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Y3 med old > CARDIOVASCULAR > Flashcards

CARDIOVASCULAR Flashcards

1
Q

What is absolute bradycardia?

A

HR is <40bpm

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2
Q

What is relative bradycardia?

A

Where HR is inappropriately slow for the haemodynamic state of the patient.

Oxford clinical handbook definition of bradycardia = <60bpm

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3
Q

Signs that may indicate haemodynamic instability?

A 
Systolic BP < 90mmHg 
HR <40 
Poor perfusion 
Poor urine output 
Ventricular arrhythmias that need suppression 
Heart failure
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4
Q

How can bradycardia be classified?

A

Based on the pacemaker that is faulty:

  • sinus node e.g. sinus bradycardia
  • AV node
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5
Q

List some causes of bradycardia

A

Physiological:
- athletes

Cardiac:

  • degenerative changes/fibrosis of conduction pathways in elderly
  • post-MI (especially inferior MI (leads II, III, aVF)
  • sick sinus syndrome
  • iatrogenic —> ablation, surgery
  • aortic valve disease e.g. infective endocarditis (rheumatic fever)
  • myocarditis, cardiomyopathy, sarcoidosis, SLE

Non-cardiac origin:

  • vasovagal
  • endocrine = hypothyroidism, adrenal insufficiency
  • metabolic = hyperkalaemia, hypoxia
  • other = hypothermia, raised ICP (Cushing’s triad - bradycardia, hypertension and irregular breathing), pericarditis, haemochromatosis,

Drug induced:

  • Beta blockers
  • amiodarone
  • verapamil
  • diltiazem
  • digoxin
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6
Q

Main management for pt with symptomatic sinus node disease (e.g. a sinus bradycardia)?

A

Pacemaker is indicated

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7
Q

What are categories of sinus node dysfunction?

A

Sinus bradycardia
Sick sinus syndrome
Sinus arrest
Part of vasovagal syncope

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8
Q

How are AV node bradycardias classified?

A

According to the degree of nodal dysfunction:

  • First degree AV block
  • Second degree AV block Mobitz Type I aka Wenckebach
  • Second degree AV block Mobitz Type II
  • Complete/Third degree AV block
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9
Q

How is First degree AV block characterised?

A

PR interval >0.2s

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10
Q

Pt has bradycardia. What rate limiting drug should you check pt is on and why?

A

Digoxin. Why? Digoxin toxicity - can worsen conduction abnormalities and worsen heart block

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11
Q

How is Second degree AV block: Wenckebach/Mobitz Type I characterised?

A

Lengthening of PR interval. Followed by failure of atrial impulse to conduct to the ventricles.

i.e. QRS is dropped after progressive lengthening of PR interval.

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12
Q

Who is more likely to have Second degree AV block: Wenckebach/Mobitz Type I?

A
  • Young fit patients with a high vagal tone

- Patients after inferior MI

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13
Q

How is Second degree AV block: Mobitz Type II characterised?

A

Constant PR interval followed by sudden failure of a p wave to be conducted to the ventricles.

i.e. PR length constant, then drop of QRS. 2 p waves for every QRS

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14
Q

How is complete heart block/ Third degree AV block characterised?

A

No conduction from atria to the ventricles. No relationship between p waves and QRS complexes

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15
Q

What does complete/ third degree heart block look like on ECG?

A

Rate is slow. Broad complex QRS escape rhythm seen, with no linkage of p waves and QRS - they are both independent.
Sometimes can look intermittent - see trifascicular or bifascicular block (RBBB, with or without prolonged PR interval) and alternating LBBB and RBBB.

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16
Q

Where can complete/third degree block occur?

A

Either:

  • above AV node at the HIS region
  • beneath AV node
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17
Q

Causes of complete/third degree AV block?

A

Anti-arrhythmic drugs - especially digoxin toxicity!!
Post- inferior STEMI (will resolve in hrs-days)
Anterior MI
Severe hyperkalaemia

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18
Q

How to treat severe hyperkalaemia causing. complete/third degree AV heart block?

A

IV calcium chloride - 10ml of a 10% solution over 3-5mins

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19
Q

How to treat a haemodynamically unstable patient with complete/third degree AV heart block?

A

Atropine - 600micrograme to 3 mg.

Isoprenaline - at rate of 5micrograms/minute

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20
Q

Main management for complete/ third degree AV heart block?

A

Urgent permanent pacemaker. Within 24hrs unless they are likely to have a recovery of conduction (e.g post inferior STEMI)

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21
Q

Types of tachycardic arrhythmias?

A

Atrial fibrillation
Supraventricular tachycardia = in atria
Ventricular tachycardia

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22
Q

Presentation of AFib?

A 
Asymptomatic 
Breathlessness 
Palpatations
Syncope/dizziness 
Chest discomfort 
Stroke or TIA
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23
Q

Complications of AFib?

A

Cardioembolic stroke
Cardiac instability
Death

Increase in healthcare costs

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24
Q

How to diagnose A fib?

A

Presence of symptoms - palpitations, dizziness/syncope, breathlessness, chest discomfort, stroke, TIA
ECG used to confirm if an irregular pulse is due to A fib.

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25
Q

What to do before treating suspected AFib just from clinical picture?

A

Do an ECG to confirm.

Why? Irregular pulse may be due to other reasons

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26
Q

Pt has intermittent AFib. What is next step in investigation?

A

Short term cardiac monitoring with 24hr cardiac monitor

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27
Q

Disadvantage of 24hr cardiac monitor to identify arrhythmia?

A

Symptoms need to be very frequent to diagnose an arrhythmia - this is a short time period - delivers low yield results.

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28
Q

What are the different types of prolonged cardiac monitors?

A

Prolonged Holter monitor

Implantable loop recorder

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29
Q

When/ In what circumstances is an echocardiogram carried out for AFib ?

A
  1. Suspected structural heart disease - from symptoms, murmer or signs of HF
  2. When considering cardioversion to control rhythm
  3. When a baseline is needed to inform long term management
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30
Q

How to manage AFib?

A
  1. Anticoagulation to prevent stroke
  2. Rate control
  3. Rhythm control
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31
Q

Scoring tool to assess whether pt with AFib needs anticoagulation? State and explain

A 
CHA2DS2-VASc
Congestive heart failure 
Hypertension 
Age >75 = 2, 65-74 = 1
Diabetes
Stroke or Tia = 2
Vascular disease 
Sex category (female)

Higher score = higher risk of stroke or embolism.

