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Y3 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is angina pectoris?

A

Symptomatic reversible myocardial ischaemia

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2
Q

What are the features of angina pectoris?

A
  1. Constricting/heavy discomfort to chest, jaw, neck, shoulder or arms
  2. Symptoms brought on by exertion
  3. Symptoms relieved within 5min by rest or GTN

All 3 = typical angina
2 = atypical angina
0-1 = non-anginal chest pain

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3
Q

What are the causes of angina?

A

Atheroma

Rarely:
Anaemia
Coronary artery spasm
Aortic stenosis
Tachyarrhythmias
Hypertrophic obstructive cardiomyopathy
Arteritis/small vessel disease
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4
Q

What are the different types of angina?

A

Stable = induced by effort, relieved by rest; good prognosis

Unstable = angina of increasing frequency or severity; occurs on minimal exertion or at rest; increased MI risk

Decubitus = precipitated by lying flat

Variant = caused by coronary artery spasm - rare

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5
Q

What is stable angina?

A

Chest pain resulting from myocardial ischaemia induced by exertion, relieved by rest

Good prognosis

Most common cause = atherosclerotic disease

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6
Q

What is unstable angina?

A

Angina of increasing frequency or severity

Occurs on minimal exertion or at rest

Increased MI risk

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7
Q

What is decubitus angina?

A

Angina precipitated by lying flat

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8
Q

What is variant angina?

A

Angina caused by coronary artery spasm

Rare

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9
Q

What are the risk factors for angina?

A 
Age (M≥ 45, W≥55)
Smoking
DM
Dyslipidemia
Family history of premature cardiovascular disease (M<55, F<65)
HTN
Kidney disease (microalbuminuria or GFR<60 mL/min)
Obesity (BMI ≥ 30 kg/m2)
Physical inactivity
Prolonged psychosocial stress
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10
Q

How is angina investigated?

A
  1. ECG - normal, may be ST depression, flat or inverted T waves, signs of past MI
2. BLOODS:
FBC
U+Es
TFTs - high ?thyrotoxicosis
Lipids - high
HbA1c - may be high in DM
  1. ECHO
  2. CXR
  3. EXERCISE ECG - ST depression or elevation
  4. ANGIOGRAPHY - using cardiac CT w contrast or transcatheter
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11
Q

How is angina managed?

A
  1. Address exacerbating factors: anaemia, tachycardia (eg fast AF), thyrotoxicosis
  2. Secondary prevention of CVD
    - Stop smoking, exercise, dietary advice, optimise HTN and diabetes control
    - Daily aspirin
    - Address hyperlipidaemia
    - Consider ACEis eg if diabetic
  3. PRN symptom relief = GTN spray or sublingual tabs
    - Advise patient to repeat dose if pain not gone in 5m and to call ambulance if still pain after 2nd dose
    - SE: headache, hypotension
  4. Anti-anginal medication
    1st line - B blocker + CCB (atenolol + amlodipine
  5. Revascularisation
    - Considered when optimal medical therapy proves inadequate
    - Percutaneous coronary intervention
    - CABG
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12
Q

What is PCI?

A

Percutaneous coronary intervention

Balloon inflated inside stenosed vessel, opening the lumen

Stent usually inserted to reduce risk of re-stenosis

Dual antiplatelet therapy (aspirin + clopidigrel) for 12 months+ after stent insertion to reduce risk of in-stent thrombosis

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13
Q

When is revascularisation (PCI/CABG) indicated?

A

Angina

Considered when optimal medical therapy proves inadequate

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14
Q

What is CABG? Compare it to PCI

A

Coronary artery bypass graft

vs PSI
Open heart surgery
Slower recovery
2 large wounds - sternal + vein harvesting
Less likely to need revascularisation
Better outcomes for those with multivessel disease

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15
Q

What is acute coronary syndrome?

A

A constellation fo symptoms caused by sudden reduced blood flow to the heart muscle

Unstable angina + MIs

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16
Q

What is myocardial infarction?

A

Myocardial cell death, releasing troponin

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17
Q

What causes ACS?

