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Applied Pharmacology > Cardiovascular Drugs > Flashcards

Cardiovascular Drugs Flashcards

1
Q

What are ACEi and what are they indicated in?

A

Angiotensin Converting enzyme Inhibitor

  • HTN
  • Chronic HF
  • Ischaemic Heart Disease
  • Diabetic Nephropathy
  • CKD
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2
Q

What is the MOA of ACEi in HTN?

A

The dug blocks the action of ACE to prevent the conversion of angiotensin I to angiotensin II.

This then inhibits aldosterone secretion causing vasodilation.

This reduces the peripheral vascular resistance (afterload) hence lowering BP.

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3
Q

What is the MOA of ACEi in Chronic HF?

A

The drug blocks the action of ACE to prevent the conversion of angiotensin I to angiotensin II.

This then reduces aldosterone secretion; promoting Na 2+ and H2O excretion which can help reduce venous return (preload)- good for treating HF

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4
Q

What is the MOA of ACEi in CKD?

A

When the BP is lowered, this causes the efferent glomerular arterioles to dilate; which reduces the intraglomerular pressure to slow the progression of CKD.

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5
Q

What are the side effects of ACEi?

A
  • Hypotension
  • Dry cough
  • Hyperkalaemia- due to lower aldosterone level that promotes K+ retention.

RARE:
- Angioedema
- allergies

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6
Q

Who are ACEi contraindicated in?

A
  • Renal artery stenosis
  • Acute kidney injury
  • Pregnant/ breastfeeding
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7
Q

What other drugs does ACEi interact with?

A

Due to risk of hyperkalaemia, avoid prescribing with other POTASSIUM-ELEVATING DRUGS, including K supplements and potassium-sparing diuretics, except under specialist advice for advanced HF

ACEi and NSAID together particularly increase the risk of nephrotoxicity

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8
Q

What is Aspirin and what is it Indicated in?

A

Aspirin is a antiplatelet drug and an NSAID.

Indicated in:
- ACS
- Acute Ischaemic Strole
- Stroke prevention

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9
Q

What is the MOA of Aspirin?

A

Irreversibly inhibits cyclooxygenase (COX) which reduces the production of thromboxane (pro-aggregatory factor) from arachidonic acid.

This then inhibits platelet aggregation and the risk of arterial occlusion.

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10
Q

What are the main side effects of Aspirin?

A
  • dyspepsia
  • peptic ulcer
  • haemorrhage
  • Allergies- bronchospasm
  • Tinnitus
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11
Q

What could happen if a patient overdosed on Aspirin?

A

Overdose – life-threatening:
- Hyperventilation
- Hearing changes
- Metabolic acidosis
- Confusion
- Convulsions
- CV collapse
- Respiratory arrest

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12
Q

What is Aspirin contraindicated in?

A
  • Not given if <16y
  • aspirin hypersensitivity
  • 3rd trimester of pregnancy
  • Peptic ulceration (give PPI)
  • gout (may trigger acute attack)
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13
Q

What drugs does Aspirin interact with?

A
  • antiplatelet agents – can lead to increased risk of bleeding (e.g. heparin, warfarin)
  • NSAIDs – ulcers (give PPI)
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14
Q

What kind of drug is Clopidogrel?

A

Antiplatlet drugs; ADP-receptor antagonist

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15
Q

What is Clopidogrel indicated in?

A
  • ACS
  • Prevent occlusion of coronary artery stents
  • Thrombotic arterial events in pts with CV, cerebrovascular and PAD
  • TIA prevention, without AF for stroke prevention
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16
Q

What is the MOA of Clopidogrel?

A

Clopidogrel prevents platelet aggregation by irreversibly binding to adenosine diphospate (ADP) receptors found on the surface of platelets

As this process is independent of COX pathway so it has a synergistic action with aspirin.

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17
Q

What are the side effects of clopidogrel?

A

Common:
- Bleeding
- Dyspepsia
- Abdominal pain
- Diarrhoea
- Haemorrhage

Rare = thrombocytopenia

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18
Q

What is clopidogrel contraindicated in?

A
  • active bleeding
  • stop taking 7 days before surgery

CAUTION:
- renal and hepatic impairment

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19
Q

What are the key interactions of Clopidogrel?

