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FINALS > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

ACS

What are the three branches of ACS and how do you differentiate them?

A
  • Unstable angina = cardiac chest pain + normal/abnormal ECG + normal troponin
  • NSTEMI = cardiac chest pain + normal/abnormal ECG + raised troponin
  • STEMI = cardiac chest pain + abnormal ECG + raised troponin
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2
Q

ACS

What are the common and uncommon causes of ACS?

A
  • Common = atherosclerotic plaque ruptures causing platelet aggregation and thrombus formation leading to coronary artery occlusion > infarction
  • Uncommon = coronary vasospasm, cocaine, coronary dissection
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3
Q

ACS

What are the unmodifiable and modifiable risk factors for cardiac pathology?

A
  • Unmodifiable = age, male, FHx

- Modifiable = smoking, DM, HTN, hypercholesterolaemia, obesity

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4
Q

ACS

How do you classify MIs in terms of ECG changes and causes?

A
  • STEMI = complete coronary artery occlusion
  • NSTEMI = partial coronary thrombus occlusion
  • Type 1 MI = spontaneous MI due to primary coronary event
  • Type 2 MI = secondary to ischaemia e.g., coronary spasm, arrhythmias, sepsis
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5
Q

ACS

How does ACS classically present?

A
  • Sudden onset, unremitting central chest pain
  • Left arm, neck and jaw radiation
  • Associated SOB, N+V, sweating
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6
Q

ACS

How may ACS atypically present?

A
  • Silent MI in elderly and patients with diabetes
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7
Q

ACS

How does unstable angina present?

A
  • Chest pain at rest
  • Doesn’t resolve with GTN
  • Crescendo pattern = more frequent, easier to provoke
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8
Q

ACS

Give some differentials for chest pain

A
  • Cardiac = myo/pericarditis, dissection
  • Resp = PE, pneumonia, pneumothorax
  • GI = reflux, peptic ulcer
  • MSK = rib #, costochondritis
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9
Q

ACS

Describe the territories and vessels on an ECG

A
  • Leads II, III, aVF = inferior so RCA
  • V1–2 = septal, V3–4 = anterior so LAD
  • I, aVL, V5–6 = lateral so left circumflex
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10
Q

ACS
What is the diagnostic criteria for a STEMI?
What ECG changes may come later?

A
  • New LBBB
  • ST elevation >2mm in adjacent chest leads or >1mm in adjacent limb leads (may have hyperacute T waves)
  • Tall R waves and ST depression in V1–3 = posterior MI (usually left circumflex or RCA)
  • T wave inversion and pathological Q waves
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11
Q

ACS

What ECG changes may be seen in an NSTEMI?

A
  • ST depression

- T wave inversion

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12
Q

ACS
How would you investigate ACS?
What is the most important test and how do you interpret it?

A
  • FBC, U&E, lipid profile, glucose, CXR
  • Serial troponins (3h after, if mildly raised repeat after 6–12h and if doubles then confirm MI)
  • May be falsely raised in peri/myocarditis, sepsis, PE, CKD
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13
Q

ACS

What are the post-MI complications?

A

DREAD

  • Death (VF arrest)
  • Rupture of myocardium
  • oEdema.
  • Arrhythmia/aneurysm
  • Dressler’s/pericarditis
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14
Q

ACS

How can post-MI rupture of myocardium present?

A
  • LV free wall = acute HF due to tamponade
  • Mitral valve papillary muscle = acute MR with pulmonary oedema + pan-systolic murmur
  • VSD = acute HF
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15
Q

ACS

How can post-MI arrhythmia/aneurysm present?

A
  • AV block after inferior MI

- LV aneurysm = weakened myocardium can present with persistent ST elevation

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16
Q

ACS

How can post-MI Dressler’s syndrome/pericarditis present?

A
  • Normal pericarditis 48h after
  • Dressler’s = 2–6w post MI with autoimmune pericarditis due to autoantibody formation against heart
  • Global saddle-shaped ST elevation, T wave inversion, echo (pericardial effusion) and raised inflammatory markers
  • Manage with high dose aspirin or NSAIDs
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17
Q

ACS

How do you manage ACS initially?

A

MONA

  • Morphine 5–10mg IV with metoclopramide 10mg IV
  • Oxygen if SpO2 <94%
  • Nitrates (sublingual GTN first, then IV, NOT if SBP <90)
  • Aspirin 300mg PO
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18
Q

ACS

What are the 2 management options of an acute STEMI and how do you determine which one to use?

A
  • Primary percutaneous coronary intervention if ≤12h since Sx onset and can deliver within 120m
  • Fibrinolysis with streptokinase or alteplase if >12h since Sx onset or cannot be delivered within 120m e.g., DGH
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19
Q

ACS

Describe the management of STEMI with PPCI

A
  • Before = DAPT with 60mg prasugrel if not on anticoagulation, 300mg clopidogrel if anticoagulated
  • During = unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (tirofiban) for radial access
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20
Q

ACS

Describe the management of STEMI with thrombolysis

A
  • During, give antithrombin fondaparniux
  • Ticagrelor 180mg post procedure
  • If ECG 60–90m shows failure of STEMI resolution, ?PCI
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21
Q

ACS

Describe the management of an NSTEMI

A
  • MONA and fondaparniux if no immediate PCI
  • Calculate GRACE 6m mortality score
  • Low risk ≤3% = ticagrelor (clopidogrel if anticoagulated)
  • High risk >3% = coronary angiography with follow-on PCI if clinically unstable or if not within 72h, give unfractionated heparin with DAPT (prasugrel/ticagrelor or clopidogrel if anticoagulated) prior to PCI
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22
Q

ACS
What secondary prevention medications should all patients be on post-MI?
What else should happen post-MI?

A
  • Aspirin 75mg
  • Another antiplatelet e.g., clopidogrel 75mg, ticagrelor 90mg
  • Atorvastatin 80mg
  • ACEi (e.g., ramipril)
  • Atenolol aka beta blockers (usually bisoprolol
  • Also, echo to assess for LVSD and refer for cardiac rehab
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23
Q

IHD

What is the pathophysiology of angina?

A
  • Symptom of oxygen supply/demand mismatch to the heart felt on exertion
  • Microvascular resistance reduces to increase flow at rest instead of during exertion and cannot fall further so flow cannot meet myocardial demand
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24
Q

IHD

What are the 4 main classifications of angina?

A
  • Stable = induced by effort, relieved by rest/GTN
  • Unstable angina = ACS, comes on at rest
  • Decubitus angina = precipitated by lying flat
  • Prinzmetal angina = vasospastic due to coronary artery spasm
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25
Q

IHD
What is the most common cause of angina?
What are the less common causes?

A
  • Atherosclerosis = atheroma causes narrowing of coronary vessels meaning increase oxygen demand leading to reversible myocardial ischaemia
  • Increased distal resistance (LVH), reduced oxygen carrying capacity (anaemia), coronary artery spasm, thrombosis
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26
Q

IHD

What is the clinical presentation of angina?

A
  • Triad of: heavy discomfort to chest, jaw, neck and arm, symptoms induced by exertion, symptoms relieved by rest/GTN (3/3 = typical, 2/3 = atypical, 1/3 = non-anginal)
  • Also SOB, sweating, palpitations
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27
Q

IHD

What baseline investigations would you do in angina?

A
  • ECG

- FBC, U&E, LFT, TFT, lipid profile, HbA1c/fasting glucose

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28
Q

IHD

What are the three lines of investigations for ischaemic heart disease?

A
  • 1st = CT coronary angiography
  • 2nd = non-invasive functional imaging (stress echo, myocardial perfusion SPECT, MR imaging)
  • 3rd = invasive coronary angiogram
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29
Q

IHD
What is the primary prevention of angina?
When is this indicated?

A
  • QRisk3 >10%, CKD or DM = atorvastatin 20mg (increase dose if non-HDL has not reduced for ≥40%)
  • Optimise RFs = smoking cessation, reduce alcohol, weight loss, optimise co-morbidities
  • Before someone has angina
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30
Q

IHD

What is the first line management of angina?