A

Plaque rupture -> thrombosis -> inflammation

Rarely: emboli, coronary spasm, vasculitis in normal coronary arteries

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18
Q

What is the biochemical difference between MIs and unstable angina?

A

MIs have a rise in troponin

Unstable anginas do not

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19
Q

What are the risk factors for ACS?

A

Non-modifiable: age, male, FHx of IHD (MI in 1st-degree relative <55)

Modifiable: smoking, HTN, DM, hyperlipidaemia, obesity, sedentary lifestyle, cocaine use

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20
Q

What are the presenting symptoms of ACS?

A

Acute-onset central, crushing chest pain lasting>20m
Radiates to arms/neck/jaw
Pallor
Sweating

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21
Q

How might ACS present in elderly and diabetic patients?

A 
'Silent' ACS
No chest pain
Syncope
Pulmonary oedema
Epigastric pain
Vomiting
Post-operative hypotension or oliguria
Acute confusional state
Stroke
Diabetic hyperglycaemic state
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22
Q

What are the signs of ACS?

A 
Distress
Anxiety
Pallor
Sweatiness
Pulse up or down
BP up or down
S4

Signs of HF: raised JVP, S3, basal creps

Pansystolic murmur: papillary muscle dysfunction/rupture, VSD

Low-grade fever

Later: pericardial friction rub, peripheral oedema

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23
Q

How is ACS investigated?

A

ECG: STEMI - tall T waves, ST elevation or new LBBB within hours; T-wave inversion + pathological Q waves over hours-days
NSTEMI/unstable angina: ST depresson, T wave inversion, non-specific changes or normal

CXR: Cardiomegaly, pulmonary oedema, widened mediastinum

BLOODS: FBC, U+Es, glucose, lipids, high troponin

ECHO: regional wall abnormalities

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24
Q

How is STEMI managed acutely?

A
  1. Attach ECG monitor and record a 12-lead ECG
  2. IV access - bloods for FBC, U+E, glucose, lipids, troponin
  3. Brief assessment:
    - Hx of CVD, RFs for IHD
    - Examination: pulse, BP both arms, JVP, murmurs, signs of CCF, upper limb pulses, scars from previous cardiac surgery, CXR if will not delay Rx
    - CIs to PCI or fibrinolysis?
  4. Aspirin: 300mg PO (unless already given by GP/paramedics) + tricagrelor 180mg (or other antiplatelet)
  5. Morphine: 5-10mg IV + metoclopramide 10mg IV (anti-emetic) w 1st dose

STEMI on ECG and PCI available within 2h?
YES - primary PCI - further management
NO - fibrinolysis –> transfer to PCI centre for either rescue PCI if fibrinolysis unsuccessful or for angiography

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25
Q

What is the prognosis of ACS?

A

50% of deaths occur with 2h of symptom onset

Up to 70% die before discharge

Worse prognosis: elderly, LVF, ST changes

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26
Q

How is ACS without ST-elevation managed acutely?

A
  1. Monitor closely; record ECG while in pain
  2. If SaO2<90% or brethless, low-flow O2
  3. Analgesia: morphine 5-10mg IC + metoclopramide 10mg IV
  4. Nitrates: GTN spray or sublingual tablets as required
  5. Aspirin: 300mg PO; consider need for 2nd antiplately agent
  6. Measure troponin and clinical parameters to risk assess, eg GRACE score

Invasive strategy (HIGH-RISK PT):

  • Rise in troponin OR
  • Dynamic ST or T-wave changes
  • Secondary criteria - DM, CKD, LVEF<40%, early angina post MI, recent PCI, prior CABG, intermediate to high-risk GRACE score)
    1. Fondaparinux or LMWH
    2. 2nd antiplatelet agent - ticagrelor, clopidogrel, prasugrel
    3. IV nitrate if pain continues
    4. Oral B blocker - bisoprolol
    5. Prompt cardiologist review for angiography

Conservative strategy (LOW-RISK PT):

  • No recurrence of chest pain
  • No signs of HF
  • Normal ECG
  • -ve baseline (+-repeat) troponin
    1. May be discharged
    2. Further outpatient investigation, eg stress test
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27
Q

What are the possible complications of IHD?

