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Advanced Pharmacy Practice > Cardiology > Flashcards

Cardiology Flashcards

1
Q

How often should patients recieving amiodarone be clinically reviewed and what should this entail?

A

Patients taking amiodarone should have a routine 6-monthly clinical review, including liver and thyroid function tests, including a review of side effects.

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2
Q

Why would CCB be used in heart failure patients? Which ones?

A

To treat hypertension or angina.
Amlodipine is drug of choice.
Verapamil, diltiazem or short-acting dihydropyridine agents should be AVOIDED.

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3
Q

When would diuretics be used in a a patient with heart failure?

A

To treat congestive symptoms and fluid retention. Diagnosis and treatment of HF with preserved ejection fraction should be made by a specialist.

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4
Q

What dose of a suitable diuretic would be used in a patient with heart failure?

A

Less than 80mg furosemide per day.

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5
Q

What monitoring accompanies the use of ARBs in HF patients? (4)

A
  1. Serum urea
  2. Serum electrolytes
  3. Creatinine
  4. eGFR

Risk of renal impairment and/or hyperkalaemia.

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6
Q

When would digoxin be used to treat a HF patient?

A

When first-line and second-line ineffective.

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7
Q

What monitoring accompanies the use of digoxin?

A

Routine monitoring of serum digoxin concentration is not recommended. A digoxin concentration measured within 8-12 hours of the last dose may be useful to confirm a clinical impression of toxicity or non-adherence.

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8
Q

What is the CCB drug of choice in the treatment of hypertension/angina in heart failure patients?

A

Amlodipine.

Avoid verapamil, diltiazem or short-acting dihydropyridine agents.

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9
Q

The use of beta blockers in HF treatment is associated with what monitoring requirements?

A

‘Start low, go slow’

  1. HR
  2. BP
  3. Clinical state after each titration.
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10
Q

ARBs are associated with what electrolyte imbalances?

A

Hyperkalaemia

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11
Q

What is the first-line treatment of HF?

A

ACEI + BBs

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12
Q

What is the second-line treatment of HF?

A

Seek specialist advice if the patient is still symptomatic despite optimal therapy with ACEI and BB.

Add in an aldosterone antagonist licensed for heart failure or an ARB or hydralazine in combination with a nitrate.

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13
Q

How do ACEI work?

A

Produce vasodilation by inhibiting the formation of angiotensin II, which is a vasocontrictor formed by the proteolytic action of renin (from the kidneys) on angiotensinogen to form angiotensin I.

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14
Q

How do ARB work?

A

They block the action of angiotensin II at its receptors on muscles surround blood vessels. As a result, blood vessels enlarge and BP is reduced.

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15
Q

How does digoxin work?

A

Increases the force of the heart muscle contraction, reducing the conductivity of the atrioventricular node and reducing the heart rate.

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16
Q

How does ivabradine work?

A

On the funny ion current, which is highly expressed in the sinoatrial node. Blocking this channel reduces cardiac pacemaker activity, selectively slowing the heart rate and allowing more time for blood to flow to the myocardium.

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17
Q

How do aldosterone antagonists such as spironolactone work?

A

Antagonise action of aldosterone at mineralcorticoid receptors which inhibits sodium resportion in the collecting duct of the nephron in the kidneys. This reduces urinary potassium excreation and weakly increases water excretion.

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18
Q

What is heart failure?

A

The condition in which the heart can’t pump enough blood to meet the body’s needs.

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19
Q

What is Class I of the NYHA HF classification?

A

Cardiac disease, but no symptoms and no limitation in ordinary physical activity, e.g. no shortness of breath when walking, climbing stairs etc.

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20
Q

What is Class II of the NYHA HF classification?

A

Mild symptoms (mild shortness of breath and/or angina) and slight limitation during ordinary activity.

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21
Q

Why does heart failure cause SOB?

A

The shortness of breath occurs because blood in the body backs up in the blood vessels that return blood from the lungs to the heart due to the heart not pumping blood out of the heart effectively. This causes fluid to leak into the lungs, also known as congestion.

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22
Q

What is angina?

A

Angina is caused by reduced blood flow to your heart muscle. Your blood carries oxygen, which your heart muscle needs to survive. When your heart muscle isn’t getting enough oxygen, it causes a condition called ischemia. The most common cause of reduced blood flow to your heart muscle is coronary artery disease (CAD).

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23
Q

What is Class III of the NYHA HF classification?

A

Class III: Marked limitation in activity due to symptoms, even during less-than-ordinary activity e.g. walking short distances (20-100m).

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24
Q

What is Class IV of the NYHA HF classification?

A

Severe limitations, experiences symptoms even while at rest. Mostly bedbound patients.

