily administration
By contrast, nifedipine has a half-life of 2-3 hours, verapamil (2-8 hours) and diltiazem (6-8 hours)
Diltiazem and nifedipine are available as SR 8-hourly, and MR taken 12-hourly
Example regimens:
Hypertension- amlodipine 5-10mg OD
Angina- diltiazem MR 90mg orally 12-hourly
Supraventricular arrhythmias- verapamil 40-120mg 8-hourly
How are CCBs monitored?
BP monitoring for hypertension
Enquire about chest pain for angina
Pulse rate from examination or ECG
What is digoxin used for?
- In AF and atrial flutter, it is used to reduce the ventricular rate. However a BB or CCB is usually more effective
- In severe heart failure, it is an option in patients who are already on an ACEi
How does digoxin work?
It is negatively chonotropic (reduces the heart rate) and positively inotropic (increases force of contraction)
In AF it increases vagal tone (parasympathetic) which reduces contraction at the AV node. However this can be lost in stress and failure exercise, so it is rarely used on its own
In heart failure, it increases contractile force by directly affecting the myocytes, causing Ca to accumulate in the cell
What are the important adverse effects of digoxin?
Bradycardia, GI disturbance, rash, dizziness, visual disturbance (blurred or yellow vision)
It has a narrow therapeutic index meaning the toxic dose is close to the therapeutic dose. Toxicity can cause a wide range of arrhyhmias
What are the warnings for taking digoxin?
It can worsen conduction abnormalities, so is contraindicated in second-degree heart block and intermittent complete heart block
It should not be used in patients with or at risk of ventricular arrhythmias
The dose should be reduced in renal failure, as digoxin is eliminated by the kidneys
Certain electrolyte abnormalities can increase the risk of digoxin toxicity, such as hypokalaemia, hypomagnesaemia and hypercalaemia
What are the important interactions of digoxin?
Loop and thiazides diuretics can increase the risk of digoxin toxicity by causing hypokalaemia
Amiodarone, CCBs, spironolactone and quinine can all increase plasma conc of digoxin and therefore increase toxicity
How is digoxin prescribed?
Available as an oral or IV preparation
The effect of IV digoxin is 30 mins, whereas 2 hours following oral
A loading dose is required for rapid effect- 500mcg of digoxin followed by 200-500mcg 6 hours later, depending on response
There after, the usual maintenance dose is 125-250mcg daily
What does an ECG show for a therapeutic dose?
ST-segment depression (the reverse tick sign)
Name some examples of loop diuretics
Furosemide, bumetanide
What are the indications for loop diuretics?
- For relief of breathlessness in acute pulmonary oedema in conjunction with oxygen and nitrates
- For symptomatic treatment of fluid overload in chronic heart failure
- For symptomatic treatment of fluid overload in other oedematous states e.g. Due to renal disease or liver failure
How do loop diuretics work?
They act of the ascending limb of the loop of Henle, where they inhibit the Na+/K+/2Cl- co-transporter
This prevents these ions leaving the lumen for the epithelial cells, so has a diuretic effect
In addition, they also have a direct effect on blood vessels, causing dilatation of capacitance veins. In acute heart failure, this reduces preload and improve some contractile function of the ‘overstretched’ heart muscle
What are the important adverse effects of loop diuretics?
Dehydration and hypotension
You can associate loop diuretics with almost any low electrolyte state
At high doses, loop diuretics can also lead to tinnitus and hearing loss
What are the warnings for loop diuretics?
They are contraindicated in patients with severe hypovolaemia or dehydration
They should be used with caution in patients at risk of hepatic encephalopathy (where hypokalaemia can cause or worsen coma) and in pts with severe hypokalaemia or hyponatraemia
Taken chronically, they can worsen gout
What are the importantly interactions for loop diuretics?
They have the potential to affect drugs that are excreted by the kidneys e.g. Lithium levels are increased due to reduced excretion
Increased risk of digoxin toxicity due to diuretic-associated hypokalaemia
They can increase the ototoxicity and neohrotoxiciyy of aminoglycosides
How are loop diuretics prescribed?
They are available in oral and IV preparations
In the management of acute pulmonary oedema, you usually prescribe the initial dose of the loop diuretic IV, due to its more rapid and reliable effect. A typical dose is furosemide 40mg IV
Then may need additional bonuses or regular oral medication
When should oral maintenance doses of loop diuretics be prescribed?