A

Efficacy may be reduced by cytochrome P450 (CYP) inhibitors as (clopidogrel is a pro-drug that requires metabolism by CYP enzymes) e.g:
- Omeprazole
- Ciprofloxacin,
- Erythromycin
- Some antifungals
- Some SSRIs

Co-prescription with the following increase bleeding risk:
- Other antiplatelet drugs
- Anticoagulants
NSAIDs

  • If gastroprotection with PPI required, prescribe lansoprazole or pantoprazole over omeprazole
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20
Q

What are Statins Indicated in?

A
  • Prevention of CV events
  • Hyperlipidaemia
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21
Q

What is the MOA of Statins?

A

In the liver, statins inhibit 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG CoA) reductase which reduces serum cholesterol levels.

  • Increase clearance of LDL from the blood to reduce LDL levels.
  • Indirectly reduce triglycerides and slightly increase HDL-cholesterol levels ?? Check if correct

^^Through these effects, slow the atherosclerotic process and may even reverse it.

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22
Q

What are the main side effects of statins?

A

Most common:
- headache
- GI disturbance

More Severe:
- muscle aches
- Myopathy
- Rhabdomylosis

Rare:
- rise in liver enzymes (ALT)

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23
Q

Who are statins contraindicated in?

A

Caution:
- existing hepatic impairment
- renal impairment

Avoid:
- pregnancy
- breastfeeding
- Hypothyroidism increases the risk of myositis with statins.

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24
Q

What other drugs does Statins interact with?

A

Metabolism of statins is reduced by:

  • CYP inhibitors e.g. amiodarone, diltiazem, itraconazole, macrolides
  • Protease inhibitors lead to the accumulation of statin in the body. Patient is at risk of adverse effects
  • Amlodipine
  • Grapefruit AVOID if on Simvastatin OR Atorvostatin
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25
Q

What are the main indications of Digoxin?

A

To reduce ventricular rate in AF and atrial flutter
- BUT BB or non-DHP CCBs usually more effective

In severe HF, it is used at an earlier stage in pts with co-existing AF. It’s an option in pts who are already taking an:
- ACEi
- BB
- AA or ARB

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26
Q

What is the MOA of Digoxin?

A
  • Negatively chronotropic
  • Positively inotropic

In AF and atrial flutter, DIgoxin reduces conduction at the AVN.

This prevents impulses from being transmitted to ventricles to reduce the ventricular rate.

  • Therapeutic effect arises mainly via an indirect pathway involving increased vagal (parasympathetic) tone (thus tends to be lost during stress and exercise so rarely used on its own for AF, although may be an option in sedentary pts)
  • In heart failure, Digoxin inhibits NA/K ATPase pumps on myocytes which causes Na+ to accumulate in the cell causing Ca accumulation in cell which increases contractile force.
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27
Q

What are the main side effects of Digoxin?

A
  • Bradycardia
  • GI disturbance
  • Rash
  • Dizziness
  • Visual disturbance (blurred or yellow vision)
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28
Q

Whom is Digoxin contraindicated in?

A

Those with conduction abnormalities:
- heart block

Ventricular arrhythmias

reduce dose in renal failure.

Certain electrolyte abnormalities increase the risk of its toxicity:
- Hypomagnesaemia
- Hypercalcaemia
- Hypokalaemia- digoxin competes with K+ to bind NA/K ATPAase pump, meaning low serum K so, reduced competition allowing for enhanced effects of digoxin.

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29
Q

What are the key drug interactions of Digoxin/

A
  • Loop and thiazide diuretics cause hypokalaemia, so can increase risk of digoxin toxicity.

Plasma concentration of digoxin can be increased by:
- Amiodarone
- CCBs
- Spironolactone
- Quinine
which Increases risk of toxicity

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30
Q

Give examples of Short-acting Nitrates and its indication?

A

Short acting nitrate (glyceryl trinitrate):
- Acute angina
- Chest pain associated with ACS

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31
Q

Give examples of Long-acting Nitrates and its indication?

A

Long acting nitrates (e.g. isosobide mononitrate, ISMN) are used as 2nd line for prophylaxis of angina
- Where a BB and/or a CCB are insufficient or not tolerated

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32
Q

What is IV nitrates indicated in?

A
  • treatment of pulmonary oedema (in conjunction with furosemide and O2)
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33
Q

What is the MOA of Nitrates?