  • Score of 2+ = significant risk. Offer anticoagulant.
  • Score of 1 in men = intermediate risk, consider anticoagulant
  • Score of 0 = low risk, not offered anticoagulant
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32
Q

Scoring tool to assess risk of major bleeding when on anticoagulation?

A 
HAS-BLED 
Hypertension 
Abnormal renal and liver function - 1 point for each  
Stroke 
Bleeding 
Labile INRs (poor INR control while on warfarin)
Elderly (65 + )
Drugs or alcohol - 1 point each
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33
Q

Anticoagulant options for AFib?

A

DOACs - apixaban, rivaroxaban, edoxaban, dabigatran

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34
Q

How does the mechanism of action of dabigatran differ to other DOACs?

A

Apixaban, rivaroxaban, edoxaban = inhibit factor Xa directly so prevent conversion of prothrombin —> thrombin.

Dabigatraan = direct thrombin inhibitor so prevents conversation of fibrinogen —> fibrin

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35
Q

Benefit of DOAC compared to warfarin?

A

Less monitoring (INR monitoring)
No restrictions on food or alcohol
Lower rates of bleeding to warfarin
Better reduction in stroke

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36
Q

How are DOACs excreted and why is this important?

A

Via kidney. Need to monitor renal function yearly

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37
Q

Other management options available for AFib, other than anticoagulants?

A

Rate control
Electrical cardioversion
Drug therapy

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38
Q

Pathophysiology of supraventricular tachycardia (SVT)?

A

AV nodal re-entry tachycardia (a re-entry within the AV node)
OR
Atrio-ventricular re-entry tachycardia (an anatomical re-entry)

Both of these depend on AV nodal conduction

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39
Q

First line treatment of supra ventricular tachycardia in haemodynamically stable patients?

A

Vagal manoeuvres

e. g. breath holding, valsalva manoeuvre
e. g. carotid massage (younger patients)

These slow down conduction in AV node so can interrupt re-entrant circuit

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40
Q

What should you do before attempting carotid massage for treating supra ventricular tachycardia?

A

Auscultate for bruits before carotid massage manoeuvre

Why? Risk of stroke from emboli

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41
Q

Short term management options for SVT if vagal manoeuvres do not help?

A

IV adenosine

CCBs

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42
Q

Route of administration and dose of adenosine for SVT?

A

IV - rapid bolus Followed by saline flush immediately.
Administered via three way stopcock.
Give 6mg stat followed by 12mg if unsuccessful. Repeat 12mg if unsuccessful after first 12mg dose.
In antecubital fossa

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43
Q

Describe half life of adenosine?

A

Very short half life

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44
Q

Why is it important that dose of adenosine is given IV and in antecubital fossa via large bore cannula?

A

Needs to reach heart quickly to minimise cellular uptake en route - so need large bore cannula and entry to be as proximal as possible.

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45
Q

ADRs of adenosine given for SVT?

A

Chest discomfort
Transient hypotension
Flushing

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46
Q

Contraindication for adenosine use in SVT management?

A

Pts with significant reversible airway disease e.g asthma or COPD - as can cause bronchospasm

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47
Q

Safety precautions to have in place before administering adenosine to a pt?

A

Crash trolley next to pt - as possibility of bradyarrhythmia or tachyarrhythmia

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48
Q

ECG findings of SVT?

A

A narrow-complex tachycardias with a QRS interval of 100 ms or less

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49
Q

When is verapamil contraindicated for SVT control?

A

Pts on B-blockers

Pts with LV dysfunction

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50
Q

If adenosine and verapamil are ineffective/contraindicated for SVT, what can be done for SVT?

A

Electrical cardioversion under GA or sedation

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51
Q

Second line drugs for SVT?

A

IV flecainide can be used if they don’t have PMH of MI
Sotalol
Amiodarone

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52
Q

ECG findings of VT?

A

Regular broad QRS

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53
Q

Management for sustained VT in haemodynamically compromised pts?

A
  • oxygen
  • IV access
  • exclude reversible factors - e.g. PA catheter in RV, hypokalaemia, hypomagnesia
  • synchronised DC shock - up to 3 attempts
  • if unsuccessful = Amiodarone 300 mg IV over 10–20 min. Repeat synchronised DC shock
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54
Q

Pharmacological options for VT?

A

B-blockers
Amiodarone
Lidocaine

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55
Q

Maximum dose of lidocaine that can be given in 1hr?

A

200-300mg

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56
Q

Presentation of stable angina?

A

Chest discomfort/ pain provoked by effort, emotion and relieved by rest

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57
Q

How may severe angina present?

A

Accompanied by autonomic features- fear, sweating and nausea

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58
Q

ddx for chest pain/discomfort

A

angina, GORD, MSK discomfort, pulmonary disease

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59
Q

What is Cardiac Tamponade? Mechanism of how it happens?

A

Accumulation of fluid, blood, purulent exudate or air in the pericardial space.

This raises intra pericardial pressure.

Diastolic filling is reduced, which reduces cardiac output.

Life threatening emergency that requires prompt diagnosis with echocardiogram and treatment.

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60
Q

How would a pt with cardiac tamponade present?

A 
Shortness of breath
Tachycardia
Confusion
Chest pain
Abdominal pain
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61
Q

What are the signs of cardiac tamponade. Hint a helpful ____ triad?

A

BECK’S Triad of signs:

  1. Hypotension
  2. Quiet heart sounds
  3. Raised JVP

Other signs:
dyspnoea

pulsus paradoxus - an abnormally large drop in BP during inspiration.

an absent Y descent on the JVP - this is due to the limited right ventricular filling

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62
Q

What are RF for cardiac tamponade?

A

malignancy,
purulent pericarditis,
severe thoracic trauma.

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63
Q

RF for angina?

A

cigarette smoking, hypertension, DM, hypercholesterolaemia, Fhx of premature coronary artery disease presence of other acquired vascular disease

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64
Q

What drugs do you prescribe to someone with angina?

A

Aspirin 75mg OD
Sublingual GTN
Statin
Beta blocker OR CCB- depending on contraindications, co-morbities and pt preference- first line. If using CCB monotherapy, use rate limiting one- verapamil or diltiazem.

