Cardiovascular Flashcards

1
Q

Atenalol/ beta blocker

A

Management angina, HT, prevention MI

Blocks stimulation of beta 1 (cardiac) adrenergic receptors. Decreases BP and HR and anginal attacks,

Contraindicated- uncompensated heart failure, pulmonary oedema, cardiogenic shock, bradycardia, heart block

Dose- 50-100mg daily

Nursing considerations- monitor BP and pulse

Caution- rental impairment (GFR <35), diabetes (masks hypo), thyrotoxicosis

Side effects-
CNS- fatigue, weakness, anxiety, depression, dizziness, drowsiness, insomnia, memory loss, mental status change, nervousness, nightmares
ENT- blurred vision, stuffy nose
Resp- bronchospasm, wheezing
CVS- Heart failure, bradycardia, pulmonary oedema, hypotension, peripheral vasoconstriction
GI- constipation, diarrhoea, increased liver enzymes, nausea, vomiting,
Genitourinary- erectile dysfunction, decreased libido, urinary frequency
Endo- hyper/hypoglycaemia
Skin- rashes
Musculoskeletal- arthralgia, backpain, joint pain

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2
Q

Labetalol/beta blocker

A

Antianginal/ anti hypertensive

Blocks stimulation of beta 1 (myocardial) and beta 2 ( pulmonary, peripheral vascularture and uterine) adrenergic receptor sites. Also has alpha 1 adrenergic blocking activity which may result in more ortho static hypotension

Dose- 100-400mg 2-3times day

Nursing considerations- monitor BP and pulse, watch for orthostatic hypotension.
IV labetalol patients must be supine for administration and 3 hours post.
Monitor intake/output and daily weight

Contraindicated in- decompensated HF, pulmonary oedema, cardiogenic shock, bradycardia or heart block

Use cautiously in: pulmonary disease, thyrotoxicosis, diabetes, renal or hepatic impairment,

Adverse reactions- CNS- fatigue, weakness, anxiety, depression, dizzy, drowsiness, insomnia, memory loss, mental status change, nightmares
CVS- arrhythmias, bradycardia, CHf, orthostatic hypotension
Skin- itching, rash
ENT- blurred vision, dry eyes, intraoperative floppy iris syndrome, nasal stuffiness
Endo- hypoglycaemia, hyperglycaemia
GI- constipation, diarrhoea, nausea
Genitourinary- decreased libido, erectile dysfunction
Musculoskeletal- arthralgia, back pain, muscle cramps
Neuro- parasthesia
Resp- pulmonary oedema, bronchospasm, wheezing

Drug interactions- digoxin, verapamil, general anaesthesia,diltiazem cause added myocardial depression, bradycardia. Thyroid meds may decrease effectiveness. May alter effects of hypoglycaemics. Effects increased with propranolol and cimetidine. NSAIDs May decrease antihypertensive effects

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3
Q

Digoxin /antiarrhythmic, inotropic

A

Indication- heart failure, Atrial fib, atrial flutter, paroxysmal atrial tachycardia

Increases force of myocardial contraction, prolongs refractory period of AV node, decreases conduction through SA and AV nodes.
Increases cardiac output (positive inotropic) and slows heart rate (negative chronotropic)

Contraindicated: uncontrolled ventricular arrhythmias, AV block (no pacemaker), idiopathic hypertrophic subaortic stenosis, constrictive pericarditis

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4
Q

Midodrine/ vasopressor

A

Used for symptom management of refractory orthostatic hypotension in patients whose livers are impaired. Can also be used for urinary incontinence

Dose- 10mg TDS

Activation of alpha 1 adrenergic receptors in arteries and veins.
Increases vascular tone and BP

Nursing responsibility- monitor sitting and standing BP during therapy, Assess for urinary incontinence, monitor renal and hepatic function

Contraindicated in urinary retention, severe organic heart disease, acute renal disease, persistent excessive supine hypertension, pheochromocytoma, thyrotoxicosis

Use cautiously in: hypertension, renal impairment, hepatic impairment, diabetes, visual impairment, concurrent fludrocortisone,

Adverse effects: CNS- anxiety, confusion, head pressure/fullness, headache, nervousness
CVS- supine hypertension, bradycardia
Urinary- urge/frequency/retention, dysuria
Skin- facial flushing, piloerection, pruritis, rash
Neuro- parasthesia
Misc- chills and pain

Drug interactions- increased risk bradycardia with digoxin, beta blockers, antipsychotics
Increased BP with ephedrine, thyroid hormones, MAO inhibitors, droxidopa,

Effects reduced with alpha adrenergic blockers (prazosin, terazosin)

