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Year 6 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Define Acute coronary syndrome

A

A set of symptoms and signs that occur due to decreased blood flow to the heart at rest, this happens when there is sudden plaque rupture and clot formation w/in diseased coronary arteries leading to either partial occlusion and ischaemia (unstable angina) or complete occlusion, hypoperfusion and infarction (NSTEMI and STEMI)

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2
Q

Define Unstable angina

A

Partial occlusion of the coronary artery leading to troponin -ve chest pain (myocardial ischaemia) at rest w/ normal/abnormal ECG signs (ST depression and T wave inversion)

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3
Q

Define Non-ST elevating myocardial infarction

A

Severe but incomplete occlusion of a coronary artery leading to troponin +ve chest pain (myocardial death) w/out ST elevation (but w/ ST depression and T wave inversion)

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4
Q

Define ST elevating myocardial infarction

A

Complete occlusion of a coronary artery leading to troponin +ve chest pain (myocardial death) and ST elevation on ECG

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5
Q

Define Type 2 myocardial infarction

A

Myocardial infarction due to cardiac hypoperfusion for reasons other than ACS - e.g. severe sepsis, hypotension, hypovolaemia or coronary artery spasm

Don’t require the usual treatment for MI’s

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6
Q

Acute coronary syndrome features

A
  • Central/left sided, sudden onset, crushing chest pain which may radiate to the left arm and jaw
  • Associated nausea, sweating, clamminess, SOB, syncope
  • Occurs are rest but is worsened by exercise/exertion and may be improved by GTN
  • Inferior infarcts can present atypically w/ epigastric pain

Diabetic pts may have silent MI’s:
- NO pain
- Acute SOB
- Palpitations
- Acute confusion
- Hyperglycaemic crisis
- Syncope

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7
Q

Acute coronary syndrome investigations

A
  • Troponin at least 3 hours after onset of pain and then 6 hours later
  • ECG - STEMI = ST elevation >2cm in adjacent chest leads, ST elevation >1cm in adjacent limp leads, new LBBB
  • CXR to rule out other causes/complications
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8
Q

Changes in which ECG leads demonstrate an inferior MI, and what coronary artery is affected?

A

Leads II, III and aVF

RCA affected

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9
Q

Changes in which ECG leads demonstrate a septal MI, and what coronary artery is affected?

A

Leads V1 and V2

Proximal LAD affected

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10
Q

Changes in which ECG leads demonstrate an anterior MI, and what coronary artery is affected?

A

Leads V3 and V4

LAD affected

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11
Q

Changes in which ECG leads demonstrate an apical MI, and what coronary artery is affected?

A

Leads V5 and V6

Distal LAD, LCx and RCA affected

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12
Q

Changes in which ECG leads demonstrate a lateral MI, and what coronary artery is affected?

A

Leads I and aVL

LCs affected

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13
Q

Changes in which ECG leads demonstrate a posterolateral MI, and what coronary artery is affected?

A

Leads V7-V9 show ST elevation, V1-V3 show ST depression

RCA/LCx affected

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14
Q

Causes of a raised troponin

A
  • MI
  • Pericarditis
  • Myocarditis
  • Arrhythmias
  • Defibrillation
  • Acute HF
  • PE
  • Type A aortic dissection
  • CKD
  • Prolonged strenuous exercise
  • Sepsis
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15
Q

STEMI management

A

Offer 300mg loading dose of aspirin ASAP, sublingual GTN and IV morphine/diamorphine and continue aspirin indefinitely unless contraindicated, then offer reperfusion therapy (PCI or fibrinolysis) if possible, or medical management if not:

Percutaneous coronary intervention:
- Offer if presenting w/in 12 hrs of symptoms and PCI can be done w/in 2 hrs
- Give prasugrel w/ the aspirin if not already taking oral anticoagulants, and less than 75
- Give Clopidogrel/ticagrelor w/ the aspirin if taking an oral anticoagulant
- PCI involves endovascular stenting or complete revascularisation

Fibrinolysis:
- Offer if presenting w/in 12 hrs of symptoms and PCI cannot be giving w/in 2 hours
- Give ticagrelor w/ the aspirin
- Give an antithrombin
- Do not repeat, offer a PCI if still not resolving

Medical:
- Give ticagrelor w/ aspirin
- Asses LV function

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16
Q

NSTEMI/unstable angina management

A
  • Loading dose of 300mg aspirin and fondaparinux
  • Calculate GRACE score (6 mon mortality risk) and all pts who aren’t low risk should be given prasugrel or ticagrelor
  • Sublingual GTN
  • IV morphine/diamorphine
  • Antithrombin e.g. Enoxaparin or fondaparinux
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17
Q

Post-MI secondary management

A

ALL pts post-MI should be started on the following 5 drugs:
1) Aspirin 75mg OD + a second anti platelet (Clopidogrel 75mg or ticagrelor 90mg OD)
- Beta blocker (normally bisoprolol)
- ACEi (normally Ramipril)
- High dose statin (normally atorvastatin 80mg ON)

All pts should have an echo to assess systolic function, as well as being referred for cardiac rehabilitation

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18
Q

MI complications

A

DARTHVARDER:

Death
Arrhythmia
Rupture
Tamponade
HF
Valve disease
Aneurysm
Dressler’s syndrome = post-infarction pericarditis 2-3 wks later
Embolism
Recurrence

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19
Q

Define Pericarditis

A

Inflammation of the pericardium (the fibroelastic sac surrounding the heard)

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20
Q

Causes of Pericarditis

A
  • Idiopathic
  • Infective = coxsackie B viruses (echovirus, CMV, HSV, HIV), bacteria (staphs, streps, pneumococcus, haemophilus, TB), rarely fungi and parasites
  • Malignancies = lung, breast and Hodgkin’s lymphoma
  • Cardiac = HF, Dressler’s syndrome
  • Radiation
  • Drugs = doxorubicin chemo, hydralazine, isoniazid, methyldopa, phenytoin, penicillin allergy
  • Rheumatological = SLE, RA, Sarcoidosis, Takayasu’s, Behcet’s
  • Uraemic renal failure
  • Hypothyroidism
  • IBD
  • Ovarian hyperstimulation
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21
Q

Pericarditis features

A
  • Pleuritic chest pain worse on inspiration
  • Worse lying flat and relieved by sitting forwards
  • Fever
  • Pericardial friction rub = high-pitched scratching noise, best heard over the left sternal border during inspiration
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22
Q

Pericarditis investigations

A
  • Serial troponins
  • ECG - Widespread saddle ST elevation (not following vascular territories) and PR depression
  • Echo
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23
Q

Pericarditis management

A

Idiopathic or viral:
- 1st line = exercise restriction and NSAIDs + PPI for 1-2 wks
- 2nd line = colchicine
- 3rd line = corticosteroids

Bacterial:
- IV abx +/- pericardiocentesis if purulent exudative present

Non-infective causes
- Corticosteroids

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24
Q

Pericarditis complications

A
  • Pericardial effusions
  • Cardiac tamponade
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25
Q

Define Acute pulmonary oedema

A

The sudden accumulation of fluid in the lungs, specifically the alveoli and interstitial spaces, leading to severe dyspnoea and hypoxia - caused by increased left heart pressure which in turn leads to a backlog of pressure into the lungs via in the pulmonary veins. This increases the hydrostatic pressure in the lungs forcing fluid out of the pulmonary capillaries

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26
Q

Causes of Acute pulmonary oedema

A
  • Left ventricular HF (most common)
  • Posterior-inferior MI leading to mitral regurgitation
  • HTN crisis
  • Iatrogenic fluid overload
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27
Q

Acute pulmonary oedema features

A
  • Severe dyspnoea
  • Orthopnoea and paroxysmal nocturnal dyspnoea
  • Sitting upright, leaning forwards and tripoding
  • Pink frothy sputum
  • Widespread crackles and wheeze
  • Raised JVP
  • Tachycradia
  • Pulsus alternans and S3 gallop
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28
Q

Define Pulsus alternans

A

An arterial pulse w/ alternating strong and weak beats - indicates severe LV dysfunction

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29
Q

Acute pulmonary oedema management

A
  • A-E
  • O2 therapy
  • Loop diuretic = IV furosemide 400mg STAT+ close fluid balance
  • CPAP (reduced hypoxia and recruits more alveoli, thus improving V/Q mismatch)
  • Furosemide infusion over 24 hrs
  • IV dopamine for vasopression
  • Intra-aortic balloon pump if pt in cardiogenic shock
  • Intubation and ventilation
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30
Q

Define Acute bradycardia

A

HR <60bpm + adverse features (shock, syncope, HF or evidence of myocardial ischaemia) - usually caused by sick sinus syndrome

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31
Q

Causes of bradycardia

A
  • Physiological
  • Sick sinus syndrome
  • Heart block
  • Post-MI
  • Aortic valve disease
  • Vasovagal
  • Hypothyroidism
  • Hypothermia
  • Electrolyte abnormalities
  • Raised ICP
  • Medication = beta blockers, CCBs, digoxin
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32
Q

