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Clinical Pharmacology > Cardiovascular Pharmacology > Flashcards

Cardiovascular Pharmacology Flashcards

1
Q

Heart Failure

  1. What are main systems targeted therapeutically in heart failure
  2. Which drug classes are commonly used?
A
  1. Systems targeted:
    1. Renin-angiotensin-aldosterone (reduce afterload and Na+ and H2O retention)
    2. Sympathetic nervous system (negative inotropes and chronotropes
  2. Drugs used:
    1. Loop diuretics
    2. ACE-i / ARBs
    3. Beta blockers
    4. Aldosterone antagonists
    5. Digoxin
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2
Q

Heart Failure

What is the role of loop diuretics. Give examples and doses.

A
  1. Reduce sodium reabsorption in the LOH, decreasing pre-load
  2. Provide **symptomatic relief **(breathlessness and oedema), but have no effect on mortality
  3. Main options:
    1. furosemide: 40mg/24h PO
    2. bumetanide: 1-2mg/24h PO
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3
Q

Heart Failure

What is the role of ACE-i? Give examples and doses?

A
  1. Decreases afterload (arteriolar dilation) and promotes sodium excretion. Improve symptoms and mortality (life extending)
  2. Lisinopril: start at 10mg/d PO in adults, and titrate to ~30-40mg/d by increasing every 2 weeks if no adverse side effects.
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4
Q

Heart Failure

What is the role of Angiotensin Receptor Blockers? Give example type and dose.

A
  1. Unclear if they should be used in combination with ACE-i; most frequently used if S/E preclude further use of ACE-i
  2. ARTANs: consider candesartan 4mg/d up to a maximum of 32mg/d
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5
Q

Heart Failure:

What is the role of beta blockers? When are they started, and give examples of type and dosing.

A
  1. Negatively inotropic and chronotropic - reduce mortality through reducing oxygen consumption
  2. Started once heart failure is stabilized: acutely they cause deterioration as negatively inotropic.
  3. Options: carvidalol, bisoprolol. Bisoprolol used most commonly due to lower cost.
  4. Begin at **very low dose **and slowly titrate up every 2 weeks. E.g 1.25mg/d up to maximum 10mg/d or until symptoms intervene
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6
Q

Heart Failure

What is the role of aldosterone antagonists. Give examples and doses.

A
  1. Act as diuretics by inhibiting aldosterone receptors in the distal tubule causing sodium and water excretion, and potassium retention
  2. The **RALES trial **showed reduced mortality by 30% when combined with ACE-i and beta blocker.
  3. Example: spironolactone** **25mg/day PO
  4. Note: eplerenone (more selective for mineralocorticoid receptor does not cause gynaecomastia, but more expensive)
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7
Q

Heart Failure

What is the role of Digoxin in managing heart failure? What is an appropriate starting dose?

A
  1. A cardiac glycoside (decreases action of Na+/K+/ATPase) , usually used in the control of AF.
  2. Provides **symptom control. **No effect on all cause mortality, but small effect to decrease all-cause-related and HF-related hospitalization (at a cost of admissions with digoxin toxicity)
  3. Dose: 0.125 - 0.25mg/24h PO. Monitor digoxin levels (narrow therapeutic window)
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8
Q

Heart Failure

What is the role of warfarin in heart failure?

A
  1. Not indicated, but a high number of patients require it for co-existing pathology.
  2. Patients with AF require warfarin
  3. LV thrombus should be considered
  4. Frequently used for LV dysfunction post MI, but not a strong evidence base.
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9
Q

Heart Failure

What management strategy would be appropriate for a patient presenting with symptomatic heart failure?

A

First Line

  1. Diuretic: Furosemide (control symptoms if symptomatic)
  2. ACE-i/ARB (Lisinopril / Candesartan): start at low dose and titrate up. ACE-i first line, ARB if contraindicated
  3. Beta-blocker (Bisoprolol): once symptoms stablised. Slowly titrate dose.

Second Line

  1. Aldosterone antagonist (spironolactone)
  2. Digoxin if remaining symptomatic

Note: if co-existing hypertension consider amlodipine (dihydropyridine), rather than non-dihydropyridine (verapamil etc.)

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10
Q

Heart Failure

Which classes of drugs are contra-indicated in heart failure?

