Cardio drugs:
Adenosine injections:
Mode of action: slows conduction time through the AV node and can interrupt the re-entry
pathways through the AV node, resulting in the restoration of normal sinus rhythm in patients
with paroxysmal supraventricular tachycardia (PSVT). It deactivates adenyl cyclase thus
decreases cAMP thus K+ channels open and Ca2+ channels close causing hyperpolarisation
of cell membrane so kinda resets the rhythm.
Indication: rapid reversion of paroxysmal supraventricular tachycardias
Side effects: Abdominal discomfort; arrhythmias; atrioventricular block; chest discomfort;
chest pain (discontinue); dizziness; dry mouth; dyspnoea; flushing; headache; hypotension
(discontinue if severe); pain; paraesthesia; throat discomfort
Therapeutic evaluation:
Interactions: https://bnf.nice.org.uk/interaction/adenosine-2.html
Monitoring: Monitor ECG and have resuscitation facilities available.
Education:
Adenosine is most commonly used to terminate supraventricular
tachycardias. The effects of adenosine are enhanced by
dipyridamole (antiplatelet agent) and blocked by theophyllines. It should
be avoided in asthmatics due to possible bronchospasm.
Mechanism of action
causes transient heart block in the AV node
agonist of the A1 receptor in the atrioventricular node, which
inhibits adenylyl cyclase thus reducing cAMP and causing
hyperpolarization by increasing outward potassium flux
adenosine has a very short half-life of about 8-10 seconds
Adenosine should ideally be infused via a large-calibre cannula due to it's
short half-life,
Adverse effects
chest pain
bronchospasm
transient flushing
can enhance conduction down accessory pathways, resulting in
increased ventricular rate (e.g. WPW syndrome)
Digoxin:
,Mode of action: a cardiac glycoside. HFIt increases the force of cardiac muscle contraction
due to inhibition of the Na+/K+ ATPase pump which leads to increase intracellular calcium
concentrations so more calcium will be released during contraction. Supraventricular
arrythmias decreases conduction through the atrioventricular node which slows the
ventricular rate in atrial fibrillation and flutter. Also stimulates vagus nerve
Indication: heart failure, supraventricular arrythmias, supraventricular tachycardia.
Contraindication: ventricular fibrillation
Side effects: arrythmias, sinus bradycardia, Nausea, vomiting, diarrhea, lower stomach pain,
dizziness, drowsiness, headache, blurred/yellow vision, depression , skin rash. Highlighted=
most common Symptoms of heart problems including: fluttering, pounding or pain in your
chest, feeling your heart skips a beat, dizziness or fainting
Interactions: amiodarone, quinidine, verapamil, diltiazem, spironolactone (competes for
secretion in distal convoluted tubule therefore reduce excretion), ciclosporin. Also drugs
which cause hypokalaemia e.g. thiazides and loop diuretics. All of these increase toxicity
Monitoring: digoxin has a narrow therapeutic index. Plasma potassium needs to be regularly
monitored
Education:
Toxicity:
Plasma concentration alone does not determine whether a patient has developed
digoxin toxicity. Toxicity may occur even when the concentration is within the
therapeutic range.
Features:
o generally unwell, lethargy, nausea & vomiting, anorexia, confusion, yellow-
green vision
o arrhythmias (e.g. AV block, bradycardia)
o gynaecomastia
Management:
o Digibind
o correct arrhythmias
o monitor potassium
Here this is in a normal cell
where when there is an action
potential, the calcium L type
channel opens and calcium
enters and binds to the RyR
which causes calcium release
from the SR.
In relaxation, the calcium that
was in the cell eaves mainly
thro the Na+/Ca2+ outside of
the cell.
In digoxin, blocks the blue
receptor (which is essential to
keep sodium low in the cell and
,thus allows the function on the sodium/ calcium pump). When the sodium/ k+ is inhibited,
the intracellular sodium conc is higher thus this will lower the ability of the sodium/ calcium
pump to remove calcium from inside the cell. So more calcium will be pumped in the sr in
response to try to remove NA out of the cell. So now we have more calcium in the SR than
before so when an action potebtial arrives, more ca2+ will be released from the sr and thus
greater contraction force.
Patient:
Digoxin works by slowing down the rate at which your heart beats but also strengthens the
force of your heartbeat. When your heart rate is brought down to normal, your heart becomes
efficient again and your symptoms usually improve.