If pt is still symptomatic on CCB or Beta blocker monotherapy, add the other. Ensure CCB is now a is long-acting dihydropyridine one e.g modified release nifedipine.

If patient on monotherapy cannot tolerate addition of a CCB or Beta blocker, consider long-acting nitrate, ivabradine ( when B blocker is not tolerated and not prescribed with verapamil or diltiazem), nicorandil or ranolazine

if a patient is taking both a beta-blocker and a calcium-channel blocker then only add a third drug whilst a patient is awaiting assessment for PCI or CABG

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65
Q

Hx for someone presenting with angina?

A 
precipitants of anginal attacks
relieving factors
stability of symptoms
risk factors (smoking history, high BP, lipids, diabetes, prior CV disease) • occupation
assessment of the intensity, length and regularity of exercise
basic dietary assessment
alcohol intake 
drug history
family history
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66
Q

Examination for someone presenting with angina?

A

weight and height (to allow calculation of BMI) or waist / hip ratio
blood pressure
presence of murmurs, especially that of aortic stenosis
evidence of hyperlipidaemia
evidence of peripheral vascular disease and carotid bruits (especially in diabetes).

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67
Q

Investigations for someone presenting with angina?

A

FBC and biochem screen incl glucose and HbA1c
Full lipid profile
Resting 12 lead ECG- provides info on rhythm, presence of heart block, previous MI, myocardial hypertrophy and iscahemia

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68
Q

What investigations for Cardiac tamponade?

A

ECG - low voltage QRS complexes or electrical alternans (alternating QRS amplitude)

Chest x-ray - show a large globular heart

ECHO - fluid around the heart and quantify the level of ventricular compromise.

Pericardiocentesis - sampling of the fluid to find the underlying cause and treat the immediate problem.

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69
Q

What is first line management for cardiac tamponade in a haemodynamically unstable pt?

A

pericardiocentesis

using a needle and small catheter to drain excess fluid

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70
Q

In a pt with cardiac tamponade when would surgical drainage be indicated as first line management ?

A

In patients with haemopericardium, associated malignancy, traumatic/purulent effusion

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71
Q

What are some complications of pericardiocentesis?

A

pneumothorax (all patients should have a CXR post procedure to exclude this)

Damage to the myocardium / coronary vessels

Thrombus

Arrhythmias/cardiac arrest

Damage to the peritoneum.

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72
Q

Causes of non-cardiac chest pain?

A 
Costo-chondritis 
Gastro-oesophageal 
PE
Pneumonia 
Pneumothorax 
Psychogenic/psychosomatic
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73
Q

When do you offer invasive coronary angiography to a pt for angina?

A

If estimated likelihood of CAD is between 61-90%

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74
Q

When do you offer functional imaging as the first- line diagnostic investigation (stress MRI, echo or myoview) of angina?

A

If the estimated likelihood of CAD is 30 - 60%

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75
Q

When do you offer CT calcium scoring as the first- line diagnostic investigation in angina?

A

If the estimated likelihood of CAD is 10 - 29%

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76
Q

How do you interpret CT calcium scoring?

A

0- minimal likelihood there is significant coronary disease
1-400: Consider CTCA or stress perfusion imaging
Above 400- coronary angiography should be seriously considered

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77
Q

What is top differencial for Cardiac tamponade?

A

Constrictive pericarditis

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78
Q

How would differentiate between cardiac tamponade and constrictive pericarditis?

A

CT

  • absent Y descent JVP - reduced RV filling
  • Pulsus paradoxus - (+ drop in BP w/inspiration)

CP

  • Y+ X present in JVP
  • no Pulsus paradoxus
  • Kussmaul’s sign +ve
  • Pericardial calcification seen on CXR
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79
Q

When should you NOT use exercise ECG to diagnose stable angina?

A

If they do NOT have known CAD

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80
Q

For men older than 70 with atypical or typical symptoms what risk do you assume of having CAD

A

> 90%

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81
Q

For women older than 70, with typical or atypical symptoms, what risk do you assume of CAD?

A

61-90%

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82
Q

When do you assume women over 70 has a risk of CAD of >90%?

A

If she has high risk factors AND typical symptoms

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83
Q

What is the danger of leaving valvular heart disease untreated? What can it lead to?

A

Irreversible ventricular dysfunction and / or pulmonary HTN

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84
Q

What are the three classic symptoms of aortic stenosis?

A

Angina
heart failure
syncope

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85
Q

What is the most common INITIAL symptom of aortic stenosis? i.e. what pt might recognise and then seek help as change in normal

A

Exercise intolerance or dyspnoea on exertion

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86
Q

What are some causes of aortic stenosis?

A

Most common: AGE -senile/degenerative calcification
congenital bicuspid valve
CKD
rheumatic fever
william’s syndrome

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87
Q

Where on the chest is best place to listen to murmur due to aortic stenosis?

A

Aortic area:

2 ICS Right sternal border

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88
Q

How would you describe aortic stenosis murmur ?

A

Ejection systolic murmur radiating to the carotid / neck

Tom says: ejection -systolic, high pitched murmur. crescendo - decrescendo character.

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89
Q

What are the indications for surgery in Aortic stenosis?

A

Symptoms (no matter severity)
Asymptomatic severe - LV systolic dysfunction
Asymptomatic severe - abnormal exercice test (drop in BP, ST elevation)
Asymptomatic severe - at time of other cardiac surgery e..g CABG

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90
Q

What extra should you consider doing for older patients with aortic stenosis? How is this implanted?

A

especially with co-morbidities

Transcatheter aortic valve implantation (TAVI)

implanted via femoral artery

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91
Q

When doing a cardio exam (yay) what special manoeuvres would you do to listen for mitral stenosis or aortic regurgitation?

A

Mitral stenosis
Listen with patient on left hand side

Aortic regurgitation
Pt sat up, leaning forward and holding exhalation

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92
Q

How does Aortic regurgitation ultimately lead to heart failure?

A

increased volume load on Left ventricle causes dilation of LV and ultimately HF

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93
Q

What is the most common initial symptom in aortic regurgitation?

A

exertional dyspnoea / reduction in exercise tolerance

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94
Q

What are the causes of aortic regurgitation ?

A 
Many!
Dilation of aorta (pulls the valve leaflets apart)
congenital (e.g. bicuspid valves)
Calcific degeneration
rheumatic disease
infective endocarditis
Marfan's
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95
Q

Where is aortic regurgitation best heard on the chest?