A 
Cardiac arrest
Cardiogenic shock
LVF
Bradyarrhythmias
Tachyarrhythmias
RVF/infarction - fluids
Pericarditis - NSAIDs
Systemic embolism - warfarin 3 months
Cardiac tamponade - pericardial aspiration, surgery
Mitral regurgitation - treat LVF, ?valve replacement
Ventricular septal defect - surgery
Late malignant ventricular arrhythmias
Dressler's syndrome - NSAIDs, steroids
Left ventricular aneurysm - anticoagulate, ?excision
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28
Q

What is infective endocarditis?

A

Infection of the endocardium, usually the valves, usually caused by a bacterial infection, but less commonly a fungal infection

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29
Q

What are the risk factors for infective endocarditis?

A
  1. Artificial heart valves
  2. Intracardiac devices
  3. Unrepaired cyanotic congenital heart defects
  4. Hx of IE
  5. Chronic rheumatic heart disease (AI response to repeated Streptococcus pyogenes infection)
  6. Age-related degenerative valvular lesions
  7. Haemodialysis (in renal failure)
  8. Coexisting conditions, especially ones that suppress immunity - DM, alcohol abuse, HIV/AIDS, IVD
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30
Q

What are the presenting symptoms of infective endocarditis?

A 
Fever
Malaise
Fatigue
Weight loss
Coughing
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31
Q

What are the causes of infective endocarditis?

A

Bacteraemia –> heart valves

Strep. viridans (usually subacute)
Staph. aureus
Strep. bovis
Enterococci + Coxiella burnetii

Rarely: HACEK Gram -ve bacteria:
Haemophilus
Actinobacillus
Cardiobacterium
Eikenella
Kingella

Diphtheroids
Chlamydia

Fungi: usually in IVD, immunocomp, prosthetic valves
Candida
Aspergillus
Histoplasma

Other:
SLE (Libman-Sacks endocarditis)
Malignancy

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32
Q

What are the signs of infective endocarditis?

A

Septic signs: fever, rigors, night sweats, malaise, weight loss, anaemia, splenomegaly, clubbing

Cardiac lesions: any new murmur, or change in old murmur

Immune complex deposition: Roth spots on retina, splinter haemorrhages, Osler’s nodes

Embolic phenomena: Janeway lesions

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33
Q

How is infective endocarditis investigated?

A

Modified Duke criteria

Blood cultures: 3 sets at different times from different sites at peak of fever

Blood tests: normochromic, normocytic anaemia, neutrophilia, high ESR/CRP, RF positive
Also check U+E, Mg, LFT

Urinanalysis: microscopic haematuria

CXR: cardiomegaly, pulmonary oedema

ECG: ?heart block

Echocardiogram: vegetations, mitral lesions + aortic root abscess

CT: emboli (spleen, brain, etc)

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34
Q

What is hypertension?

A

Blood pressure over 135/85mmHg

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35
Q

What are the presenting symptoms of hypertension?

A

Usually asymptomatic

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36
Q

How is hypertension investigated?

A

To confirm diagnosis: ABPM or week of home BP monitoring

To help quantify overall risk: fasting glucose, cholesterol

To look for end-organ damage:

  • Urinanalyis: protein, blood
  • ECG or echo (any LV hypertropgy? past MI?

To exclude secondary causes: U+E (eg low K in Conn’s); Ca (high in hyperPT)

Special tests: Renal US/arteriography (RAS); 24h urinary meta-adrenaline; urinary free cortisol; renin; aldosterone; MR aorta (coarction)

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37
Q

How is hypertension managed conservatively?

A 
Lifestyle changes:
Reduce concomitant RFs
Stop smoking
Low-fat diet
Reduce EtOH and salt intake
Increase exercise
Reduce weight if obese
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38
Q

What are the complications of hypertension?

A

CVD

Death

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39
Q

What is mitral regurgitation?