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25
Why are aldosterone antagonists used in congestive heart failure?
They are used in addition to other drugs for additive diuretic effect, which reduces oedema and the cardiac workload.
26
A typical initial dose and dosing regimen for ramipril in heart failure____
Initially 2.5mg od, increased as tolerated to 10mg max daily (divided doses). Increased at intervals of 1-2 weeks.
27
What is a typical initial dose and dosing regimen for losartan and when would it be used in heart failure?
Initially 12.5mg od, increased if tolerated to max 150mg daily in divided doses, at intervals of at least 2 weeks. Used when ACEI unsuitable/ not tolerated.
28
What is a typical dose of bisprolol as an adjunct in heart failure?
Initially 1.25mg once daily (in morning) for 1 week then, if tolerated, increased to 2.5mg once daily for 2 week etc.
29
What is the first line symptom control medication for heart failure?
Diuretics to deal with the fluid imbalances, oedema. Loop diuretics such as furosemide and bumetanide.
30
What is the second line symptom control medication for heart failure?
Aldosterone antagonists like spironolactone for the oedema etc.
31
What is the third line treatment for symptom control in heart failure?
Digoxin, concentration monitoring not really needed unless suspected adverse effects: nausea and vomitting etc. Need to monitor Ca2+, Mg2+ and K+ very closely.
32
If a patient is over 60 and has heart failure and hypertension, what is first-line?
They should be on ACEI as works for both heart failure and hypertension, not CCB as would be expected RE NICE guidance for hypertension over 55s.
33
What is a vascular assessment, who is offered them?
All people over 40 should have a routine cardiovascular risk assessment. A risk factor calculator is used by doctors and nurses to assess the risk of a patient developing a cardio diseas.
34
What are the modifiable risk factors for primary prevention of CHD? (6)
``` Smoking status Hypertension Physical inactivity Uncontrolled diabetes BMI High Cholesterol ```
35
What is/ are Acute Coronary Syndromes (ACS)?
A range of disorders, includes heart attack and unstable angina: caused by sudde reduction of blood flow to part of the heart muscle.
36
What is an STEMI?
ST elevation MI
37
How would a STEMI patient by stabilised?
S/L GTN (IV if needed) for chest pain --> vasodilator. Morphine for pain if needed. (+anti-emetic --> Metoclopramide)
38
How would we reduce the damage in a STEMI patient?
``` Antiplatelets etc. Dual antiplatelet. STAT aspirin and clopidogrel. Aspirin: 300mg, 75mg lifelong. Clopidogrel: 300/600mg (unlicensed but maybe local guidelines), 75mg for 12 months post STEMI. ```
39
Why are anticoagulants used with PCI?
There is a risk of clotting downstream due to disturbance of the plaque/break down.
40
What secondary prevention treatment needs to be initiated for a patient post STEMI?
ACEI Dual antiplatelet therapy (for a year, aspirin for life) Beta-blocker Statin.
41
A positive Exercise Tolerance Test (ETT) result means what?
Highly likely the patient has coronary heart disease.
42
What is the GRACE risk scoring tool used for?
Calculating a patient's risk of future CV events.
43
What does the GRACE tool take into account? (10)
``` Tropinin levels. Renal function. Age. Heart rate. Systolic mmHg. CHF class. Use of diuretics. Renal failure Y/N. ST-segment deviation Y/N. Cardiac arrest at admission Y/N. ```
44
Treatment should be offered to those with a GRACE score of _____
3.5% and above
45
Why would someone on dual antiplatelets also be on a PPI?
To protect the GI due to risk of GI bleeds.
46
What PPI would not be used in patients on dual antiplatelet therapy?
Omeprazole interacts with Clopidogrel (theoretically) - so lansoprazole instead.
47
What percentage drop in kidney function is acceptable when initiating ACEI?
20% drop.
48
What are main symptoms of heart failure? (4)
1. Fatigue 2. Breathlessness - pulmonary oedema 3. Decreased exercise tolerance. 4. Paroxysmal Nocturnal Dyspnoea
49
What are the clinical signs of heart failure? (3)
1. Fluid retention (oedema) 2. Raised venous pressure (elevated JVP) 3. Abnormal heart sounds.
50
When is it possible for a patient to recover completely from heart failure?
When it is caused by a viral agent.
51
Echocardiogram diagnosis of heart failure is based on what? (3)
1. Ejection fraction %, 60% and greater = normal. <30% severe dysfunction. 2. Size of chambers, particularly LV. 3. Presence of regional wall abnormalities. Modern ECHO allows repeatable measurement of parameters removing operator dependence.
52
Do all people with LV dysfunction have heart failure/cardio problems?
High variation in the degree of systolic dysfunction and symptoms that patients present with.
53
What are the aims of heart failure treatment? (4)
1. Reduce symptoms 2. Improve QoL 3. Improve life expectancy 4. Reduce hospital admissions.
