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CVS Flashcards

1
Q

SA node is …

A

The dominant pacemaker with an intrinsic rate of 60-100 bpm (NORMAL HEART RATE) - the fastest depolarising tissue

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2
Q

ECG paper scale

A
  • Horizontally:
    • One small box = 0.04s/40ms
    • One large box = 0.20s - Vertically:
    • One large box = 0.5mV
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3
Q

Cardiac output equation + unit

A

(L/min) = Stroke volume (L) x Heart rate (BPM)

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4
Q

Heart sounds

A
  • S1 - mitral and tricuspid valve closure
  • S2 - aortic and pulmonary valve closure
  • S3 - in early diastole during rapid ventricular filling, normal in children and pregnant women, associated with mitral regurgitation and heart failure
  • S4 - ‘Gallop’, in late diastole, produced by blood being forced into a stiff hypertrophic ventricle - associated with left ventricular hypertrophy
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5
Q

ASPIRIN

  • used for treating …
  • info …
A

Angina

  • Antiplatelet effect (inhibits platelet aggregation) in coronary arteries
    thereby avoiding platelet thrombosis
  • To reduce events
  • E.g. salicylate
  • COX inhibitor - reduces prostaglandin synthesis including thromboxane A2 resulting in reduced platelet aggregation
  • Side effects - gastric ulceration
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6
Q

Angina drug treatment:

A

Aspirin
Statins
Betablockers - 1st line antianginal:
-Reduce force of contraction of heart
-E.g. Bisoprolol and atenolol
-Act on B1 receptors in the heart as part of the adrenergic sympathetic pathway
-B1activation→Gs→cAMPtoATP→contraction
• Glyceryl Trinitrate (GTN) spray - 1st line antianginal:
- Nitrate that is a venodilator
- Dilates systemic veins thereby reducing venous return to right heart
- Reduces preload
- Thus reduces work of heart and O2 demand
- Also dilates coronary arteries
- Side effect: profuse headache immediately after use
• Ca2+ channel antagonists/blocker:
- Primary arterodilators
- Dilates systemic arteries resulting in BP drop
- Thus reduces afterload on the heart
- Thus less energy required to produce same cardiac output - Thus less work on heart and O2 demand
- E.g. verapamil

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7
Q

ACS (acute coronary syndrome) drug treatment:

A

Pain relief: GTN spray + IV opioid
Aspirin
P2Y12 inhibitors - E.g. Clopidogrel, Prasugrel & Ticagrelor
Glycoproteins IIIb/IIIa antagonist (IV) - E.g. Abciximab, Tirofiban and Eptifbatide
Beta-blockers (IV & oral) • E.g. Atenolol (IV then oral) or Metoprolol (IV then oral)
Statins • E.g. Simvastatin, Pravastatin and Atorvastin
ACE inhibitors: Ramipril and Lisonopril

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8
Q

ACI (acute myocardial infarction) drug treatment:

A 
Pre-hospital:
• Aspirin 300mg chewable 
• GTN (sublingual)
• Morphine
Hospital:
• IV morphine
• Oxygen if their sats are below 95% or are breathless 
• Beta-blocker - Atenolol
• P2Y12 inhibitor - Clopidogrel
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9
Q

Cardiac failure def:

A

• The inability of the heart to deliver blood and thus O2 at a rate that is commensurate with the requirement of metabolising tissue of the body

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10
Q

Cardia failure drug treatment:

A

Diuretics:
• Promote sodium and thus water loss thereby reducing ventricular filling pressure (preload) decreasing systemic and pulmonary congestion
• Loop diuretic - furosemide
• Thiazide diuretic - bendroflumethiazide (inhibit sodium reabsorption in the distal convoluted tubule)
• Aldosterone antagonist (thereby inhibiting ADH release resulting in water loss) - spirolactone & epelerone - note with these beware of renal impairment and hyperkalaemia
ACE inhibitors:
• Ramipril, enalipril, captopril
• Side effects: cough (since inhibit ACE and thus the breakdown of substance P and bradykinin which results in cough), hypotension, hyperkalaemia and renal dysfunction
• If cough is a problem then can give angiotensin receptor blockers (not as effective as ACE-inhibitors) e.g. canderstan or valsartan
Beta-blockers:
• Bisoprolol, nebivolol, carvedilol
• Start at low dose and titrate upwards
• DO NOT GIVE TO ASTHMATICS
-Digoxin
-Inotropes

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11
Q

• CLINICAL SCENARIO:
- 84 yr old frail woman of Asian origin with dizziness, low blood pressure and
shortness of breath
- She also has swollen legs (leg oedema) which have become more swollen
over the past few days
• In the context of her shortness of breath and swollen legs, her low BP is
most likely to be indicative of?