Acute bradycardia management

A
  • A-E
  • 1st line = 500 micrograms atropine IV (atropine blocks the vagus nerve which increases firing rate of the SAN) - can give repeat doses up to a total of 3mg
  • 2nd line = Transcutaneous pacing, isoprenaline, adrenaline
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33
Q

Causes of Myocarditis

A

Viral:
- Cocksackie B viruses (echovirus, CMV, HSV, HIV)
- COVID-19
- Adenovirus
- EBV

Bacterial:
- Diphtheria
- Clostridia
- N. Gonorrhoea

Protozoa = Trypanosoma cruzi

AI:
- Kawasaki disease
- Scleroderma
- SLE
- Sarcoid
- Systemic vasculitides

Drug reactions:
- Antipsychotics e.g. clozapine
- Immune-checkpoint inhibitors
- Mesalazine

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34
Q

Myocarditis features

A
  • Chest pain = sharp, stabbing
  • SOB
  • Palpitations
  • Light-headedness
  • Syncope
  • Fever and viral prodrome
  • Severe cases can cause unexplained cardiac death
  • Dull heart sounds
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35
Q

Myocarditis investigations

A
  • ECG = non-specific changes, arrhythmias, tachycardia, ectopic beats
  • Bloods = raised troponin and CK-MB
  • Echo
  • Cardiac biopsy = gold standard (shows inflammatory infiltrates and myocardial necrosis)
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36
Q

Myocarditis management

A
  • Treat underlying cause
  • ITU support
  • Corticosteroids if viral
  • Limit activity for a few months post-recovery
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37
Q

Myocarditis complications

A
  • HF
  • Arrhythmias
  • Dilated cardiomyopathy
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38
Q

Define Aortic dissection

A

When a tear in the tunica intima of the aorta creates a false lumen where blood can flow between the inner and outer layers of the walls of the aorta

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39
Q

Aortic dissection risk factors

A
  • HTN
  • Marfan’s
  • Valvular heart disease
  • Cocaine/amphetamine use
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40
Q

Aortic dissection Stanford classifications

A
  • Type A = involves the ascending aorta and/or arch of the aorta
  • Type B = involves the descending aorta
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41
Q

Aortic dissection features

A

Symptoms:
- Sudden onset tearing chest pain or interscapular pain which radiates to the back
- Bowel/limp ischaemia
- Renal failure
- Syncope

Signs:
- Radio-radial delay
- Radio-femoral delay
- BP difference between arms

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42
Q

Aortic dissection investigations

A

CT angiogram to diagnose

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43
Q

Aortic dissection management

A

Initial:
- Resuscitation if necessary
- Cardiac monitoring
- Strict BP control e.g. IV metoprolol infusion

Definitive:
- Type A = Surgical management e.g. aortic graft
- Type B = conservatively w/ BP control - endovascular/open repair if signs of end organ damage

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44
Q

Causes of aortic regurgitation

A

Acute:
- Infective endocarditis
- Aortic dissection (due to dilation of the aortic root)
- Blunt/penetrating trauma to the valve leaflets
- Iatrogenic (balloon valvotomy)
- Non-native aortic valve regurgitation

Chronic:
- Rheumatic heart disease
- Age-related calcification
- Congenital bicuspid aortic valve
- CTD e.g Marfan’s, Ehler’s Danlos
- Infective endocarditis
- Rheumatological = RA, ankylosing spondylitis, APLS, GCA

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45
Q

Aortic regurgitation features

A

Symptoms:
- Exertional dyspnoea
- Orthopnoea
- Stable angina in the absence of coronary artery disease (due to reduction in diastolic coronary perfusion)

Signs:
- Early diastolic murmur heard best at the aortic region, leaning forwards and on expiration
- De Quicke’s sign = nail bed pulsations
- Waterhammer pulse
- De Musset’s sign = head bobbing in time to heart beat
- Corrigan’s sign = dancing carotids
- Muller’s sign = pulsation of the uvula
- Traube’s sign = femoral bruit
- Widened pulse pressure

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46
Q

Aortic regurgitation investigations

A

Transthoracic echo + investigate for infective endocarditis and Group A strep

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47
Q

Aortic regurgitation management

A
  • Conservative = no treatment for mild-moderate AR
  • Medical = Beta blockers +/- losartan to lower BP in higher risk pts (e.g Marfan’s or bicuspid valves)
  • Surgical = for pts with symptomatic AR, asymptomatic w/ LVEF <=50%, refractory IE, significant enlargement of ascending aorta
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48
Q

Aortic stenosis causes

A
  • Age-related calcification
  • Congenital bicuspid valve
  • Rheumatic heart disease
  • William’s syndrome (supravalvular stenosis)
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49
Q

Aortic stenosis features

A

Symptoms:
- Severe = syncope, angina, dyspnoea
- Palpitations
- Signs of left ventricular failure
- Sudden cardiac death

Signs:
- Ejection systolic murmur heard best at the second intercostal space in the mid clavicular line, which radiates to the carotids
- Slow-rising carotid pulse
- Narrow pulse pressure
- Heaving, non-displaced apex beat
- Soft S2

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50
Q

Aortic stenosis investigations

A

Echo is definitive - CXR may show cardiomegaly in severe cases

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51
Q

Aortic stenosis management

A
  • Conservative = for asymptomatic and stable cases - echo monitoring every 6 months for severe cases, and yearly for mild-moderate cases
  • Medical = symptom management of LV failure = diuretics, beta blockers, ACEi
  • Surgical = Transcatheter/surgical aortic valve replacement - for all symptomatic pts, or asymptomatic pts with LVEF <=50%
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52
Q

Define Aortic sclerosis

A

Thickening and calcification of the aortic valve, but without obstruction of ventricular outflow - causes an ejection systolic murmur that DOESN’T radiate to the carotids

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53
Q

Define Atrial flutter

A

A common supraventricular tachycardia characterised by an abnormal cardiac rhythm w/ an atrial rate of 300 bpm and a ventricular rate that can be fixed or variable - caused by an aberrant re-entrant circuit w/in the right atrium which cycles at 300 bpm - produces a classical saw-tooth appearance of ECG

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54
Q

Causes of Atrial flutter

A
  • Pulmonary diseases = COPD, OSA, PE, pulmonary HTN
  • Ischaemic heart disease
  • Sepsis
  • Alcohol
  • Cardiomyopathy
  • Thyrotoxicosis
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55
Q

Atrial flutter management

A

In haemodynamically unstable pts:
- Synchronised DC cardioversion +/- amiodarone

In haemodynamically stable pts:
- 1st line = bisoprolol or CCB (dilitiazem, verapamil)
- 2nd line = cardioversion
- 3rd line = ablation of the aberrant circuit

Use CHADVASC to decide on giving anticoagulation

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56
Q

Define Atrial fibrillation

A

Irregular, uncoordinated contractions at a rate of 300-600 bpm - delays at the AVN means that only some of the irregular impulses are conducted resulting in an irregularly irregular ventricular response

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57
Q

Atrial fibrillation classifications

A
  • Acute = lasts <48 hrs
  • Paroxysmal = lasts <7 days and is intermittent
  • Persistent = lasts >7 days but is amendable to cardioversion
  • Permanent = lasts >7 days and is not amendable to cardioversion

Also can be fast (>=100bpm) or slow (<=60bpm)

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58
Q

Causes of Atrial fibrillation

A

Cardiac:
- IHD
- HTN
- Rheumatic heart disease
- Peri/myocarditis

Non-cardiac:
- Dehydration
- Endocrine causes e.g. hyperthyroidism
- Sepsis and other infections
- Pulmonary causes = PE, pneumonia
- Alcohol abuse
- Electrolyte disturbances e.g. hypokalaemia, hypomagnesaemia

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59
Q

Atrial fibrillation features

A

Symptoms:
- Palpitations
- Chest pain
- SOB
- Syncope
- Light-headedness

Signs:
- Irregularly irregular pulse
- A single waveform on JVP (due to loss of a-wave which signifies atrial contraction)
- ECG changes = absent P waves, irregularly irregular rhythm

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60
Q

Atrial fibrillation acute management

A

Acute unstable pt:
- Synchronised DC cardioversion +/- amiodarone

Stable pt w/ onset <48 hrs:
- Rhythm control w/ DC cardioversion or anti-arrhythmics (flecainide if no heart disease, amiodarone otherwise)
- Heparin if DC cardioversion is delayed
- Alternatively can use rate control (below)

Stable pt w/ onset >48hrs:
- Rate control only w/ bisoprolol, diltiazem or digoxin
- Can try cardioversion later if its persisting, but need to anticoagulated for 3 wks prior to this due to the risk of throwing off a clot

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61
Q

Atrial fibrillation chronic management

A

Rate control:
- 1st line = bisoprolol or rate limitng CCB (diltiazem or verapamil)
- 2nd line = dual therapy
- Digoxin monotherapy in sedentary pts w/ non-paroxysmal AF, who are hypotensive or who have HF

