hypertension and heart block and WPW

Question 1

MOA of ACEi

Answer 1

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

Question 2

tall tented t waves what hypertensive drug causes this

Answer 2

ramipril

Question 3

malignant hypetension with encephalopathy and papilloedema

Answer 3

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.

Question 4

hypertensive encephalopathy

Answer 4

V Labetalol or IV infusion Sodium Nitroprusside.

Question 5

indapamide CI when

Answer 5

severe rena failure

Question 6

why is bendroflumethiazide not used

Answer 6

others suhc as indapamide reduced cardio events and strokes

Question 7

hypertensive retinopathy what would be seen on fundoscopy

Answer 7

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

Question 8

gold standard test for paeochromocytoma - can cause high BP

Answer 8

urien metanephrines

Question 9

malignnat hypertension above

Answer 9

180/120 and symptomatic

Question 10

cuases of 1st degree

Answer 10

High vagal tone (e.g. athletes)
Acute inferior MI
Electrolyte abnormalities (e.g. hyperkalaemia)
Drugs: NHP-CCBs, beta-blockers, digoxin, cholinesterase inhibitors

Question 11

MX of 1st degree

Answer 11

First degree heart block itself is benign and does not need treating. However, any pathological underlying cause should be reversed.

Question 12

causes of mobitz type 1

Answer 12

MI (mainly inferior)
Drugs such as beta/calcium channel blockers, digoxin
Professional athletes due to high vagal tone
Myocarditis
Cardiac surgery

Question 13

mx morbitz 1

Answer 13

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.

Question 14

causes mobitz type 11

Answer 14

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

Question 15

mx morbitz 2

Answer 15

Definitive management is with a permanent pacemaker as these patients are at risk of risk of complete heart block and becoming haemodynamically unstable

Question 16

mx of third degree

Answer 16

Definitive management of Third Degree Heart Block
Permanent pacemaker due to the risk of sudden death.

Question 17

what drug that treats dementia can cause heart block

Answer 17

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.

Question 18

heart block most common cuse

Answer 18

RCA disease as this supplies AVnode - 1st degree

Question 19

what two drugs used to together can cause heart block

Answer 19

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

Question 20

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

Answer 20

seen in those with increased resting vagal tone (e.g. in athelets)

Question 21

what is WPW

Answer 21

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)

Question 22

accesory pathway in WPW leads to

Answer 22

This accessory pathway leads to the potential for re-entrant circuits to form leading to supraventricular tachycardias.

Question 23

WPW mx

Answer 23

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

Question 24

ST segment depression in leads V1-3 seen in

Answer 24

posterior MI - left circumflex or RCA

Question 25

Reciprocal changes seen in leads V1-V3 include: to inferiro lead

Answer 25

Horizontal ST depression
Tall, dominant R waves with R wave/S wave ratio >1 in lead V2
uprigth t waves

Question 26

A 35 year old man presents to the emergency department with severe central chest pain and shortness of breath whilst he was on a run this morning. He mentions that this has happened before and the pain is relieved by rest. The patient is not on any prescribed drugs, but admits to taking cocaine with his friends recently.

On examination he is distressed and sweating. His pulse rate is 115 beats per minute and blood pressure is 118/68 mmHg. His respiratory rate is 28 breaths per minute with normal breath sounds in both sides of the chest. An ECG is conducted and shows only sinus tachycardia.

What is the most likely diagnosis?

Answer 26

cocaine - coroary artery vasospasm

Question 27

PCCI within how many hours

Answer 27

12

Primary percutaneous coronary intervention (PCI)

If a patient with an ST-elevation myocardial infarction presents within 12 hours of symptom onset and there is ongoing pain or cardiovascular instability, then they are eligible for primary percutaneous coronary intervention. Ideally, PCI should be performed within 120 minutes of the time when fibrinolysis could have been given

Question 28

what is unstbael angina

Answer 28

This is the correct answer. A diagnosis can be made in the presence of cardiac chest pain, with or without ECG changes and a normal troponin. It is characterised by prolonged (>20 minutes) angina at rest, new onset of severe angina or angina that is increasing in frequency/duration. The patient is a Type-2 diabetic and a smoker which are all risk factors for Acute Coronary syndrome. As with NSTEMI, unstable angina is caused by partial occlusions. Partial (or incomplete) occlusion mean that there is still some passage for blood to flow within the artery

Question 29

A 56-year old female attends the Emergency department with central chest pain. She underwent percutaneous coronary intervention (PCI) which was successful. She experiences a similar chest pain six days later.

Which is the most useful blood test in this scenario?

Answer 29

Creatine kinase MB (CK-MB)

This is correct. The CK-MB remains elevated for 3-4 days following a myocardial infarction (MI). It is therefore useful in detecting re-infarction between 4-10 days post initial MI. Although creatinine kinase is found within both skeletal and cardiac muscle, CK-MB is found in higher concentrations within cardiac muscle, making it more specific to cardiac damage. Skeletal muscle is mostly composed of CK-MM

troponin I stays up up to 10 days post MI - best 6-12 hours post onset

also CK - BB - brian and MM - muscles

Question 30

The ECG of this lady shows pathological Q waves and T wave inversion in the inferior leads (II, III and aVF). This indicates that this lady has had an

Answer 30

inferioro MI

300mg aspriin is loadign dose
75 in maintainance

Question 31

inferior MI can lead to heart block complete blood supply to av so can cause cannon

Answer 31

Cannon A waves are the result of the right atrium contracting against a closed tricuspid valve. This can occur in patients with complete heart block. An inferior myocardial infarction can lead to complete heart block, as the occlusion that causes an inferior MI also affects the blood supply to the AV node and the SA node

Question 32

what is colporrhaphy - gynae

Answer 32

surgery to fix weakness in vaginal walls