A
  • Aspirin 75mg, atorvastatin 80mg (2ndary prevention)
  • Sublingual GTN (reliever)
  • Beta-blocker (bisoprolol) OR rate limiting CCB (diltiazem, verapamil)
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31
Q

IHD

What advice should be given to patients regarding their GTN spray?

A
  • Take when Sx start, wait 5m, repeat spray, wait 5m > ambulance
  • SEs = headaches, flushing, dizziness
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32
Q

IHD
If a patient is on monotherapy as they cannot tolerate dual therapy, or they are on dual therapy awaiting PCI, what options may you consider?

A
  • Long-acting nitrates e.g., isosorbide mononitrate, ivabradine, nicorandil, ranolazine)
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33
Q

IHD

What is the second line management of angina?

A
  • Beta-blocker AND long-acting DHP CCB (e.g., amlodipine)
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34
Q

IHD

What are the options for third line management and their relative pros/cons?

A
  • Percutaneous coronary intervention with coronary angioplasty = cost-effective, quicker recovery
  • Coronary artery bypass graft (CABG) = major surgery, more complications, mortality advantage if >65, have DM or complex 3 vessel disease
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35
Q

IHD

What are the indications for procedural interventions?

A
  • Complex 3 vessel disease

- Significant left main stem stenosis

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36
Q

HEART FAILURE

What is heart failure?

A
  • Failure of the heart to generate sufficient cardiac output to meet the metabolic demands of the body
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37
Q

HEART FAILURE

How does the heart respond to the initial reduced cardiac output?

A
  • Compensatory hypertrophy as Starling effect dilates heart to enhance contractility
  • Sympathetic and RAAS activation
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38
Q

HEART FAILURE

Over time, what happens to the initial compensatory mechanisms?

A
  • Dilatation = impaired contractility and valve regurg
  • Hypertrophy = myocardial ischaemia
  • RAAS = Na and fluid retention (oedema)
  • Sympathetic activation = increased afterload so decreased CO
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39
Q

HEART FAILURE

What are the broad main types of heart failure?

A
  • Systolic failure (HFrEF <40%) = inability of ventricles to contract normally = low CO
  • Diastolic failure (HFpEF >40%) = inability of ventricles to relax and fill normally = low CO
  • Left and right heart failure
  • High output heart failure
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40
Q 
HEART FAILURE
What are some causes of...
i) HFrEF?
ii) HFpEF?
iii) left heart failure?
iv) right heart failure?
v) high output heart failure?
A

i) IHD, dilated cardiomyopathy, myocarditis and infiltration (e.g., haemochromatosis, sarcoidosis)
ii) HOCM, restrictive cardiomyopathy/pericarditis, cardiac tamponade
iii) increased LV afterload (aortic stenosis) or preload (aortic regurg)
iv) increased RV afterload (pulmonary HTN) or preload (tricuspid regurg)
v) anaemia, pregnancy, thyrotoxicosis

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41
Q

HEART FAILURE

What is the New York Heart Association Classification of heart failure?

A
  • Class I = no Sx/limitations (asymptomatic)
  • Class II = mild Sx/limitations (mild heart failure)
  • Class III = marked limitation, only asymptomatic at rest (moderate heart failure)
  • Class IV = symptomatic at rest (severe heart failure)
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42
Q

HEART FAILURE
What is the consequence of left heart failure?
What are the signs and symptoms of left heart failure?

A
  • Pulmonary congestion and systemic hypoperfusion
  • Sx = nocturnal cough ± pink frothy sputum, PND, orthopnoea and SOBOE
  • Signs = bi-basal fine crackles, tachypnoea, S3 gallop rhythm, ‘cardiac wheeze’, prolonged CRT, hypotension and cyanosis
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43
Q

HEART FAILURE
What is the consequence of right heart failure?
What are the signs and symptoms of right heart failure?

A
  • Venous congestion and pulmonary hypoperfusion
  • Sx = peripheral oedema, weight gain, ascites, nausea
  • Signs = raised JVP, pitting oedema, hepatomegaly, ascites, (bilat) transudative pleural effusions
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44
Q

HEART FAILURE

What is the first-line investigation for heart failure and how would you interpret the results?

A
  • N-terminal pro-B-type natriuretic peptide (NT-proBNP)
  • 400–2000 = 6w referral for assessment + echo
  • > 2000 = urgent 2w referral for assessment + echo
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45
Q

HEART FAILURE

What is the diagnostic investigation for heart failure?

A

Echocardiogram

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46
Q

HEART FAILURE

What other investigations may you perform in heart failure?

A
  • ECG may identify cause

- CXR

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47
Q

HEART FAILURE

What are the features of heart failure on a CXR?

A

ABCDEF –

  • Alveolar oedema (bat-wing perihilar shadowing)
  • kerley B lines (interstitial oedema)
  • Cardiomegaly (CT ratio >0.5)
  • upper lobe Diversion
  • pleural Effusion
  • Fluid in horizontal fissure
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48
Q

HEART FAILURE

What lifestyle advice is offered in heart failure?

A
  • Annual flu and one off PCV vaccination
  • Smoking + alcohol cessation, optimise weight, salt and fluid restrictions
  • Supervised cardiac rehab
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49
Q

HEART FAILURE

What is the initial management of acute heart failure?

A

POUR SOD –

  • POUR (stop) any IVI and monitor fluid balance
  • Sit patient upright
  • Oxygen if hypoxic
  • Diuretics (IV furosemide 40mg STAT, ? more)
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50
Q

HEART FAILURE

What is the advanced management of acute heart failure?

A
  • SBP >100mmHg = ?IV nitrate infusion under senior guidance, CPAP
  • SBP <100mmHg = ICU input with inotropes (dopamine), CPAP
  • Consider furosemide infusion, ultrafiltration
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51
Q

HEART FAILURE

What is the first line management of chronic heart failure?

A
  • BOTH ACEi (prolongs life in LVSD) and beta-blocker

- Can add loop diuretics for symptomatic relief e.g., furosemide or bumetanide

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52
Q

HEART FAILURE

What is the second line management of chronic heart failure?

A
  • Aldosterone antagonist e.g., spironolactone or eplerenone

- Monitor U&E as with ACEi can cause hyperkalaemia

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53
Q

HEART FAILURE

What is the third line management of chronic heart failure?

A
  • Hydralazine and nitrate in Afro-Carribbean
  • Ivabradine if sinus >75bpm and EF <35%
  • Sacubitril/valsartan if EF <35% + after ACEi/ARB washout
  • Cardiac resynchronisation therapy if widened QRS on ECG
  • Digoxin esp. if AF
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54
Q

HEART FAILURE

What drugs should be avoided in heart failure?

A
  • Rate limiting CCBs in HFrEF as negatively inotropic
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55
Q

AF

What is the pathophysiology of AF?

A
  • Chaotic electrical activity from SAN leads to uncontrolled atrial contraction
  • Delayed AVN response means only some atrial impulses conduced to ventricles
  • Irregular ventricular response
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56
Q

AF

How can AF be sub-classified?

A
  • Acute <48h
  • Paroxysmal if <7d and is intermittent
  • Persistent if lasts >7d but amenable to cardioversion
  • Permanent if lasts >7d but not amenable to cardioversion
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57
Q

AF

What are the causes of AF?

A

“AF affects Mrs. SMITH”

  • Sepsis
  • Mitral valve disorders (stenosis, regurg, rheumatic heart disease)
  • IHD
  • Thyrotoxicosis
  • HTN
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58
Q

AF

What is the clinical presentation of AF?

A
  • Palpitations, SOB, syncope, chest pain

- Signs = irregular pulse

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59
Q

AF

What investigations would you perform in someone with AF?

A
  • FBC, U&E, LFT, TFTs, CRP/ESR, lipid profile, ?cultures
  • ECG
  • Echo for structural abnormalities
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60
Q

AF

What are the ECG findings in AF?

A
  • Absent P waves
  • Irregularly irregular rhythm
  • Narrow QRS complex
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61
Q

AF

What is a potential complication of AF?