A
  • Biventricular failure:
    • Shortness of breath due to right ventricular failure
    • Leg oedema due to left ventricular failure
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12
Q

Mitral valve disease drug treatment:

A
  • Beta-blockers e.g. Atenolol and digoxin which control heart rate and thus prolong diastole for improved diastolic filling
  • Diuretics for fluid overload e.g. Furosemide
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13
Q

Mitral regurgitation drug treatment:

A

Vasodilators such as ACE-inhibitors e.g. Ramipril or Hydralazine (smooth muscle relaxer)
• Heart rate control for atrial fibrillation with Beta blockers (Atenolol), Calcium channel blockers and digoxin
• Anticoagulation in atrial fibrillation and flutter
• Diuretics for fluid overload e.g. Furosemide

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14
Q

Ineffective endocarditis is caused by:

A 
Staphylococcus aureus (IVDU, diabetes and surgery) - most common cause
Pseudomonas aeruginosa
 Streptococcus viridans (dental problems) - GRAM POSITIVE, alpha haemolytic and optochin resistant (Strep. mutans, strep, sanguis, strep. milleri & strep. oralis)
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15
Q

Ineffective endocarditis drug therapy:

A
  • Antibiotic treatment (which one is decided on organism ascertained from cultures) for 4-6 weeks
  • If not staphylococcus then use penicillin ideally Benzylpenicillin & Gentamycin (doesn’t work on own since cannot get through bacterial cell wall)
  • If staphylococcus then use Vancomycin & Rifampicin (if MRSA)
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16
Q

Hypertrophic cardiomyopathy (HCM) drug therapy:

A

Amiodarone - anti-arrythmatic medication, if at high risk of arrhythmia then can place an implantable cardiac defibrillator
• Calcium channel blocker e.g. Verampil
• Beta-blocker e.g. Atenolol

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17
Q

Arrythmogenic right ventricular cardiomyopathy:

A

• Beta-blockers e.g. Atenolol for patients with non-life-threatening arrhythmias
• Amiodarone for symptomatic arrhythmias
• Occasionally cardiac transplant indicated i.e. in cardiac failure or
devastating arrhythmia

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18
Q

Ventricular septal defects (VSD) drug treatment:

A

If moderately sized lesion; furosemide, ACE inhibitor e.g. ramipril and digoxin may suffice

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19
Q

Patent ductus arteriosus drug treatment:

A

Indometacin (prostaglandin inhibitor) can be given to stimulate duct closure

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20
Q

Acute pericarditis def:

A

Acute inflammation of the pericardium; with or without effusion

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21
Q

Acute pericarditis drug treatment:

A

NSAID e.g Ibuprofen for two weeks or Aspirin for two weeks
- Colchicine for 3 weeks however is limited by nausea and diarrhoea but does reduce recurrence
• Recurrent or relapsing pericarditis:
- About 20% of cases of acute pericarditis go on to develop idiopathic relapsing pericarditis
- This may occur within 6 weeks during weaning off NSAIDs or intermittently i.e. recurs more than 6 weeks after the initial presentation
- The first line treatment is oral NSAIDs e.g. Ibuprofen
- Colchicine has been proven to be more effective than Aspirin alone

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22
Q

Hypertension:

Normotensive=

A

Less than 140/90mmHg

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23
Q

Hypertension values -stages …

A

Stage 1 hypertension:
- More than or equal to 140/90mmHg clinic BP
- Daytime average Ambulatory blood pressure monitoring (ABPM - 24hr BP monitor) or Home blood pressure monitoring (HBPM); greater than or equal to 135/85mmHg
Stage 2 hypertension:
- More than or equal to 160/100mmHg clinic BP
- Daytime average ABPM or HBPM greater than or equal to 150/95mmHg
Severe hypertension:
- Clinic systolic BP greater than or equal to 180mmHg and/or
diastolic BP greater than or equal to 110mmHg
- Start immediate anti-hypertensive drug treatment!

