You are working in the general medical clinic where a 42 year old woman comes for review following a recent, short admission to hospital where she was treated for a paracetamol overdose. She has a past history of depression but denies any other previous problems.
During the review, she is found to have a manual blood pressure reading of 165/85 mmHg. Clinical examination of cardiovascular and respiratory systems are normal, as is urine dip and fundoscopy. Given this information what should be your next course of management in relation to her blood pressure.
- Start ramipril
- Offer ambulatory blood pressure monitoring
- Arrange to check blood pressure again following a two week interval
- Start amlodipine
- Screen for causes of secondary hypertension
Offer ambulatory blood pressure monitoring
A 21 year old gentleman is under the cardiologists for investigation of prolonged QT-syndrome. He presents to your surgery with a 5 day history of cough productive of thick, green sputum, fevers and lethargy. Examination reveals a temperature of 39ºC, oxygen saturations of 96% on air and crackles at the right lung base. Which of the following drugs should be avoided in the management of his condition?
Co-amoxiclav
Metronidazole
Doxycyline
Erythromycin
Amoxicillin
Eythromycin
What is a normal corrected QT interval?
A normal corrected QT interval is less than 430 ms in males and 450 ms in females.
What is long QT syndrome and what can it lead to?
A rare inherited or acquired disorder where delayed repolarisation of the ventricles increases propensity to ventricular tachyarrhythmias. This may lead to syncope, cardiac arrest, or sudden death.
How is long QT diagnosed?
It may be diagnosed as an incidental finding on ECG, following a cardiac event (eg, syncope, cardiac arrest) or after sudden death of a family member
What is the usual mechanism that leads to prolonged QT in the context of drugs?
the usual mechanism by which drugs prolong the QT interval is blockage of potassium channels
Drugs that cause prolonged QT
Acquired Medical causes of prolonged QT
Management of Lonq QT
- avoid drugs which prolong the QT interval and other precipitants if appropriate (e.g. Strenuous exercise)
- beta-blockers***
- implantable cardioverter defibrillators in high risk cases
A 65-year-old man presents to the emergency department complaining of palpitations. He is noted to have a regular broad complex tachycardia on his ECG. Observations show temperature 36.3ºC, heart rate 155bpm, blood pressure 115/78mmHg, respiratory rate 18/min, and oxygen saturations 98% in room air. He denies chest pain or dizziness. Recently, he had several days of diarrhoea. His only past medical history is ischaemic heart disease.
What is the first-line treatment for this patient?
- Adenosine
- Amiodarone
- Atropine
- Direct Current Cardioversion (DCCV)
- Metoprolol
- IV amiodarone is the first-line treatment for regular broad complex tachycardias without adverse features
- Adenosine is incorrect because it is used for the treatment of supraventricular tachycardia (SVT) with narrow QRS complexes, not for regular broad complex tachycardia.
- Atropine is incorrect because it is used for the treatment of bradycardia and not for regular broad complex tachycardia.
- Direct Current Cardioversion is incorrect. This patient is stable and has no adverse features
- Metoprolol is incorrect because it is not recommended as a first-line treatment for regular broad complex tachycardias. Metoprolol is most commonly used to manage atrial fibrillation with fast ventricular response to obtain rate control
What classifies a peri-arrest tachycardia as unstable?
Following basic ABC assessment, patients are classified as being stable or unstable according to the presence of any adverse signs:
- shock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness
- syncope
- myocardial ischaemia
- heart failure
How many shocks can be given in unstable tachyarrythmias
- ## Up to 3 synchronized DC shocks can be given; after this expert help should be sought.
Adult tachycardia management algorithm
A 52-year-old female who you see regularly represents to your clinic after routine blood tests having recently been started on ramipril for her hypertension. Her blood pressure (BP) prior to initiation of ramipril in the clinic was 145/98mmHg and her baseline creatinine prior to treatment was 100umol/L. On review today her clinic BP appears to be well controlled at 132/84mmHg and her bloods show her creatinine has risen to 125umol/L. What is the most appropriate step in the management of her hypertension?