Rhythm control:
- Either DC cardioversion or medical w/ flecainide, amiodarone or sotalol
- For pts who have AF secondary to a reversible cause, HF associated w/ AF, new-onset AF

Catheter ablations

CHADVASC to calculate the need for anticoagulation (DOAC 1st line)

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62
Q

Define Broad complex tachycardias

A

Dysrhythmias that have a heart rate greater than 100bpm and a QRS complex that is greater than 120ms

Examples:
- VT
- VF
- Torsade’s de pointes
- SVT w/ aberrancy

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63
Q

Ventricular Tachycardia features

A

A regular broad complex tachycardia that occur w/ or w/out a pulse

ECG features:
- Tachycardia >100bpm
- Absent P waves
- Monomorphic regular QRS complexes >120ms

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64
Q

Pulseless Ventricular Tachycardia management

A
  • This is a shockable rhythm = 200J bi-phasic unsynchronised shock should be administrated
  • IV adrenaline (1mg in 10ml of 1:10,000 solution) and IV amiodarone (300mg) should be administered after delivery of the 3rd shock
  • Adrenaline should be administered every 3-5 min thereafter
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65
Q

Pulsed Ventricular Tachycardia management

A

With adverse features:
- Synchronised DC shocks (up to 3) - need to sedate the pt if their awake
- 300mg IV amiodarone over 10-20 min, followed by 900mg infusion over 24 hrs

With no adverse features:
- 300mg IV amiodarone over 10-60 min
- If that doesn’t work, the synchronised DC shocks (up to 3)

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66
Q

Ventricular fibrillation features

A

An irregular broad complex tachycardia - this is always pulseless

ECG features:
- Tachycardia >100bpm
- QRS complexes are polymorphic and irregular (>120ms)

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67
Q

Ventricular fibrillation management

A
  • This is a shockable rhythm = 200J bi-phasic unsynchronised shock should be administrated
  • IV adrenaline (1mg in 10ml of 1:10,000 solution) and IV amiodarone (300mg) should be administered after delivery of the 3rd shock
  • Adrenaline should be administered every 3-5 min thereafter
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68
Q

Define Brugada syndrome

A

A genetic condition caused by a sodium channelopathy that predisposes pts to ventricular fibrillation/tachycardia - most common in SEA males

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69
Q

Brugada syndrome triggers

A
  • Sleep
  • Eating heavy meals
  • Dehydration
  • Excess alcohol
  • Drugs = flecainide, verapamil, TCAs
  • Electrolyte abnormalities
  • Fevers
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70
Q

Brugada syndrome investigations

A

Characteristic ECG changes + at least 1 clinical criterion

ECG changes = RBBB and ST elevation in V1-V3

Criteria:
- VF or polymorphic VT
- FHx of sudden cardiac death under 45 yrs
- Syncope or ECG signs in family
- Inducible VT
- Nocturnal agonal breathing (gasping or grunting in sleep)

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71
Q

Brugada syndrome management

A

Conservative = lifestyle measures and avoiding triggers

Definitive = insertion of an ICD to reduce risk of sudden cardiac death from VT/VF - can add quinidine (anti-arrhythmic) in pts who still have arrhythmias

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72
Q

Define Bundle branch block

A

When the electrical impulses to the ventricles are slower than normal, leading to a widened QRS complex >120ms

Can be left or right BBB

Incomplete BBB is when there is a partial delay and the QRS complex is between 110-120ms

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73
Q

How do you identify right vs left BBB?

A

In both, the QRS complex will b > 120ms

Look at V1 and V6 - then use WiLLiaM and MaRRoW:
- In LBBB, V1 QRS complexes will look like W, and V6 will look like an M
- In RBBB, V1 complexes will look like an M and V6 will look like a W

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74
Q

Causes of LBBB

A
  • Aortic stenosis
  • IHD
  • Hyperkalaemia
  • Digoxin toxicity
  • MI - new LBBB can indicate STEMI
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75
Q

Causes of RBBB

A
  • RB hypertrophy
  • PE
  • IHD
  • Atrial septal defect
  • Normal variant
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76
Q

Define Cardiac tamponade

A

When pericardial fluid accumulates and intrapericardial pressure rises compressing the IVC and heart chambers - this compromises ventricular filling and leads to reduced cardiac output

Caused by the accumulation of:
- Blood
- Fluid
- Purulent exudate
- Air

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77
Q

Cardiac tamponade features

A

Symptoms:
- SOB
- Tachycardia
- Confusion
- Chest pain
- Abdo pain

Signs:
- Beck’s triad = hypotension, quiet heart sounds, raised JVP
- Pulsus paradoxus (pulse fades on inspiration)

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78
Q

Cardiac tamponade investigations

A
  • ECG = low voltage QRS
  • CXR = may show large globular heart
  • Echo = will demonstrate the amount of fluid and quantify the level of ventricular compromise
  • Pericardiocentesis = will allow for sampling of the fluid to find the underlying cause and treat the immediate problem
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79
Q

Cardiac tamponade management

A

If haemodynamically unstable = pericardiocentesis

If stable = careful observation w/ repeat echo’s and IV fluid treatment to maintain ventricular filling

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80
Q

Most common reversible causes of cardiac arrest

A

4 H’s:
1) Hypoxia
2) Hypovolaemia
3) Hypo/hyperkalaemia
4) Hypo/hyperthermia

4T’s:
1) Tamponade
2) Toxins
3) Tension pneumothorax
4) Thrombosis

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81
Q

Indications for cardiac catheterisation

A
  • Imaging = inject contrast dye into the coronary vessels to image anatomy and blood supply
  • Angioplasty = balloon dilatation and stenting (PCI)
  • Valvuloplasty = transcatheter aortic valve implantation (TAVI)
  • Repair = transcatheter repair of septal defects
  • Electrophysiology = studies and catheter ablations
  • Measurements = accurate measures of pressures w/in heat and great vessels
  • Biopsy
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82
Q

Define Cardiac myxoma

A

Benign tumours of the cardiac cells composed of unspecialised mesenchymal cells w/in a mucopolysaccharide stroma - this causes it to look smooth and gelatinous

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83
Q

Cardiac myxoma features

A

Symptoms:
- Fever
- WL
- Dyspnoea
- Orthopnoea
- Cough
- A. fib
- Can rarely embolize and cause ACS

Signs:
- Tumour plop on auscultation

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84
Q

Cardiac myxoma investigations

A
  • Raised inflammatory markers
  • Echo = mobile mass
  • Cardiac MRI
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85
Q

Cardiac myxoma management

A

Surgical resection

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86
Q

Define Carney complex

A

A genetic condition of benign connective tissue tumours - characterised by cardiac/cutaneous myxomas, schwannomas, endocrine tumours and abnormal skin pigmentation

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87
Q

What is the purpose of temporary cardiac pacing?

A

To restore haemodynamic stability to a pt

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88
Q

How is temporary pacing done?

A

Transcutaneous = using electrode pads on the skin - used as a bridge to transvenous pacing

Transvenous pacing = inserting a pacemaker wire into a vein and then passing it to the right atrium or ventricle - wire is then connected to an external pacemaker box and may be kept in place until a permanent pacemaker is inserted, or its no longer required

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89
Q

Indications for permanent pacemaker insertion

A
  • Complete heart block
  • Mobitz type 2 heart block
  • Symptomatic Mobitz type 1 heart block
  • Symptomatic sick sinus syndrome
  • Permanent bradyarrhythmias due to MI
  • Tachyarrhythmias resistant to therapy
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90
Q

Define Constrictive pericarditis

A

The loss of elasticity in the pericardial sac due to scarring - this prevents normal cardiac filling and leads to restriction of ventricular volume, stroke volume and cardiac output

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91
Q

Constrictive pericarditis features

A

Symptoms = symptoms of HF:
- Fatigue
- Reduced exercise tolerance
- Exertional dyspnoea
- Peripheral oedema

Signs:
- Raised JVP
- Kussmaul’s sign = paradoxical rise in JVP w/ inspiration
- Pulsus paradoxus
- Quiet heart sounds (if pericardial effusion present)
- Pericardial knock = high pitched, early diastolic sound that occurs when stiff pericardium results in sudden arrest of ventricular filling

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92
Q

Constrictive pericarditis investigations

A
  • CXR = small heart +/- pericardial calcifications
  • Echo = ventricular filling defect and heart failure w/ preserved ejection fraction
  • Cardiac MRI = helps differentiate from restrictive cardiomyopathy
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93
Q

Constrictive pericarditis management

A

Surgical excision of the fibrosed pericardium (pericardiectomy)

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94
Q

Define Cor pulmonale

A

Right ventricular failure as a result of long standing lung disease

Chronic arterial vasoconstriction occurs due to hypoxia, in order to overcome this increased pressure in the pulmonary circulation, the right side of the heart has to work harder - when it can no longer compensate this leads to right HF