A
  1. CCBs:
    1. Non-dihydropyridines (verapamil, diltiazem) are negatively inotropic
    2. Dihydropyridines (amlodipine) tend to promote **salt and water retention **(but may be necessary if uncontrolled hypertension)
  2. Alpha-blockers (e.g. doxazosin, tamsulosin): increase mortality
  3. NSAIDs: salt and water retention, and impair renal function particularly with ACE-i and diuretics
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11
Q

Acute pulmonary oedema

What is the management strategy for acute pulmonary oedema

(Note: may be a first presentation of HF, or exacerbation of known HF. Requires treatment of underlying condition, as well as pulmonary oedema)

A
  1. Sit patient upright
  2. High flow oxygen via facemask
  3. ECG, CXR, Pulse oximetry, ABG
  4. **IV Furosemide: **40-80mg IV, or 2.5 normal dose
  5. IV isosorbide or GTN: titrated to BP
  6. Consider **slow I.V morphine **with an anti-emetic (metoclopramide), but cautiously in those who are drowsy, exhausted or hypotensive
  7. Consider CPAP if severe LVF and por response to furosemide and nitrates
  8. No improvement / significant hypotension - seek senior help. Note combination of pulmonary oedema and cardiogenic shock are difficult to manage and require ICU
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12
Q

Stable angina

Medical treatment for stable angina involves both symptom control and cardioprotection. What are the options for symtom control?

A
  1. GTN PRN for chest pain or before exertion
  2. EITHER** beta blocker** OR CCB as first line. If one is insufficient or poorly tolerated, switch or use a combination of the two. e.g
    1. Atenolol 50-100mg/24h PO OR
    2. Amlodipine 10mg/24h - particularly used if betablockers contraindicated
  3. NOTE: **do not combine beta blockers and non-dihydropyridines **(verapamil / diltiazem) as bradycardia and negative inotropy results
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13
Q

Stable Angina

If Beta Blockers or CCBs are not tolerated or contraindicated for symptom control, what further agents could be considered?

Note: 3 drugs not recommended; patients not controlled on two assessed for revascularization.

A
  1. Long acting nitrate e.g isosorbide mononitrate.(20-40mg PO BD) Note: give doses separated by 8h, not 12h to give a nitrate free period to prevent tolerance developing. S/E: headache, flushing, hypotension
  2. **Nicorandil: **K+ channel activator causing arterial and venous vasodilation. Similar S/E to isosorbide
  3. Ivabradine (selective inhibitor of sinus node pacemaker activity)
  4. **Ranolazine **(decreases ischaemia by acting on intracellular sodium currents)
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14
Q

Stable Angina

Medical treatment for stable angina involves both symptom control and cardioprotection. What are the options for cardioprotection?

A
  1. Treat risk factors (BP, Smoking, Diabetes)
  2. Aspirin: 75mg / 24h
  3. Statin: NICE recommends Simvastatin 40mg / 24h. Target serum cholesterol <4mmol/L, LDL <2mmol/L
  4. **ACE-i: **controversial - clearly indicated if HTN or LV dysfunction, but may reduce mortailty even if these are not present.
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15
Q

Acute Coronary Syndrome: STEMI

What management is appropriate before patient is taken to PCI (though immediate transfer is priority)

A
  1. Morphine: 5 - 10mg, slow IV injection +- metoclopramide 10mg IV
  2. Oxygen: if SpO2 is below 94%
  3. Nitrate: GTN sub-lingually
  4. Aspirin: 300mg soluble aspirin, or 75mg if already taking regularly
  5. Clopidogrel: 600mg PO loading dose, then 75mg /24h OR Ticagralor.
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16
Q

Acute Coronary Syndrome: NSTEMI / Unstable Angina

What is the initial management for NSTEMI (i.e. BEFORE TIMI/GRACE score has been done)

A
  1. **Morphine **5-10mg slow IV +- metoclopramide 10mg IV
  2. Oxygen if Sp02 < 94%
  3. Nitrate (GTN sublingual)
  4. Aspirin (300mg loading dose, chewed)
  5. Fondaparinux unless PCI planned within 24h in which case Heparin
  6. Beta-blocker (e.g. atenolol 5mg IV) unless contraindicated
  7. TIMI Score to stratify risk
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17
Q

Acute Coronary Syndrome: Ongoing Management

What medications should all patients with ACS (regardless of types) be considered for following acute treatment?