A
  • Embolic stroke as stagnation of blood in atria due to ineffective mechanical action can lead to thrombus formation
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62
Q

AF

When managing AF, when would you consider rate control or rhythm control?

A
  • Rate = >65y/o, Hx of IHD
  • Rhythm = first onset, co-existent heart failure, obvious reversible cause or immediately if haemodynamically unstable (shock, CP, syncope, pulmonary oedema)
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63
Q

AF
How do you choose between immediate and elective rhythm control?
How do you perform immediate rhythm control?

A
  • Immediate = AF <48h or haemodynamically stable

- Synchronised DC cardioversion with sedation

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64
Q

AF

How do you perform elective rhythm control?

A
  • Anticoagulate 3w prior due to embolism risk or TOE to exclude thrombus
  • DC cardioversion preferred if AF >48h and stable
  • Pharmacological is either flecainide (regular/pill in pocket if young with no structural heart disease) or amiodarone (older and structural heart disease)
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65
Q

AF

What is the rate management for AF?

A
  • Beta blockers or rate-limiting CCB (asthma)

- Second line is digoxin

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66
Q

AF

How are decisions about anticoagulation made in AF?

A
  • CHA2DS2-VaSc score = CCF, HTN, Age 64-75 (1) or ≥75 (2), DM (1), Stroke/TIA (2), Vascular disease (1), F(1)
  • Males scoring 1 or females scoring 2 should be anticoagulated
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67
Q

AF

How are decisions about bleeding risk made in AF?

A

ORBIT –

  • Hb (<13 in men, <12 in females) (2)
  • Age >74
  • Bleeding Hx (2)
  • eGFR <60 (1)
  • Concomitant use of anti-platelets (1)
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68
Q

AF

How is anticoagulation in AF managed?

A
  • First line = DOAC e.g., apixaban, rivaroxaban

- Second line = warfarin

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69
Q

ATRIAL FLUTTER

What is atrial flutter?

A
  • Aberrant macro-circuit in the right atrium which cycles at 300bpm and the AVN gives a degree of block giving a regular rhythm at variable rates (e.g., 2:1, 3:1)
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70
Q

ATRIAL FLUTTER

What is the ECG pattern of atrial flutter?

A
  • Regular rhythm where rate is dependent on block (if irregular ?flutter with variable block vs. AF)
  • ‘Sawtooth’ appearance of p waves
  • Narrow QRS complex
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71
Q

ATRIAL FLUTTER

What is the management of atrial flutter?

A
  • Same as AF but emphasis on electrical cardioversion

- Radio frequency ablation of tricuspid valve isthmus mostly curative

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72
Q

TACHYARRHYTHMIAS

What are the two types of tachyarrhythmias?

A
  • Narrow complex (SVTs) = atrioventricular re-entrant tachycardia, atrioventricular node re-entrant tachycardia, atrial tachyarrhythmias (AF/flutter)
  • Broad complex = regular being VT, irregular being polymorphic VT, AF with BBB and VF
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73
Q

TACHYARRHYTHMIAS

What is the difference between AVRT and AVNRT?

A
  • AVRT = accessory pathway can lead to pre-excitation of ventricles (e.g., Wolff-Parkinson-White bundle of Kent)
  • AVNRT = commonest where circuits form within the AVN and can be triggered by exertion, stress, coffee + alcohol
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74
Q

TACHYARRHYTHMIAS
What are some causes of…
i) VT?
ii) polymorphic VT?

A

i) MI #1, digoxin, cardiomyopathy,

ii) Prolonged QT = antipsychotics, citalopram, myocarditis, low Ca/Mg/K, SAH, hypothermia

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75
Q

TACHYARRHYTHMIAS
What are the ECG findings in:
i) Wolff-Parkinson White syndrome?
ii) AVNRT?

A

i) Slurred upstroke to QRS (delta wave), short PR interval, P wave between QRS complexes
ii) normal QRS, P waves not present

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76
Q

TACHYARRHYTHMIAS
What is the initial management of tachyarrhythmias and what are you looking for?
If you are unhappy at this stage, how would you manage this?

A
  • ABCDE approach
  • Adverse signs = syncope, shock, HF or CP
  • Synchronised DC shock up to 3x > 300mg IV amiodarone + repeat DC shock
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77
Q

TACHYARRHYTHMIAS

There are no adverse features, the QRS is narrow and regular. What is the diagnosis and management?

A
  • SVT
  • Vagal manoeuvres (carotid sinus massage or modified Valsalva)
  • IV adenosine 6mg > 12mg > 18mg
  • Verapamil or beta blocker
  • DC shock up to 3 attempts
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78
Q

TACHYARRHYTHMIAS

There are no adverse features, the QRS is narrow and irregular. What is the diagnosis and management?

A
  • AF or flutter

- Treat as AF for rate control (e.g., bisoprolol vs. verapamil or ?digoxin/amiodarone if heart failure)

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79
Q

TACHYARRHYTHMIAS

There are no adverse features, the QRS is broad and regular. What is the diagnosis and management?

A
  • Ventricular tachycardia
  • Pulseless = cardiac arrest algorithm
  • Pulse = IV amiodarone 300mg followed by 900mg infusion, DC shock up to 3 attempts
  • Do NOT use verapamil, may need ICD afterwards
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80
Q

TACHYARRHYTHMIAS

There are no adverse features, the QRS is broad and irregular. What are some differentials and how would you manage?

A
  • AF with BBB (#1), polymorphic VT

- Expert help, if polymorphic VT then IVI magnesium sulfate 2g

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81
Q

BRADYARRHYTHMIAS

What are some causes of bradycardia?

A
  • Cardio = degenerative fibrosis of conduction pathways, sick sinus syndrome, heart block, iatrogenic (beta blockers, digoxin)
  • Normal variant
  • Hypothyroidism
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82
Q

BRADYARRHYTHMIAS

What is first degree heart block? How does it present and how is it managed?

A
  • Delayed AV conduction with fixed prolonged PR interval >0.2s
  • Often asymptomatic
  • No treatment
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83
Q

BRADYARRHYTHMIAS
What is second degree heart block?
What two types are there?

A
  • Some atrial activity fails to conduct to the ventricles so there are more P waves than QRS complexes
  • Mobitz I (Wenckebach) = progressively increasing PR Intervals until dropped QRS and pattern resets
  • Mobitz II (Wenckebach) = sustained PR intervals with occasional dropped QRS
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84
Q

BRADYARRHYTHMIAS
Which type of second degree heart block is more dangerous and why?
How is it managed?

A
  • Mobitz II
  • Can progress to complete heart block
  • PPM insertion
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85
Q 
BRADYARRHYTHMIAS
What is third degree heart block?
Give a potential cause for it.
How can you determine where the issue is?
How is it managed?
A
  • Complete dissociation between atrial and ventricular activity where P waves and QRS complexes appear independently of each other
  • Post-inferior MI
  • Narrow QRS = originates in HIS bundle (junctional)
  • Broad QRS = originates below HIS bundle (ventricular)
  • PPM insertion
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86
Q

BRADYARRHYTHMIAS

What is the difference between a bifascicular and trifascicular block?

A
  • Bifascicular = RBBB + LAD

- Trifascicular = RBBB + LAD + 1st degree heart block

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87
Q

BRADYARRHYTHMIAS
How does left bundle branch block appear on ECG?
What are some causes?

A
  • WiLLiaM = ‘W’ in V1 (rSlurred), ‘M’ in V6 (R)

- New = always pathological (MI, HTN, aortic stenosis, cardiomyopathy

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88
Q

BRADYARRHYTHMIAS
How does right bundle branch block appear on ECG?
What are some causes?

A
  • MaRRoW = ‘M’ in V1 (rSR), ‘W’ in V6 (qRslurred)

- Normal variant, RVH, PE and MI

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89
Q

BRADYARRHYTHMIAS
What is the initial management of bradyarrhythmias and what are you looking for?
If you are unhappy at this stage, how would you manage this?

A
  • ABCDE approach
  • Adverse signs = syncope, shock, HF or CP
  • IV atropine 500mcg up to maximum of 3mg (6 doses)
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90
Q

BRADYARRHYTHMIAS

The IV atropine has not helped. What are your next stages in management?