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95
Q

Cor pulmonale features

A

Symptoms:
- Fatigue
- Peripheral oedema
- Ascites
- Symptoms of chronic lung condition

Signs:
- Cyanosis
- Raised JVP w/ prominent a and v waves
- RV heave
- Loud P2
- Pansystolic murmur w/ tricuspid regurgitation
- Pulsatile hepatomegaly
- Graham-Steel murmur = functional pulmonary regurgitation as the chronic HTN stretches the valvular attachments, whilst the valve itself is healthy

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96
Q

Cor pulmonale investigations

A
  • ECG = Right axis deviation
  • CXR = enlarged right atrium and ventricle w/ prominent pulmonary arteries
  • Echo = diagnostic - look to see right ventricular function
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97
Q

Cor pulmonale managemet

A

No specific treatments other than optimise management of respiratory condition w/ O2 therapy to reduce pulmonary HTN- can give diuretics for symptomatic relief

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98
Q

Define Coronary artery bypass graft

A

A revascularisation technique used to treat coronary artery disease - a healthy vein (usually harvested from the leg or chest) is attached to the heart so blood can get around the narrowed coronary artery

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99
Q

Coronary artery bypass graft indications

A

In pts with:
- Symptoms of CAD that are not controlled by optimal medical management
- Complex 3 vessel disease and/or significant left main stem on CTCA

PCI is more cost effective than CABG, but CABG confers a mortality benefit in pts >65, with DM or complex 3 vessel disease

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100
Q

Define Pansystolic murmur

A

A systolic murmur that is of uniform intensity, as opposed to the crescendo-decrescendo ejection systolic murmurs - they start at S1 and extend up to, and may merge with, S2

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101
Q

Causes of pansystolic murmurs

A
  • Mitral regurgitation (most common) = loudest at the axilla and on expirations, radiates to the axilla
  • Tricuspid regurgitation = loudest at the left lower sternal edge and on inspiration
  • Ventricular septal defect = loudest at the lower sternal edge
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102
Q

Define Ejection systolic murmurs

A

A systolic murmur that is described as a high-pitched, crescendo=decrescendo mid-systolic murmur

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103
Q

Causes of ejection systolic murmurs

A
  • Aortic stenosis (most common) = loudest in aortic region and on expiration, radiates to the carotids
  • Aortic sclerosis = loudest in aortic region and on expiration, no radiation
  • Pulmonary stenosis = loudest in pulmonary region and on inspiration
  • Flow murmur = in anaemia, pregnancy and thyrotoxicosis
  • HOCM
  • Pulmonary stenosis
  • Supravalvular aortic stenosis (Williams syndrome)
104
Q

Indications for digoxin

A

Atrial fibrillation/flutter who may be in HF or hypotensive

105
Q

Digoxin mechanism of action

A

Inhibits Na/K/ATPase ion pump inhibitor in the myocardium and has parasympathetic affects on the AV node - its negatively chronotropic and positively ionotropic (slows down the heart but increases contractility)

106
Q

Risk factors for digoxin toxicity

A
  • Hypokalaemia
  • Hypomagnesaemia
  • Hypercalcaemia
  • Elderly pts
107
Q

Digoxin toxicity features

A
  • N&V
  • Diarrhoea
  • Blurred vision
  • Yellow/green discolouration of vision
  • Haloes in vision
  • Confusion
  • Fatigue
  • Palpitations
  • Syncope

ECG changes:
- Down sloping ST depression - reverse tick
- T wave inversion
- Biphasic/flattened and shortened QT interval
- Slight PR prolongation

108
Q

Digoxin toxicity manegement

A
  • Stop digoxin
  • Correct electrolyte imbalance
  • Administer digifab = digoxin-specific antibody)
109
Q

ECG changes in hyperkalaemia

A

Typically occurs w/ levels => 6

-Tall tented T waves (that would hurt to sit on)
- PR prolongation
- P wave flattening
- Bradyarrhythmia - sinus bradycardia, high-grade AV block or slow AF
- QRS broadening w/ unusual morphology

110
Q

ECG changes in hypokalaemia

A

Typically occurs w/ levels < 2.7

  • Widened P wave
  • Prolonged PR interval
  • ST depression
  • T wave inversion
  • U waves ( a second wave after the T wave due to repolarisation of the perkinje fibres)
  • Long QT/U interval
  • Supraventricular complexes
  • Supraventricular arrhythmias - atrial fibrillation/flutter
  • Ventricular arrhythmias - Torsade’s de pointes, VT, VF
111
Q

Hypokalaemia management

A
  • 3-3.5 = replace w/ oral K if
  • < 3 = replace w/ IV K over 10-12 hours if pt asymptomatic and there are no ECG changes
  • < 3 = IV K over 3-4 hrs if pt symptomatic and there are ECG changes
112
Q

Examples of supraventricular (narrow complex) tachycardias

A

Atrial fibrillation/flutter, AV re-entry tachycardia (AVRT), AV nodal re-entry tachycardia (AVNRT)

113
Q

What are the adverse features of SVT?

A

HISS

  • Heart failure
  • Ischaemia
  • Shock
  • Syncope
114
Q

Management of SVT with adverse features

A

Synchronised DC shock

115
Q

Management of stable SVT

A

Depends on if the rhythm is regular or irregular

Regular:
- Vagal manoeuvres = carotid sinus massage or Valsalva manoeuvre
- If those don’t work - give 6mg IV adenosine (temporarily blocks conduction through the AV node)

Irregular:
- Go down Atrial fibrillation/flutter management pathway

116
Q

How is adenosine given?

A

Given IV rapidly over 1-3 seconds, followed by 20ml of normal saline bolus

Pts should be warned that they might have difficulty breathing, chest tightness and flushing - but this should resolve w/in seconds

117
Q

Contraindications for giving adenosine

A
  • Pts with a central line
  • Pts on dipyridamole or carbamazepine as these can potentiate its effects
  • Pts w/ asthma - use verapamil instead
118
Q

1st degree Heart block definition and features

A

Prolonged conductivity through the AVN - can be identified by PR interval of >200ms

119
Q

Causes of 1st degree Heart block

A
  • High vagal tone (e.g. athletes)
  • Acute inferior MI
  • Electrolyte abnormalities e.g. hyperkaelemia
  • Drugs = NHP-CCB, beta blockers, digoxin, cholesterase inhibitors
120
Q

1st degree Heart block management

A

Mostly benign and doesn’t need treating - but treat any underlying pathologies

121
Q

Mobitz type I heart block definition and features

A

A type of 2nd degree heart block due to reversible conduction block at the AVN - characterized by progressive lengthening of the PR interval until a QRS complex is skipped

122
Q

Causes of Mobitz type I heart block

A
  • Inferior MI
  • Drugs = beta blockers, CCBs, digoxin
  • High vagal tone (e.g. athletes)
  • Myocarditis
  • Cardiac surgery
123
Q

Mobitz type I heart block management

A

It’s generally asymptomatic and thus doesn’t require treatment - if there are symptoms (e.g. bradycardia) then monitor ECGs and if they have adverse features give atropine

124
Q

Mobitz type II heart block definition and features

A

A type of 2nd degree heart block usually caused by a block in the His-Perkinje system - characterized by intermittent non-conductive P waves, the PR interval is constant (normal or prolonged) and there is commonly a fixed ration of P waves to QRS complexes (e.g. 2:1 or 3:1)

125
Q

Causes of Mobitz type II heart block

A
  • Anterior MI
  • Surgery = mitral valve repair or septal ablation
  • Inflammatory = rheumatic heart disease, SLE, systemic sclerosis, myocarditis
  • Lenegre’s disease = progressive fibrosis of the conduction system
  • Infiltrations = sarcoidosis, haemochromotosis, amyloidosis
  • Drugs = beta blockers, CCBs, digoxin, amioderone
126
Q

Mobitz type II heart block management

A

Permanent pacemaker as these pts are at risk of complete heart block

127
Q

3rd degree heart block definition and features

A

This is complete heart block where the atrial impulses are not conducted to the ventricles, cardiac output is due to a ventricular or junctional escape impulses - ECG shows bradycardia and a complete dissociation between P waves and QRS complexes

128
Q

What are the risks of 3rd degree heart block

A
  • Asytole
  • VT
  • Cardiac arrest
129
Q

Causes of 3rd degree heart block

A
  • MI’s (esp inferior)
  • Drugs acting at the AVN = beta blockers, dihydropyridine CCBs, adenosine
  • Idiopathic fibrosis
130
Q

3rd degree heart block management

A

Manage acute bradycardia and then insert a permanent pacemaker

131
Q

Define Heart failure

A

The failure of the heart to generate sufficient cardiac output to meet the metabolic demands of the body

132
Q

What are the 3 classification systems for Heart failure ?