This drug is prescribed for heart failure and some other heart conditions.
Digoxin can cause unwanted side-effects although not everyone experiences them:
feeling dizzy
feeling sick
diarrhoea
skin rash
blurry/yellow vision or Symptoms of heart problems including: fluttering, pounding
or pain in your chest, feeling your heart skips a beat, dizziness or fainting stop and
seek urgent medical advise
Make sure that you take the right dose.
Plasma potassium needs to be regularly monitored
beta blockers:
ALL- patient:
Beta-blockers work by blocking the transmission of certain nerve impulses. Normally these
impulses send signals to the heart to increase the force and rate of it’s contraction so by
giving this medication, we block this signals which slows down the rate or the heart and the
force of contraction reducing the load on the heart. Thus the heart will work more efficiently.
The ends of some nerves release a chemical (neurotransmitter) called noradrenaline when the
nerve is stimulated. This chemical then stimulates beta-adrenergic receptors. These receptors
are tiny structures which occur on cells in various parts of the body, including the heart,
brain, and blood vessels. When these receptors are stimulated, they cause various effects. For
example, nerve impulses to the heart can stimulate beta-adrenergic receptors on heart cells.
This causes an increase in the force and rate of the heartbeat. The beta-blocker medicine 'sits'
on beta-adrenergic receptors and stops (blocks) the receptor from being stimulated. So, for
example, if beta-adrenergic receptors in the heart are blocked, the force and rate of the
heartbeat are reduced.
Most people who take beta-blockers have no side-effects, or only minor ones. However,
because of their action in various parts of the body, some people have unwanted side-effects.
For example:
, Sometimes the heart rate can go too slowly. This can make you dizzy or feel faint.
If you have diabetes you need to be aware that beta-blockers may dull the warning
signs of a low blood sugar level (hypoglycaemia - often called a hypo). For example,
you may not develop the sensation of rapid, irregular or forceful heartbeats
(palpitations) or tremor, which tend to occur as the blood sugar is going too low.
Some people develop cool hands and feet when taking beta-blockers. This is because
they can narrow (constrict) small blood vessels and reduce the circulation to the skin
of the hands and feet.
Tiredness, depression, inability to achieve a proper erection (impotence).
The most common side effects are dizziness, tiredness and headaches
Monitor lung function in obstructive
Bisoprolol
Mode of action: Bisoprolol is a competitive, cardioselective β1-adrenergic antagonist. When
β1-receptors (located mainly in the heart) are activated by adrenergic neurotransmitters such
as epinephrine, both the blood pressure and heart rate increase, leading to greater
cardiovascular work, increasing the demand for oxygen. Bisoprolol reduces cardiac workload
by decreasing contractility and the need for oxygen through competitive inhibition of β1-
adrenergic receptors.
Bisoprolol is also thought to reduce the output of renin in the kidneys, which normally
increases blood pressure.
Indication: hypertension, angina, Adjunct in heart failure
Side effects: Constipation, Abdominal discomfort; bradycardia; confusion; depression;
diarrhoea; dizziness; dry eye
Interactions: amlodipine, Viagra, digoxin, ibuprofen
Contraindications: for all beta blockers - asthma, hypotension, bradycardia, diabetics- not
sure- check
Monitoring: Monitor lung function (in patients with a history of obstructive airway disease)-
risk of bronchospasm
Education:
Propranolol-beta blocker:
Mode of action: Nonselective beta-adrenergic blocker (class II antiarrhythmic); competitively
blocks response to beta1- and beta2-adrenergic stimulation (sympathetic stimulation) which
results in decreases in heart rate, myocardial contractility, blood pressure, and myocardial
oxygen demand.
Indication: hypertension, angina, anxiety tachycardia, arrythmias
Side effects: Abdominal discomfort; bradycardia; confusion; depression; diarrhoea; dizziness;
dry eye (reversible on discontinuation); dyspnoea; erectile dysfunction; fatigue; headache;
heart failure; nausea; paraesthesia; peripheral coldness; peripheral vascular disease; rash
(reversible on discontinuation); sleep disorders; syncope; visual impairment; vomiting.
Therapeutic evaluation: caution with renal and hepatic impairment.
Interactions: mainly adrenaline but also https://bnf.nice.org.uk/interaction/propranolol.html
Monitoring: Monitor lung function (in patients with a history of obstructive airway disease).