A

Converted to NO:
- Increases cGMP synthesis
- Reduces intracellular Ca in vascular SMCs  SMCs relax
 venous, and to a lesser extent, arterial vasodilatation  relaxation of the venous capacitance vessels reduces cardiac preload and LV filling  reduces cardiac work and myocardial O2 demand  relieves angina and cardiac failure

  • Can relieve coronary vasospasm and dilate collateral vessels  improves coronary perfusion
  • Relax systemic arteries  reduces peripheral resistance and afterload
  • Most of the antianginal effects are mediated by reduction in preload
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34
Q

what are the main side effects of nitrates?

A

Due to the vasodilation:
- Flushing
- headaches
- light-headedness
- Hypotension

when taken regularly, there is the risk of tolerance (tachyphyalxis)

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35
Q

What is Nitrates contraindicated in?

A
  • aortic stenosis
  • haemodynamic instability (hypotension)
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36
Q

What other drugs does Nitrates interact with?

A

Must NOT be used with phosphodiesterase (PDE) inhibitors (e.g. Sildenafil)
- These enhance and prolong the hypotensive effects of nitrates

Use with caution in pts taking antihypertensive medications, in whom they may precipitate hypotension

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37
Q

Give an example of MRA and what does it stand for?

A

Mineralocorticoid Receptor Antagonists.

Spironolactone

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38
Q

What are the main indications of Spironolactone?

A

1st line diuretic for:
- Ascites
- Oedema due to liver cirrhosis

  • CHF: of at least moderate severity or arising within 1 month of a MI, usually as an addition to a beta blocker and an ACEi/ARB
    ^if showing signs of fluid overload e.g. peripheral oedema, weight gain
  • Primary hyperaldosteronism for pts awaiting surgery or for whom surgery is not an option
  • 4th line for hypertension??
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39
Q

What is the MOA of Spironolactone?

A

Competitively bind to the aldosterone receptor which prevents the binding of aldosterone (produced by adrenal cortex) to the MR in distal tubules of the kidney.

This decreases the activity of the luminal epithelial Na+ channels (ENaC) to decrease BP, and increase Na and water excretion, and K retention

Effect is greatest when circulating aldosterone is increased, e.g. in:
- Primary hyperaldosteronism
- Cirrhosis

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40
Q

What are the main side effects of different types of Nitrates?

A

Hyperkalaemia which can lead to:
- Muscle weakness
- Arrhythmias
- Cardiac arrest

Spironolactone
- Gynecomastia

Eplerenone
- Less likely to cause endocrine SEs (used for HF only)

Aldosterone antagonists can cause:
- Liver impairment
- Jaundice
- Stevens-Johnson syndrome (T-cell mediated hypersensitivity reaction) that causes a bullous skin eruption.

41
Q

Whom are nitrates contraindicated in?

A
  • severe renal impairment
  • Hyperkalaemia
  • Addisons disease
  • pregnancy
  • breastfeeding
42
Q

What are the key interactions of Nitrates?

A

Combination with other K-elevating drugs, including ACEi and ARBs increases the risk of hyperkamaemia
- BUT could be a beneficial combination in HF

  • Should not be combined with potassium supplements except in specialist practice
  • Relatively weak diuretic that takes several days to start having an effect, therefore prescribed in combination with loop or thiazide diuretic, where it both counteracts K wasting and potentiates the diuretic effect
43
Q

What are some examples of alpha-blockers?

A
  • Doxazosin
  • Tamsulosin
  • Alfuzosin
44
Q

What are the main indications of alpha blockers?

A
  • 1st line in benign prostatic hyperplasia
  • add on treatment for resistant HTN (when other medications are insufficient)
45
Q

What is MOA of alpha blockers?

A

The drug binds and inhibits Alpha-1 adrenoreceptors in the smooth muscle (including blood vessels and the urinary tract – bladder neck and prostate).

This causes muscle relaxation causing:
- Vasodilation
- Fall in BP
- Reduced resistance to bladder outflow

Highly selective for the alpha1 adrenoceptor:
- Doxazosin (for benign prostatic enlargement AND hypertension)
- Tamsulosin (for benign prostatic enlargement only)

46
Q

What are the main side effects of Alpha Blockers?

A
  • Postural Hypotension
  • dizziness
  • Syncope
47
Q

Whom is alpha blockers contraindicated in?

A
  • patients with existing POSTURAL HYPOTENSION
48
Q

What other drugs does Alpha blockers interact with?

A

Combining this drug with antihypertensive drugs can cause BP lowering effects.

49
Q

What are thiazide diuretics indicated in?