A

Left sternal edge 3rd ICS

96
Q

Where is aortic regurgitation best heard on the chest?

A

Left sternal edge

Early diastolic blowing murmur (associated with collapsing pulse + headbobbing -De Musset’s Sign)

97
Q

What is the role of ACEi in aortic regurgitation?

A

Reduces afterload so can slow LV dilatation - standard therapy for pt with severe AR and LV dilation

98
Q

Which 2 heart murmurs often have delayed presentation?

A 
Mitral regurgitation (16 years from onset to diagnosis)
Aortic regurgitation (many pt do not know they have it despite large LV dilation)
99
Q

Most pt with Mitral regurgitation will never need surgical intervention - TRUE or FALSE

A

TRUE!

most pts have mild - moderate disease and wont need surgery

100
Q

What are some causes of Mitral regurgitation?

A 
Mitral valve prolapse - (Marfans)
pts with pectus excavatum
Rheumatic heart disease
IHD
Infective endocarditis
drugs 
collagen vascular disease
2ndary to dilated annulus from LV dilatation
101
Q

What are some of the few cases where mitral regurgitation may be acute and severe?

A

Ruptured chordae
ruptured papillary muscle
Infective endocarditis

102
Q

Where is mitral regurgitation best heard? How would you characterise it?

A

Mitral area - 5th ICS in midclavicular line

Pan-systolic blowing murmur radiates to axilla

TOM: cause congestive heart failure -leaking valve = reduced ejection fraction + backlog of blood. May hear 3rd heart sound (stiff / weak ventricles + chordae “guitar string twang”)

103
Q

What are the indications for surgery in mitral regurgitation?

A

Symptomatic pts
Asymptomatic w/ mild/mod LV dysfucntion (EF 30-60%)

mitral valve replacement or repair

104
Q

What is the drug treatment for mitral regurgitation?

A

Diuretics

ACEI used in pt w/ dilated / ischaemic cardiomyopathy

LV dysfunction ? Give: ACEi and B-blockers e.g. bisoprolol and CRT reduced severity pg MR

105
Q

What are some causes of mitral stenosis?

A

Rheumatic heart disease

infective endocarditis

106
Q

What kind murmur does mitral stenosis cause? Where should you listen to it?

A

Mid-diastolic low pitched rumbling murmur

Large S1- thick valves need big systolic force to shut.

Listen at apex
Palpate a ‘tapping’ apex beat - due to loud SI

107
Q

What other examination findings is mitral stenosis associated with and why?

A

Malar flush: back pressure of blood into pulmonary system causing increase in C02 and vasodilation

Atrial fib: Left atrium struggling to push blood through stenosed valve - strain - electrical disruption - fibrillation

108
Q

What are the acute coronary syndromes?

A

STEMI
NSTEM
Unstable angina

109
Q

What is a STEMI ?

A

Cardiac sounding chest pain
with: ST segment elevation >1mm in limb >2mm in chest
or
New LBBB on ECG

hs-Tnl (Troponin I ) - >100ng/L
CK usualluy > 400

110
Q

What is an NSTEMI ?

A

Cardiac sounding chest pain
with: ST depression, T wave inversion (can be normal)

hs-Tnl (Troponin I ) - >100ng/L

+ previous ECG changes: old MI (pathological Q waves), LV hypertrophy / Afib may be present on ECG

111
Q

What is unstable angina?

A

Cardiac sounding chest pain
with ST depression, T wave inversion (can be normal)

hs-Tnl (Troponin I ) - NORMAL RANGE

112
Q

Apart from Troponin I (Tnl) levels what else should be measured in STEMI pts?

A

Creatinine Kinase

113
Q

What levels of Tnl (troponin) in men and women suggest high likelihood of myocardial necrosis?

A

men: hs-Tnl levels >34 ng/L
women: hs-Tnl levels >16 ng/L

114
Q

if suspect ACS when should you take a Tnl (troponin)?

A

1 on admission and then 1 hour later

only 1 needed if onset of symptoms was >3 hours ago

115
Q

What other conditions can cause a rise in Tnl (Troponin) and therefore give a false positive result when investigating for suspected ACS?

A 
Non cardiac: 
sepsis
Advanced renal failure (rhabdmyolysis - CTF)
Large PE
Congestive cardiac failure 
malignancy 
stroke 
Cardiac:
Myocarditis - post tacchyarrythmias
aortic dissection 
aortic stenosis 
hypertrophic cardiomyopathy
116
Q

What ECG findings do you need for a STEMI diagnosis?

A

ST elevation on 2 or more leads from the same zones e.g. II, III , AVF (inferior)

or

presence of LBBB

117
Q

What conditions can mimic STEMI on ECG?

A

Early repolarisation causes up-sloping ST elevation V1-V2 -Younger athletic / afro Caribbean pts.

Pericarditis - concave ST elevation. Widespread changes

118
Q

If there are raised troponins, and / or ECG changes such as ST depression, T wave inversion, pathological Q waves) what is diagnosis?

A

NSTEMI

119
Q

If troponin is normal and ECG shows no pathological changes, what is diagnosis?

A

Unstable angina

or

musculoskeletal chest pain

120
Q

If a pt presents with a STEMI within 12 hours of onset of symptoms what are the two treatment options that are time dependant ?

A

PCI - Percutaneous coronary intervention w/in 2 hours of presentation

Thrombolysis
- if PCI not available w/in 2 hours

121
Q

How is PCI for STEMI performed?

A

catheter is fed through pts femoral / brachial artery up to the coronary arteries.

A dye is injected so that the blockage can be visualised.

Balloons to widen or devices to aspirate and remove the blockage are performed.

Stent is then placed to keep the artery open

122
Q

What does thrombolysis involve?

A

Fibrinolytic material is injected to rapidly break down clots

e.g. alteplase
streptokinase
tenectplase

123
Q

What is the management for an STEMI -? This is workbook one

A
  1. IV access
  2. Pain relief (morphine + antiemetic)
  3. O2 (ONLY IF hypoxic aim >94%)
  4. Aspirin (300mg loading dose)
    4 a. Prasugrel (Ticagrelor if contra)
    4 b. Clopidogrel
  5. PCI
  6. Biochem - lipid progile, glucose, HbA1c, FBC
  7. Meds (Bblocker, statin, ACEi)
  8. Diabetic control
  9. HTN control
  10. Smoking cessation
  11. Triple therapy - AF pts
  12. complication monitoring - HF diuretics etc.
124
Q

What is the risk with pts who have AF and then get a STEMI in terms of their drug regimine?