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24
Q

Hypertension treatment

A

Reach 140/90mmHg
ACD pathway:
A - ACE-inhibitor e.g. Ramipril or Enalapril, or Angiotensin receptor blocker (ARB) (use if ACEi is contraindicated e.g. due to cough) e.g. Candesartan or Losartan
C - Calcium channel blocker (CCB) e.g. Nifedipine or Amlodipine D - Diuretics e.g. Bendroflumethiazide (thiazide, distal tube - less
potent) or Furosemide (loop diuretic, loop of henle - more potent)
NOTE: Beta-blocker e.g. Bisoprolol or Metoprolol (B1 selective) are NOT the FIRST LINE TREATMENT FOR HYPERTENSION but consider in young people especially if they are intolerant of ACEi/ARB
Less than 55 yrs old:
- Ramipril/Candesartan - + Nifedipine
- + Bendroflumethiazide - + Furosemide
Older than 55 yrs/black/African-Caribbean origin:
- Ramipril/Candesartan + Nifedipine - + Bendroflumethiazide
- + Furosemide

25
Q

Cardiac arrhythmias may cause:

A
  • Sudden death
  • Syncope
  • Heart failure
  • Chest pain
  • Dizziness
  • Palpitations
  • No symptoms at all
26
Q

AF (atrial fibrillation) drug treatment:

A

Cardioversion:
- Conversion to sinus rhythm achieved electrically by DC shock e.g. defibrillator - NOTE: give low molecular weight heparin e.g. Enoxaparin or Dalteparin to minimise the risk of thromboembolism associated with cardioversion
- If this fails then achieved medically by IV infusion or anti- arrhythmic drug such as flecainide or amiodarone
Ventricular rate control:
- Achieved by drugs that block AV node:
• Calcium channel blocker e.g. Verapamil • Beta-blocker e.g. Bisoprolol
• Digoxin
• Anti-arrhythmic e.g. Amiodarone
- Long term & stable patient management:
• Two strategies; which to choose should be decided based on individual
patient needs
• Rate control:
- AV nodal slowing agents plus oral anticoagulation
- Beta-blocker e.g. Bisoprolol
- Calcium channel blocker e.g. Verapamil or Diltiazem
- If above fails then try Digoxin and then consider Amiodarone
• Rhythm control:
- Advocated for younger, symptomatic and physically active
patients
- Cardioversion to sinus rhythm and use Beta-blockers e.g.
Bisoprolol to suppress arrhythmia
- Can use pharmacological cardioversion e.g. Flecainide if no structural heart defect or use IV Amiodarone instead if there is structural heart disease
- Appropriate anti-coagulation e.g. Warfarin due to thromboembolism risk with cardioversion

27
Q

Atrial flutter drug treatment:

A

Electrical cardioversion but anticoagulate before e.g low molecular weight heparin e.g. Enoxaparin or Dalteparin if acute i.e. atrial flutter started less than 48 hours ago

  • Catheter ablation - creating a conduction block to try an restore rhythm and block offending re-entrant wave
  • IV Amiodarone to restore sinus rhythm and use a beta-blocker e.g. Bisoprolol to suppress further arrhythmias
28
Q

Atrioventricular block causes:
First degree AV block:
Second degree …:

Third degree…:

A

1: • Hypokalaemia
• Myocarditis
• Inferior MI
• Atrioventricular node (AVN) blocking drugs e.g. beta blockers (Bisoprolol), calcium channel blockers (Verapamil) and Digoxin
2: - Atrioventricular node (AVN) blocking drugs e.g. beta blockers
(Bisoprolol), calcium channel blockers (Verapamil) and Digoxin - Inferior MI

Complete AV block

29
Q

AV block narrow-complex escape rhythm

A

QRS complex less than 0.12 seconds
Implies block originates in the His bundle and thus the region of block lies
more proximally in the AV node
Recent-onset, narrow-complex AV block that has transient causes may
responses to IV atropine
Chronic narrow-complex AV block requires permanent pacemaker if it is symptomatic