A

Backflow through the mitral valve during systole

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40
Q

What causes mitral regurgitation?

A 
Functional - LV dilatation
Annular calcification (elderly)
Rheumatic fever
Infective endocarditis
Mitral valve prolapse
Ruptured chordae tendinae
Papillary muscle dysfunction/rupture (eg post-MI)
Connective tissue disorders (E-D, Marfan's)
Cardiomyopathy
Congenital
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41
Q

Which drugs can cause mitral regurgitation?

A

Appetite suppressants - fenfluramine, phentermine

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42
Q

What are the presenting symptoms of mitral regurgitation?

A 
Dyspnoea
Fatigue
Decreased exercise tolerance
Palpitations
Symptoms of causative factor (eg fever)
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43
Q

What are the signs of mitral regurgitation?

A

Holosystolic (between S1 and S2), blowing murmur at apex that radiates to axilla

Laterally displaced apical impulse

Dimished S1

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44
Q

How is mitral regurgitation investigated?

A

Transthoracic echocardiogram:
determine presence, severity + mechanism of flail, as well as evaluating LV size + function, LA size, other valvular abnormalities, and RV systolic pressure

CXR: big LA and LV, mitral valve calcification, pulmonary oedema

Transoesophageal echocardiogram: to assess LV function and MR severity and aetiology

ECG: AF, P-mitrale if in sinus rhythm (may mean increased LA size), LVH

Cardiac catheterisation to confirm Dx, exclude other valve disease and assess CAD

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45
Q

What can be seen on a CXR of a patient with mitral regurgitation?

A

Big LA and LV
Mitral valve calcification
Pulmonary oedema

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46
Q

What can be seen on an ECG of a patient with mitral regurgitation?

A

AF
P-mitrale if in sinus rhythm (may mean increased LA size)
LVH

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47
Q

What are the risk factors for mitral regurgitation?

A 
Mitral valve prolapse
Hx of rheumatic heart disease
Infective endocarditis
Hx of cardiac trauma
Hx of MI
Hx of congenital heart disease
Hx of IHD
LV systolic dysfunction
hypertrophic cardiomyopathy
Anorectic/doapminergic drugs
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48
Q

What is the worldwide prevalence of mitral regurgitation?

A

> 5 million

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49
Q

What causes mitral regurgitation?

A

Mitral valve apparatus = anterior + posterior leaflets, chordae tendineae, anterolateral, and posteromedial papillary muscles + mitral annulus, atrial + ventricular myocardium

Mitral valve dysfunction may result from aberrations of any portion of the mitral valve apparatus, due to mechanical, traumatic, infectious, degenerative, congenital, or metabolic causes. MR can be either acute or chronic.

Typical causes of acute MR: infective endocarditis, ischaemic papillary muscle dysfunction or rupture, acute rheumatic fever, acute dilation of LV due to myocarditis or ischaemia

Common causes of chronic MR include those already listed as well as myxomatous degeneration of the mitral leaflets or chordae tendineae, mitral valve prolapse, and mitral annular enlargement.

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50
Q

What is mitral stenosis?

A

Narrowing of the mitral valve orifice

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51
Q

Explain the aetiology of mitral stenosis

A

Cause in >95% of cases: rheumatic fever leading to rheumatic heart disease

Rarer causes: congenital deformity of the valve, carcinoid syndrome, use of ergot and/or serotogenic drugs such as fenfluramine, SLE, mitral annular calcification due to ageing, and amyloidosis.

Theory:

  • Some M antigens are held in common by heart and some strains of group A streptococci
  • Streptococcal M protein may bind directly to valvular collagen, inciting an inflammatory response
  • The endocardium containing heart valves receives the most inflammatory damage
  • During an attack of acute rheumatic fever, the mitral valve becomes thickened and retracted leading to mitral regurgitation
  • However, years later, fusion of mitral leaflet commissures and thickening of leaflets and sub-valvular apparatus cause mitral stenosis
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52
Q

What are the risk factors for mitral stenosis?