A

AF taking anticoagulation (not
anti-platelets such as asprin).

They will be on 3 medications - increasing the risk of bleeding.

SO - limit time on all 3 drugs and give a PPI

125
Q

What is NSTEMI treatment? Dr Tom mnemonic

A

BATMAN

B – Beta-blockers unless contraindicated

A – Aspirin 300mg stat dose

T – Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative if higher bleeding risk)

M – Morphine titrated to control pain

A – Anticoagulant: Fondaparinux (unless high bleeding risk)

N – Nitrates (e.g. GTN) to relieve coronary artery spasm

Give oxygen only if their oxygen saturations are dropping (i.e. <95%).

SANDILANDS PLUS:
repeat ECG
Grace score for elevated troponins

126
Q

What are some complications of MI?

A

(Heart Failure DREAD)

D – Death

R – Rupture of the heart septum or papillary muscles

E – “Edema” (Heart Failure)

A – Arrhythmia and Aneurysm

D – Dressler’s Syndrome

127
Q

Secondary Prevention Medical Management for Acute Coronary Syndromes / STEMI DR TOM

A

Aspirin 75mg once daily

Another antiplatelet: e.g. clopidogrel or ticagrelor for up to 12 months

Atorvastatin 80mg once daily

ACE inhibitors (e.g. ramipril titrated as tolerated to 10mg once daily)

Atenolol (or other beta blocker titrated as high as tolerated)

Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)

128
Q

What is some secondary Prevetion lifestyle advice for ACS (acute coronary syndromes - STEMI/ NSTEM/UA)

A

Stop smoking
Reduce alcohol consumption
Mediterranean diet
Cardiac rehabilitation (a specific exercise regime for patients post MI)
Optimise treatment of other medical conditions (e.g. diabetes and hypertension)

129
Q

What is Grace score ? who is used for ?

A

gives a 6-month risk of death or repeat MI after having an NSTEMI:

<5% Low Risk
5-10% Medium Risk
>10% High Risk

If they are medium or high risk they are considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease.

130
Q

Coronary arteries anatomy :

The Left Coronary Artery becomes the _____1___and _____2_____

A

The Left Coronary Artery becomes the ___Circumflex___and __Left anterior descending (LAD)___

131
Q

What part of the heart does the Right Coronary Artery (RCA) supply?

A

Curves around the right side and under the heart and supplies the:

Right atrium
Right ventricle
Inferior aspect of left ventricle
Posterior septal area

132
Q

What part of the heart does the Circumflex Artery supply?

A

curves around the top, left and back of the heart and supplies the:

Left atrium
Posterior aspect of left ventricle

133
Q

What part of the heart does the Left Anterior Descending (LAD) supply?

A

it travels down the middle of the heart and supplies the:

Anterior aspect of left ventricle
Anterior aspect of septum

134
Q

What ECG leads correspond with Left Coronary Artery?

A

I, aVL, V3-6

Anterolateral

135
Q

What ECG leads correspond with LAD Artery?

A

V1-4

Anterior

136
Q

What ECG leads correspond with Circumflex Artery?

A

I, aVL, V5-6

Lateral

137
Q

What ECG leads correspond with the Right Coronary Artery?

A

II, III, aVF

Inferior

138
Q

What is stage 1 HTN?

A

Clinical BP is 140/90 mmHg or higher.

Ambulatory BP monitor or home BP monitor averages out at 135/85 mmHg

139
Q

What is stage 2 HTN?

A

Clinical BP is 160/100 mmHg or higher

ABPM or HBPM average is 150/95 mmHg or higher

140
Q

What is severe HTN?

A

Clinical systolic BP is 180 mmHg or higher.

Clinical diastolic Bp is 110 mmHg or higher.

141
Q

When should ambulatory BP readings be offered?

A

If BP is >140/90.

142
Q

How to manage pt with severe HTN (S=>180mmHg or= 110mmHg)?

A

Consider treatment immediately.

No need to do ABPM or HBPM

143
Q

Signs and symptoms of pt with HTN?

A

Asymptomatic

144
Q

Main ddx of pt with HTN, sweating, headache, palpatations, anxiety?

A

Phaeochromocytoma

145
Q

Main ddx of pt with HTN, muscle weakness and tetany?

A

Hyperaldosteronism

146
Q

CVS RF that may lead to HTN?

A

TIA, stroke, DM, previous renal disease, smoking, cholesterol, NSAID excess

147
Q

Pt has HTN. What may be present in PMH?

A

Angina, CCF, palpatations, syncope, valvular heart disease

148
Q

Pt has HTN. What should you cover in FHx?

A

FHx of HTN?
FHx of premature coronary disease
FHx of polycystic kidney disease

149
Q

What are secondary causes of HTN?

A 
Cushing's syndrome
Polycystic kidney disease 
Renal bruits 
Radio-femoral delay (coarctation)
Phaechromocytoma 
Hyperaldosteronism
150
Q

What investigations would you fo for pt with HTN?

A

Urinanalysis - albumin:creatinine ratio
Urinanalysis - haematuria
Blood glucose, U+Es = creatinine and eGFR
Lipid profile - serum total cholesterol, HDL cholesterol
U+Es for secondary cause too - low potassium and high sodium = hyperaldosteronism
12 lead ECG
ECHO - if LVH, valve disease, LVSD, diastolic dysfunction

151
Q

How to do a CVS risk assessment?

A

Use Q risk calculator

152
Q

When should pts with stage 1 HTN (under age of 80) be offered treatment?

A
  • if they have evidence of: target organ damage
  • if they have evidence of: established CVD
  • have renal impairment
  • have DM
  • have 10 year risk >20%
153
Q

When should pts with stage 2 HTN be offered treatment?

A

Always offer if have stage 2 HTN

154
Q

What is target BP in low-moderate risk pts with HTN?

A

<140 mmHg systolic

155
Q

What is target BP in pts who have HTN with a background of either DM, stroke, TIA, IHD, CKD?

A

<130/80 mmHg

156
Q

Elderly pt with systolic >160mmHg should have target BP of ??

(a) if under 80
(b) if over 80

A

(a) 140-150mmHg if under 80, ideally <140mmHg

(b) 140-150mmHg

157
Q

What is target diastolic BP in:

1) all pts with HTN?
2) diabetics specifically?