30
Q

AV block drug treatment:

A

IV atropine

31
Q

Right bundle branch block (RBBB) on ECG:

A
  • Looks like maRRow
  • maRRow - Right bundle branch block - MarroW:
    • M-QRSlookslikeanMinleadV1
    • W-QRSlookslikeWinV5&V6
    • Causes wide physiological splitting of the SECOND HEART SOUND
32
Q

Left bundle branch block (LBBB) on ECG:

A
  • Looks like wiLLiam
  • wiLLiam - Left bundle branch block
  • WilliaM:
    • W-QRSlookslikeaWinleadsV1&V2 • M - QRS looks like an M in leads V4-V6
33
Q

Sinus tachycardia drug treatment:

A

Beta-blocker like bisoprolol

34
Q

ATRIOVENTRICULAR RE-ENTRANT TACHYCARDIA (AVRT):

A
  • If stable then vagal manoeuvres:
    • Breath-holding
    • Carotid massage
    • Valsalva manoeuvre - abrupt voluntary increase in intra-abdominal and intrathoracic pressure by straining - several seconds after the release of the strain, the resulting intense vagal effect may terminate the AVNRT or AVRT
  • If manoeuvres unsuccessful then IV adenosine - causes complete heart block for a fraction of a second and is highly effective at terminating AVNRT and AVRT
35
Q

Ventricular ECTOPICS OR TACHYCARDIA drug treatment:

A
  • Give beta-blockers e.g. Bisoprolol if symptomatic
36
Q

SUSTAINED VENTRICULAR TACHYCARDIA

A
  • Haemodynamically unstable (e.g. hypotensive or pulmonary oedema):
    97
    KP

All information is taken from lectures and textbooks, there may be mistakes!!
• Emergency electrical cardioversion - Stable:
• IV beta-blocker e.g. Esmolol
• IV Amiodarone

37
Q

Lone QT syndrome drug treatment:

A
  • Treat underlying cause
  • If acquired long QT then give IV isoprenaline (contraindicated for congenital
    long QT)
38
Q

Aneurysmal disease

A

An aneurysm is defined if there is a permanent dilatation of the artery to TWICE the normal diameter

39
Q

THORACICABDOMINALANEURYSM(TAA) drug treatment:

A
  • Rigorous BP control using beta-blockers e.g. Bisoprolol -
40
Q

Aortic dissection drug treatment:

A
  • At least 50% are hypertensive and may require urgent antihypertensive medication to reduce blood pressure to less than 120mmHg - give IV beta- blockers e.g. IV metoprolol or vasodilators e.g. IV GTN
  • Adequate analgesia e.g. morphine
  • Surgery to replace aortic arch
  • Endovascular intervention with stents
41
Q 
- PERIPHERAL VASCULAR DISEASE (PVD):
   Thrombotic disease (more common nowadays):

Symptoms:

Treatment:

A 
- Symptoms:
• The 6 P’s:
- Pain
- Pallor
- Perishing cold
- Pulseless
- Paralysis
- Paraesthesia - abnormal tingling or prickling - ‘pins & needles’
- The more P’s present the more sudden and the more complete your ischaemia

• Antiplatelet agent such as P2Y12 inhibitor e.g. Clopidogrel to prevent
progression and minimise risk

42
Q

SHOCK def

A

Shock is the term used to describe acute circulatory failure with inadequate or inappropriately distributed tissue perfusion (meaning there is inadequate substrate (glucose & oxygen) for aerobic cellular respiration), resulting in generalised hypoxia and/or an inability of the cells to utilise oxygen

43
Q

Recognising shock:

A
  • Skin is pale, cold, sweaty and vasoconstricted
  • Pulse is weak and rapid
  • Pulse pressure reduced - mean arterial pressure (MAP) may be maintained - NOTE; ARTERIAL BP is NOT A GOOD INDICATOR OF SHOCK since it will be maintained until a very large amount of blood loss
  • Reduced urine output
  • Confusion, weakness, collapse and coma
44
Q

Effects of shock

A

Prolonged hypotension which can lead to life threatening organ failure after recovery from the acute event

45
Q

Causes of shock:

Anaphylactic shock- how?