Taken in the morning, with 2nd dose in early afternoon, to avoid nocturia
How are loop diuretics monitored?
Improvement in symptoms, tachycardia, hypertension and oxygen requirement
In longer term therapy, monitor symptoms, signs and body weight
For safety, regularly monitor serum sodium, potassium and renal function particularly in the 1st few weeks
Name some examples of thiazide and thiazide-like diuretics?
Bendroflumethazide, indapamide, chlortalidone
What are thiazides diuretics used for?
- As an alternative treatment for hypertension where a CCB would otherwise be used; bunks unsuitable due to oedema or there are features heart failure
- Add-on treatment for hypertension in patients whose BP is not adequately controlled by a CCB plus a ACEi/ARB
How do thiazide diuretics work?
They inhibit the Na+/Cl- co-transporter in the distal convoluted tubule of the nephron. This prevents reabsorption of sodium and its osmotically associated water. This resulting diuresis causes an initial fall in extracellular fluid volume. Over time, compensatory change from the RAS tends to reverse this. The longer-term anti hypertensive effect may be mediated by vasodilatation
What are the important adverse effects of thiazide diuretics?
- Preventing sodium reabsorption from the nephron can cause hyponatraemia
- This can also lead to hypokalaemia, which in turn can lead to cardiac arrhythmias
- Can also cause impotence in men
What are the warnings surrounding thiazide diuretics?
They should be avoided in patients with hypokalaemia and hyponatraemia. As they reduce uric acid excretion, they may precipitate acute attacks in patients with gout
What are the important interactions with thiazide diuretics?
They effectiveness may be reduced by NSAIDs (not aspirin though)
Should not be combined with other potassium lowering drugs such as loop diuretics
Why is combining ACEi/ARBs and thiazide diuretics useful?
Thiazides cause hypokalaemia
ACEi/ARBs cause hyperkalaemia
They also have a synergistic BP lowering effect, therefore combination is useful for BP control and maintaining potassium balance
How are thiazides prescribed?
Orally, best taken in the morning so it doesn’t wake them up at night needing a wee
Indapamide (e.g. 2.5mg daily) and chlortalidone (12.5-25mg daily) are recommended for hypertension
What should be monitored during prescription of thiazide diuretics?
Measure patients BP and severity of oedema
Measure the patient’s serum electrolyte concentrations before starting the drug, at 2-4 weeks into therapy, and after any change in therapy that might alter electrolyte balance
What is lidocaine indicated for?
- Local anaesthetic e.g. urinary catheterisation and minor procedures e.g. suturing
- Uncommonly as an anti-arrhythmic drug in VT and VF refractory to electrical cardioversion
How does lidocaine work?
Blocks voltage-gated sodium channels on the surface membrane
In the heart, it reduces the action potential, slows conduction velocity and increases the refractory period. These effects may terminate VT and improve the chances of successfully treating VF
What are the important adverse effects of lidocaine?
Initial stinging sensation
Also drowsiness, restlessness, tremor and fits in systemic administration
In overdose it can cause hypotension and arrhythmias
What are the warnings with lidocaine?
It depends heavily in hepatic blood from for its elimination therefore a lower dose should be used in states of reduced cardiac output
What are the important interactions with lidocaine?
As the duration of action of LA depends on how long they stay in contact with the neurons, co-administration produces a desirable interaction that may prolong the LA effect
How is lidocaine prescribed?
For urinary catheterisation, it is a gel with an antiseptic agent- called Instillagel (dose is 6-11mL in the once-only section)
For minor procedures, usually use a 1% (10mg/mL) solution of lidocaine hydrochloride. The max dose is 200mg or 3mg/kg, whichever is lower (7mg/kg or up to 500mg is permitted with it is combined with adrenaline)
Name some examples of nitrates?
Isosorbide mononitrate, glyceryl trinitrate
What are nitrates used for?
- Short-acting nitrates e.g. glyceryl trinitrate are used in the treatment of acute angina and chest pain associated with acute coronary syndrome (ACS)
- Long-acting nitrates e.g. isosorbide mononitrate are used for the prophylaxis of angina where a B-blocker and/or a calcium channel bocker are insufficient or not tolerated
- IV nitrates are sued in the treatment of pulmonary oedema, usually in combination with furosemide and oxygen
How do nitrates work?
Nitrates are converted into (NO. NO increases cyclic guanosine monophospate (cGMP) synthesis and reduces intracellular Ca2+ in vascular smooth muscle cells, causing them to relax. This results in venous and, to a lesser extent, arterial vasodilatation.