54
What is Sucabitril?
Novel antihypertensie used in conjunction with Valsartan.
55
What is the mode of action of Sucabitril?
Neprilysin inhibitor, neprilysin is responsible for the degradation of atrial and brain natriuretic peptide, two blood pressure-lowering peptides that work mainly by reducing blood volume.
56
Sucabitril/Valsartan use leads to______
Increased salt and water excretion via kidneys and reduced blood volume.
57
What is cardiac resynchronisation therapy?
CRT is the implantation of a special pacemaker device to improve the efficieny of existing pump function.
58
What are intra cardiac defibrilators?
Implanted device to terminate or shock patients who develop life-threatening heart rhythms, often combined with CRT device.
59
What is the pathogenesis of ACS?
1. Initiated by the disruption or rupture of an atherosclerotic plaque. 2. Exposure of the unstable core of the atheroma leads to the local generation of thrombin and deposition of fibrin. 3. This promotes platelet aggregation and adhesion and the formation of an intracoronary thrombus. 4. UA and NSTEMI's are associated with partially occlusive thrombus. 5. STEMI's typically result from an occlusive thrombus.
60
What is the pathogenesis of an NSTEMI?
Partially occlusive thrombus.
61
What is the pathogenesis of a STEMI?
Occlusive thrombus.
62
What cardiac markers can indicate cardiac damage?
``` Cardiac tropinins (TnT and Tnl) Creatinine kinase (CK, CK-MB) ```
63
Why are cardiac tropinins prefered to creatinine kinase?
Cardiac tropinins are sensitive and specific for myocardial damage. While creatinine kinases may also be inidicative of heart damage, they are present when ANY muscle damage occurs. Hence, if a patient has suffered other damage there may be a false positive etc.
64
When are levels of cardiac tropinins taken?
On arrival, at 6 hours and 12 hours. Some places are increasingly taking measurements at arrival and then after 30mins/1 hour. Levels peak within 12 hours and fall slowly for up to two weeks.
65
Which cardiac marker is most useful for indicating if a re-infarction has occured?
CK-MB
66
ST-segment modificaton is an indication of_____
Elevation or suppression is a signal marker for ischaemia in the heart.
67
What does ACS encompass?
Unstable angina, NSTEMI STEMI
68
How does the ST segment differ between NSTEMI and STEMI?
NSTEMI = ST segment is depressed or the T wave is inverted. STEMI: ST segment elevated.
69
How will the tropinin results differ for UA/NSTEMI/STEMI?
UA: tropinin negative | STEMI/NSTEMI: tropinin positive
70
What is a coronary angiography?
A procedure that uses contrast dye, usually containing iodine, and x-ray pictures to detect blockages in the coronary arteries that are caused by plaque buildup.
71
What is a coronary angioplasty?
Widen blocked or narrowed coronary arteries (the main vessels supplying the heart). Uses balloons and small stents.
72
How does stenting work?
Inserted through radial artery (more difficult but easier on patient) or the femoral artery (more straightforward route but more hassle for patient due to location) then inflated with a balloon to crush plaque to wall of artery, balloon the deflated and the stent is left in place.
73
Why would thrombolysis be given during/following PCI?
Due to the risk of clots travelling from the site of the plaque to other areas and causing thrombus.
74
Why is thrombolysis no longer used as often in treatment for STEMI?
Superceded by primary PCI directly on admission.
75
What are glycoprotein 2B/3A inhibitors?
They are antiplatelet drugs that act on one of the final stages of platelet activation.
76
How many types of glycoprotein 2B/3A inhibitors are there? What are they?
Two. 1. MAb: Abciximab - permanently inactivates bound platelets 2. Small molecule e.g. Tirofiban, Eptifibatide - reversible inhibition of platelets whilst bound.
77
When are glycoprotein 2B/3A inhibitors used?
Used in the management of NSTEMI and UA patients with high risk factors. Also used post PCI to reduce thrombotic complications due to plaque disruption.
78
What is Tirofiban?
Small molecule reversible inhibitor of glycoprotein 2B/3A.
79
What is Abiciximab?
MAb which permantently inactivates bound platelets. Inhibitor of glycoprotein 2B/3A inhibitors.
80
What is Eptifitibatide?
Small molecule reversible inhibitor of glycoprotein 2B/3A.
81
What is a coronary artery bypass graft?
Treatment of choice for those with severe multi-vessel disease or with co-morbities such as diabetes. Vein grafts, radial grafts or internal mammary artery grafts.
82
What is the overall mortality for CABG?
3-4% but proven to reduce long-term CV mortality in patients with significant coronary disease. Often carried out at the same time if valve replacement/repair surgery is necessary.
83
Why may clopidogrel have variability of effect from patient to patient?