A
  • Intense allergic
  • Massive release of histamine and other vasoactive mediators causing haemodynamic collapse
  • Accompanied by breathlessness and wheeze (due to bronchospasm)
46
Q

Haemorrhagic Shock Classification (Tennis Score):

A 
- Class I:
• 15% blood loss
• Pulse below 100 bpm • BP normal
• Pulse pressure normal
• Resp rate; 14-20
• Urine output greater than 30ml/hr • Slightly anxious
 Class II:
• 15-30% blood loss
• Pulse greater than 100 bpm (tachycardia - earliest sign)
• BP normal due to autonomic response (increased sympathetic activity) • Pulse pressure decreased
• Resp rate; 20-30
• Urine output: 20-30ml/hr
• Mental status: mildly anxious
-Class III:
• 30-40% blood loss
• Pulse above 120 bpm
• BP decreased
• Pulse pressure decreased • Resp rate; 30-40
• Urine output: 5-15ml/hr
• Mental status: confused
47
Q

Clinical presentation of cardia shock:

A

• Increased sympathetic tone
• Tachycardia - narrow pulse pressure and weak pulse • Sweating
• BP may be maintained initially but later hypotension
• Bradycardia
- Cardiogenic shock:
• Signs of myocardial failure
• Raised jugular venous pressure (JVP) • Gallop rhythm
• Basal crackles and pulmonary oedema

48
Q

Hypertension def

A

as a clinical BP of 140/90mmHg or higher

49
Q

Factors controlling BP and thus targets for BP control therapy:

A

Since; Cardiac output x Peripheral resistance = BP - can target peripheral resistance to alter BP

50
Q

Hypertension drug treatment:

A

ANGIOTENSIN CONVERTING ENZYME (ACE) INHIBITORS:
• Indicated for; hypertension, heart failure and diabetic nephropathy • ACE inhibitor end in ‘pril’
• Also REDUCE circulating levels of ALDOSTERONE
• Examples:
- RAMIPRIL
- ENALAPRIL
- PERINDOPRIL
- LISINOPRIL
- TRANDOLAPRIL
ANGIOTENSIN II RECEPTOR BLOCKERS (ARB):
• Indicated for; hypertension, diabetic neuropathy and heart failure (when ACE inhibitor is contraindicated
• ARB’s end in ‘sartan’
• Angiotensin receptor blocker acts on AT-1 receptor (angiotensin receptor)
• Examples:
- CANDESARTAN - LOSARTAN
- VALSARTAN
- IRBESARTAN
- TELMISARTAN
- CALCIUM CHANNEL BLOCKERS (CCB):
Indicated for; hypertension, ischaemic heart disease (IHD) i.e. angina and arrhythmia (tachycardia)
A lot but not all end in ‘pine’ - these are vasodilators Diltiazem & Verapamil have effects on electrical conductivity Examples:
- AMLODIPINE - DILTIAZEM
- VERAPAMIL - NIFEDIPINE
- FELODIPINE - LACIDIPINE
BETA-ADRENOCEPTOR BLOCKERS (BETA-BLOCKERS):
Lower down list in terms of use
Indicated for; ischaemic heart disease (IHD) - angina, heart failure,
arrhythmia and hypertension A lot end in ‘olol’
Examples:
- BISOPROLOL
- CARVEDILOL
- PROPRANOLOL
- METOPROLOL
- ATENOLOL (antagonist at beta-1 adrenoceptor) - NADOLOL