A
  • Transcutaneous pacing
  • Isoprenaline/adrenaline infusion titrated to response
  • Specialist help for ?transvenous pacing
  • ?Glucagon if beta-blocker overdose
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91
Q

BRADYARRHYTHMIAS

There are no adverse features, what do you do next?

A
  • Assess for risk of asystole = complete heart block with broad QRS, recent asystole, Mobitz II block, ventricular pause >3s
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92
Q

BRADYARRHYTHMIAS
There are no adverse features and…

i) risk of asystole present
ii) no risk of asystole present

how do you manage this?

A

i) Same management as if adverse features

ii) Monitor with cardiology input

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93
Q

CARDIAC ARREST

What are the reversible causes of cardiac arrest?

A

4Hs and 4Ts

  • Hypoxia
  • Hypovolaemia
  • Hypo/hyperkalaemia
  • Hypothermia
  • Thrombosis (coronary/pulmonary)
  • Tension pneumothorax
  • Tamponade (cardiac)
  • Toxins
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94
Q

CARDIAC ARREST

What is the initial management of cardiac arrest?

A
  • ABCDE approach, IV (or IO) access, ABG, fluids
  • No or agonal breathing or no palpable central pulse = cardiac arrest
  • Chest compressions 30:2, ONLY stop when analysing rhythm and shocking
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95
Q

CARDIAC ARREST
What are the shockable rhythms?
How do you manage an arrest with shockable rhythms?

A
  • Pulsless VT and VF
  • Deliver single shock > 2m CPR unless witnessed in monitored patient (CCU) then 3x quick shocks then CPR
  • After 3 shocks > 300mg amiodarone IV/IO and 1mg adrenaline 1:10,000 IV/IO repeat adrenaline 3–5m
  • After 5 shocks give further 150mg amiodarone IV/IO
  • Lidocaine is an alternative to amiodarone
96
Q

CARDIAC ARREST
What are the non-shockable rhythms?
How do you manage an arrest with non-shockable rhythms?

A
  • Asystole and pulseless electrical activity

- Immediately give 1mg adrenaline 1:10,000 IV/IO then every 3–5m

97
Q

CARDIAC ARREST

What is the management of an arrest that is thought to be due to a PE?

A
  • Consider thrombolytic drugs

- Continue CPR for 60–90m

98
Q

AORTIC STENOSIS

What is aortic stenosis?

A
  • Narrowing of aortic valve > LV outflow obstruction and so increased LV pressure and increased pressure gradient between LV + aorta
  • Leads to compensatory LVH and increased oxygen demand
99
Q

AORTIC STENOSIS

What are some causes of aortic stenosis?

A
  • Degeneration + calcification of a normal valve (>65y)
  • Calcification of congenital bicuspid aortic valve (<65y)
  • William’s syndrome (supravalvular)
100
Q

AORTIC STENOSIS

What are the symptoms of aortic stenosis?

A
  • Syncope
  • Angina
  • Dyspnoea (exertional with reduced exercise tolerance)
101
Q

AORTIC STENOSIS

What are the signs of aortic stenosis?

A
  • Slow rising carotid pulse (pulsus tardus)
  • Narrow pulse pressure (SBP – DBP)
  • ESM = harsh, best heard 2nd ICS R sternal border and radiates to the carotids
  • Soft S2 heart sound and sometimes ejection click
102
Q

AORTIC STENOSIS

What are some differentials of an ejection systolic murmur?

A
  • Pulmonary stenosis
  • HOCM
  • Aortic sclerosis
  • Pregnancy
103
Q

AORTIC STENOSIS

What investigations would you do for aortic stenosis?

A
  • ECG = ?LVH
  • CXR = ?cardiomegaly
  • ECHO = diagnostic
104
Q

AORTIC STENOSIS

What would you measure on the echo and how would this guide follow-up?

A
  • Doppler echo can quantify stenosis by estimating gradient across valves
  • Peak gradient >40mmHg = severe
  • Regular follow up every 6m if severe or yearly if mild-moderate
105
Q

AORTIC STENOSIS

What is the management of aortic stenosis?

A
  • Asymptomatic = observe
  • Symptomatic = aortic valve replacement
  • Asymptomatic but valvular gradient >40mmHg and LVSD = aortic valve replacement
106
Q

AORTIC STENOSIS

What are the two options for aortic valve replacement and when would you favour them?

A
  • Transcatheter aortic valve implantation = severe comorbidities, previous heart surgery, frailty, restricted mobility and >75y
  • Surgical aortic valve replacement = low risk patients <75
107
Q

AORTIC REGURGITATION

What is aortic regurgitation?

A

Backflow of blood to LV via an ineffective aortic valve during diastole leading to volume overload > LV dilatation

108
Q

AORTIC REGURGITATION

What are the causes of aortic regurgitation?

A
  • Valve disease = rheumatic fever, infective endocarditis, bicuspid valve
  • Aortic root disease = dissection, Marfan’s/EDS, HTN
109
Q

AORTIC REGURGITATION

What is the clinical presentation of aortic regurgitation?

A
  • Exertional dyspnoea, angina, orthopnoea
  • Early diastolic murmur (heard best learnt forward in exhalation)
  • Collapsing (Corrigan’s/waterhammer) pulse
  • Wide pulse pressure
  • De Musset’s sign (head bobbing)
  • Quincke’s sign (nailbed pulsation)
110
Q

AORTIC REGURGITATION

What is the management of aortic regurgitation?

A
  • Echocardiogram for diagnosis and monitoring
  • Medical Mx to reduce HTN useful in slowing aortic root dilatation
  • Surgical aortic valve replacement if symptomatic, EF<50% or significant enlargement of ascending aorta
111
Q

MITRAL STENOSIS

What is mitral stenosis and the consequence of this?

A
  • Obstruction of LV inflow leading to elevated LA pressures and enlargement causing AF
112
Q

MITRAL STENOSIS
What is the most common cause of mitral stenosis?
What are some other causes of mitral stenosis?

A
  • Rheumatic fever

- Age-related mitral annular calcification, infective endocarditis

113
Q

MITRAL STENOSIS

What are the symptoms of mitral stenosis?

A
  • Dyspnoea
  • Haemoptysis
  • Palpitations
  • Chest pain
114
Q

MITRAL STENOSIS

What are the signs of mitral stenosis?

A
  • Mid-late low pitched rumbling diastolic murmur = heard best in exhalation lying on left with bell
  • Loud S1 opening snap
  • Low volume pulse
  • Malar flush
  • Irregular pulse (AF)
115
Q

MITRAL STENOSIS

What are the investigations for mitral stenosis and what might they reveal?

A
  • ECG = p-mitrale and AF
  • CXR = LA enlargement
  • ECHO = diagnostic, cross sectional area <1sq cm
116
Q

MITRAL STENOSIS

What is the management of symptomatic mitral stenosis?

A
  • Balloon valvuloplasty if valve pliable and non-calcified
  • Percutaneous mitral valvotomy if moderate disease
  • Open valve repair/replacement if severe disease
117
Q

MITRAL REGURGITATION

What is mitral regurgitation?

A
  • Blood leaks back through the mitral valve on systole meaning a less efficient heart as less blood pumped to body which can ultimately lead to heart failure
118
Q

MITRAL REGURGITATION

What are the causes of mitral regurgitation?

A
  • Degenerative mitral valve prolapse = #1 developed world
  • Rheumatic fever = #1 developing world
  • Ischaemic = papillary muscle rupture post MI
  • Infective endocarditis = vegetations prevent valve closing
  • Connective tissue disorders = Marfan’s/EDS
119
Q

MITRAL REGURGITATION

What are the investigations for mitral regurgitation and what might they reveal?

A
  • ECG = LA enlargement, p-mitrale
  • CXR = LA enlargement, cardiomegaly
  • Echocardiogram = diagnostic
120
Q

MITRAL REGURGITATION

What is the management of symptomatic mitral regurgitation?