Reduce dose of ramipril
Continue current dose of ramipril
Stop ramipril and consider angiotensin receptor blocker
Increase dose of ramipril
Stop ramipril and consider calcium channel blocker
The main consideration here is the renal function, which shows an increase in creatinine by 25%. Her BP appears to be well controlled. The BNF recommends the angiotensin-converting enzyme inhibitors should only be stopped if the creatinine increases by 30% or eGFR falls by 25% or greater. This lady’s results are within these limits and have shown good effect. It would therefore be pertinent to continue the ramipril at the current dose and monitor the renal function as per normal protocol
Examples of common ACE inhibitors
ramipril
enalapril
lisinopril
Monitoring requirements ACE inhibitors
- urea and electrolytes should be checked before treatment is initiated and after increasing the dose
- Check renal function and serum electrolytes 1–2 weeks after starting treatment and 1–2 weeks after each dose increase. Thereafter, check renal function and serum electrolytes annually unless clinical judgement or abnormal blood testing parameters indicate a need for more frequent monitoring.
- Check blood pressure 4 weeks after each dose titration.
- a rise in the creatinine and potassium may be expected after starting ACE inhibitors
acceptable changes are an increase in serum creatinine, up to 30% from baseline and an increase in potassium up to 5.5 mmol/l. - significant renal impairment may occur in patients who have undiagnosed bilateral renal artery stenosis
In which patients should specialist advice be sought before starting ACE inhibitor?
specialist advice should be sought before starting ACE inhibitors in patients with a potassium >= 5.0 mmol/L
Side effects of ACE inhibitors
- cough: occurs in around 15% of patients and may occur up to a year after starting treatment
thought to be due to increased bradykinin levels. If this happens then switch to ARB - angioedema: may occur up to a year after starting treatment
- hyperkalaemia
- first-dose hypotension: more common in patients taking diuretics
ACE I contraindications
Hereditary or idiopathic angioedema; history of angioedema associated with prior ACE inhibitor therapy; the combination of an ACE inhibitor with aliskiren (renin inhibitor) is contra-indicated in patients with an eGFR less than 60 mL/minute/1.73 m2; the combination of an ACE inhibitor with aliskiren is contra-indicated in patients with diabetes mellitus
ACE I cautions
- Concomitant diuretics; diabetes (may lower blood glucose; increased risk of hyperkalaemia)
- first dose hypotension (especially in patients taking high doses of diuretics, on a low-sodium diet, on dialysis, dehydrated, or with cerebrovascular disease, ischaemic heart disease, or heart failure)
- patients of black African or African-Caribbean origin (may respond less well to ACE inhibitors)
- peripheral vascular disease or generalised atherosclerosis (risk of clinically silent renovascular disease)
- primary aldosteronism (patients may respond less well to ACE inhibitors)
- the risk of agranulocytosis is possibly increased in collagen vascular disease (blood counts recommended)
- use with care in patients with aortic or mitral valve stenosis (risk of hypotension)
- use with care in patients with hypertrophic cardiomyopathy
A 54-year-old man is referred to the medical team for management of community-acquired pneumonia with associated postural hypotension causing collapse. He denies any head or long-bone injuries. He has a past medical history of hypertension, type 2 diabetes mellitus, and ischaemic heart disease. He is alcohol-dependent and has no fixed abode currently. Bloods show:
Na+ 128 mmol/L (135 - 145)
K+ 3.0 mmol/L (3.5 - 5.0)
Urea 19 mmol/L (2.0 - 7.0)
Creatinine 245 µmol/L (55 - 120)
What is the most likely medication to cause this derangement from the list below?
Amlodipine
Bumetanide
Labetalol
Metformin
Spironolactone
This patient is presenting with pneumonia - due to his history of alcohol dependence, it is likely to be an atypical organism, such as Klebsiella. He is also noted to be hyponatraemic and hypokalaemic - this may be due to the bacterial infection as well as his bumetanide use. While he is unwell and hypokalaemic, his bumetanide should be held and fluid balance monitoring, regular blood tests, and potassium supplementation. With his potassium being 3.0mmol/L, he is at risk of cardiac arrhythmias secondary to his hypokalaemia and should have ECG and cardiac monitoring
Loop diuretic examples
Furosemide and bumetanide
How do loop diuretics work?
inhibiting the Na-K-Cl cotransporter (NKCC) in the thick ascending limb of the loop of Henle, reducing the absorption of NaCl
Which patients may require higher doses of loop diuretics?
As loop diuretics work on the apical membrane they must first be filtered into the tubules by the glomerulus before they can have an effect. Therefore patients with poor renal function may require escalating doses to ensure a sufficient concentration is achieved within the tubules.