A
  1. GTN Spray PRN
  2. **Aspirin 75mg daily + **clopidogrel (for 1 year)
  3. Beta-blocker: titrated to decrease pulse to <60 fpr 1 at least 1 year. CCB if contraindicated (non-dihydropyridine - verapamil / diltiazem)
  4. ACE inhibitor (e.g. lisinopril 2.5mg)
  5. Statin: (e.g. simvastatin 40mg)
  6. Control other risk factors:
    1. Smoking cessation / Weight management
    2. Diabetes
    3. HTN
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18
Q

Coronary Stent Implantation:

What are drug eluting stents, and what management is in place to prevent thrombus formation which MUST NOT BE DISCONTINUED

A
  1. Placed into coronary arteries to treat focal stenosis. Release anti-fibrotic drugs to prevent a proliferative response. The drugs release **suppress endothelialization **therefore increase thrombus risk.
  2. Two different anti-platelets (typically **aspirin and clopidogrel) **are required for atleast 1 year - premature discontinuation even for a few days is associated with a high rate of stent thrombosis. Never discontinue prematurely with discussion with an interventional cardiologist
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19
Q

Hypertension

Which classes of drugs are available for the treatment of hypertension?

A
  • ACE-inhibitors (-pril)
  • AR Blockers (-artan)
  • **Alpha blockers **(-osin)
  • **Beta-blockers **(-lol)
  • **CCB **(dihydropyridines (-dipines) and non-dihydropyridines (verapamil, diltiazem)
  • Diuretics
    • **​Thiazides **(bendroflumethiazide etc.)
    • **Thiazide like diuretics **(indapamine, spironolactone)
20
Q

Hypertension: Thiazides

What are the compelling indications, contraindications, and side effects of **Thiazide Diuretics **(e.g. bendroflumethiazide)

A
  1. Compelling Indications:
    1. ​Heart failure, advanced age, volume-dependent HTN, low-renin HTN, systolic HTN
  2. Contra-indications:
    1. ​Gout
  3. Side Effects
    1. ​Hypokalemia, hyperuricaemia, glucose intolerance, hypercalcaemia, impotence
21
Q

Hypertension: Aldosterone Antagonists

What are the compelling indications, contraindications, and side effects of aldosterone antagonists (e.g. spironolactone)

A
  1. Compelling Indications
    1. ​Primary aldosteronism, resistant HTN, sleep apnoea
  2. Contraindications
    1. ​Reduced GFR, hyperkalaemia
  3. Side-effects
    1. ​Hyperkalaemia, increased creatinine, painful gynaecomastia, menstrual irregularities, GI distress
22
Q

Hypertension: ACE-i

What are the compelling indications, contraindications, and side effects of ACE-inhibitors (e.g. lisinopril)

A
  1. Compelling Indications
    1. ​Heart failure, LV dysfunction, post-MI, proteinuria, diabetic nephropathy, CKD
  2. Contraindications
    1. ​Pregnancy, hyperkalaemia
  3. Side effects
    1. ​Cough, angioedema, hyperkalaemia, potential raised creatinine in those with renal artery stenosis, rash, loss of taste
23
Q

Hypertension: ARBs

What are the compelling indications, contraindications, and side effects of angiotensin receptor blockers (e.g. losartan)

A
  1. Compelling Indications
    1. ​(As ACE-i - usefull when not tolerated) Heart Failure, LV dysfunction, post-MI, diabetic nephropathy, CKD, proteinuria
  2. Contraindications
    1. Pregnancy, hyperkalaemia
  3. Side effects
    1. ​(as ACE-i but no cough): angioedema, hyperkalaemia, potential raised creatinine in those with bilateral renal artery stenosis
24
Q

Hypertension: CCBs

What are the compelling indications, contraindications, and side effects of calcium channel blockers (e.g. amlodipine, verapamil, diltiazem etc.)

A
  1. Compelling indications
    1. Systolic hypertension, angina, coronary heart disease, (cyclosporine induced HTN)
  2. Contraindications
    1. ​Heart block (for nondihydropyridines verapamil and diltiazem)
  3. Side effects
    1. ​Headache, flushing, gingival hyperplasia, oedema, constipation
25
Q

Hypertension: Beta Blockers

What are the compelling indications, contraindications, and side effects of Beta-blockers (e.g. propranolol)

A
  1. Compelling indications
    1. Angina, heart failure, post-MI, tachyarrthymias, migraine
  2. Contraindications
    1. ​Asthma, COPD, heart block
  3. Side effects
    1. ​Bronchospasm, bradycardia, heart failure, impaired peripheral circulation, decreased exercise tolerance, fatigue
26
Q