A

1) Low-output vs High-output
2) Systolic VS Diastolic
3) New York Heart Association symptom severity

133
Q

Low-output vs High-output heart failure

A

Low-output HF occurs when cardiac output is reduced due to a primary problem in the heart (more common)

High-output HF occurs when there is a normal cardiac output , but there is an increased peripheral metabolic demand that the heart is unable to meet

134
Q

Causes of high-output HF

A

AAPPTT

  • Anaemia
  • AV malformations
  • Paget’s disease
  • Pregnancy
  • Thyrotoxicosis
  • Thiamine deficiency
135
Q

Systolic VS Diastolic heart failure

A

Systolic HF occurs when the ventricles fill well, but are unable to sufficiently pump blood around the body due to impaired myocardial contractility during systole - this leads to HF with reduced ejection fraction

Diastolic HF occurs when the ventricles are unable to properly relax and fill during diastole, thus it is able to pump blood normally, but pumps out less blood per contraction - this leads to HF with preserved ejection fraction

136
Q

Causes of HF with reduced ejection fraction

A

Anything which reduces the ventricles ability to contract

  • IHD
  • Dilated cardiomyopathy
  • Myocarditis
  • Infiltrates = sarcoidosis, haemochromatosis
137
Q

Causes of HF with preserved ejection fraction

A

Anything which stops the ventricles filling properly

  • Uncontrolled chronic HTN = leads to LV hypertrophy
  • Hypertrophic cardiomyopathy
  • Cardiac tamponade
  • Constrictive pericarditis
138
Q

What is a normal ejection fraction?

A

50%

Anything less than 40% is heart failure

139
Q

New York Heart Association (NYHA) Classification of HF

A
  • Class I - no limitation in physical activity, and activity does not cause undue fatigue, palpitations or dyspnoea
  • Class II - slight limitation of physical activity, and comfort at rest. Ordinary physical activity causes fatigue, palpitations and/or dyspnoea
  • Class III - marked limitation in physical activity, but comfort at rest. Minimal physical activity causes fatigue (less than ordinary)
  • Class IV - inability to carry on any physical activity without discomfort, with symptoms occurring at rest. If any activity takes place, discomfort increases
140
Q

Left HF features

A

Left HF causes pulmonary congestion (pressure builds up on the left side of the heart leading to back pressure into the pulmonary circulation and lungs) and hypoperfusion

Symptoms:
- SOB on exertion
- Orthopnoea
- Paroxysmal nocturnal dypnoaea
- Nocturnal cough +/- pink frothy sputum
- Fatigue

Signs:
- Tachyapnoea
- Bibasal crackles on the lungs
- Cyanosis
- Prolonged CRT
- Hypotension

141
Q

Right HF features

A

Right HF causes venous congestion (back pressure through the vena cava) and pulmonary hypoperfusion (reduced right ventricle output)

Symptoms:
- Peripheral oedema
- Weight gain
- Ascites
- Anorexia and nausea
- Fatigue

Signs:
- Raised JVP
- Pitting oedema
- Tender, smooth hepatomegaly
- Ascities
- Transudative pleural effusion (usually bilaterally)

142
Q

Define Congestive cardiac failure

A

When left-sided HF causes significant enough pulmonary congestion that the right-side of the heart can no longer overcome the pressure and goes into failure

Pts present w/ signs of both LHF and RHF

143
Q

Heart failure investigations

A
  • 1st line = NT-pro-BNP levels =a molecule released by the ventricles in reponse to myocardial stretch
  • ECG
  • Echo = to assess ejection fraction
  • CXR
  • Bloods = U&E, LFT, TFT, glucose and lipid profile
144
Q

What are the key CXR findings in a pt w/ heart failure?

A

ABCDEF

  • Alveolar oedema = bat wing perihilar shadowing
  • Kerley B lines = interstitial oedema
  • Cardiomegaly
  • Upper lobe blood Diversions
  • Plueral effusions
  • Fluid in the horizontal fissure
145
Q

Heart failure management

A

Conservative:
- WL if BMI >30
- Smocking cessation
- Salt and fluid restriction
- Exercise
- Annual and one-off influenza vaccines

Medical:
- Loop diuretics (furosemide or bumetanide) for fluid overload
- For mortality benefits in HFrEF BASH = beta blockers, ACEi/ARBs, spirinolactone, hydralazine
- There are no medical treatments to improve mortality in HFpEF
- Can concider gicing SGLT2 inhibitors in pts with optomised meds

Surgical:
- Implantable cardiac defibrillators if at risk of sudden cardiac death, or with wide QRS complexes

146
Q

Define Hypertrophic obstructive cardiomyopathy

A

An autosomal dominant condition resulting in asymmetrical septal hypertrophy which leads the LV hypertrophy and diastolic dysfunction w/out an obvious cause

147
Q

HOCM features

A

Symptoms:
- Asymptomatic
- Exertional syncope
- Syncope
- Sudden cardiac death
- Exertional dyspnoea
- Fatigue
- Chest pain - anginal or atypical

Signs:
- Jerky pulse
- Double apex beat
- Harsh ejection systolic murmur
- Apical thrill
- A wave in JVP

148
Q

HOCM investigations

A

ECG

Echo (definitive) = signs can be remembered usiuing MR SAM ASH:
-Mitral regurgitation
- Systolic anterior motion of the mitral valve leaflets
- Asymmetrical septal hypertrophy

Cardiac MRI = if echo is clear but still suscpect HOCM (20% of cases missed on echo)

149
Q

HOCM management

A

Conservative:
- Avoid especially strenuous activity or competitive sports

Medical:
- Beta blockers 1st line
- Verapamil
- Amiodarone

Surgical (for those w/ severe LV outflow obstructions, or serve symptoms):
- Surgical septal myectomy
- Alcohol septal ablation
- ICD insertion

150
Q

Hypothermia classification

A
  • Mild = 32-35 degrees - tachyapnoea, tachycardia, vasoconstriction and shivering
  • Moderate = 28-32 degrees - cardiac arrhythmias, hypotension, respiratory distress, confusion, stop shivering
  • Severe = <28 degrees - markedly reduced consciousness/coma, apnoea, arrythmias, fixed and dilated pupils
151
Q

ECG features of hypothermia

A
  • Bradyarrhythmias
  • Osborne waves (J waves) = positive deflection points between the end of the QRS complex and beginning of the ST segment
  • Prolonged PR, QRS and ST
  • Shivering artifacts
  • Ventricular ectopics
  • Cardiac arrest
152
Q

Infective endocarditis classification

A
  • Acute = symptoms for < 6 wks (usually Staph. A)
  • Subacute = symptoms for 6 wks - 3 months
  • Chronic = sumptoms for > 3 months
153
Q

Common organisms in Infective endocarditis

A
  • Staph aureus = most common
  • Strep viridans = in pts w/ poor dentition
  • Enterococci
  • Staph epidermidis = common in prosthetic valves
  • Strep bovis = linked w/ colorectal cancer - pts need endoscopy
  • Fungal
  • HACEK organisms = culture negative IE
  • Non-infective = marantic endocarditis (pancreatic cancer), Libman-Sacks (SLE)
154
Q

Infective endocarditis features

A

Symptoms:
- Fever
- NS
- Anorexia and WL
- Myalgia
- Other signs of systemic unwellness

Signs:
- New murmur
- Vascular phenomenon = spetic emboli, Janeway lesions (palms and soles)
- Immune phenomenon = splinter haemorrhages, Osler’s nodes (end of fingers), Roth spots (retinal haemorrhages), glomerulonephritis

155
Q

Infective endocarditis investigations

A

Use modified Dukes criteria - need 2 majors, 1 major and 3 minor or all 5 minor to have IE

Pneumonic = BE FIVE PM

Major:
- Blood cultures (2x positive)
- Evidence of vegetation on echo

Minor:
- Fever
- Immune phenomena
- Vascular phenomena
- Electrocardiogram suggestive but not definitive
- Predisposing features
- Microbiology suggestive but not definitive

156
Q

Infective endocarditis management

A

6 wks IV antibiotics

  • Native valve S. aureus = fluclox or vanc + rif
  • Prosthetic valve S. aurues = fluclox + rif + gent
  • Strep viridans = benzylpen or vanc + gent
  • HACEK = ceftriaxone
  • Surgery if indicated
157
Q

What are the indications for surgical management in Infective endocarditis?