Prodrug - cytochrome p450 system - genetic variation in populations.
84
What is eplerenone?
Aldosterone antagonist licensed for use in patients with evidence of heart failure post MI (ejection fraction <40%).
85
How are beta-blockers of benefit in the management of ACS?
1. Reduce sympathetic drive - reduced myocardial contractility and oxygen demand = reduced stress on myocardium and prevention of further ischemic damage. 2. Reduces BP by vasodilation and prevents sudden spikes in pressure from stress or anxiety.
86
Tropinin-T levels of greater than what are consistent with a diagnosis of ACS?
30ng/L
87
Patients with ACS, and a predicted 6-month mortality of >1.5% should be prescribed what anticoagulants?
Both aspirin 75mg od indefinitely and clopidogrel 75mg od for 12 months.
88
What are the two types of heart failure?
1. Systolic heart failure. 2. Diastolic heart failure. S-HF: reduced ejection fraction, ventricles can't pump fully. D-HF: preserved ejection fraction, but the heart cannot fill properly with blood. Biventricular = both sides.
89
Why is the ejection fraction in diastolic heart failure normal?
Although there is low stroke volume, there is also a reduced 'preload' (low total volume entering ventricle)
90
Blood backed up to the lungs is a sign of
Left sided heart failure.
91
When is the JVP often seen?
Jugular venus pressure is often seen in right sided heart failure.
92
Why are enlarged livers and spleens often seen in heart failure?
Fluid leaks out into the interstital space and leads to enlarged livers and spleens, can cause liver cirrhosis.
93
What is pitting oedema?
Fluid builds up in the legs and when you press it, it dissappears - leaving a pit. It then takes a while to come back.
94
What are troponins?
Specific cardiac structural proteins - if there is myocyte injury troponin will be released. levels of >30ng/l indicate possible MI.
95
What classes of drugs can precipitate HF?
BBs Rate-limiting CCBS (Diltiazem/Verapamil - never used with BB) Corticosteroids. Antiarrythmics (class 1) NSAIDS Lithium Gaviscon Analgesics with high sodium content.
96
What is BNP?
B-type natriuretic peptide is secreted from the ventricles of the heart in response to excess stretching of myocytes. Plasma concentrations of BNP are elevated in HF. Measure serum natriuretic peptides (B-type natriuretic peptide [BNP] or N-terminal pro-B-type natriuretic peptide [NTproBNP]) in patients with suspected heart failure without previous MI. Because very high levels of serum natriuretic peptides carry a poor prognosis, refer patients with suspected heart failure and a BNP level above 400 pg/ml (116 pmol/litre) or an NTproBNP level above 2000 pg/ml (236 pmol/litre) urgently, to have transthoracic Doppler 2D echocardiography and specialist assessment within 2 weeks.
97
If patients are still symptomatic after initial treatment with an ACEI and B-blocker, what is the next step in pharmacological treatment?
Adding in an aldosterone antagonist --> Spironolactone or eplerenone. These have been shown to reduce symptoms and hospitilisation in HF, whilst increasing patient survival.
98
What is the role of diuretics in HF?
Symptom control. | Oedema and SoB etc.
99
When would you use tirofiban in acute treatment of NSTEMI?
If GRACE >6% or significant ECG changes --> NICE says it prevents thrombus extension
100
Name one extra medication use for high risk NSTEMI not used in intermediate risk NSTEMI
Tirofiban
101
What heart rate do you aim for post NSTEMI?
50-60bpm
102
When using aldosterone antagonists such as spironolactone or eplerenone what should you be cautious of
Hyperkalaemia
103
If patients have evidence of heart failure post MI (ejection fraction <40%) what should they be started on within 3-14 days of the event?
Aldosterone antagonist such as eplereone (if already on spironolactone then remain on this).
104
The acute management of ACS consists of
Dual antiplatelets: 300mg aspirin stat oral/rectal, 300mg clopidogrel stat (some trusts 600mg). Anticoagulant: fondaprinux sodium 2.5mg s/c or UFH if eGFR <20ml. Morphine for pain 5-10mg IV + antiemetic like metoclopramide. GTN spray/nitrates. Oxygen? Fluids? Thombolysis if not able to get angioplasty.
105
First line morbidity/mortality control for HF
ACEI and BB (Cardioselective)
106
Second line morbidity/mortality control for HF
1st: ACEI and BB 2nd: Add on aldosterone antagonists or hydralazine nitrate (black heritage, low renin) or ARB
107
What is 3rd line morbidity/mortality control for HF?
1st: ACEI and BB 2nd: Aldosterone antagonists or hydralazine nitrate (black heritage, low renin) or ARB 3rd: Digoxin All of the drugs.
108
What is the 1st line symptom control treatment for HF?
1. Loop diuretic (80mg furosemide) in morning, restrict salt. 2. Thiazide like diuretic (bendro) 3. Aldosterone antagonist (step 2 of morbitity?)

Advanced Pharmacy Practice (29 decks)

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