Hypertension: Alpha Blockers

What are the compelling indications, contraindications, and side effects of alpha blockers (e.g. tamsulosin)

A
  1. Compelling indications
    1. Prostatic hyperplasia
  2. Contraindications
    1. Orthostatic hypotension
  3. Side effects
    1. Headache, drowsiness, fatigue, weakness, postural hypotension
27
Q

Hypertension

What is the management strategy for commencing medications for individuals with hypertension

A
  1. Initiate based upon compelling indications or contraindications.
  2. If none exist, follow algorithm:
28
Q

Hypertension

Which agents are considered first line for HTN in:

  1. Pregnancy
  2. Renal disease
A
  1. Methyldopa. Note: Beta-blockers and CCBs probably safe. ACE-i contraindicated (teratogenic in first trimester and affect renal blood flow in fetus)
  2. ACE-i and AR Blockers have some renoprotective effects and are first line except in renovascular disease. Thiazides are usually not effective at conventional doses.
29
Q

Lipid Lowering Drugs: Statins

What is the mechanism of statins, and what are the adverse effects?

A
  1. HMG Co-A reductase inhibitor, reducing cholesterol synthesis in the liver
  2. Contraindications:
    1. Raised LFTs; measure before commencing and at 3 & 12 months
    2. Myopathy (pain / weakness with raised CK) is rare (1/10,000), and rhabdomyolysis (extremely rare - 1/100,000 treatment years). Higher risk if renal impairment, elderly, hypothyroidism, diabetes.
30
Q

Lipid Lowering Drugs: Statins

What is the general strategy for starting statins in terms of which drugs used, targets and switching drugs.

A

No evidence of efficacy between commonly prescribed statins:

  1. Start simvastatin 40mg at night. If higher dose required:
  2. Atorvastatin 80mg (higher dose of simvastatin increases risk of rhabdomyolysis)
  3. If intolerent to simvastatin, try another agent e.g. pravastatin

Note: amlodipine and macrolides decrease statin metabolism, increase risk of muscle damage. Reduce / stop dose in this situation

31
Q

**Lipid Lowering Drugs: **Fibrates

What is the mechanism, indication and adverse affects of fibrates

A
  1. Mechanism: acts on intracellular receptors (peroxisome proliferator-active receptor (PPAR)) to modify genes involved in regulating lipid metabolism
  2. Indications: predominantly for reducing high triglyceride levels but may replace statin in situation of statin intolerance or inadequate effect
  3. Side effects: as statin; rare myopathy, rhabdomyolysis, more frequently GI symptoms. Can cause renal impairment, deranged LFTs.
32
Q

Lipid Lowering Drugs: Ezetimibe

What is the mechanism, indication and adverse affects of ezetimibe

A
  1. Mechanism: inhibits intestinal absorption of cholesterol; those with high natural absoprtion may benefit
  2. Indications: can be used alone or in combination with a statin to reduce cholesterol. Used in treatment of familial hypercholesterolaemia
  3. Side effects: LFTs may increase. Some GI disturbance. Otherwise adverse effects rare.
33
Q

Lipid Lowering Drugs

Lipid therapy can be indicated as both **primary and secondary prevention. **In which situations is it indicated for primary prevention?

A
  1. Primary prevention: if 10 year risk of cardiovascular disease > 20% and have not responded to dietary / lifestyle advice
  2. **Diabetics: **age > 40, or younger with particularly high risk.

Note: lowering LDL by 1mmol/L reduces risk of heart attack / stroke / revascularisation by 21%.

34
Q

Lipid Lowering Drugs

Lipid therapy can be indicated as both primary and secondary prevention. In which situations is it indicated for secondary prevention?

A

Indicated in all patients with:

  1. Coronary artery disease
  2. Peripheral vascular disease
  3. Stroke
  4. TIA

NICE recommends starting **simvastatin 40mg OD **(taken at night). This has demonstrated a

35
Q

Familial Hypercholesterolaemia

What treatment strategy is recommended for individuals with familial hypercholesterolaemia?

A
  1. High intensity statin (dose equivalent >40mg simvastatin) aiming for a 50% LDL reduction from baseline
  2. Refer to lipid clinic for cascade testing of family members
36
Q

Adult Tachycardia

What is the initial management of adult tachycardia, and separation into stable and unstable categories?