A
  • Mitral valvuloplasty = preserve all components of native valve
  • Mitral valve replacement = if mechanical then need anticoagulation but lasts longer
121
Q

INFECTIVE ENDOCARDITIS
What is infective endocarditis?
What valve is most affected?

A
  • Infection of endovascular structures in heart

- Mitral, then aortic

122
Q

INFECTIVE ENDOCARDITIS

What are the most common causative organisms of infective endocarditis?

A
  • Staph aureus = #1
  • Strep viridans was #1, associated with poor dentition
  • Coagulase -ve staph epidermidis commonly colonise indwelling lines <2m post prosthetic valve surgery
  • Strep bovis associated with colorectal cancer
123
Q

INFECTIVE ENDOCARDITIS

What are some risk factors for developing infective endocarditis?

A
  • Strongest = previous endocarditis
  • Rheumatic valve disease
  • Prosthetic valves
  • Congenital heart defects
  • IVDUs (typically tricuspid lesion)
124
Q

INFECTIVE ENDOCARDITIS
What clinical presentation should raise alarms for infective endocarditis?
How is it diagnosed?

A
  • Fever and new murmur (due to valve regurgitation)

- Modified Duke criteria = 2x major, 1 major/3 minor or 5 minor criteria

125
Q

INFECTIVE ENDOCARDITIS

What are the Dukes modified major criteria?

A

Positive cultures:
- 2x +ve with typical bacteria OR persistent bacteraemia from 2x cultures >12h apart OR ≥3x cultures +ve with less specific pathogen
Positive imaging for endocardial involvement or new valve regurgitation:
- Transthoracic echo first-line before more sensitive transoesophageal

126
Q

INFECTIVE ENDOCARDITIS

What are the Dukes modified minor criteria?

A
  • Microbiological evidence not meeting major criteria
  • Fever >38
  • Predisposing heart condition or IVDU
  • Immunological phenomena
  • Vascular phenomena
127
Q

INFECTIVE ENDOCARDITIS

What immunological phenomena is there in infective endocarditis?

A
  • Glomerulonephritis = microscopic haematuria
  • Osler’s nodes = tender nodules on fingers/toes
  • Roth spots = retinal infarcts
128
Q

INFECTIVE ENDOCARDITIS

What vascular phenomena is there in infective endocarditis?

A
  • Major emboli
  • Splinter haemorrhages
  • Janeway lesions (painless erythematous palms/soles)
129
Q

INFECTIVE ENDOCARDITIS

What investigations would you do in infective endocarditis?

A
  • ECG (prolonged PR if aortic root abscess)
  • Inflammatory markers (raised)
  • 3x blood cultures
  • Echocardiogram
130
Q

INFECTIVE ENDOCARDITIS

What is the management of infective endocarditis?

A
  • High dose IV amox (vanc if pen allergic) and low-dose gent for at least 6w
  • Prophylactic Abx not recommended
  • Surgical repair if HD instability, severe HF, severe sepsis despite Abx, infected prosthetic valve or aortic root abscess
131
Q

AORTIC DISSECTION

What is aortic dissection?

A
  • Tear in the tunica intima (inner lining) of aorta and creates a false lumen whereby blood can flow between the inner and outer layers of the walls of the aorta
132
Q

AORTIC DISSECTION

What are some risk factors for aortic dissection?

A
  • HTN = #1
  • Connective tissue disease like Marfan’s
  • Valvular heart disease
  • Cocaine/amphetamine use
133
Q

AORTIC DISSECTION

What are the 2 different classifications for aortic dissection?

A

Stanford –
- A = ascending aorta, 2/3rds cases, CP
- B = descending aorta, 1/3rds cases, back pain
DeBakey –
- I = starts ascending aorta, propagates at least to aortic arch
- II = starts + confined to ascending aorta
- III = originates in descending aorta

134
Q

AORTIC DISSECTION

What is the clinical presentation of aortic dissection?

A
  • Sudden onset ‘tearing’ chest pain which radiates to the back often in men >50y
  • Signs = radial-radial/femoral delay, >20mmHg BP discrepancy in arms, CRT>2s, absent/weak peripheral pulses
135
Q

AORTIC DISSECTION

What are some investigations you would consider in aortic dissection?

A
  • ECG = ?territorial ST-elevation if involves coronaries
  • Trop and d-dimer may be raised
  • CXR = widened mediastinum
  • CT aortic angiogram = diagnostic if stable (false lumen)
  • Transoesophageal echo more suitable in HD unstable
136
Q

AORTIC DISSECTION

What is the management of aortic dissection?

A
  • Type A = surgical and control SBP of 100–120mmHg.

- Type B = conservative, reduce BP with IV labetalol to prevent progression

137
Q

AORTIC ANEURYSM

What are the two types of aortic aneurysms?

A
  • True = abnormal dilatations that involve all layers of arterial wall
  • False/pseudo = involve a collection in the adventitia only which communicates with the lumen (e.g., after trauma)
138
Q

AORTIC ANEURYSM

What is the aetiology of aortic aneurysm?

A
  • Commonest group = HTN, DM or smokers (atherosclerosis)

- Connective tissue disorders such as Marfan’s syndrome, Ehlers Danlos

139
Q

AORTIC ANEURYSM

What is the clinical presentation of aortic aneurysm?

A

Majority asymptomatic until rupture –

  • Severe, central abdominal pain which radiates to back
  • Signs = pulsatile and expansile abdo mass, clinical shock
140
Q

AORTIC ANEURYSM

Describe the surveillance programme for aortic aneurysms

A

Single abdominal USS for males aged 65 –

  • <3cm = normal, no further action
  • 3–4.4cm = small, USS every 12m
  • 4.5–5.4cm = medium, USS every 3m
  • ≥5.5cm = large, urgent 2w vascular referral for intervention
141
Q

AORTIC ANEURYSM

What determines a low rupture risk and how is it managed?

A
  • Asymptomatic and aortic diameter <5.5cm

- Abdominal USS surveillance and CVS risk factor modification

142
Q

AORTIC ANEURYSM
What determines a high rupture risk and how is it managed?
How is a rupture managed?

A
  • Symptomatic, aortic diameter ≥5.5cm or rapidly enlarging >1cm/y
  • Urgent 2w vascular referral for intervention with either endovascular repair (EVAR) or open repair
  • Surgical emergency with immediate vascular review
143
Q

HYPERTENSION

What are the main types of hypertension?

A
  • Primary/essential (95%) with no known cause
  • Secondary suspected in younger, severe or resistant HTN and electrolyte issues
  • Malignant HTN = severe BP elevation (>180SBP, >120DBP) resulting in end organ damage
144
Q

HYPERTENSION

What are some causes of secondary HTN

A

ROPE

  • Renal (PKD, glomerulonephritis, renal artery stenosis)
  • Obesity
  • Pregnancy-induced/pre-eclampsia
  • Endo (Conn’s, Cushing’s, acromegaly, pheochromocytoma)
145
Q

HYPERTENSION

When would you suspect HTN and how would you diagnose it?

A
  • Suspected = 2x clinical BP ≥140/90

- Confirmed = ABPM/HBPM ≥135/85 for stage 1 HTN

146
Q

HYPERTENSION

Once HTN is suspected, what other investigations should be performed?

A
  • QRisk3 calculation
  • Urinalysis looking for proteinuria + haematuria
  • First urine of day albumin creatinine ratio (ACR)
  • Fundoscopy for hypertensive retinopathy
  • ECG for LVH
  • Bloods for U&E, HbA1c and lipids
147
Q

HYPERTENSION

What are the three stages of HTN?

A
  • 1 = clinical ≥140/90, ABPM ≥135/85
  • 2 = clinical ≥160/100, ABPM ≥150/95
  • Severe HTN = SBP >180 or DBP >110
148
Q

HYPERTENSION

When would you be concerned if the BP was ≥180/120 and what would you do?

A
  • End organ damage e.g., retinal haemorrhage, papilloedema, new confusion (encephalopathy), chest pain, heart failure, AKI
  • Admit for specialist assessment
  • Control BP drop to 160/100 over 24h with CCB as risk of ischaemic stroke if too quick
149
Q

HYPERTENSION

If the BP was ≥180/120 but you had no immediate concerns, what would you do?