A

1) <90 mmHG

2) <85mmHg

158
Q

What is target systolic BP in pt with CKD and overt proteinuria?

A

<130mmHg

159
Q

Non-pharmacological treatment for HTN?

A
  • lose weight if BMI >25 kg/m2. (for every kg lost = reduce BP by 3/2 mmHg)
  • reduce salt intake (can reduce BP by 8/5mmHg)
  • minimise alcohol intake
  • exercise
  • smoking cessation
160
Q

Initial pharmacological treatment for HTN in pt under 55?

A

ACEi or ARB

161
Q

Initial pharmacological treatment for HTN in pt 55+, or black person of African or Carribean family origin of any age?

A

CCB

162
Q

Pt is already on ACEi for HTN. It isn’t reducing BP. What to add next ?

A

ACEi + CCB

163
Q

Pt is already on CCB for HTN. It isn’t reducing BP. What to add next ?

A

CCB + ACEi

164
Q

Pt is already on ACEi and CCB for HTN which is not helping. What to consider adding next?

A

Thiazide like diuretic

165
Q

Pharmacological treatment for resistant HTN?

A

ACEi, CCB, Thiazide like diuretic + one of the following:

  • spironolactone
  • higher dose of thiazide like diuretic
  • alpha or beta blocker if the above 2 do not work.
166
Q

What is a hypertensive crisis?

A

An increase in BP which if sustained over the next few hours, will lead to irreversible end-organ damage

E.g. encephalopathy, LV failure, aortic dissection, unstable angina, renal failure.

167
Q

Distinguish between a hypertensive emergency and a hypertensive urgency

A

Hypertensive emergency:
= high BP associated with a critical event (e.g. encephalopathy, pulm oedema, AKI, MI)

Hypertensive urgency:
= high BP without a critical illness but may include malignant hypertension.

168
Q

What is main target BP aim of treating a HTN emergency?

A

Reduce diastolic BP to 110mmHg in 3-12hrs

169
Q

What is main target BP aim of treating a HTN urgency?

A

Reduce diastolic BP to 110mmHg in 24hrs.

170
Q

What IV drugs should be started in hypertensive emergency?

A
  1. Sodium nitroprusside
  2. Labetalol
  3. GTN (1-10mg/hr)
  4. Esmolol
171
Q

Oral treatment options for hypertensive urgency?

A

Amlodipine - 5-10mg OD
Diltiazem - 120-300mg daily
Lisinopril - 5mg OD
Note: ACEi and CCB is effective and well tolerated

172
Q

What is the safest and most effective oral treatment for hypertensive urgency (according to CVS booklet)?

A

Nifedipine 20mg BD + Amlodipine 10mg OD for 3 days.

After 3 days, continue with amlodipine 10mg OD.

173
Q

Triad of symptoms in pheochromocytoma?

Most common sign?

A

The triad:
Episodic headache
sweating
tachycardia

most common sign: sustained or paroxysmal HTN

174
Q

Investigation for phaeochromocytoma?

A

24hr urine collection.
Measure urinary metanephrines and catecholamines.
Measure plasma fractionated metanephrines and catecholamines.
CT scan or MRI of abdomen and pelvis - detect adrenal tumours. If these do not show, can do MIBG scan.

175
Q

Management of phaeochromocytoma?

A

Resection

176
Q

How to manage phaeochromocytoma before surgery?

A

Alpha adrenergic blockade and beta adrenergic blockade.

177
Q

Name of commonly used alpha adrenergic blockage used for phaeochromocytoma?

A

Phenoxybenzamine

178
Q

Which order are alpha adrenergic blockade and beta adrenergic blockades given to pt for phaeochromocytoma?
Describe dosage.

A

Alpha first - ALWAYS. Phenoxybenzamine is used. Initial dose is 10mg OD/BD. Dose is increased every 2-3days to control BP. Final dose is 20-100mg daily.

After use of alpha adrenergic blockade is achieved, can start beta-adrenergic blockade - usually 2-3 days pre-operatively.

179
Q

Investigations and findings for Cushing’s syndrome with HTN?

A

Blood glucose = hyperglycaemia
24hr urine cortisol excretion = elevated by 3x
Adrenal CT
Low dose - dexamethasone suppression test. = Show high cortisol.

180
Q

Investigations for primary aldosteronism with HTN?

A

Aldosterone:renin - plasma renin will be low, aldosterone will be high
Adrenal CT

181
Q

What are some cardiac RF for developing Infective endocarditis?

A 
Mitral valve prolapse
Prosthetic (valves + patches NOT stents)
bicuspid aortic valve disease
rheumatic heart disease
congenital heart disease
182
Q

How are normal heart valves often involved in infective endocardiits?

A

previously normal heart valves can be infected due to a intravascular device e.g. central line?

183
Q

What are the most common organisms involved in native-valve Infective Endocarditis?

A 
Strep viridans (50%)
Staph aureus (20%)
184
Q

What is the most common organism for Infective Endocarditis in IV drug users?

A

Staph aureus (50-60%) of cases

185
Q

What is the organism most commonly involved in ‘early’ (up to 1 year) Infective Endocarditis, post prosthetic heat valve operation?

A

Peri-operative contamination- mainly staphylococci

especially coagulase - negative e.g. staph epidermis

186
Q

What is the organism most commonly involved in ‘late’ Infective Endocarditis, post prosthetic heat valve operation?

A

Viridans streptococci

Staph aureus

coagulase negatvie staph e.g. staph epidermis

187
Q

In Infective Endocarditis, what organisms might suggest concurrent disease of GU / GI tract?

A

Enterococcal infective carditis 10% of all cases

e.g. Enterococcus feacalis

188
Q

Which groups of people at risk of contracting Infective Endocarditis due to Fungi (+ which types) ?

A

E.g. Candidas / Aspergillus sp.

Immunosuppression
IV drug use 
cardiac surgery 
prolonged exposure to AB
IV feeding
189
Q

Why might blood cultures be negative in cases of infective endocarditis?

A

5% of those with IE is negative

often due to recent exposure to AB

or

Infection with slow growing / fastidious organisms e.g. streptococci, Coxiella Burnetii or Brucella

190
Q

What is the main causes of mortality in Infective Endocarditis?