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5
Q

Telimisartan- micardis

Angiotensin II receptor antagonist

A

Antihypertensive

Dose- 40-80mg daily

Reduces risk of MI, stroke, cardiovascular death in patients over 55 who are at risk of cardiovascular events and can’t take ACE inhibitors

Blocks vasoconstrictor and aldosterone secreting effects of angiotensin II at various receptor sites including vascular smooth muscle and the adrenal glands

Nursing responsibility- assess lying and standing BP, pulse, assess signs of angioedema, monitor renal function, monitor potassium

Contraindicated- hypersensitivity, bilateral renal artery stenosis, concurrent use with aliskirin in patients with diabetes or mod-severe kidney disease

Use cautiously in- volume or salt depleted patients, use of diuretics, impaired renal function caused by primary renal disease or heart failure, obstructive biliary disorder or hepatic impairment, women of childbearing age,

Adverse reactions- CNS- dizziness, fatigue, headache,
CVS- hypotension
ENT- sinusitis
Metabolic- hyperkalaemia
GI- abdo pain, diarrhoea, dyspepsia
Renal- impaired renal function
Muscle- myalgia, back pain
Misc- angioedema

Drug-drug- risk hypotension with other antihypertensive, risk of hyperkalaemia with diuretics/potassium supplement, risk of hyperkalaemia/hypotension/renal impairment with use of ACE inhibitors, NSAID can decrease antihypertensive effect and increase risk of renal impairment

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6
Q

Milrinone

A

Use- inodilator, selectively inhibits cAMP PDE 3 (responsible for breakdown of cAMP) therefore increasing cAMp levels in cardiac and vascular muscle improving myocardial contractility independent of beta stimulation

Positive inotrope as increases calcium influx to cardiac muscle and vasodilator little chronotropic effect

-slight enhancement of AV node conduction

  • increases velocity and magnitude of ventricular contraction, increased cardiac output
  • increased rate ventricular relaxation and enhanced diastolic function
  • arterial and venous dilation (reduced afterload and PVR)

Half life- 2.5-2.4hrs
Onset- 5-15mins

Usual dose- 5-50mcg/min= 1-10ml/hr

Prep- 10mg in 33mls glucose 5%
- 300mcg/ml= 5mcg/min

Indications- cardiogenic shock secondary to ADHF
- low output states post cardiac surgery

Contraindications- severe obstructive aortic or pulmonary vascular disease

Nursing considerations- correct electrolytes, continuous cardiac monitoring, monitor (CO index, PCWP, MAP, SVR, PVR if able )
- never cease abruptly, wean everyone 2-3hrs

Side effects- arrhythmias, hypotension, angina, headache, nausea, tremor, hypokalaemia, thrombocytopenia

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7
Q

Amiodarone

A

-Prep
- low sorb IV line
-loading dose 150mg in 250ml glucose 5% , give over 1hr
Dose range 5mg/kg -(150-350mg)

  • 900mg in 100mls (remove 28ml) of glucose 5%
    10mg/ml

Dose range 1-5ml/hr

Central line or large peripheral vein.
Sideline of normal saline/glucose

300mg can be given via push in emergency situations- 20mls glucose pre and post- saline of cardiac arrest

Class 3 antiarhythmic that prolongs the action potential duration and refractory period of atrial, nodal, ventricular tissues and accessory bypass pathways
- slows HR and AV conduction
- vasodilators action to increase coronary blood flow, decrease cardiac workload and myocardial oxygen consumption
-half-life 9-36 days for IV

Contraindications- brady, sick sinus, AV block, not given with antipsychotics that prolong QT

Precautions- hypotension and circulatory collapse, excessive doses may lead to atropine resistant bradycardia, caution with hepatic failure/lung disease, hypersensitivity to iodine, hypo/hyperthyroidism

Nursing consider- baseline ECG, baseline thyroid tests

Side effects- prolonged QT, bradycardia, AV block, hypotension, N&V, metallic taste, proarrhythmogenic atypical ventricular tachycardia

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8
Q

Labetalol

A

Initial dose 10-20mg over 1-2min
Rpt in 10min if high BP
20-40mg every 10-15min
Max 160mg in 1/24
Max with infusion 300mg in 24hrs

Prep- 100ml N/S or glucose 5%. remove 20mls, add 100mg labetalol
1mg/ml

Infusion rate commence at 20mg/hr then increase by 20mg every 15min till desired BP- max 200mg/hr

Half rate every 30min until off

If BP increases then restart at last effective rate or increase by 20mg/hr every 15min

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9
Q

Lignocaine

A

VT/VF 1-1.5mg/kg (usual 75-100mg)
Over 1-2min slow IV bolus
Can repeat at half dose every 5-10min
Max dose 300mg/hr

Infusion- 1200mg lignocaine (12mls of 500mg in 5mls) in 100mls N/S or glucose 5%. Remove 12mls.

