Flashcards in Cardiology Deck (15)
Which of the following is a cause of high output heart failure?
1. Ischaemic heart disease
4. Valvular heart disease
High output heart failure occurs when the pump function of the myocardium is insufficient to meet the oxygen requirements of the tissues due to increase demand of the tissues.
Causes: pregnancy, thyrotoxicosis, anaemia, beriberi & Paget's disease of the bone
Low output HF - failure of "supply" due to disease of the heart itself
Causes:IHD, valvular HD, pericardial disease, cardiomyopathies, hypertension
Which investigation is the most useful in a patient with peripheral pitting oedema, hepatomegaly, displaced apex beat & SOB
ECHO - most useful test in diagnosis of HF and assesses the left ventricular ejection fraction, left and right ventricular structure and functionality, heart valves and pericardium.
Presence of regional wall motion abnormality suggests underlying coronary artery disease
Systolic HF - reduced ejection fraction (stroke vol/ end diastolic vol)
Diastolic HF - stiffening of the ventricle wall, HF with preserved ejection fraction - reduced ventricular filling
Which of the following blood tests is useful in the diagnosis of HF?
low levels have a high negative predictive value.
High levels have a high positive predictive value.
Other blood tests are not helpful but U&Es need to be monitored to detect complications of diuretic therapy. Additionally, hyponatraemia is strongly assoc with adverse outcomes in HF
A man with diagnosed HF can walk 80m without becoming fatigued and breathless and having to rest. What NYHA classification is he?
III - marked limitation of activity (walking 100m)
III - marked limitation
IV - symptoms at rest
68 yr old man with orthopnoea and paroxysmal nocturnal dyspnoea and a cough with pink frothy sputum. What sign would you not expect to see?
1/ bilateral creptitations on respiratory auscultation
2. bats wings shadowing on CXR
3. cardiomegaly on CXR
4. polyphonic wheeze
5. pleural effusions, upper lobe diversion and Kerley B lines
6. additional HS (S3 and/or S4)
Polyphonic wheeze - characteristic of asthma and COPD
The rest are common signs in HF
68yr old man with orthopnoea and PND and cough with pink frothy sputum. What would be the first line of treatment?
2. IV GTN
4. Intubation and mechanical ventilation
5. IV furosemide
IV furoremide (loop diuretic) - immediate effect in HF is through venodilatation.
If furosemide is insufficient add IV GTN infusion.
If insufficient - CPAP
Useful adjuncts include IV opioids such as morphine (venodilates and reduces feeling of breathlessness and anxiety)
Occasionally digoxin (+ve inotrope) in pmts who are hypotensive due to caridogenic shock
If pnt still hypoxic or tiring refer to ITU for intubation and mechanical ventilation
Initial management of a pnt diagnosed with HF,
1. ACE I, atenolol and lifestyle changes
2. lifestyle changes, ACEI, bisoprolol and amlodipine
3. Lifestyle changes alone
4. Lifestyle changes, furosemide, bisoprolol, ramipril
5. lifestyle changes, furosemide, atenolol, enalapril
Initial management of chronic heart failure
(i) Optimal long-term treatment of patients newly diagnosed with heart failure should include a combination of: lifestyle changes, loop diuretics, ACE inhibitors and β-blockers.
(ii) Lifestyle changes. Patients should be advised to stop smoking and excessive alcohol intake, restrict dietary salt intake, perform aerobic exercise, and lose weight if overweight or obese.
(iii) Loop diuretics:
a. Most patients are started on oral furosemide, which is then up-titrated until oedema is controlled.
b. Occasionally you will encounter patients on a different loop diuretic, bumetanide. This is 40x more potent that furosemide (i.e. 1mg bumetanide = 40mg furosemide). Bumetanide is said to be better absorbed (i.e. have higher oral bioavailability) in patients with severe right heart failure because of mucosal oedema in the bowel, although the evidence for this is weak.
c. Loop diuretics improve symptoms in heart failure but do not alter prognosis.
(iv) ACE inhibitors:
a. ACE inhibitors (-pril) drugs improve prognosis in heart failure. Start at low dose and aim to up-titrate as much as tolerated.
b. The effect is class-specific (i.e. any ACE inhibitor can be used and there is no particular advantage to one over the other).
c. Common ACE inhibitors you will encounter include ramipril, enalapril and lisinopril.
a. β-blockers also improve prognosis in heart failure. Start at low dose and aim to up-titrate as much as tolerated.
b. The effects are drug-specific (i.e. only a few are proven to be effective). These are bisoprolol, metoprolol and carvedilol. Other β-blockers such as atenolol and propranolol do not work in this scenario.
Patient with HF who is on furosemide, ramipril and bisoprolol but has very swollen legs and is very SOB. You are taking daily weights but he is not losing weight. which of the following is not a sensible management plan?
1. switch from furosemide to bumetanide
2. Switch from oral to iv furosemide
3. Switch from oral to iv ramipril
4. Add metolazone
5. Add bendroflumethiazide
6. Add digoxin
Daily weights - aim to lose 1kg / 24hrs.
If this is difficult with oral furosemide, options include:
a. Switching furosemide from oral to IV.
b. Switching furosemide to bumetanide (said to have greater oral bioavailability; see above).
c. Adding in a thiazide diuretic (such as metolazone or high dose bendroflumethiazide).
d. Adding in digoxin (demonstrated to improve symptoms and reduce hospital admissions, but does not alter overall prognosis).
Mr R is on furosemide, ramipril and bisoprolol for his HF. He has developed a nasty dry cough. What has caused this and what could you do?
Ramipril SE is cough
Switching to an angiotensin receptor blocker (ARB, -artan drug), such as losartan, candesartan or valsartan.
Switching to a combination of hydralazine and isosorbide mononitrate.
(ii) Both of these approaches improve prognosis. There is no benefit of additive therapy (i.e. being on both an ACE inhibitor and an ARB, or an ACE inhibitor and hydralazine/nitrate).
Patient presents with SOB
If a patient presents with NYHA stage III-IV heart failure, there is a prognostic benefit in adding in an aldosterone antagonist such as spironolactone.
(ii) Approximately 25% of men taking spironolactone develop painful gynaecomastia.
(iii) If gynaecomastia is severe enough that patients cannot tolerate spironolactone, alternative drugs include eplerenone or amiloride.
(iv) If despite optimal medical management, symptoms are still not controlled, further options include:
a. Mechanical options such as ultrafiltration, cardiac resynchronisation therapy or left ventricular assist devices. The evidence base for some of these interventions is limited at present but data collection is ongoing. Knowledge of these is beyond the scope of the undergraduate curriculum.
b. Heart transplantation. Definitive but rarely available or appropriate.
c. Palliative care input. End-stage heart failure has a worse prognosis than most cancers, and symptom burden is high. Involve the palliative care team early as this approach can work well alongside ongoing active medical therapy.
Which of the following is not a SE of furosemide?
Which of the following is not a SE of bendroflumethiazide?
What is the most common SE of ACE I?
2. Postural hypotension
4. flash pulmonary oedema
These are all SE of ACE I e.g. ramipril
cough is the most common ~10%
Which of these is not a SE of ARBs e.g. losartan?
2. Postural hypotension
4. flash pulmonary oedema