A

Heart failure
CNS emboli
uncontrolled infection

191
Q

What features should make you immediately suspect Infective Endocarditis in a pt?

A

Unexplained fever
Bacteraemia
systemic illness
and / or new murmur

192
Q

What initial investigations should be performed on a pt with suspected Infective Endocarditis you have just admitted to hospital?

A

Bloods:
FBC
ESR / CRP
U&E
LTF
urine dip analysis and MSU for microscopy / culutre.
BLOOD CULTURES - 3 SETS FROM 3 DIFFERENT SITES **

Imaging:
CXR
ECG
ECHOCARDIOGRAM - TRANS OESOPHAGEAL ECHOCARDIOGRAM **

193
Q

How many blood cultures, over how long and where should you take in a pt with Infective Endocarditis?

A

at least 3 (ideally 6) from different sites over several hours.

Sampling during temperature peak does not make cultures more sensitive

194
Q

In a pt who is STABLE and has Infective Endocarditis, is it reasonable to delay AB treatment to take blood cultures - TRUE / FALSE

A

TRUE

once AB have been given harder to identify a causative organism

195
Q

What imaging modality should you use to visualise Infective Endocarditis?

A

Echocardiogram

Transthoracic echo - 65% of vegetations

Transoesophageal echo (TOE) - 95% of vegetations

196
Q

Which type of echocardiography is better for detecting mitral valve and prosthetic valve vegetations?

A

Transoesophageal echocardiography (TOE)

Also better at detecting aortic root, septal abscesses and leaflet perforations

197
Q

Diagnostic criteria for Infective Endocarditis: How many of major / minor criteria do you need to make a diagnosis?

A

2 major

or

1 major + 3 minor

or

5 minor

198
Q

What are the major criteria for diagnosing Infective Endocarditis?

A
  1. +ve blood cultures
    - typical org from 2 BC
    - +ve BCs >12 hrs apart
    - >3 +ve BCs >1hour
  2. Endocardial involvement
  3. +ve echo findings (abscess / vegetations)
  4. New valvular regurgitation
  5. dehiscence of prosthesis
199
Q

What are the minor criteria for diagnosing Infective Endocarditis?

A
  1. Predisposing valvular or cardiac abnormality
  2. IV drug user
  3. Pyrexia > 38°C
  4. Embolic phenomenon
  5. Vasculitic phenomenon
  6. Blood cultures suggestive (grown but not achieving major criteria)
  7. Suggestive echo findings (but not meeting major criteria)
200
Q

In terms of the management of Infective Endocarditis, what is the general principal? (before organism specific)

A

AB therapy

tunnelled central venous line good for prolonged IV AB (discuss regimens with duty microbiologist)

201
Q

What AB therapy is recommended for Infective Endocarditis caused by Viridans streptococci?

A

IV Benzylpenicillin

(+ low dose IV gentamicin 80 mg BD)

(Vancomycin if penicillin allergic)

202
Q

What AB therapy is recommended for Infective Endocarditis caused by Enterococci e.g. Enterococcus faecalis?

A

IV amoxicillin

(+ low dose IV gentamicin 80 mg BD)

(Vancomycin if penicillin allergic)

203
Q

What AB therapy is recommended for Infective Endocarditis caused by staphylocci, e.g. Staph aureus / Staph epidermis?

A

Flucloxacillin

Vancomycin if penicillin allergic

plus gentamicin / fusidic acid

204
Q

How would you recommend response to AB therapy in a pt with Infective Endocarditis? imaging, bloods etc

A
  1. bedside reviews of clinical status
  2. Echo 1 x weekly
    (vegetation size, complications e.g. abscess / valve destruction)
  3. ECG 2 x weekly
    conduction disturbances- aortic root abscess / valve infection
  4. Blood tests 2 x weekly
    ESR / CRP/ FBC / U&Es

AB - 6 weeks depending on response

205
Q

Referral for surgery is indicated for pts with Infective Endocarditis who have …..

A
  • Cardiac failure (valve compromise)
  • Valve dehiscence
  • Uncontrolled infection despite AB
  • Fungal / Coxiella burnetii infection
  • Relapse after medical therapy
  • Threatened / actual systemic embolism
  • Para-valvular infection (aortic root abscess)
  • Valve obstruction

Common exam question: PR interval prolongation in a patient with Infective Endocarditis is an indication for surgery as it can be secondary to aortic root abscess

206
Q

Examination findings in cardiac tamponade?

A

Becks triad present - raised JVP, Hypotension, muffled heart sounds
Kussmaul’s sign - raised JVP with inspiration
Pulsus paradoxus - reduced systolic BP with inspiration
ECG - may show alternating heights of QRS

207
Q

What type of shock can you get from cardiac tamponde and why?

A

Mechanical shock

Why? CTamponade is where there is a build up of fluid/blood in pericardial space. This restricts filling of heart. Get high central venous pressure and low arterial BP = mechanical shock.

208
Q

Causes of heart failure?

A 
Ischaemic heart disease 
Hypertension 
Valvular heart disease 
AF 
Chronic lung disease 
Cardiomyopathy 
Previous cancer chemo drugs 
HIV
209
Q

What is heart failure with normal ejection fraction (HFNEF) ?

A

Pts with heart failure who have clinical picture of HF but have echo that shows mild impairment or even normal systolic function

210
Q

Who suffers from heart failure with normal ejection fraction?

A

They are usually more elderly, overweight and have hypertension and atrial fibrillation

211
Q

What is the HFNEF pathophysiology?

A

Expected that relates to impaired filling or diastolic dysfunction

212
Q

Worst prognostic indicators for HF?

A 
Severe fluid overload
very high NT-proBNP levels
severe renal impairment 
advanced age 
multi- morbidity 
frequent admissions with heart failure
213
Q

Investigations for HF and why?

A

Renal function (baseline and for diuretic effect),
FBC (anaemia should be treated as consequence of bone marrow issue)
LFT’s hepatic congestion
TFT’s Thyroid disease
Ferritin and transferrin (Younger patients with possible haemochromatosis)
Brain natriuretic peptide (NT-proBNP)- identification of LV dysfunction

214
Q

When should you measure NTproBNP

A

Only when there is doubt about the diagnosis of HF
Above normal range does not equate to HF–> the levels will be increased in anything that causes cardiac strain e.g. AF or right heart strain

215
Q

CXR findings in HF?