A
  • Urgent end-organ damage investigations (urinalysis and urine ACR, fundoscopy, ECG, bloods like U&E, HbA1c, lipids)
150
Q

HYPERTENSION

What is the first line treatment of HTN and when would you consider a different management?

A
  • Lifestyle advice (smoking and alcohol cessation, reduce caffeine, exercise, diet reduce salt <6g/d and saturated fat)
  • Stage 1 HTN: <80 with end organ damage, CVS or renal disease, DM, QRisk3 >10% or stage 2 HTN
151
Q

HYPERTENSION
What is the first line medical treatment for HTN ..

i) with T2DM in caucasian 56 year old?
ii) with T2DM in Black African 57 year old?
iii) in caucasian 48 year old?
iv) in caucasian 58 year old?
v) in African-Carribbean 45 year old?
vi) in caucasian 48 year old who has dry cough after trialling an antihypertensive medication?

A

i) ACEi (ramipril)
ii) ARB (candesartan, preferred in Black African/African-Carribbean to ACEi)
iii) ACEi
iv) CCB (amlodipine)
v) CCB
vi) ARB

152
Q

HYPERTENSION
What is the second line medical treatment for HTN…

i) in Black African on CCB?
ii) in white caucasian on ACEi?
iii) in white caucasian on CCB?

A

i) ARB (preferred in Black African/African-Carribbean to ACEi) or thiazide-like diuretic (indapamide)
ii) CCB or thiazide-like diuretic
iii) ACEi or thiazide-like diuretic

153
Q

HYPERTENSION

What is the third line medical treatment for HTN?

A
  • ACEi/ARB + CCB + thiazide-like diuretic
154
Q

HYPERTENSION

What is the fourth line medical management for HTN?

A
  • Low dose spironolactone if K <4.5mmol/L

- Alpha or beta-blocker if K >4.5mmol/L

155
Q

HYPERTENSION

When starting someone on ACEi/ARB what must you do?

A
  • Check renal function about 2w after to monitor electrolytes and kidney function
156
Q

HYPERTENSION

What are the treatment targets in HTN?

A
  • <80 = clinical <140/90, ABPM <135/85

- >80 = clinical <150/90, ABPM <145/85

157
Q

DVT
What risk tool can be used to determine how to investigate a DVT?
How can it be split in terms of history taking?

A
  • Well’s score

- History of presenting complaint, past medical history and alternative Dx more likely (–2 points)

158
Q

DVT

What are the HPC aspects of the Well’s score?

A
  • Entire leg swollen = 1
  • Pitting oedema on symptomatic leg = 1
  • Calf size discrepancy >3cm (10cm below tibial tuberosity) = 1
  • Collateral superficial veins present = 1
  • Localised tenderness (calf pain) along deep venous system = 1
  • Paralysis, paresis or recent immobilisation = 1
159
Q

DVT

What are the PMHx aspects of the Well’s score?

A
  • Bedridden >3d or major surgery (esp. orthopaedic) <12w = 1
  • Active cancer (treatment or palliation <6m) = 1
  • Previous DVT = 1
160
Q

DVT

What are some other risk factors for DVTs?

A
  • Thrombophilias
  • Pregnancy or COCP/HRT
  • Dehydration
  • Long-distance travel
161
Q

DVT
What Well’s score is classified as DVT unlikely?
How do you manage an unlikely DVT?

A
  • ≤1

- D-dimer as highly sensitive meaning it’s good for exclusion (ruling out)

162
Q

DVT
What Well’s score is classified as DVT likely?
How do you manage a likely DVT?

A
  • ≥2
  • Doppler USS of leg
  • If cannot be done <4h = interim therapeutic anticoagulation
  • If scan -ve but d-dimer +ve then stop anticoagulation but re-scan in 1/52
163
Q

DVT

What are some complications of DVTs?

A
  • PE
  • DVT recurrence
  • Post-thrombotic syndrome
164
Q

DVT
What is post-thrombotic syndrome?
How does it present?
What is the management?

A
  • Chronic venous HTN due to venous outflow obstruction + venous insufficiency
  • Features = painful calves, pruritus, swelling, varicose veins and venous ulceration
  • Management = compression stockings, elevate legs
165
Q

DVT

How can DVTs be prevented in hospitals?

A
  • VTE prophylaxis including LMWH and TED stockings for high risk or TED stockings if low risk or LMWH is C/I
166
Q

DVT
What is the first line treatment for DVT?
Alternative in severe renal impairment?
How long should patients be treated for?

A
  • DOAC such as apixaban or rivaroxaban
  • Unfractionated heparin if severe renal impairment
  • ALL patients for at least 3m then if provoked can stop, if unprovoked a further 3m
167
Q

DVT
What is the second line treatment for DVT?
What treatment may be considered if anticoagulation is contraindicated and why?

A
  • LMWH or warfarin (bridged with LMWH)

- IVC filter to prevent PEs

168
Q

PE

What is the clinical presentation of PE?

A
  • Classic sudden onset triad of = pleuritic chest pain, dyspnoea and haemoptysis
  • Signs = tachypnoea (#1), crackles, tachycardia and fever >37.8
169
Q

PE

What risk tool can be used to investigate how to manage a PE?

A

PE Well’s score

  • Clinical signs of DVT = 3
  • Alternative Dx less likely = 3
  • Tachycardia = 1.5
  • Immobilisation >3d or surgery in <4w = 1.5
  • Previous VTE = 1.5
  • Haemoptysis = 1
  • Malignancy (Rx, treated <6m or palliative) = 1
170
Q

PE

What routine investigations would you do for someone suspected of having a PE?

A
  • Routine bloods (FBC, U&E, CRP and clotting)
  • ABG = T1RF ± respiratory alkalosis
  • ECG
171
Q

PE
What is the most common ECG finding in PE?
What ECG finding is highly suggestive of PE?
What ECG finding indicates RV strain in PE?

A
  • Sinus tachycardia
  • Deep S wave in I, Q wave in III, T wave inversion in III (S1Q3T3)
  • RAD and deep T wave inversion in precordial leads
172
Q

PE
What PE Well’s score is classified as PE unlikely?
How do you manage an unlikely PE?

A
  • ≤4 points

- D-dimer, if elevated > CTPA if normal > stop anticoagulation and search alternative diagnosis

173
Q

PE
What PE Well’s score is classified as PE likely?
How do you manage a likely PE?

A
  • > 4 points
  • CTPA, if delay then interim therapeutic anticoagulation with DOAC until scan
  • If negative but clinical DVT suspected > doppler USS leg
  • V/Q scanning in renal impairment
174
Q

PE

What is the management of PE and hypotension?

A
  • Massive PE with circulatory failure = thrombolysis
175
Q

PE
What is the first-line management of PE?
How long should the treatment be for?
What setting should the treatment be delivered?

A
  • DOAC (apixaban or rivaroxaban) or unfractionated heparin if severe renal impairment
  • 3m for ALL, if provoked stop, unprovoked = 3m more
  • Outpatient in low-risk PE on Pulmonary Embolism Severity Index (PESI) = HD stability, lack of co-morbidities and home support
176
Q

PE

What is the second-line management of PE?

A
  • LMWH or LMWH followed by warfarin with INR target of 2.5 unless recurrent VTE then 3.5
177
Q

PE

What other management may be considered for PE?

A
  • IVC filter if repeated PE despite adequate anticoagulation or anticoagulation is C/I
178
Q

PERIPHERAL VASCULAR DISEASE

What are the risk factors for PVD?

A
  • Smoking
  • DM
  • HTN
  • Hyperlipidaemia
  • Physical inactivity and obesity
179
Q

PERIPHERAL VASCULAR DISEASE

What are the three main types of PVD?

A
  • Intermittent claudication
  • Critical limb ischaemia
  • Acute limb-threatening ischaemia
180
Q

PERIPHERAL VASCULAR DISEASE
What causes intermittent claudication?
How does it present?