A
  • Haemodynamic instability
  • Severe HF
  • Refractory severe sepsis
  • Valve obstruction
  • Infected prosthetic valve
  • Persistent bacterameia
  • Repeated emboli
  • Aortic root abscess (will give new PR prolongation)
158
Q

Define Long QT syndrome

A

Individuals with persistent prolonger QT intervals

This is >440ms in men and >460ms in women

QT prolongation predisposes pts to Torsade’s de Pointes ad VF

159
Q

Causes of QTc prolongation

A

Congenital = Romano-Ward syndrome, Jervell and Lange-Nielson syndrome

Acquired = TIMES
- Toxins (clarithromycin, anti-arrhythmics, anti-psychotics, TCAs)
- Ischaemia
- Myocarditis/mitral valve prolapse
- Electrolyte abnormalities (hypokalaemia, hypocalcaemia, hypomagnesaemia)
- Subarachnoid haemorrhage

160
Q

Long QT syndrome management

A

Acquired = adress underlying cause

Congenital:
- 1st line = beta blockers if no bradycardia
- 2nd line = ICD insertion or cardiac pacing

161
Q

Define Malignant hypertension

A

A medical emergency where there is a relatively rapid increase in BP that leads to end organ damage - there is a rapid increase in systemic vascular resistance by vasoconstriction leading to hypoperfusion of organs

Occurs at SBP =>180 and DBP =>120

162
Q

Causes of Malignant hypertension

A
  • Anti-hypertensive non-compliance
  • Drugs = cocaine, amphetamines, sympathomimetics
  • Renovascular disease = renal artery stenosis or Takayasu arteritis
  • Renal parenchymal disease = glomerulonephritis, SLE, systemic sclerosis
  • Endocrine = pheochromocytoma, Cushing’s, Conn’s
  • CNS = head injury, stroke
163
Q

Malignant hypertension features

A

SBP =>180 and DBP =>120 + evidence of end organ damage:
- Papilledema and/or retinal haemorrhages
- New onset confusion )encephalopathy)
- Occipital pulsatile headache +/- visual disturbance
- Seizures
- Chest pain
- Signs of HF
- AKI

164
Q

Malignant hypertension management

A
  • Aim for a controlled drop in BP to around 160/100 over at least 24hrs
  • 1st line = CCBs e.g. amlodipine or nifedipine

PO is preferred to IV unless there is evidence of encephalopathy, HF or aortic dissection

An uncontrolled drop can result in ischaemic stroke due to poor cerebral autoregulation and perfusion

165
Q

Hypertensive encephalopathy management

A

IV labetalol or IV sodium nitroprusside

166
Q

What are the shockable rhythms?

A
  • VT w/out a pulse
  • VF
167
Q

What are the non-shockable rhythms?

A
  • Pulseless electrical activity
  • Asystole
168
Q

Management of non-shockable rhythms

A
  • CPR 30:2
  • Give 1mg IV adrenaline as ASAP
  • Give further adrenaline very 3-5 min (after 2 2-min loops of CPR)
169
Q

Define Mitral valve prolapse

A

Abnormal systolic displacement of one or both leaflets of the mitral valve into the left atrium - over time this leads to mitral regurgitation

Specifically displacement >2mm above the annular plane or echo

170
Q

Mitral valve prolapse classifications

A

Primary = caused by the degeneration of the valve leaflets in the absence of an identifiable cause

Secondary = occurs due to a CTD e.g. Marfan’s, Ehlers-Danlos, Turner’s

171
Q

Mitral valve prolapse features

A

Symptoms:
- Mostly assymtomatic
- Palpitaions - development of AF due to dilated L atium
- Lightheadedness
- SOB
- Fatigue

Signs:
- Mid systolic click on auscultation = results from the sudden tensing of the mitral valve apparatus as the leaflets prolapse into the L atrium
- Pansystolic mitral regurgitation murmur

172
Q

Mitral valve prolapse management

A

Conservative = if asymptomatic it requires no treatment, can council on increased risk of IE

Medical and surgical - only if mitral regurgitation develops:
- Loop diuretics and management of HF
- Valve replacement

173
Q

Define Mitral regurgitation

A

Back flow of blood into the L atrium during systole die to the incompetence of the mitral valve

Overtime this leads to enlargement of the L atrium, volume overload in the left side of the heart and leads to LV failure

174
Q

Causes of acute Mitral regurgitation

A
  • Papillary muscle rupture secondary to a posterio-inferior MI
  • Rupture of the chordae tendinea = due to myoxomatous disease, IE, rheumatic heart disease, trauma
  • Damage to a prosthetic valve
175
Q

Causes of chronic Mitral regurgitation

A

Leaflet causes:
- Mitral valve prolapse
- Degenerative causes
- Rheumatic fever
- IE
- SLE/scleroderma
- CTD
- Congenital causes e.g. mitral valve clefts
- Hypertrophic cardiomyopathy
- Drug-related damage

Chordae causes:
- Myxomatous disease
- Trauma

Papillary muscle causes:
- MI
- Dilated cardiomyopathy

Annular causes:
- Calcification
- Dilation due to cardiomyopathy or CTD

176
Q

Mitral regurgitation features

A

Acute symptoms = sudden onset:
- SOB
- Exertional dyspnoea
- Fatigue
- Weakness
- Signs of pulmonary oedema, hypotension and cardiogenic shock

Chronic symptoms:
- Asymptomatic until significant systolic dysfunction then pulmonary HTN or symptomatic AF
- Fatigue
- Exertional dyspnoea

Signs:
- Pansystolic murmur, loudest at the apex, radiates to the axilla, louder on exertion and on rolling to the left
- S1 may be quiet or absent
- Signs of LHF

177
Q

Mitral regurgitation management

A

Conservative = if asymptomatic then regular echo’s for monitoring

Medical = treatment of complications:
- AF w/ rate control and anticoagulation
- HF w/ diuretics, ACEi and beta blockers

Surgical:
- Mitral valvuloplasty = repair of the valve (preferred)
- Mitral valve replacement

178
Q

Define Mitral stenosis

A

The narrowing of the mitral valve resulting in reduced blood flow to the left ventricle, usually due to calcification and thickening

The leads to increased volume in the left atrium, atrial dilation (which predisposes to AF), pulmonary congestion and RHF

179
Q

Causes of Mitral stenosis

A

Rheumatic heart disease

180
Q

Mitral stenosis features

A

Asymptomatic until valve area falls to < 1.5cm^2

Symtpoms:
- Gradual exertional dyspnoea
- Haemoptysis due to pulmonary congestion
- AF
- Chest pain
- Hoarseness - large L atrium can compress the recurrent laryngeal nerve (Ortner’s syndrome)
- Peripheral oedema due to RHF

Signs:
- Malar flush due to CO2 retention
- Mid-to-late diastolic murmur, most prominent at the apex, loudest on expiration, heard best when pt lying on left side and with the bell

181
Q

Mitral stenosis management

A

Conservative = no treatment if asymptomatic

Medical = symptomatic management

Surgical:
- Balloon valvuloplasty if valve pliable and not calcified
- Percutaneous mitral valvotomy if moderate disease
- Valve replacement

182
Q

Define Narrow complex tachycardia

A

A dysrhythmia with a HR > 100pbm and QRS complexes <120ms

Can be:
- Supraventricular = starts suddenly and then stays at the same rate until it ends
- Sinus = frequently changes rate and speeds up/slow down over seconds-minutes

183
Q

Types of Narrow complex tachycardia

A

Regular NCT’s:
- Sinus tachycardia = physiological or pathological
- Focal atrial tachycardia
- Atrial flutter
- Atrioventricular re-entry tachycardia (AVRT)
- Atrioventricular nodal re-entry tachycardia (AVNRT)
- Junctional tachycardia

Irregular NCT’s:
- Atrial fibrillation
- Atrial flutter w/ variable block
- Multifocal atrial tachycardia

184
Q

Define Focal atrial tachycardia

A

When there is autonomous atrial cells acting like the SAN

Causes abnormal p wave morphology

185
Q

Define Atrioventricular re-entry tachycardia

A

Where there is an accessory pathway between the atria and the ventricles that is not filtered by the AVN

Associated w/ Wolff-Parkinson White

186
Q

Define Atrioventricular nodal re-entry tachycardia

A

Where there is are re-entry circuits w/in or near the AVN causing a supraventricular tachycardia

187
Q

Define Junctional tachycardia

A

When the AVN becomes the pacemaker and causes ventricular contraction >100bpm

188
Q

Define Multifocal atrial tachycardia:

A

Where there are multiple groups of autonomous atrial cells acting as the SAN leading to an irregular rhythm

Commonly found in pts w/ severe COPD

189
Q

Narrow complex tachycardia management

A
  • A-E
  • If adverse signs = synchronised DC cardioversion +/- amiodarone
  • If no adverse signs, consider if its regular or irregular

Regular:
- 1st line = vagal manoeuvres
- 2nd line = IV adenosine 0 initially a 6mg bolus, if that’s unsuccessful give 12mg, if that’s unsuccessful give 18mg
- 3rd line = verapamil or beta-blocker
- 4th line = synchronised DC cardioversion

Irregular:
- Beta blockers
- If HF - trial digoxin
- If onset >48hrs then anticoagulated

190
Q

What are the 4 main types of cardiomyopathy?