Adenosine injections:
Mode of action: slows conduction time through the AV node and can interrupt the re-entry
pathways through the AV node, resulting in the restoration of normal sinus rhythm in patients
with paroxysmal supraventricular tachycardia (PSVT). It deactivates adenyl cyclase thus
decreases cAMP thus K+ channels open and Ca2+ channels close causing hyperpolarisation
of cell membrane so kinda resets the rhythm.
Indication: rapid reversion of paroxysmal supraventricular tachycardias
Side effects: Abdominal discomfort; arrhythmias; atrioventricular block; chest discomfort;
chest pain (discontinue); dizziness; dry mouth; dyspnoea; flushing; headache; hypotension
(discontinue if severe); pain; paraesthesia; throat discomfort
Therapeutic evaluation:
Interactions: https://bnf.nice.org.uk/interaction/adenosine-2.html
Monitoring: Monitor ECG and have resuscitation facilities available.
Education:
Adenosine is most commonly used to terminate supraventricular
tachycardias. The effects of adenosine are enhanced by
dipyridamole (antiplatelet agent) and blocked by theophyllines. It should
be avoided in asthmatics due to possible bronchospasm.
Mechanism of action
causes transient heart block in the AV node
agonist of the A1 receptor in the atrioventricular node, which
inhibits adenylyl cyclase thus reducing cAMP and causing
hyperpolarization by increasing outward potassium flux
adenosine has a very short half-life of about 8-10 seconds
Adenosine should ideally be infused via a large-calibre cannula due to it's
short half-life,
Adverse effects
chest pain
bronchospasm
transient flushing
can enhance conduction down accessory pathways, resulting in
increased ventricular rate (e.g. WPW syndrome)
Digoxin:
,Mode of action: a cardiac glycoside. HFIt increases the force of cardiac muscle contraction
due to inhibition of the Na+/K+ ATPase pump which leads to increase intracellular calcium
concentrations so more calcium will be released during contraction. Supraventricular
arrythmias decreases conduction through the atrioventricular node which slows the
ventricular rate in atrial fibrillation and flutter. Also stimulates vagus nerve
Indication: heart failure, supraventricular arrythmias, supraventricular tachycardia.
Contraindication: ventricular fibrillation
Side effects: arrythmias, sinus bradycardia, Nausea, vomiting, diarrhea, lower stomach pain,
dizziness, drowsiness, headache, blurred/yellow vision, depression , skin rash. Highlighted=
most common Symptoms of heart problems including: fluttering, pounding or pain in your
chest, feeling your heart skips a beat, dizziness or fainting
Interactions: amiodarone, quinidine, verapamil, diltiazem, spironolactone (competes for
secretion in distal convoluted tubule therefore reduce excretion), ciclosporin. Also drugs
which cause hypokalaemia e.g. thiazides and loop diuretics. All of these increase toxicity
Monitoring: digoxin has a narrow therapeutic index. Plasma potassium needs to be regularly
monitored
Education:
Toxicity:
Plasma concentration alone does not determine whether a patient has developed
digoxin toxicity. Toxicity may occur even when the concentration is within the
therapeutic range.
Features:
o generally unwell, lethargy, nausea & vomiting, anorexia, confusion, yellow-
green vision
o arrhythmias (e.g. AV block, bradycardia)
o gynaecomastia
Management:
o Digibind
o correct arrhythmias
o monitor potassium
Here this is in a normal cell
where when there is an action
potential, the calcium L type
channel opens and calcium
enters and binds to the RyR
which causes calcium release
from the SR.
In relaxation, the calcium that
was in the cell eaves mainly
thro the Na+/Ca2+ outside of
the cell.
In digoxin, blocks the blue
receptor (which is essential to
keep sodium low in the cell and
,thus allows the function on the sodium/ calcium pump). When the sodium/ k+ is inhibited,
the intracellular sodium conc is higher thus this will lower the ability of the sodium/ calcium
pump to remove calcium from inside the cell. So more calcium will be pumped in the sr in
response to try to remove NA out of the cell. So now we have more calcium in the SR than
before so when an action potebtial arrives, more ca2+ will be released from the sr and thus
greater contraction force.
Patient:
Digoxin works by slowing down the rate at which your heart beats but also strengthens the
force of your heartbeat. When your heart rate is brought down to normal, your heart becomes
efficient again and your symptoms usually improve.