A
  • Significant narrowing of arteries distal to the arch of the aorta due to atherosclerosis
  • Aching/burning in the leg muscles after walking, not present at rest (iliac = butt, femoral = calf)
  • Pain relieved within minutes of stopping
  • Skin may look shiny with hair loss + atrophic nails
181
Q

PERIPHERAL VASCULAR DISEASE
What causes critical limb ischaemia?
How does it present?

A
  • Inadequate blood supply to limbs at rest
  • ≥1: rest pain in foot >2w, ulceration or gangrene
  • May report hanging legs out of bed at night to ease pain
182
Q

PERIPHERAL VASCULAR DISEASE
What is acute limb-threatening ischaemia?
How does it present?
What causes it?

A
  • Rapid onset limb ischaemia
  • 6Ps: Pale, Pulseless, Painful, Paralysed, Paraesthesia, Perishingly cold
  • Thrombus or embolus
183
Q

PERIPHERAL VASCULAR DISEASE

How can you differentiate between the thrombus and embolus aetiologies of acute limb-threatening ischaemia?

A
  • Thrombus = pre-existing claudication w/ sudden deterioration, no emboli source, reduced/absent pulses in contralateral limb, vascular disease
  • Embolus = sudden onset <24h, no Hx of claudication, emboli source, no evidence of PVD (normal pulses) and evidence of proximal aneurysm (e.g., abdo, popliteal)
184
Q

PERIPHERAL VASCULAR DISEASE

What clinical examination test can you do in PVD and what will it show?

A
  • Buerger’s test = elevate leg 45 degree for 1–2m and see if there is pallor and then rest legs off the bed
  • White > blue (ischaemic tissue deoxygenates blood) > dark red (reactive hyperaemia)
185
Q

PERIPHERAL VASCULAR DISEASE
What is the first line investigation for PVD?
What other investigation may you consider and why?

A
  • Duplex USS with ABPI
    – >1.2 = artery calcification (DM), 1-1.2 = normal, 0.8–0.9 = mild disease (claudication), 0.5–0.79 = mod disease (severe claudication) and <0.5 = severe disease (critical limb ischaemia)
  • MR angiography before any intervention
186
Q

PERIPHERAL VASCULAR DISEASE

What is the initial management of peripheral vascular disease?

A
  • Lifestyle = stop smoking, optimise co-morbidities, exercise training
  • High dose atorvastatin 80mg + clopidogrel 75mg
187
Q

PERIPHERAL VASCULAR DISEASE

What is the management of severe peripheral vascular disease or critical limb ischaemia?

A
  • Endovascular revascularisation = percutaneous transluminal angioplasty ± stent if short segment stenosis <10cm + high risk
  • Surgical revascularisation = bypass or endarterectomy if >10cm, multifocal lesions or involve common femoral artery + purely infrapopliteal disease
  • Naftidrofuryl oxalate vasodilator if not for surgery
188
Q

PERIPHERAL VASCULAR DISEASE
What is the management of acute limb-threatening ischaemia?
What are the potential complications from this management?

A
  • ABCDE, analgesia with IV opioids
  • IV unfractionated heparin to prevent thrombus propagation if not suitable for immediate surgery and vascular review
  • Definitive = intra-arterial thrombolysis, surgical embolectomy, angioplasty, bypass surgery or amputation if irreversible ischaemia
  • Reperfusion injury and compartment syndrome
189
Q

PERICARDIAL DISEASE

What are some causes of acute pericarditis?

A
  • Viral (Coxsackie), bacterial (TB)
  • Renal failure (uraemia causes fibrinous pericarditis)
  • Malignancy (lung, breast)
  • Post-MI and Dressler’s syndrome
190
Q

PERICARDIAL DISEASE

What is the clinical presentation of acute pericarditis?

A
  • Chest pain (pleuritic, relieved on sitting forward, worse lying down)
  • Pericardial friction rub
  • Tachypnoea + tachycardia
  • Flu-like Sx e.g., dry cough, fever
191
Q

PERICARDIAL DISEASE

What investigations would you do in acute pericarditis?

A
  • ECG
  • Troponin (often raised)
  • All patients for transthoracic echo
192
Q

PERICARDIAL DISEASE

What ECG changes might you see in acute pericarditis?

A
  • Widespread saddle-shaped ST elevation

- PR depression (most specific marker)

193
Q

PERICARDIAL DISEASE

What are some potential complications of acute pericarditis and what are they?

A
  • Cardiac tamponade = accumulation of fluid under pressure restricting diastolic filling and so CO
  • Constrictive pericarditis = rigid pericardial fibrotic sac which prevents diastolic filling
  • Pericardial effusion = accumulation of fluid in pericardial sac
194
Q

PERICARDIAL DISEASE

What is the presentation of cardiac tamponade?

A
  • Beck’s triad = hypotension, raised JVP + muffled HS
  • Pulses paradoxus = abnormally large BP drop during inspiration
  • Raised JVP (absent Y descent)
195
Q

PERICARDIAL DISEASE
What are the investigations and management of cardiac tamponade?
What is a potential complication?

A
  • ECG = electrical alternans, CXR = globular heart, echocardiogram
  • Urgent pericardiocentesis
  • Pneumothorax (CXR after pericardiocentesis)
196
Q

PERICARDIAL DISEASE

What is the presentation of constrictive pericarditis?

A
  • RHF (SOB, raised JVP with prominent X + Y descent, oedema)

- Kussmaul’s sign = paradoxical rise in JVP during inspiration

197
Q

PERICARDIAL DISEASE

What are the investigations and management of constrictive pericarditis?

A
  • CXR = pericardial calcification

- Surgical excision of pericardium

198
Q

PERICARDIAL DISEASE

What is the presentation of pericardial effusion?

A
  • SOB
  • Raised JVP
  • Bronchial breathing at L base
199
Q

PERICARDIAL DISEASE

What are the investigations and management of pericardial effusion?

A
  • ECG = low voltage QRS, CXR = large globular heart + echo diagnostic
  • Treat underlying cause and pericardiocentesis
200
Q

PERICARDIAL DISEASE

What is the management of acute pericarditis?

A
  • First-line = combination NSAIDs and colchicine if idiopathic or viral
  • If C/I and infection rule out, consider low dose corticosteroid
201
Q

MYOCARDITIS

What are the causes of myocarditis?

A
  • Viral = coxsackie B, HIV

- Autoimmune = SLE, scleroderma, granulomatosis with polyangiitis

202
Q

MYOCARDITIS

How does myocarditis present?

A
  • Young patient
  • Acute history pulmonary oedema (SOB) post-viral infection
  • Chest pain
203
Q

MYOCARDITIS

What investigations would you do for myocarditis and what might they show?

A
  • Raised inflammatory markers, troponin and BNP
  • ECG = tachycardia, arrhythmias or ST elevation and T wave inversion
  • Endomyocardial biopsy via cardiac catheterisation is gold standard
204
Q

MYOCARDITIS
What are some complications of myocarditis?
What is the management?

A
  • HF, arrhythmias + dilated cardiomyopathy (late complication)
  • Treat underlying cause + symptomatic control
205
Q

CARDIOMYOPATHIES

What are the four types of cardiomyopathies?

A
  • Hypertrophic obstructive cardiomyopathy (HOCM)
  • Dilated cardiomyopathy
  • Restrictive cardiomyopathy
  • Arrhythmogenic right ventricular cardiomyopathy
206
Q

CARDIOMYOPATHIES

What is HOCM?

A
  • Autosomal dominant disorder leading to LVH which causes decreased compliance with impaired diastolic filling + decreased CO
207
Q

CARDIOMYOPATHIES

How does HOCM present?

A
  • Sudden cardiac death in young (ventricular arrhythmias)
  • Angina
  • Exertional dyspnoea
  • Exertional syncope due to subaortic hypertrophy of ventricular septum causing functional aortic stenosis and so ESM at LLSE
208
Q

CARDIOMYOPATHIES

What investigations would you do in HOCM

A
  • ECG (LVH and T wave inversion)
  • Echo
  • Biopsy
209
Q

CARDIOMYOPATHIES

What would an echo show in HOCM?