A
  1. Cardiomegaly
  2. Could be pleural effusions
  3. Perihilar shadowing/consolidations
  4. Alveolar oedema
  5. Air bronchograms
  6. Increased width of vascular pedicle
216
Q

What investigations do you do in HF?

A

Echocardiography: THE KEY INVESTIGATION. It will confirm whether the diagnosis is correct.

Cardiac MRI: May elaborate cause for heart failure as echo may miss right ventricle.

217
Q

What would you find on an echo in HF?

A

Possibly: dilated poorly contracting left ventricle (systolic dysfunction) ; stiff, poorly relaxing, often small diameter left ventricle(diastolic dysfunction); valvular heart disease; atrial myxoma; pericardial disease

218
Q

What lifestyle advice would you give to someone with HF?

A

Smoking cessation
Restrict alcohol consumption
Salt restriction
Fluid restriction especially in the presence of hyponatraemia

219
Q

What would you prescribe to a pt with Chronic HF?

A

1st line treatment: ACE inhibitor and beta blocker (diuretics for symptomatic relief)

2nd line treatment: aldosterone antagonist

3rd line treatment:
ivabradine: sinus rhythm > 75/min and a left ventricular fraction < 35%

sacubitril-valsartan: left ventricular fraction < 35%
Considered in heart failure with reduced ejection fraction who are symptomatic on ACE inhibitors or ARBs
Initiated following ACEi or ARB wash-out period

Digoxin: not proven to reduce mortality may improve symptoms due to its inotropic properties
strongly indicated if there is coexistent atrial fibrillation

hydralazine in combination with nitrate
this may be particularly indicated in Afro-Caribbean patients

cardiac resynchronisation therapy
indications include a widened QRS (e.g. left bundle branch block) complex on ECG

220
Q

What is the purpose of Implantable cardiac defibrillators in HF?

A

Not to improve symptoms, but to prevent sudden cardiac death by delivering electroshock if pt in VT/VF

221
Q

What is the acute management for HF?

SODIUM mnemonic

A

IV loop diuretics- symptoms relief

Oxygen: 94-98% sats
Vasodilators- nitrates, not to all patients but inconcomitant myocardial ischaemia, severe hypertension or regurgitant aortic or mitral valve disease.

If pt is hypotensive/ cardiogenic shock:
Inotropic agents e.g. dobutamine
Vasopressor agents e.g norepinephrine
Mechanical circulatory assistance

S – Sit up
O – Oxygen
D – Diuretics
I – Intravenous fluids should be stopped
U – Underlying causes need to be identified and treated (e.g., myocardial infarction)
M – Monitor fluid balance

222
Q

How does GTN spray help alleviate symptoms of angina

CVS revision

A

1) Nitric oxide causes vascular smooth muscle relaxation. NO activates granulate cyclase which increases cGMP. this lowers intracellular calcium levels so causes relaxation of vascular smooth muscle.
2) It acts primarily on veins - ventilation will lower preload. So the heart will fill less so force of contraction is reduced. This lowers oxygen demand needed.
3) GTN also acts on coronary collateral arteries - so improves oxygen delivery to the ischaemic heart muscle.

223
Q

ECG findings in PE?

A

Sinus tachycardia
“S1Q3T3” pattern of acute cor pulmonale is classic; this is termed the McGinn-White Sign.
—> A large S wave in lead I, a Q wave in lead III and an inverted T wave in lead III together indicate acute right heart strain

224
Q

Diagnostic investigations for infective endocarditis?

A 
Blood cultures (3 different sites over several hours)
Echocardiogram (transoesophageal)
225
Q

Symptoms of digoxin toxicity?

A
  • abdo pain
  • nausea
  • vomitting
  • arrythmia
  • yellow-green tint to vision
  • diarrhoea
  • confusion
  • fatigue
  • palpitations
226
Q

RF for digoxin toxicity?

A
  • hypokalaemia
  • hypomagnesia
  • hypercalcaemia
  • elderly
227
Q

ECG changes in digoxin toxicity?

A
  • Downsloping ST depression - ‘Reverse Tick’
  • T wave changes (inversion)
  • Biphasic/flattened and shortened QT interval
  • Slight PR interval prolongation
228
Q

Treatment for digoxin toxicity?

A

Stop digoxin
Correct dyselectrolytaemia
Administer digifab (digoxin specific antibody indicated in lifethreatening digoxin toxicity).

229
Q

What is dresslers syndrome?

A

central, pleuritic chest pain and fever 4 weeks following a myocardial infarction. The ESR is elevated - Dressler’s syndrome

230
Q

What is acute pericarditis?

A

inflammation of the pericardial sac, lasting for less than 4-6 weeks.

231
Q
A
232
Q

Causes of acute pericarditis?

A
  • viral infections (Coxsackie)
  • tuberculosis
  • uraemia
  • post-myocardial infarction
  • early (1-3 days): fibrinous pericarditis
  • late (weeks to months): autoimmune pericarditis (Dressler’s syndrome)
  • radiotherapy
  • connective tissue disease
  • systemic lupus erythematosus
  • rheumatoid arthritis
  • hypothyroidism
  • malignancy
    lung cancer
    breast cancer
  • trauma
233
Q

Features of pericarditis?

A
  • chest pain: may be pleuritic. Is often relieved by sitting forwards
  • other symptoms include a non-productive cough, dyspnoea and flu-like symptoms
  • pericardial rub: heard as a scratching or creaking noise at the left lower sternal border.
234
Q

Inv for acute pericarditis?

A

Bedside:
* ECG: widespread saddle shaped ST elevation, PR depression
Bloods:
* FBC- for WBCs
* CRP
* Troponins (may be elevated, this could be myocrditis)
Imaging:
* Transthoracic echocardiography

235
Q

Management of acute pericarditis?

A
  • the majority of patients can be managed as outpatients
    patients who have high-risk features such as fever > 38°C or elevated troponin should be managed as an inpatient
  • treat any underlying cause
    most patients however will have pericarditis secondary to viral infection, meaning no specific treatment is indicated
  • strenuous physical activity should be avoided until symptom resolution and normalisation of inflammatory markers
  • a combination of NSAIDs and colchicine is now generally used for first-line for patients with acute idiopathic or viral pericarditis
  • until symptom resolution and normalisation of inflammatory markers (usually 1-2 weeks) followed by tapering of dose recommended over
236
Q
A

Y3 med old (8 decks)

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