Relaxation of the venous capacitance vessels reduces cardiac preload and left ventricular filling. These effects reduce cardiac work and myocardial oxygen demand, relieving angina and cardiac failure
Nitrates can relieve coronary vasospasm and dilate collateral vessels, improving coronary perfusion
What are the important adverse effects of nitrates?
As vasodilators, nitrates commonly cause flushing, headaches, light-headedness and hypotension.
Sustained use of nitrates can lead to tolerance, with reduced symptom relief despite continued use. To prevent this, time doses to ensure that there is a ‘nitrate-free period’ every day during a time of inactivity, usually overnight. E.g take doses morning and early afternoon rather than morning and night
What are the warnings surrounding nitrates?
They are contraindicated in patients with severe aortic stenosis, in whom they may cause cardiovascular collapse
Nitrates should also be avoided in patients with haemodynamic instability, particularly hypotension
What are the important interactions with nitrates?
They must NOT be used with phosphodiesterase (PDE) inhibitors (e.g. sildenafil) because these enhance and prolong the hypotensive effects of nitrates
They should also be used in caution in patients take antihypertensive medication
How are nitrates prescribed?
GTN is taken sublingually as tablets or spray for immediate relief of chest pain
In patients with ACS or heart failure, it is prescribed as a continuous IV infusion. ISMN has a plasma half-life of 4-5 hours and is prescribed 2-3 times a day as immediate-release tablets for the prevention of current angina. ISMN is also available as MR tablets or transdermal patches, which are prescribed once-daily
How is GTN administered?
Usually administered as 50mg in 50mL (1mg/mL). Give nursing staff clear instructions on the starting dose e.g 1ml/hr. You should provide instructions on how to increase the dose to relieve symptoms e.g. increase rate by 0.5mg/hour every 15-20 mins until chest pain is relieved while avoiding hypotension (systolic BP >90mmHg)
What should be monitored during nitrate prescription?
The best indicator of efficacy are the patients symptoms. When administering nitrates by IV infusion, blood pressure should be monitored frequently, and the infusion rate adjusted to ensure the systolic BP does not drop below 90mmHg
Name some examples of strong opioids
Morphine, oxycodone
What are strong opioids prescribed for?
- Rapid relief of acute severe pain, including post-operative pain and pain associated with acute MI
- Relief of chronic pain, when paracetamol, NSAIDs and weak/moderate opioids are insufficient
- Relief of breathlessness in the context of end-of-life care
- Relief
How do strong opioids work?
Opiates- morphine
Synthetic analogues- oxycodone
They work by activating opioid u-receptors in the CNS. They reduce neuronal excitability and pain transmission, therefore reducing sympathetic nervous system- which can also reduce cardiac work and oxygen demand in acute MI and pulmonary oedema
What are the important adverse effects of strong opioids?
- They cause respiratory depression by reducing respiratory drive. This may cause euphoria and detachment, and in higher doses, neurological depression
- Can cause N&V at the beginning of use
- Pupillary constriction can occur
- Constipation due to increased smooth muscle tone and reduced motility
- Tolerance and dependence over time, withdrawal reaction
What are the warnings surrounding opioids?
Doses should be reduced in hepatic failure and renal impairment and in the elderly
Don’t give opioids in resp failure except under senior guidance e.g. palliative care
Avoid opioids in biliary colic, as they may cause spasm of the sphinctor of Oddi, which may worsen pain
What are the important interactions for strong opioids?
They should ideally not be used with other sedating drugs e.g. antipsychotics, benzodiazepines, TCAs
How are strong opioids prescribed?
Acute severe pain- IV morphine 2-10mg
Chronic pain- oral route. Immediate release oral morphine is preferred initially (e.g. Oramorph 5mg every 4 hours). Then, having found the optimum dose, this is converted to a MR form (e.g. MST Continus 15mg every 12 hours). Alongside regular treatment, ‘breakthrough analgesia’ should be prescribed. Prescribe Oramorph IM about 1/6th of the total daily regular dose (e.g. 5mg 2-hourly) in the as-required section
What can be given for the nausea and constipation experienced with opioid prescription?
Metocloproamide for nausea
Senna for constipation
What are the clinical features of opioid withdrawal?
Anxiety, pain, breathlessness, pupil dilatation, cool and dry skin (hence the phrase ‘cold turkey’)