A
  • 1st line alternative treatment for HTN or there are features of HF
  • Add-on treatment for HTN in pts whose BP is not adequately controlled by a CCB+ACEi/ARB
50
Q

What are some examples of thiazide diuretic?

A
  • Bendroflumethiazide
  • Indapamide
  • Chlortalidone
51
Q

What is the MOA of Thiazide Diuretics?

A

Thiazides inhibit the Na+/Cl- co-transporter in the distal convoluted tubule of the nephron which prevents reabsorption of Na. Also, it is osmotically associated with water leading to diuresis causing an initial fall in extracellular fluid volume.

Over time, compensatory changes (e.g. activation of RAAS) tend to reverse this, at least in part.

52
Q

What are the main side effects of Thiazide Diuretics?

A
  • Hyponatraemia
  • Hypokalaemia causing cardiac arrhythmias.
  • increase glucoses, LDL, triglycerides
  • erectile dysfunction in men
53
Q

What are the key contraindications of Thiazide Diuretics?

A
  • Hypokalaemia
  • Hyponatraemia
  • As they reduce uric acid excretion, they may precipitate acute attacks in patients with gout.
54
Q

What other drugs may Thiazide interact with?

A
  • NSAIDS (not aspirin)
  • Loop diuretics
  • ACEi/ ARBs
55
Q

Give an example of loop diuretic?

A

Furosemide
Bumatenide

56
Q

What are the main indications of Loop diuretics?

A
  • relief of breathlessness in acute PULMONARY OEDEMA (with O2 and nitrates).
  • symptom relief of fluid overload in CHRONIC HF, RENAL DISEASE, LIVER FAILURE.
57
Q

What is the MOA of loop diuretics?

A

Inhibit the Na+/K+/2Cl- co-transporter on the ascending limb of the loop of Henle which inhibits Na and K reabsorption from the tubular lumen into the epithelial cell.

So, as water follows by osmosis, this inhibits water reabsorption meaning that water, K, Na is excreted in urine - potent diuretic affect.

ALSO, have a direct effect on blood vessels, causing dilation of capacitance veins.
- In Acute HF, this reduces preload and improves contractile function of the ‘overstretched’ heart muscle.

58
Q

What are the main side effects of loop diurectics?

A
  • Dehydration
  • Hypotension
  • Hyponatraemia
  • Hypokalaemia
  • Hypochloraemia
  • Hypocalcaemia
  • Hypomagnesaemia
  • Metabolic acidosis

At high doses, loop diuretics can affect Na+/K+/2Cl- co-transporter responsible for regulating endolymph composition in the inner ear causing:
- Hearing loss
- Titinus

59
Q

What are the key contraindications of Loop diuretics?

A
  • Severe Hypovolemia
  • Severe dehydration

Used with caution in pts:
- At risk of hepatic encephalopathy
- With severe hypokalaemia
- With severe hyponatraemia

  • Taken chronically, they inhibit uric acid excretion which can worsen gout
60
Q

What are the key interactions of Loop Diuretics?

A

Have the potential to affect drugs that are excreted by kidneys
- E.g. lithium levels are increased due to reduced excretion

  • The risk of digoxin toxicity may also be increased, because diuretic-associated hypokalaemia
  • Can increase the ototoxicity and nephrotoxicity of aminoglycosides
61
Q

What are Beta blockers indicated in?

A
  • Ischaemic Heart Disease
  • Chronic HF
  • Atrial Fibrillation
  • Supraventricular Tachycardia
  • HTN
62
Q

What is the MOA of Beta blockers?

A

The drug binds to beta-1 adrenoreceptors in the heart which reduces the force of contraction and speed of conduction (prolongs refractory period of AVN) in the heart.

This reduces cardiac work and O2 demand to increase myocardial perfusion which then relieves myocardial ischemia.

  • Protect the heart from chronic sympathetic stimulation which improves prognosis in HF

Prolong the refractory period of AVN:
- Slows ventricular rate in AF
- May terminate SVT if this is due to a re-entry circuit that takes in the AVN

  • In hypertension lower BP through a variety of means e.g. reducing renin secretion from kidney
63
Q

What are the main side effects of Beta Blockers?

A
  • Fatigue, low exercise tolerance
  • Cold extremities
  • Headache
  • GI disturbance e.g. nausea
  • Intermittent claudication

Can cause:
- Sleep disturbance
- Nightmares
- Impotence in men

64
Q

What are beta blockers contraindicated in?