A
  • Dilated
  • Restrictive
  • Arrhythmogenic
  • Hypertrophic
191
Q

Define Dilated cardiomyopathy

A

A dilated heart w/ impaired systolic function (HFrEF) - most common cardiomyopathy

192
Q

Causes of Dilated cardiomyopathy

A
  • Ischaemic changes
  • Congenital
  • Toxin-related = excessive alcohol, cocain use, doxorubicin chemo, cyclophosphamide, chloroquine, clozapine
  • Infiltrative = haemochromatosis, amyloidosis, sarcoidosis
  • Peripartum
  • Thyrotoxicosis
  • Secondary to myocarditis
  • HIV
  • Lyme disease
  • Chagas disease
  • Idiopathic
193
Q

Dilated cardiomyopathy features

A

Symptoms = signs of HF

Signs:
- Displaced apex beat
- S3 gallop rhythm (rapid ventricular filling)
- Mitral regurgitation
- Signs of HF

194
Q

Dilated cardiomyopathy investigations

A
  • ECG = poor R wave progression
  • Echo (diagnostic) = globular, dilated heart w/ reduced EF
195
Q

Dilated cardiomyopathy management

A
  • Address underlying issue
  • HF management = loop diuretics, beta blockers, ACEi
196
Q

Define Restrictive cardiomyopathy

A

Non-dilated, non-hypertrophied ventricles w/ impaired diastolic filling but w/ near-normal systolic function

197
Q

Causes of Restrictive cardiomyopathy

A
  • Familial non-infiltrative cardiomyopathy
  • Infiltrative = amyloidosis, sarcoidosis, fatty infiltration
  • Storage = haemochromatosis, Fabry disease, glycogen storage disorders
  • Diabetic cardiomyopathy
  • Scleroderma
  • Radiation
  • Doxorubicin chemo
198
Q

Restrictive cardiomyopathy features

A

Signs and symptoms of RHF

Most will have associated AF

Difficult to distinguish between this and constrictive pericarditis clinically

199
Q

Restrictive cardiomyopathy investigations

A
  • Echo = shows thickened ventricular walls and valves, w/ impaired ventricular filling and preserved systolic function
  • Cardiac MRI to distinguish from contractive pericarditis
200
Q

Restrictive cardiomyopathy management

A
  • Resolve underlying cause
  • Loop diuretics and anticoagulation for symptomatic relief
201
Q

Define Arrhythmogenic Right Ventricular Cardiomyopathy

A

When fatty, fibrous material replaces the myocardium due to a a. dominant defect in the desmosomes

Primarily involves the right ventricle and can be seen on echo w/ hypokinetic segments of the free wall of the RV

202
Q

Arrhythmogenic Right Ventricular Cardiomyopathy features

A
  • Palpations
  • Syncope
  • Sudden cardiac death

All due to development of dangerous arrhythmias

203
Q

Define Takotsubo cardiomyopathy

A

Non-ischaemic cardiomyopathy associated w/ transient apical ballooning of the myocardium usually due to stress

Suspect in pts w/ troponin +ve chest pain, ST elevation but normal coronary angiography with a Hx of a significant stressor

Self resolves in around 2 months

204
Q

Define Pericardial effusion

A

Accumulation of fluid w/in the pericardial sac of >50mL - results in compression of the ventricles, possible haemodynamic compromise and cardiac tamponade

205
Q

Causes of Pericardial effusion

A

Any cause of pericarditis can cause pericardial effusion

The fluids can be:
- Serous = in acute viral pericarditis
- Blood = in hemopericardium from a penetrating chest wound
- Pustulent = secondary to a bacterial infection

206
Q

Pericardial effusion features

A

Symptoms:
- Can be asymptomatic and picked up on echo
- Dyspnoea
- Chest pain
- Local structure compression = phrenic nerve causing hiccups, diaphragmatic pressure causing nausea

Signs:
- Ewarts sign = bronchial breathing at L lower base
- Muffled heart sounds
- Signs of cardiac tamponade = Becks triad, hypotension, raised JVP

207
Q

Pericardial effusion management

A
  • Address the underlying cause
  • Pericardiocentesis to remove fluid = either for further diagnostic reasons, or to treat symptoms in a large volume effusion
208
Q

Causes of Essential hypertension

A

Physiological:
- Reduction of elasticity of large arteries
- Age/atherosclerosis-related calcifications
- Degradation of arterial elastin

Pathological = conditions associated w/ increased CO:
- Anaemia
- Hyperthyroidism
- Aortic regurgitation

209
Q

Essential hypertension classification

A
  • Stage 1 = Clinic => 140/90, ABPM => 135/85
  • Stage 2 = Clinic =>160/100, ABPM => 150/95
  • Stage 3 = Clinic systolic => 180, or diastolic =>120
210
Q

Essential hypertension investigations

A

24hr halter to establish HTN

Do a QRISK2 and assess for signs of end organ damage:
- Urine dip and albumin:creatinine level
- Blood glucose, lipids and renal function
- Fundoscopy
- ECG to look for evidence of LV hypertrophy

Refer for same-day specialist assessment in pts with:
- Clinic BP of 180/120 or higher w/ signs of retinal haemorrhages or papilledema
- Life threatening symptoms e.g. new onset confusion, chest pain, HF or AKI

211
Q

Essential hypertension management

A

Give treatment to all pts w/ Stage 2 disease, and pts w/ Stage 1 disease who are <80 w/ end organ damage/QRISK >10%

Step 1:
- If T2DM or <55 = ACEi or ARB
- If >55 or of Black afro-caribbean origin = CCB

Step 2:
- Add the other drug from step 1 or a thiazide-like diuretic (e.g. indapamide)

Step 3:
- Use all 3 types of medication

Step 4 = resistant HTN:
- If blood potassium <4.5 then add spironolactone
- If >4.5 yhen increase thiazide-like diuretic dose or add an alpha blocker (doxazosin), beta blocker (atenolol) or refer to cardia

212
Q

What are the blood pressure targets for pts w/ Essential hypertension?

A
  • Age >80 ABPM target <145/85 (due to risk of postural drop)
  • Age <80 ABPM target <135/85
  • T1DM w/ end organ damage = <130/80
213
Q

Define Pulmonary stenosis

A

Narrowing of the pulmonary valve, reducing the blood flow from the RV into the pulmonary bed - this results in a pressure gradient >10mmHg across the pulmonary valve during systole and reduced blood flow into the pulmonary circulation

214
Q

Causes of Pulmonary stenosis

A
  • Tetralogy of Fallot (valvular)
  • Noonan syndrome (valvular)
  • Williams syndrome (supravalvular)
  • Congenital rubella

Very rarely due to carcinoid syndrome

215
Q

Pulmonary stenosis features

A

Symptoms = causes RHF:
- Dyspnoea
- Fatigue
- Peripheral oedema
- Ascites

Signs:
- Raised JVP
- RV heave
- Ejection systolic murmur that radiates to the left shoulder and is best heard on expiration
- Widely split S2 w/ a delayed P2

216
Q

Pulmonary stenosis investigations

A
  • ECG = p pulmonale, RAD, LV hypertrophy
  • CXR = prominant pulmonary arteries and post-stenotic dilation
  • Echo = to look at the degree of stenosis and ventricular function
217
Q

Pulmonary stenosis management

A
  • Usually asymptomatic and doesn’t need treatment
  • Valvuloplasty (valvular) or balloon angioplasty (supravalvular) in pts w/ a transvalvular pressure gradient of >50 mmHg
218
Q

Define Rheumatic fever

A

An AI complication of Group A Strep infection (usually pharyngitis or scarlet fever) that occurs 2-4 weeks post infection

Abs formed as a result of the infection cross-react w/ the endocardial tissue, leading to valvular disease

219
Q

Rheumatic fever features

A

Jones criteria say that diagnosis is likely if there is evidence of a recent strep infection plus either:
- 2 major criteria
- 1 major and 2 minor criteria

Major criteria:
- Arthritis = a migratory polyarthritis
- Pancarditis = inflammation of all layers of the myocardium - causes tachycardia, new murmur or a new conduction defect
- Sydenham’s chorea = abrupt, non-rhythmic involuntary movements along w/ muscle weakness and emotional disturbances
- Erythema marginatum = pink/red, non-pruritic rash on the trunk, thighs and arms - has raised, sharp outer edges ad a diffuse clear centre making a ring
- Subcut nodules = firm, mobile, painless lesions on extensor surfaces

Minor criteria:
- Fever
- Arthralgia
- Raised ESR and CRP
- Prolonged PR interval on ECG

220
Q

Rheumatic fever management

A
  • STAT dose of IV Benzylpenicillin followed by a 10 day course of phenoxymethylpenicillin to eradicate the Strep
  • Aspirin/NSAIDs for arthritis
  • Prednisolone +/- diuretics if the carditis is causing HF
  • Haloperidol or Diazepam for Sydenham’s chorea
  • Antihistamines for erythema marginatum
221
Q

Causes of right heart strain

A

Anything which increases the pressure w/in the pulmonary circulation:

  • PE
  • Pulmonary HTN
  • Chronic lung disease
  • Pulmonary stenosis
  • Pneumothorax
222
Q

What are the characteristic ECG features of right heart strain?