12mg/ml
1ml/hr= 0.2mg/min
1mg/min= 5ml/hr

Commence 4mg/min (20ml/hr) for 1/24 then
3mg/min (15ml/hr) for 1/24 then
2mg/min (10ml/hr) for 24hrs

Action- class 1B antiarrythmic, sodium channel blocker, reduces Automacity of myocardial tissue with little effect on cardiac conduction- may favourably depress conduction in ischaemic myocardium

Half life for bolus 8-11min, for infusion 1.5-2 hours (prolonged in hepatic/heart failure)

Indication- ventricular arrhythmias associated with MI, VF/VT and symptomatic PVC, torsades de pointes

Contraindications- SVT, ventricular escape rhythm, severe heart blocks, stokes-adams syndrome, uncontrolled epilepsy, known hypersensitivity to local anaesthetics

Nursing considerations- resus equipment available, correct hypovolaemia and electrolyte imbalances, baseline ECG

Cease 24hrs after last episode of ventricular arrhythmia. Can be stopped abruptly, no weaning required

Side effects- lignocaine toxicity(drowsy, tingling, nystagmus-stop immediately), headache, dizzy, drowsy, confusion, N&V, tongue numbness, twitching/tremor, visual disturbances, tinnitus, resp arrest, hypotension, Brady, AV block, asystole

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10
Q

Metarominol

A

Dose range 0.25-0.5mg (1ml)
Rpt every 5min until effect

Infusion- 1-5mg/hr
20mg (2ml) made to 40mld of N/S or glucose 5%
0.5mg/ml

Potent synthetic sympathomimetic amine that acts on alpha and beta 1 receptors but no effect on beta 2 receptors

Peripheral vasoconstriction and positive inotropic effect causing increase in systemic blood pressure

No chonotropic effect and may cause reflex bradycardia

Uses- acute hypotension

Life span 20min-1hr
Onset 1-2mins

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11
Q

Clonidine

A

Prep- 900mcg in 100mls (remove 16ml) of N/S
10mcg/ml

25mcg/hr increase every 30min to effect
Wean by 25-50mg/hr

Dose range 50-200mcg/hr

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12
Q

GTN

A

Peripheral- 150mg (30ml) in 500mls N/S or glucose 5%
300mcg/ml
5mcg/min= 1ml/hr

Central access- 30mg (6mls) in 50mls N/S or glucose 5%
600mcg/ml
10mcg/min= 1ml/hr

Dose range 5-200mcg/min
Wean down 5mcg every 15min

Action- organic nitrate that relaxes smooth muscle, it causes dilation of arterial and predominately venous beds.
Venous dilation will reduce venous return (preload) to the heart and decrease myocardial O2 requirement.
Arterial dilation will reduce systemic vascular resistance and arterial pressure (after load) to reduce left ventricular workload.
Dilated coronary arteries to increase coronary perfusion and oxygen supply.
Increases collateral flow to coronary arteries.
Reduces systolic, diastolic and MAP

Half life- 1-4min

Indications- unstable angina and NSTEMI, reduce workload in MI/heart failure, acute HTN, reduce grafted vessel resistance post CABGS

Contraindications- hypersensitivity to nitrate, hypotension or hypovolaemia uncorrected, increased ICP, ICH, constrictive pericarditis, severe aprtic or mitral stenosis, severe anaemia and arterial hypoxaemia, use of sidenafil, hypotrophic obstructive cardiomyopathy

Nursing considerations- continuous cardiac monitoring, baseline ECG, review at 24hrs as tolerance may develop

Side effects- hypotension, headache, flushing, palpitations, reflex tachycardia, decreased arterial oxygen tension, abdominal pain, restlessness, peripheral oedema,

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13
Q

Hydralazine

A

100mg in 100ml N/S
1mg/ml

Bolus 5-10mg over 1minute rpt every 10mins
Max 40mg in 24hrs

Infusion- (no bolus =12-18mg/hr)
(Bolus 3mg/hr)

Titrate 3mg/hr every 10-15min to achieve target BP
Decrease rate when BP achieved

Typical dose range 3-9mg/hr
Max 18mg/hr

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14
Q

Noradrenaline

A

3mg in 50ml syringe of N/S

16mg in 26l glucose 5%

60mcg/ml
1mcg/min

Naturally occurring sympathomimetic amine
-acts on alpha 1& 2 (peripheral vasoconstriction)
- some beta 1 (increased contractility)
-some beta 2 (coronary vasodilation)