A
  • Asthma: can cause bronchospasm
  • Heart block
  • In COPD, should choose relatively beta1 selective (e.g. bisoprolol, metoprolol) rather than non-selective (e.g. propranolol, carvedilol)
  • Avoided in pts with hemodynamic instability
  • Generally require dosage reduction in significant hepatic failure
  • In HF, should be started at a very low dose and increased slowly, as they may initially impair cardiac function.
65
Q

What are the key interactions of Beta blockers?

A
  • Do not use with non-DHP CCBs as it can cause HF, bradycardia and asystole
66
Q

what is Warfarin Given to patients for?

A
  • treatment and secondary prevention of VTE
  • prevent arterial embolism in patients with AF, prostetic heart valves
67
Q

What is the MOA of Warfarin?

A

Inhibits vitamin K epoxide reductase which inhibits hepatic production of vitamin-K dependent Coagulation factors (II, VII, IX, X) and Proteins C and S

VitK epoxide reductase functions to restore vitamin K to its reduced form – imp co-factor in the synthesis of these clotting factors.

68
Q

What are the main side effects of Warfarin?

A
  • increased risk of bleeding
69
Q

Whom is Warfarin contraindicated in?

A
  • those who are at immediate risk of haemhorrage
  • those with liver disease
  • 1st trimester of pregnancy
  • later pregnancy
70
Q

What other drugs does Warfarin interact with?

A
  • CYP enzymes
  • CYP inducers (e.g. phenytoin, carbamazepine, rifampicin) increase warfarin metabolism and risk of clots
  • CYP inhibitors (e.g. fluconazole, macrolides) decrease warfarin metabolism and increase bleeding risk
71
Q

What does DOACs stand for?

A

Direct oral anticoagulants

72
Q

What are the main interactions of DOACs?

A
  • Treatment and secondary prevention of VTE
  • Primary prevention of VTE in pts undergoing elective hip or knee replacement surgery
  • Prevent stroke and systemic embolism in pts with non-valvular AF who have at least one risk factor.
73
Q

What are some examples of common DOACs?

A
  • Apixabam
  • Edoxaban
  • Rivaroxaban
  • Dabigatran
74
Q

What is the MOA of DOACs?

A
  • DOACs act on the final pathways of the coagulation cascade, comprising factor X, thrombin and fibrin.
  • Inhibit fibrin formation which prevents clot formation or extension in the veins and heart.
  • Apixaban, edoxaban and rivaroxaban directly inhibit activated factor X (Xa)
    which prevents conversion of prothrombin to thrombin.
  • Dabigatran directly inhibits thrombin which prevents conversion of fibrinogen to fibrin
  • Less effective in the arterial circulation where clots are lately platelet driven (antiplatelet agents better here)
75
Q

What are the main side effects of DOACs?

A

Bleeding:
- Epistaxis
- GI distubances
- Genitourinary haemorrhage

Adverse effects:
- Anaemia
- GI upset
- Dizziness
- elevated Liver enzymes

76
Q

What are DOACs contraindicated in>

A
  • Avoid in people with active, clinically significant bleeding

Avoid in people with risk factors for major bleeding e.g:
- Peptic ulceration, cancer, and recent surgery or trauma (esp in brain, spine or eye)

  • Contraindicated in pregnancy and breastfeeding (risk of harm to offspring unknown)

Dose reduction or alternative agent may be required in:
- Hepatic disease
- Renal disease
^^as excreted by multiple routes including CYP metabolism and elimination in faeces and urine)

77
Q

What are the key interactions of DOACS?

A

Risk of bleeding is increased by concurrent therapy with other antithrombotic agents:
- Heparin
- Antiplatelets
- NSAIDs

Metabolism affected by:

Anticoagulant effect can be increased by CYP inhibitors)
- Macrolides
- Protease inhibitors
- Fluconazole

Anticoagulant effect can be decreased by CYP inducers:
- Rifampicin
- Phenytoin

  • With drugs that affect their excretion (through induction/ inhibition of transport proteins)
78
Q

What Is Heparin given to patients for?

A
  • primary prevention of VTE
  • ACS
79
Q

What is the MOA of Heparin?

A

They enhance the anticoagulant effect of antithrombin (AT).

AT inactivates clotting factors (IIa and Xa) causing a break in clotting process.

80
Q

What does UFH stand for?

