hypertension and heart block and WPW Flashcards
MOA of ACEi
ACE-inhibitors result in reduced angiotensin II production, and thereby efferent (away from kidney) arteriolar vasodilation. This reduces glomerular pressure and filtration rate. ACE-inhibitors can also cause a rise in serum potassium levels by inhibiting the production of aldosterone, reducing Sodium reabsorption and Potassium efflux. Therefore, a fall in eGFR and hyperkalaemia are known effects of ACE-inhibitors. These effects are only problematic if they surpass empirically determined thresholds. NICE stipulates that the dose of ACE-inhibitors should not be modified if either the GFR decrease from pre-treatment baseline is less than 25%, or the serum creatinine increase from baseline is less than 30%.
As this patient’s reduction in eGFR and rise in serum potassium are relatively small, and to be expected when commencing Ramipril, his medications should be left unchanged
tall tented t waves what hypertensive drug causes this
ramipril
malignant hypetension with encephalopathy and papilloedema
IV labetalol
Guidelines in treatment suggest aiming for controlled drop in blood pressure, to around 160/100mmHg over at least 24 hours.
Uncontrolled drops can lead to ischaemic stroke due to poor cerebral autoregulation and perfusion.
Oral medication is preferred to IV, unless there is encephalopathy, heart failure or aortic dissection. Oral calcium channel blockers such as amlodipine or nifedipine are often used first line.
hypertensive encephalopathy
V Labetalol or IV infusion Sodium Nitroprusside.
indapamide CI when
severe rena failure
why is bendroflumethiazide not used
others suhc as indapamide reduced cardio events and strokes
hypertensive retinopathy what would be seen on fundoscopy
Flame haemorrhages and cotton wool spots
This is the correct answer. This is the third stage of hypertensive retinopathy. Other signs include arteriolar narrowing in 1, arteriovenous nipping in grade 2 and papilloedema in grade 4
gold standard test for paeochromocytoma - can cause high BP
urien metanephrines
malignnat hypertension above
180/120 and symptomatic
cuases of 1st degree
High vagal tone (e.g. athletes)
Acute inferior MI
Electrolyte abnormalities (e.g. hyperkalaemia)
Drugs: NHP-CCBs, beta-blockers, digoxin, cholinesterase inhibitors
MX of 1st degree
First degree heart block itself is benign and does not need treating. However, any pathological underlying cause should be reversed.
causes of mobitz type 1
MI (mainly inferior)
Drugs such as beta/calcium channel blockers, digoxin
Professional athletes due to high vagal tone
Myocarditis
Cardiac surgery
mx morbitz 1
It is generally asymptomatic and does not require any specific management as the risk of high AV block/ complete heart block is low. If symptoms do arise, ECG monitoring may be required, exclude precipitating drugs and if bradycardic may require atropine.
causes mobitz type 11
Infarction: particularly anterior MI which damages the bundle branches
Surgery: mitral valve repair or septal ablation
Inflammatory/autoimmune: rheumatic heart disease, SLE, systemic sclerosis, myocarditis
Fibrosis: Lenegre’s disease
Infiltration: sarcoidosis, haemochromatosis, amyloidosis
Medication: beta-blockers, calcium channel blockers, Digoxin, amiodarone
mx morbitz 2
Definitive management is with a permanent pacemaker as these patients are at risk of risk of complete heart block and becoming haemodynamically unstable
mx of third degree
Definitive management of Third Degree Heart Block
Permanent pacemaker due to the risk of sudden death.
what drug that treats dementia can cause heart block
This ECG shows a complete heart block. Donepezil is an anticholinesterase inhibitor, it is licensed for the use in mild-to-moderate dementia. As it increases acetylcholine levels, it can contribute to or lead to heart block. It is therefore important to stop this drug, as it may be the underlying cause of this patient’s ECG. It is, however, necessary to also refer this patient to A&E - as complete heart block increases the risk of ventricular pause and sudden cardiac arrest.
heart block most common cuse
RCA disease as this supplies AVnode - 1st degree
what two drugs used to together can cause heart block
This is the correct answer. The patient’s ECG shows complete heart block as there is dissociation between the P waves and the QRS complexes. Verapamil is a negative inotrope as it blocks calcium channels mainly in the SAN and AVN. Bisoprolol has a similar mechanism but the site of action is the adrenergic receptors and when used in conjunction can cause AV block
Mobitz type I, also known as the Wenckebach phenomenon refers to the progressive prolongation of the PR interval until a P wave is followed by a non-conducted QRS complex (dropped beat). In this rhythm, the PR interval is longest before the dropped beat, and it is shortest immediately after the dropped beat. Mobitz type I is usually caused by reversible conduction block at the level of the AV node, it is also a phenomenon
seen in those with increased resting vagal tone (e.g. in athelets)
what is WPW
Presence of an accessory pathway, causing early activation of the ventricles
This ECG shows delta waves in V1-V6. Those waves are pathognomonic of WPW. In WPW there’s an accessory pathway (known as the Bundle of Kent), that bypasses the AV node and causes premature excitation of the ventricles, hence creating the delta wave
The ventricles are pre-excited resulting in a slurred upstroke of the QRS complex. This is known as a delta wave (which can be seen here)
accesory pathway in WPW leads to
This accessory pathway leads to the potential for re-entrant circuits to form leading to supraventricular tachycardias.
WPW mx
Radiofrequency ablation of the accessory pathway
Drug treatment (such as amiodarone or sotalol) to avoid further tachyarrhthmias. These are contraindicate din structural heart disease.
Surgical (open heart) ablation - rarely done and only used in complex cases
Digoxin and NDP-CCBs (e.g. verapamil) are contraindicated for long term use because they may precipitate ventricular fibrillation.
If the patient is experiencing supraventricular tachycardia the management depends on whether the patient is stable or unstable, and if stable the type of arrhythmia:
Management of WPW in unstable patients
Unstable patients (blood pressure <90/60mmHg or with signs of systemic hypoperfusion or fast atrial fibrillation) require urgent direct current (DC) cardioversion.
Management of WPW in stable patients
If the patient is stable they are managed according to the rhythm:
In patients with an orthodromic AV reciprocating tachycardia (narrow QRS complex with short PR interval) management is with vagal manoeuvres (carotid sinus massage or Valsalva manoeuvre) in the first instance. If this fails IV adenosine should be administered.
Note that in orthodromic AV reciprocating tachycardias one limb of the aberrant circuit involves the AV node so slowing conduction through the AV node helps terminate the tachycardia.
In patients with antidromic AV reciprocating tachycardia (wide QRS complex), atrial fibrillation, or atrial flutter intravenous anti-arrhythmics (such as procainamide or flecainide) help prevent rapid conduction through the accessory pathway.
DC cardioversion may be used if symptoms persist.
if no respond cathter ablation of the accessory pathway conduction pathway
ST segment depression in leads V1-3 seen in
posterior MI - left circumflex or RCA