This drug is prescribed for heart failure and some other heart conditions.
Digoxin can cause unwanted side-effects although not everyone experiences them:
feeling dizzy
feeling sick
diarrhoea
skin rash
blurry/yellow vision or Symptoms of heart problems including: fluttering, pounding
or pain in your chest, feeling your heart skips a beat, dizziness or fainting stop and
seek urgent medical advise
Make sure that you take the right dose.
Plasma potassium needs to be regularly monitored
beta blockers:
ALL- patient:
Beta-blockers work by blocking the transmission of certain nerve impulses. Normally these
impulses send signals to the heart to increase the force and rate of it’s contraction so by
giving this medication, we block this signals which slows down the rate or the heart and the
force of contraction reducing the load on the heart. Thus the heart will work more efficiently.
The ends of some nerves release a chemical (neurotransmitter) called noradrenaline when the
nerve is stimulated. This chemical then stimulates beta-adrenergic receptors. These receptors
are tiny structures which occur on cells in various parts of the body, including the heart,
brain, and blood vessels. When these receptors are stimulated, they cause various effects. For
example, nerve impulses to the heart can stimulate beta-adrenergic receptors on heart cells.
This causes an increase in the force and rate of the heartbeat. The beta-blocker medicine 'sits'
on beta-adrenergic receptors and stops (blocks) the receptor from being stimulated. So, for
example, if beta-adrenergic receptors in the heart are blocked, the force and rate of the
heartbeat are reduced.
Most people who take beta-blockers have no side-effects, or only minor ones. However,
because of their action in various parts of the body, some people have unwanted side-effects.
For example:
, Sometimes the heart rate can go too slowly. This can make you dizzy or feel faint.
If you have diabetes you need to be aware that beta-blockers may dull the warning
signs of a low blood sugar level (hypoglycaemia - often called a hypo). For example,
you may not develop the sensation of rapid, irregular or forceful heartbeats
(palpitations) or tremor, which tend to occur as the blood sugar is going too low.
Some people develop cool hands and feet when taking beta-blockers. This is because
they can narrow (constrict) small blood vessels and reduce the circulation to the skin
of the hands and feet.
Tiredness, depression, inability to achieve a proper erection (impotence).
The most common side effects are dizziness, tiredness and headaches
Monitor lung function in obstructive
Bisoprolol
Mode of action: Bisoprolol is a competitive, cardioselective β1-adrenergic antagonist. When
β1-receptors (located mainly in the heart) are activated by adrenergic neurotransmitters such
as epinephrine, both the blood pressure and heart rate increase, leading to greater
cardiovascular work, increasing the demand for oxygen. Bisoprolol reduces cardiac workload
by decreasing contractility and the need for oxygen through competitive inhibition of β1-
adrenergic receptors.
Bisoprolol is also thought to reduce the output of renin in the kidneys, which normally
increases blood pressure.
Indication: hypertension, angina, Adjunct in heart failure
Side effects: Constipation, Abdominal discomfort; bradycardia; confusion; depression;
diarrhoea; dizziness; dry eye
Interactions: amlodipine, Viagra, digoxin, ibuprofen
Contraindications: for all beta blockers - asthma, hypotension, bradycardia, diabetics- not
sure- check
Monitoring: Monitor lung function (in patients with a history of obstructive airway disease)-
risk of bronchospasm
Education:
Propranolol-beta blocker:
Mode of action: Nonselective beta-adrenergic blocker (class II antiarrhythmic); competitively
blocks response to beta1- and beta2-adrenergic stimulation (sympathetic stimulation) which
results in decreases in heart rate, myocardial contractility, blood pressure, and myocardial
oxygen demand.
Indication: hypertension, angina, anxiety tachycardia, arrythmias
Side effects: Abdominal discomfort; bradycardia; confusion; depression; diarrhoea; dizziness;
dry eye (reversible on discontinuation); dyspnoea; erectile dysfunction; fatigue; headache;
heart failure; nausea; paraesthesia; peripheral coldness; peripheral vascular disease; rash
(reversible on discontinuation); sleep disorders; syncope; visual impairment; vomiting.
Therapeutic evaluation: caution with renal and hepatic impairment.
Interactions: mainly adrenaline but also https://bnf.nice.org.uk/interaction/propranolol.html
Monitoring: Monitor lung function (in patients with a history of obstructive airway disease).