A

Unfractioned Heparin

81
Q

What does LMWH stand for?

A

Low molecular weight heparin?

82
Q

What is the difference between UFH and LMWH?

A

UFH- large and small molecules which promote the inactivation of both IIa and Xa factors.

LMWH- smaller molecules which are more specific for promoting the inactivation of factor Xa.

83
Q

What are the main side effects of Heparin?

A
  • Haemorrhage
  • bruising
  • Hyperkalaemia
  • Heparin induced thrombocytopenia (RARE)
84
Q

What is Heparin Contraindicated in?

A

Used with caution in pts at increased risk of bleeding, including:
- Clotting disorders
- Severe uncontrolled hypertension
- Recent surgery or trauma

  • Should be withheld immediately before and after invasive procedures, esp lumbar puncture and spinal anesthesia

in renal impairment, use lower dose OR use UFH instead
- LMWH and fondaparinux accumulate

85
Q

What other drugs does Heparin interact with?

A

Combining heparins with other antithrombotic drugs (e.g. antiplatelets/ warfarin) has an additional effect
- This is sometimes desirable e.g. in treating ACS
- But is associated with an increased risk of bleeding, so should otherwise be avoided

In major bleeding, protamine is an option to reverse heparin anticoagulation
- This is effective for UFH but less for LMWH, and ineffective against fondaparinux

  • Andexanet alpha is in development and appears to be an effective reversal agent
86
Q

What are the two types of Calcium Channel Blockers and give examples for both:

A

DHP- Amlodipine, Nifedipine
Non-DHP- Diltiazem, Verapamil

87
Q

What is DHP Calcium Channel Blockers indicated in?

A
  • HTN
  • stable angina
88
Q

What is NON-DHP Calcium Channel Blockers indicated in?

A
  • control cardiac rate in patients with supraventricular arrhythmias
89
Q

What is the difference between DHP and Non-DHP Calcium Channel Blockers?

A
  • DHP = relatively selective for vasculature (e.g. amlodipine and nifedipine) leading to vasodilatation
  • Non-DHP = more selective for the heart (verapamil is most cadioselective, diltiazem also has some effects on BVs
90
Q

What is the MOA of Calcium channel blockers in HTN?

A

Decrease Ca ions entry into vascular and cardiac cells which reduce intracellular Ca concentration.

This leads to the relaxation and vasodilation in arterial smooth muscle hence decreasing BP.

91
Q

What is the MOA of Calcium channel blockers in Stable Angina?

A

In the heart: CCBs reduce myocardial contractility by:
- Decreasing Ca ions entry into cardiac cells which reduces intracellular Ca concentration causing reduced contractility
- Also suppress cardiac conduction (esp across AVN) so, it slows ventricular rate causing:
- Reduced cardiac rate
- Reduces afterload
- Reduces Contractility
^^reduces myocardial O2 demand  prevents angina

92
Q

What are the main side effects of DHP calcium channel blockers?

A
  • Ankle swelling
  • Flushing
  • Headache
  • Palpitations
    (caused by vasodilation and compensatory tachycardia)
  • Gum disease
93
Q

What are the main side effects of Verapamil?

A

Verapamil commonly causes constipation and less often but more seriously can cause:
- Bradycardia
- Heart block
- Cardiac failure

94
Q

What are the main side effects of Diltiazem?

A

Diltiazem can cause any of these adverse effects (due to mixed vascular and cardiac actions)
- Ankle swelling
- Flushing
- Headache
- Palpitations
- Gum disease
- Bradycardia
- Heart block
- Cardiac failure

95
Q

What is DHP calcium channel blockers contraindicated in?

A

Avoid:
- Unstable angina (vasodilation causes a reflex in contractility and tachycardia which increases myocardial O2 demand)
- Severe aortic stenosis (can provoke collapse)

96
Q

What is NON- DHP calcium channel blockers contraindicated in?

A

Verapamil and diltiazem:
- Used in caution in pts with poor LV function (can worsen HF)
- Avoided in people with AV nodal conduction delay (can provoke complete heart block)

97
Q

What are the key drug interactions of Calcium channel blockers?

A
  • Non-DHPs should NOT be prescribed with BB except under close specialist supervision
  • Both anegatively inotropic and chronotropic (HR) which may cause HF, bradycardia and systole
98
Q

What are ARBs and what are they indicated in?

A

Applied Pharmacology (7 decks)

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