A 
Streptococcal infection (usually pharyngitis)
Female (3x)

Weak:
Ergot medications (for migraine) - methysergide, ergotamine
Serotogenic medications (appetite suppressants) - fenfluramine
SLE
Amyloidosis
Bronchial carcinoid syndrome

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53
Q

What are the presenting symptoms of mitral stenosis?

A

Dyspnoea

Orthopnoea

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54
Q

What are the signs of mitral stenosis?

A 
Malar flush
Low-volume pulse
Tapping, non-displaced apex beat
Palpable S1
RV heave
Loud S1
Opening snap
Rumbling mid-diastolic murmur (heard best on expiration w patient on left side)
Loud P2 (L parasternal 2nd ICS)
Raised JVP
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55
Q

How is mitral stenosis investigated?

A

ECG: AF, LA enlargement, RVH
CXR: double right heart border –> enlarged LA, prominent pulmonary artery, Kerley B lines

56
Q

What are varicose veins?

A

Subcutaneous, permanently dilated veins 3mm or more in diameter when measured in a standing position

Long, tortuous and dilated veins of the superficial venous system

57
Q

Explain the aetiology of varicose veins

A

Usually caused by venous valve incompetence

Blood pools when valves do not function properly, leading to increased pressure and distension of the veins

Also
Progesterone is believed to lead to passive venous dilation, which may then lead to valvular dysfunction.

Oestrogen produces collagen fibre changes and smooth muscle relaxation, which both lead to vein dilation.

58
Q

What are the risk factors for varicose veins?

A 
Increasing age
Female
Hx of DVT
FHx
Pregnancy
Prolonged standing
Obesity
59
Q

What are the presenting symptoms of varicose veins?

A 
'My legs are ugly'
Leg fatigue or aching with prolonged standing
Pain
Cramps
Tingling
Heaviness
Restless legs
60
Q

What are the signs of varicose veins?

A 
Haemosiderin deposition
Oedema
Eczema
Ulcers
Haemorrhage
Phlebitis
Atrophie blanche (white scarring at site of healed ulcer)
Lipodematosclerosis
61
Q

How are varicose veins investigated?

A

Duplex ultrasound: assesses for reversed flow

Roughly, valve closure time >0.5 second = reflux in superficial system

Valve closure time >1.0 second = reflux in deep system

62
Q

How are varicose veins managed?

A

Graducated compression stockings

Phlebectomy or sclerotherapy

Ablative procedures

Perforator surgery

63
Q

What are the possible complications of varicose veins?

A 
Chronic vein insufficiency
Haemorrhage
Venous ulceration
Lipodermatosclerosis
Haemosiderin deposition
64
Q

What is the prognosis for varicose veins?

A

Symptom resolution in >95% of patients

Patients need to be counselled that new varicosities will very likely occur with time

65
Q

What is pericarditis?

A

Inflammation of the pericardium

66
Q

What is acute pericarditis?

A

New-onset inflammation of the pericardium lasting <4-6 weeks

67
Q

What is constrictive pericarditis?

A

Inflammation of the pericardium that impedes normal diastolic filling

The heart is encased in a rigid pericardium

68
Q

What are the risk factors for pericarditis?

A 
Male
20-50yo
Transmural MI
Cardiac surgery (CABG)
Neoplasm
Viral and bacterial infections
Uraemia or on dialysis
Systemic AI disorders - RA, SLE
69
Q

What are the presenting symptoms of pericarditis?

A

Central chest pain worse on inspiration or lying flat +- relief by sitting forward

Trapezius ridge pain

Fever

Myalgias

Malaise

RHF: fatigue, ankle oedema

70
Q

What are the signs of pericarditis?

A

Pericardial rub - high-pitched, squeaky, heard best at L sternal edge w patient leaning forward at end-expiration

Signs of RHF: ankle oedema, ascites

71
Q

How is pericarditis investigated?

A

ECG: concave (saddle-shaped) ST elevation globally w PR depressions

Bloods: elevated serum troponin, elevated ESR, elevated CRP, elevated urea (if uraemic cause), elevated WCC

Pericardiocentesis: positive pericardial fluid culture

Blood culture: positive

CXR: cardiomegaly (-> pericardial effusion)

Echo: pericardial effusion, absence of LV wall motion abnormalities

CMR/CT: localised inflammation

72
Q

How is pericarditis managed?