A

ST depression and T wave inversion in right ventricle (V1-V3) and inferior leads (II, III and aVF)

223
Q

Define Secondary hypertension

A

A persistent high BP due to an identifiable cause

Should suspect in younger pts

224
Q

Causes of Secondary hypertension

A

Primary intrinsic renal diseases (most common):
- CKD
- Glomerulonephritis
- Diabetic nephropathy
- Polycystic kidney disease
- Chronic pyelonephritis

Vascular disease:
- Renal artery stenosis = atherosclerosis in older pts, fibromuscular hyperplasia in younger pts
- Aortic coarctation = narrowing of the aortic arch forces the LV to pump harder leading to HTN
- Vasculitis’s

Endocrine:
- Conn’s disease = hypokalaemia and hypernatraemia
- Cushing’s disease = excess cortisol leads to increased absorption of sodium and increased vascular sensitivity to catecholamines and angiotensin II driving HTN
- Pheochromocytoma = triad of sweating, headaches and tachycardia

Drugs:
- NSAIDs
- Corticosteroids (Cushing’s syndrome)
- Mineralocorticoids
- Clozapine/olanzapine
- Cocaine/amphetamines

225
Q

When do you suspect secondary hypertension?

A
  • Pts <40 w/ few comorbidities
  • Severe HTN/ treatment resistant
  • New HTN in pts w/ previously low readings
  • HTN associated w/ symptoms of electrolyte disturbances
226
Q

Define Sick sinus syndrome

A

The clinical manifestations of intrinsic SAN dysfunction

227
Q

Sick sinus syndrome features

A

Symptoms:
- Dizzy spells
- Syncope
- Chest pain
- Palpitations
- Angina
- Low-output heart failure

Signs:
- Sinus bradycardia
- Sinoatrial block
- Periods of sinus arrest
- Abnormally long pause after a premature beat

228
Q

Sick sinus syndrome management

A

Atrial or dual-chamber pacemaker - but only if there are significant symptoms

229
Q

Define Stable angina

A

Typical chest pain triggered by a mismatch of myocardial O2 supply and demand resulting in myocardial ischaemia - usually due to coronary artery disease

Typical chest pain is defined by:
1) Constriction/heavy discomfort to the chest that may radiate to the jaw/neck/arm
2) Brought on by exertion
3) Alleviated by rest (<5 min) or GTN spray

  • 3/3 = typical angina pain
  • 2/3 = atypical angina pain
  • 0-1/3 = non-anginal pain
230
Q

Stable angina classification

A

Classed by its limitations on day-to-day activity:

  • Class I = non angina w/ normal activity, only strenuous
  • Class II = angina pain causes slight limitation on normal physical activity
  • Class III = angina pain causes marked limitation on normal physical activity
  • Class IV = angina occurs w/ any physical activity and may become unstable
231
Q

Stable angina investigations

A
  • ECG to rule out MI
  • 1st line = CTCA =-if typical/atypical anginal pain or ECG shows ischaemic changes
  • 2nd line = if CTCA inconclusive - stress echo, myocardial perfusion SPECT, cardiac MRI
  • 3rd line = invasive coronary angiography
232
Q

Stable angina management

A

Conservative:
- Smocking cessation
- Glycaemic control
- HTN control
- Hyperlipidaemia control
- WL
- Reduce alcohol intake

Medical:
- Secondary prevention =Aspirin 75 OD and statin 80mg ON
- GTN spray for symptom relief

Emergency management (pain not subsiding after 2 GTN sprays):
- 1st line = bisoprolol or verapamil/diltiazem
- 2nd line = bisoprolol and amlodipine/nifedipine
- 3rd line = bisoprolol and amlodipine/nifedipine and long-acting nitrate (ivabradine/nicorandil/ranolazine)

CABG/PCI in pts with uncontrolled symptoms or complex 3 vessel disease

233
Q

Define Cardiac syncope

A

Transient loss of consciousness as a result of inadequate CO leading to cerebral hypoperfusion

234
Q

Causes of Cardiac syncope

A

Structural:
- Aortic stenosis
- Ischaemic cardiomyopathy
- HOCM
- Cardiac tamponade

Electrical:
- Tachyarrhythmias = SVT or VT/VF
- Bradyarrhythmia’s = sick sinus syndrome or AVN block
- Brugada syndrome

235
Q

What is the target INR for pt w/ atrial fibrillation?

A

2-3

236
Q

What is the target INR for pt w/ metallic valve replacement?

A

Aortic = 2-3

Mitral = 2.5-3.5

237
Q

What is the target INR for pt following VTE?

A

2-3

238
Q

Define Torsades des pointes

A

A specific form of polymorphic VT that occurs in the context of QT prolongation

Has a characteristic ECG morphology where the QRS complex twists around the isoelectric line

239
Q

Torsades des pointes management

A

TdP often self-reverts back into sinus rhythm, but due to the risk of degeneration into VF or cardiac arrest sustain TdP needs to be terminated

  • If haemodynamically unstable = DC cardioversion
  • If stable = 2mg IV magnesium sulfate over 1-2 mins
240
Q

Define Tricuspid regurgitation

A

When the tricuspid valve fails to prevent blood leaking back into the R atrium during systole - this causes an increase in the pressure inside the RA and forces the RV to pump harder

Severe tricuspid regurgitation can lead to RHF over time

241
Q

Causes of Tricuspid regurgitation

A
  • Infective endocarditis
  • Rheumatic heart disease
  • Chronic lung disease
  • PE
  • Secondary to pulmonary stenosis
242
Q

Tricuspid regurgitation features

A
  • Tends to be asymptomatic even when severe, but can cause symptoms of RHF
  • Pansystolic murmur, loudest in the left parasternal area and on inspiration
243
Q

Tricuspid regurgitation management

A

Conservative = if asymptomatic, monitor with echos

Medical:
- Traet underlying cause
- Treat RHF and loop duiretics for fluid overload

Surgical - if severe, symptomatic and refractory:
- Ring annuloplasty
- Valve replacement

244
Q

Which congenital heart defects occur in Turner’s syndrome?

A

Bicuspid aortic valve (most common)

Coarctation of the aorta

245
Q

Define Ventricular septal defects

A

A cardiac defect where there is a hole in the septum allowing blood to flow from the LV to the RV (due to the larger pressure of the LV) - either congenital (most common) or acquired post-MI

This leads to increased load to the LV (as blood passes through the lungs twice) and increases the pressure in the right side of the heart

In severe cases, the pressure in the RV exceeds that of the LV, leading to a reversal of the shunt (right to left) and deoxygenated blood entering systemic circulation = Eisenmenger’s syndrome

246
Q

Ventricular septal defects features

A

Symptoms:
- Small = asymptomatic
- Large = childhood SOB, faltering growth and fatigue
- Undetected = decompensated HF or Eisenmenger’s (cyanosis)

Signs:
- Loud, harsh panstolic murmur at the left lower sternal edge
- Signs of HF
- Eisenmenger’s = cyanosis, clubbing

247
Q

Ventricular septal defects management

A
  • Majority will self resolve by 6 years old
  • Closure via catheter insertion if doesn’t close by itself
248
Q

Define Wellen’s syndrome

A

An ECG pattern caused by severe proximal LAD stenosis

It poses a major risk of a major anterior MI

249
Q

Wellen’s syndrome features

A

ECG:
- Biphasic, inverted T waves in leads V2 and V3
- Can have an absence of Q waves and minimal ST elevation

Commonly have a Hx of resolved chest pain or unstable angina

250
Q

Wellen’s syndrome management

A

PCI in the LAD coronary artery

251
Q

Define Wolff-Parkinson-White syndrome

A

The presence of a congenital accessory electrical pathway between the atria and the ventricles

Predisposes pts to supraventricular tachycardia, esp AVRT

252
Q

Wolff-Parkinson-White syndrome classification

A

Type A = accessory pathway between LA and LV

Type B = accessory pathway between RA and RV

253
Q

Wolff-Parkinson-White syndrome features

A

ECG:
- Delta wave (slurred upstroke in the QRS)
- Short PR interval <120ms
- Broadened QRS
- Narrow complex tachycardia

Symptoms:
- Mostly asymptomatic
- Symptoms of supraventricular tachycardia

254
Q

Wolff-Parkinson-White syndrome management

A

Long-term:
- Monitored w/ ECGs if asymptomatic
- Amiodarone/sotalol if paroxysmal SVT
- Radiofrequency ablation of the accessory pathway is definitive

Emergency:
- Adverse signs = DC cardioversion
- Stable NCT = vagal manouvers then IV adenosine
- Stable BCT = Flecainide then DC cadioversion

255
Q

What drugs are contraindicated in Wolff-Parkinson-White syndrome?

A

AVN blockers as this causes more electrical activity to be conducted down the accessory pathway, increasing risk of arrhythmias

  • Digoxin
  • Adenosine
  • Verapamil or diltiazem

Year 6 (8 decks)

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