51
Q

Calcium channel blockers (CCB) Action and adverse effects

A
  • L-type calcium channel blockers (block ion channels and NOT RECEPTORS):
    • Dihydropyridines: nifedipine, amlodipine, felodipine, lacidipine:
  • Preferentially affect vascular smooth muscle
  • Peripheral arterial vasodilators
    • Phenylalkylamines: verapamil:
  • Main effect is on heart
  • Reduce HR (negatively chronotropic) and force of
    contraction of the heart (negatively inotropic)
    • Benzothiozepines: diltiazem:
  • ## Intermediate heart/peripheral vascular effects • Adverse effects:Due to peripheral vasodilation (mainly dihydropyridines e.g. nifedipine and amlodipine):
    • Flushing
    • Headache
    • Oedema - swelling, typically around ankles due to gravity
    • Palpitations - due to vasodilation there is decreased BP so body tries to correct by increasing HR (known as reflexive tachycardia)
    Due to negatively chronotropic effects (heart rate) mainly verapamil and diltiazem:
    • Bradycardia (low HR)
    • Atrioventricular block
    • POSTURAL HYPOTENSION
    Due to negatively inotropic effects (force of contractility) mainly verapamil:
    • Worsening of cardiac failure
    Verapamil causes constipation - since it affects Ca2+ and thus smooth muscle contraction in the intestines
    Diuretics… see flash card
52
Q

Diuretics

A

• Indicated for; hypertension and heart failure • Classes & Examples:
-Thiazides (cause Na+ and thus water loss in urine) and related drugs - act on DISTAL TUBE - LESS POTENT, tend to end in ‘thiazide’:
• BENDROFLUMETHIAZIDE • HYDROCHLOROTHIAZIDE • CHLOROTHALIDONE
Loop diuretics (act on LOOP OF HENLE - MORE POTENT): • FUROSEMIDE - blocks NA/K/2Cl (NKCC2) transporter • BUMETANIDE
Potassium-sparing diuretics:
SPIRONOLACTONE EPLERENONE
Note these two have the potential to antagonise aldosterone (anti-aldosterone)
- Aldosterone antagonists • Main adverse effects:
- Hypovolaemia (mainly loop diuretics e.g. furosemide)
- Hypotension (mainly loop diuretics e.g. furosemide)
- Hypokalaemia
- Low serum sodium (hyponatraemia)
- Low serum magnesium (hypomagnesaemia)
- Low serum calcium (hypocalcaemia)
- Raised uric acid (hyperuricaemia - can result in gout (extremely painful)
- Erectile dysfunction (mainly thiazides e.g. bendroflumethiazide)
- Impaired glucose tolerance i.e. diabetes (mainly thiazides e.g.
bendroflumethiazide)

53
Q

Other antihypertensives

A

• Alpha-1 adrenoceptor blockers:
- DOXAZOSIN
• Centrally acting (i.e. on brain) anti-hypertensives: - MOXONIDINE
- METHYLDOPA - CAN BE USED IN PREGNANCY • Direct renin inhibitor:
- ALISKIREN

54
Q

Chronic heart failure drug treatmetn

A

Basic pharmacology:
- Symptomatic treatment of congestion:
• Diuretics usually loop diuretics e.g. Furosemide
- Disease influencing therapy - neurohumoral blockade:
• Inhibition of renin-angiotensin-aldosterone system e.g. ACE-inhibitors and ARB’s
• Inhibition of the sympathetic nervous system e.g. beta-blockers such as BISOPROLOL which are effective at blocking reflex sympathetic responses which stress the failing heart
- First line treatment:
• ACE inhibitors e.g. Ramipril and beta-blocker e.g. Bisoprolol • Low dose and slow uptitration
- Second line:
• Aldosterone antagonists
• If ACE-inhibitor intolerant then give ARB’s (not as good as ACE-i) e.g. Candesartan
• If ACE-I and ARB intolerant then give Hydralazine/nitrate combination (peripheral vasodilators)
- Consider digoxin or ivabradine (rate-limiting drug)

55
Q

• CARDIAC NATRIURETIC PEPTIDES:

Explained

A

Cardiac natriuretic peptides are metabolised by Neutral Endopeptidase (NEP or neprilysin)
NEP inhibition increases levels of natriuretic peptides
Sacubitril - is a neprilysin inhibitor
Valsartan - is a ARB
Entresto - is a combination of sacubitril and valsartan - VERY EFFECTIVE IN HEART FAILURE
NITRATES:
- Arterial and venous dilators
- Reduce preload and afterload
- Lower BP
- Indicated for; ischaemic heart disease (angina) and heart failure - Examples:
• ISOSORBIDE MONONITRATE - long-acting!!
• GTN (GLYCERYL TRINITRATE) SPRAY - sublingual spray, potent vasodilator, commonly give headache
• GTN infusion
- Main adverse effects are headache and GTN spray syncope as well as POTENTIAL TOLERANCE to the drug