Half life 3mins
Onset- 1-2min
Duration 5-10mins

Use- low C/O, decreased SVR, vasodilatory/cardiogenic shock

Precautions with- hypotension with hypovolaemia, peripheral vascular thrombus, MAOI, hyperthyroid, IHD, glaucoma

Side effects- reflex bradycardia due to increased BP, arrhythmia, ischaemia, necrosis with extravasation, urinary retention, anxiety,

Signs of overdose- sweating, hypertension, headache, photophobia, vomiting

Assess for organ perfusion

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15
Q

Sodium nitroprusside

A

Usual dose 20-400mcg/min
2-40ml/hr

Prep- 50mg in 100ml glucose 5%, CSL or N/S (remove 19mls) total 83mls
600mcg/ml
10mcg/min

Cover with black bag
Wean gradually over 10-30min

Infusion at max dose only for 10min to avoid cyanide toxicity

Action- relaxes vascular smooth muscle to cause arterial and venous vasodilation- reduces preload and afterload

Onset action- 2mins, half life 2mins

Contraindications- compensatory HTN, uncorrected hypovolaemia, high ICP, severe renal disease

Side effects- hypotension, rebound HTN when ceased, cyanide toxicity (Venous hyeroxemia, metabolic lactic acidosis, air hunger, confusion, death), ischaemia, GIT disturbances, headache, tachycardia, rash, flushing

Nursing considerations- BP through artline, cardiac monitoring, serum thiocyanide for infusions >48hrs

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16
Q

Vasopressin

A

CVC only

Dose 0.6-2unit/hr

Prep- 40unit (2ml) in 40mls N/S or glucose 5%
1unit/ml
1unit/hr

Analogue of posterior pituitary hormone ADH

Vasoconstriction through V1 vascular receptors

Uses- shock (cardiogenic and vasodilatory), cardiac arrest

17
Q

Aspirin

A

NSAID and Antiplatelet

Blocks pain impulse by blocking Cox 1 in CNS. Reduces inflammation and inhibits prostaglandin synthesis
Antipyretic from peripheral vasodilation and decrease platelet aggregation

Side effects- thrombocytopenia, tinnitus, rash, N&V

Metabolised by liver excreted in kidneys
Half life 15/20mins, peak 1-2, duration 4-6hrs

Nursing considerations- LFT, renal, bloods, skin checks

18
Q

Metoprolol

A

Beta blocker

19
Q

Atorvastatin

A

HMG COA reductase enzyme inhibitor
Reduces cholesterol synthesis
High doses lead to plaque regression

Side effects- constipation, abdo cramps diarrhoea, rhabdomyolosis, headache

Peak 1-2hrs
Metabolised in the liver
Half life 14hrs

Nurse consideration- stool chart, watch for rhabdo

20
Q

Adrenaline

A

Non selective adrenergic agonist with potent beta 1 and moderate alpha and beta 2 receptor activity

Increased force of myocardial contraction and HR from beta 1 stimulation

Increased platelet aggregation

SVR increases due to alpha receptors in peripheral vessels and counters the vasodilation of beta 2 receptors

Beta 2 receptors relax bronchial smooth muscle and stabilise mast cells

Uses- shock, cardiac arrest, bronchospasm/anaphylaxis, symptomatic bradycardia

21
Q

Dobutamine

A

Beta agonist resulting in increased myocardial contractility with variable effect on HR

Beta vasodilation in skeletal smooth muscle can lead to hypotension

Use- low C/O (decompensating HF, cardiogenic shock, sepsis induced myocardial dysfunction)

22
Q

Dopamine

A

Naturally occurring catecholamine that acts directly on alpha, beta and dopaminergic receptors and indirectly by releasing noradrenaline

Increased renal and mesenteric blood flow that increases GFR, sodium excretion and urine output

Beta 1 actions increase myocardial contractility increasing stroke volume and C/O

Alpha actions- vasoconstrict resulting in increased SVR and blood pressure

23
Q

Isoprenaline

A

Synthetic sympathomometic amine acts on beta 1&2 receptors causing increased HR, contractility, automacity, blood pressure, myocardial oxygen demand and bronchodilation

Uses- heart block and brady arrhythmias

24
Q

Levosimendan

A

Enhances calcium sensitivity of contractile fibres by binding to cardiac troponin C in a calcium dependant manner

Increases contractile force but does not impair ventricle relaxation

Opens ATP sensitive potassium channels in vascular smooth muscles causing vasodilation of systemic and coronary arterial resistance vessels and systemic venous capacitance vessels

In patients with heart failure the positive inotropic and vasodilatory actions result in increased contractility and a reduction in preload and afterload without affecting diastolic function