A

MR SAM ASH

  • Mitral Regurg
  • Systolic Anterior Motion (of anterior mitral valve leaflet)
  • ASymmetrical Hypertrophy
210
Q

CARDIOMYOPATHIES
What is the management of HOCM?
What should you avoid in HOCM?

A
  • ICD, exercise restriction and reduction of outflow obstruction with beta-blockers/verapamil
  • Nitrates, ACEi and inotropes
211
Q

CARDIOMYOPATHIES
What is dilated cardiomyopathy?
What causes it?

A
  • Dilated heart leading to poor contractions mostly systolic dysfunction
  • Alcohol, coxsackie B virus, IHD and HTN or infiltrative (sarcoid)
212
Q

CARDIOMYOPATHIES
What is the presentation of dilated cardiomyopathy?
What is the management?

A
  • Heart failure, S3, balloon appearance of heart on CXR, echo diagnostic
  • ICD or cardiac transplantation
213
Q

CARDIOMYOPATHIES
What is restrictive cardiomyopathy?
What causes it?

A
  • Very rigid ventricular walls which impairs diastolic ventricular filling
  • Amyloidosis (most common), sarcoid, systemic sclerosis
214
Q

CARDIOMYOPATHIES
What is the presentation of restrictive cardiomyopathy?
What is the management?

A
  • Heart failure

- ICD or cardiac transplantation

215
Q

CARDIOMYOPATHIES
What is arrhythmogenic right ventricular cardiomyopathy (ARVC)?
How does it present?
What unique disease is associated with it?

A
  • RV myocardium replaced by fatty + fibrofatty tissue
  • Palpitations, syncope and sudden cardiac death
  • Naxos disease = autosomal recessive triad of ARVC, palmoplantar keratosis and woolly hair
216
Q

CARDIOMYOPATHIES

What investigations would you do in AVRC and how would you manage it?

A
  • ECG = epsilon wave (terminal notch in QRS, V1–3 changes), MR shows fibrofatty tissue
  • Sotalol, catheter ablation to prevent VT, ICD
217
Q

CARDIOGENIC SHOCK

What is cardiogenic shock?

A
  • Reduced CO leads to inability to perfuse organs + tissues leading to acute hypoperfusion and hypoxia despite adequate intravascular volume
218
Q

CARDIOGENIC SHOCK

What are some causes of cardiogenic shock

A
  • Acute MI
  • Cardiac tamponade
  • Pulmonary embolism
  • Tension pneumothorax
  • Trauma
219
Q

CARDIOGENIC SHOCK

What is the clinical presentation of cardiogenic shock?

A
  • Hypotension and tachycardia (shock)
  • Raised JVP
  • Mottled skin + cold peripheries
  • Reduced urine output
220
Q

CARDIOGENIC SHOCK
What investigations would you do in cardiogenic shock?
What is the management?

A
  • FBC, U&E, trop, ECG, ABG, CXR, TTE
  • ABCDE, diamorphine for pain/anxiety
  • Optimise filling pressure with either plasma expander if under-filled or inotropes like dobutamine if well/over-filled
221
Q

CARDIO PHARMACOLOGY
What is the mechanism of ACEi for HTN?
How does it aid in CKD?

A
  • Inhibits ACE so less angiotensin I > II so less aldosterone > retention
  • Dilates efferent arterioles (reduced GFR) + so slows progression
222
Q

CARDIO PHARMACOLOGY
What is the mechanism of action of ARBs?
What are the adverse effects of both and ACEi only?

A
  • Angiotensin-I receptor blockers which block action of angiotensin-II
  • Hypotension, AKI, hyperkalaemia, C/I in pregnancy
  • ACEi = high bradykinin > dry cough, rash
223
Q

CARDIO PHARMACOLOGY
What is the mechanism of action of calcium channel blockers?
What are the different types?

A
  • Act on L-type Ca2+ channels
  • Dihydropyridines (amlodipine, nifedipine) = preferentially affects vascular smooth muscle
  • Non-dihydropyridines (diltiazem, verapamil) = more cardiac effects as negatively chronotropic + inotropic
224
Q

CARDIO PHARMACOLOGY

What are some adverse effects of the different types of CCBs?

A
  • Dihydropyridines = flushing, oedema, headache, postural hypotension
  • Cardiac targeting = bradycardia (AV block), hypotension + heart failure
225
Q

CARDIO PHARMACOLOGY
What is the mechanism of beta blockers?
What are the side effects?
What are the contraindications?

A
  • Binds to beta-adrenergic receptors
  • Bronchospasm, cold peripheries, fatigue, sleep disturbances + ED
  • Asthma, concurrent non-dihydropyridines
226
Q

CARDIO PHARMACOLOGY
What is the mechanism of action of thiazide diuretics?
What are some side effects?

A
  • Blocks Na+ reabsorption at DCT by blocking Na/Cl symporter
  • Low Na+, K+, HIGH Ca2+ but hypocalciuria (useful in renal stones), pancreatitis, impaired glucose tolerance + impotence
227
Q

CARDIO PHARMACOLOGY
What is the mechanism of action of loop diuretics?
What are some side effects?

A
  • Inhibits Na-K-Cl (NKCC) co-transporter in the thick ascending limb of the loop of Henle, reducing absorption of NaCl
  • Low Na+, K+, Mg2+, Ca2+, ototoxicity, AKI
228
Q

CARDIO PHARMACOLOGY
What is the mechanism of action of the 2 types of K-sparing diuretics?
What is a key side effect?

A
  • Amiloride = inhibits ENaC in DCT > Na/H20 excretion and K retention
  • Spironolactone/eplerenone = aldosterone antagonists
  • Hyperkalaemia
229
Q

CARDIO PHARMACOLOGY

What is the mechanism of action of digoxin?

A
  • Cardiac glycoside which inhibits Na/K ATPase pump (positively inotropic) and decreases conduction through AVN (negatively chronotropic)
230
Q

CARDIO PHARMACOLOGY
What are some side effects of digoxin?
What is a complication with digoxin?

A
  • SE = bradycardia, narrow therapeutic range, gynaecomastia

- Toxicity = confusion, yellow-green vision, N+V

231
Q

CARDIO PHARMACOLOGY
When would you do a digoxin level?
What can precipitate digoxin toxicity?

A
  • Within 8–12h last dose but not routinely measured

- Hypokalaemia as binds on pump to same side as K+

232
Q

CARDIO PHARMACOLOGY

What is the mechanism of action of amiodarone

A
  • Class III anti-arrhythmic agent = blocks K+ channels inhibiting repolarisation and prolongs action potential
233
Q

CARDIO PHARMACOLOGY

What are some adverse effects of amiodarone?

A
  • Hyper or hypothyroidism
  • Corneal deposits
  • Pulmonary/liver fibrosis
  • Photosensitivity
  • Slate-grey appearance
234
Q

CARDIO PHARMACOLOGY
What is the mechanism of action of aspirin?
How does this compare to clopidogrel?
What are some adverse effects?

A
  • Non-reversible inhibitor of cyclo-oxygenase (both COX1 + 2) reducing production of thromboxane so reduces platelet aggregation
  • P2Y12 antagonist inhibiting activation of platelets
  • GI irritations, bleeding, ulceration in aspirin
235
Q

CARDIO PHARMACOLOGY
What is the mechanism of action of statins?
What are some adverse effects?
What are some important interactions/contraindications?

A
  • HMG CoA reductase inhibitor reducing amount of LDL-cholesterol
  • Myopathy, liver impairment
  • Macrolides, pregnancy, avoid grapefruit juice
236
Q

CARDIO PHARMACOLOGY

What liver monitoring is required for statins?

A
  • Baseline, 3m and 12m

- Discontinue if serum transaminase concentrations rise to and persist at 3x the upper limit of reference range

237
Q

CARDIO PHARMACOLOGY
What is the mechanism of action of adenosine?
How quick does it have effect and how is it given?
What are some adverse effects?

A
  • Transient heart block in AVN as A1 receptor agonist
  • Very short half-life (8-10s), push fast into large cannula
  • Chest pain, bronchospasm (C/I asthma, use verapamil), transient flushing

FINALS (20 decks)

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