56
Q

• CHRONIC STABLE ANGINA TREATMENT:

A 
Antiplatelet therapy:
• ASPIRIN
• CLOPIDOGREL (P2Y12 inhibitor) - use if aspirin intolerant
131
KP

All information is taken from lectures and textbooks, there may be mistakes!!
- Lipid-lowering therapy:
• Statins e.g. SIMVASTATIN, ATORVASTATIN, ROSUVASTATIN &
PRAVASTATIN
- Short acting nitrate:
• GTN spray for acute attack - DILATES veins to reduce the preload of the heart
- First line treatment:
• Beta blocker e.g. BISOPROLOL
• Calcium channel blocker e.g. AMLODIPINE
- If intolerant then SWITCH i.e. if using beta-blocker then switch to calcium channel blocker
- If not controlled then COMBINE
- If intolerant and uncontrolled then consider monotherapy or combination
with:
• Long acting nitrates:
- Ivabradine - Nicorandil - Ranolazine

57
Q

• ACUTE CORONARY SYNDROMES (NSTEMI & STEMI) TREATMENT:

A

Pain relief:
• GTN spray
• Opiates - DIAMORPHINE (also helps calm patient) Dual antiplatelet therapy:
• Aspirin plus P2Y12 inhibitor (oral) e.g. TICAGRELOR, PRASUGREL or CLOPIDOGREL
Antithrombin therapy:
• Heparin e.g. FONDAPARINUX (injection)
Consider a glycoprotein IIb/IIIa inhibitor (IV) e.g. TIROFIBAN, EPTIFBATIDE or ABCIXIMAB
Background angina therapy:

All information is taken from lectures and textbooks, there may be mistakes!!
• Beta blocker e.g. BISOPROLOL:
- Beta blockers help to relieve pain from angina by:
• Reducing O2 demand by slowing heart rate and reducing myocardial contractility
• Improve O2 distribution by slowing heart rate • Long acting nitrate e.g. IVABRADINE
• Calcium channel blocker e.g. AMLODIPINE - Lipid lowering therapy:
• Statins e.g. SIMVASTATIN
- Therapy for LVSD/heart failure as required:
• ACE-I e.g. RAMIPRIL
• Beta blocker
• Aldosterone antagonist

58
Q

ANTIARRHYTHMIC DRUGS:

A
  • Vaughan Williams Classification:
    • Classes 1 & 3 = Rhythm control • Classes 2 & 4 = Rate control
    • Class 1:
  • Sodium channel blocker e.g. FLECAINIDE • Class 2:
  • Beta-adrenoceptor blockers (Beta-blockers):
    • Class 3:
    Non-selective e.g. PROPRANOLOL, NADOLOL & CARVEDILOL
    Selective (B-1) e.g. BISOPROLOL and METOPROLOL
    NOTE: PROPRANOLOL is the most useful beta blocker to help control the arrhythmias which occur immediately following a MI since it also BLOCKS SODIUM CHANNELS
  • Prolong the action potential: • AMIODARONE
    • SOTALOL
    • Has potential for SIGNIFICANT SIDE EFFECTS - see below • Class 4:
  • Calcium channel blockers:
    • VERAPAMIL (more effective than amlodipine since it DOES
    NOT effect the calcium channel at rest)
    • DILTIAZEM
    • AMLODIPINE
  • Sympathetic drive e.g. adrenaline worsens arrhythmia - DIGOXIN:
59
Q

DIGOXIN:

Explained

A

• Cardiac glycoside
• Inhibits the Na/K pump - found everywhere in body
• Main effect on heart:
- Bradycardia (due to increased vagal (parasympathetic) tone)
- Increased ectopic activity - can trigger extra heartbeats i.e. minor
arrhythmias
- Increased force of contraction (DIRECT POSITIVE INOTROPIC
EFFECT on heart muscle) by increased intracellular Ca2+ - Slowing of AV conduction
• Narrow therapeutic range - need to have precise amount to have desired effects otherwise get side effects:
- Nausea, vomiting, diarrhoea and confusion
• Used in atrial fibrillation to reduce ventricular rate response
• Used in severe heart failure as a positive inotropic (increases heart contractility)

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