A
37
Q

Adult Tachycardia

In a stable patient with a broad complex tachycardia, what are the next management steps?

A
38
Q

Adult Tachycardia

In a stable patient with a narrow complex tachycardia, what are the next management steps?

A
39
Q

Adult Bradycardia

What is the protocol for adults who are bradycardic (inappropriately slow rate for haemodynamic state)

A
40
Q

Acute Atrial Fibrillation

What options are available for treatment of recent onset, symptomatic AF?

A
  1. DC Cardioversion: if haemodynamic compromise, or AF for <48h (when risk of embolism is low). If unstable may require cardioversion, even if thromboembolism risk. If stable, defer for 4-6 weeks whilst anti-coagulated
  2. Chemical cardioversion: **flecainide **has highest chance of success, but only used in structurally normal hearts
  3. Rate control: older patients and those with structural heart disease. Beta blockers, rate limiting CCBs (non-dihydropyridines: verapamil, diltiazem), and digoxin options.

50% patients revert spontaneously to sinus

41
Q

Atrial Fibrillation

What options exist for rate control in AF, and when is each appropriate?

A
  1. Beta Blockers: first line, particularly if co-existing hypertension or angina. Reduce ventricular rate during exercise and rest.
  2. **CCB **(non-dihydropyridine): diltiazem used in prefence to verapamil, as verapamil also has negative inotropic effects and drug interations. Reduce ventricular rate during exercise and rest.
  3. Digoxin: second line, preferred if co-existing heart failure**. **Can be used in combination with beta-blocker / CCB if monotherapy insufficient. Rate control at rest, but less effective during exercise.
42
Q

Atrial Fibrillation

Which scoring system is used to assess need to anticoagulation requirements in AF, and how does it inform management?

A

CHADS2VASC: score >1; benefit of anticoagulation (aspirin, warfarin) outweighs risk. Higher score = greater absolute benefit of anti-coagulation

  • Congestive heart failure: 1 point
  • Hypertension: 1 point
  • Age > 75: 1 point
  • Diabetes mellitus: 1 point
  • Previous stroke or TIA: 2 points
  • Vascular disease (MI, PVD, aortic atheroma): 1 point
  • Age 65-74: 1 point
  • Sex category (only evaluate if > 65, 1 point for female)

Note: effectively, if age <65 and “lone” AF, anticoagulation not required. Most other patients should be considered for anticoagulation.

43
Q

Adenosine

What are the indications for adenosine use, and what are adverse effects?

A
  1. Indication: used I.V for acute termination of SVT. Note: has a very short half-life
  2. Side effects:
    1. Chest pain
    2. Bronchospasm (use cautiously if asthmatic)
    3. Flushing
    4. 3-5% chance of inducing AF (particularly if accessory pathway)
44
Q

Amiodarone

What is the mechanism of amiodarone, and what are the pharmacokinetics? When is it indicated, and what are adverse effects?

A
  1. Mechanism: class 3 anti-arrhythmic
  2. Pharmacokinetics: half-life of several weeks; requires loading dose
  3. Indications: can treat ventricular and supraventricular arrhythmias. It is not a cardiodepressant; helpful in patients with LV dysfunction.
  4. **Adverse effects **(in up to 50%)
    1. Thyroid and Liver; monitor TFTs and LFTs
    2. CXR prior to treatment: can cause pneumonitis
    3. Reversible corneal deposits, skin pigmentation
    4. High number of drug interactions (particularly warfarin, digoxin)
    5. Can cause phlebitis and necrosis I.V - given via central line if possible
45
Q

Flecainide

What is the mechanism of flecainide, and what are the indications, contra-indications and adverse effects?

Note: used as chemical cardioversion in recent onset disease.

A
  1. Mechanism: Class Ic antiarrhythmic - regulates Na+ channels, prolonges action potential.
  2. Indication:
    1. Paroxysmal AF (with **structurally normal heart - **the CAST trial increased mortality using flecainide to suppress ventricular ectopy following MI by proarrythmic and negative inotropic effects. DO NOT GIVE if LV dysfunction or ischaemic heart disease)
    2. Paroxysmal SVT
    3. Ventricular tachycardia
  3. Contra-indications: HF, abnormal LV function, history of MI, long-standing AF where conversion to sinus has not been attempted
  4. Adverse effects: oedema, pro-arrythmic effects, dyspnoea, dizziness, asthenia, fatigue, fever, visual disturbance

Clinical Pharmacology (11 decks)

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