A

Ibuprofen/aspirin w omeprazole for 1-2 weeks

+ Colchicine for 3 months to reduce recurrence risk

Treat cause

Exercise restriction

If not improving or AI, consider steroids or other immunosuppressants

73
Q

What causes constrictive pericarditis?

A

Often unknown in UK

Elsewhere - TB

Or after any pericarditis

74
Q

What are the possible complications of pericarditis?

A

Pericardial effusion +- cardiac tamponade

Chronic constrictive pericarditis

75
Q

What is the prognosis for pericarditis?

A

Depends on underlying cause and disease severity

Major poor prognostic factors:
- Evidence of large pericardial effusion
- High fever >38
Sub-acute course
- Failure to respond within 7 days to NSAID
76
Q

What is vasovagal syncope?

A

A syndrome characterised by a relatively sudden, temporary and self-terminating loss of consciousness, associated with the inability to maintain postural tone, with rapid and spontaneous recovery due to

77
Q

What is heart failure?

A

Failure of heart to maintain CO required to meet body’s requirements

78
Q

What is the equation for CO?

A

CO = HR x SV

79
Q

Compare chronic and acute HF

A

Chronic:
Develops and progresses slowly
Arterial pressure maintained until later/decompensation

Acute:
Decompensation/exacerbation of chronic disease, or can be new onset
Develops and progresses quickly
Needs urgent Tx
Evidence of peripheral hypo-perfusion
Peripheral/pulmonary oedema
80
Q

What causes left HF?

A
  1. Heart valves: AR, AS, MR
  2. Heart muscle: IHD, MI, cardiomyopathy (eg HOCM), myocarditis, arrhythmias (eg AF)
  3. Systemic: HTN, amyloidosis
  4. Drugs: alcohol, cocaine
81
Q

What causes right HF?

A
  1. Heart valves: tricuspid regurg, pulmonary valve disease
  2. Lungs: pulmonary HTN, PE, pulmonary fibrosis, ILD, CF
  3. Cor pulmonale: enlargement and failure of RV due to increased pressure in lungs/vascular resistance
82
Q

What causes a high-output state and what does it lead to?

A 
NAP MEALS
Nutritional - B1/thiamine
Anaemia
Pregnancy
Malignancy - multiple myeloma
Endocrine - hypothyroidism
AV malformation
Liver cirrhosis
Sepsis

Can lead to HF

83
Q

What are the risk factors for heart failure?

A 
Older men
PMH of HD - especially MI
DM
FHx of HD
Dyslipidaemia
Drug abuse
84
Q

What are the signs and symptoms of LHF?

A 
LHF -> fluid congestion in lungs -> resp symptoms:
Exertional dyspnoea
Orthopnoea
Paroxysmal noctural dyspnoea
Fatigue
Nocturnal cough +- pink frothy sputum
Wheeze (cardiac asthma)

Heart O/E: high HR, high RR, irregularly irregular heart beat, displaced apex beat, gallop rhythm (S3), murmur (AS, MR)

Lungs O/E: bibasal crackles, wheeze

85
Q

What are the signs and symptoms of RHF?

A 
RHF -> fluid congestion in system -> peripheral symptoms:
Swelling - ankles, face, abdomen
Fatigue
Weight gain
Decreased exercise tolerance
Anorexia
Nausea
Nocturia

Face/neck: raised JVP, facial swelling
Chest: Parasternal heave, TR murmur, high HR, high RR
Abdo: ascites, hepatomegaly
Other: pitting oedema

86
Q

What are the appropriate investigations for HF?

A

Bedside:
History and examination
ECG

Bloods:
FBC - anaemia is cause
U&amp;E
LFTS - abdominal congestion
TFTs - hyperthyroidism is cause
Glucose - DM is RF
BNP - high

Imaging:
Transthoracic echocardiogram - EF<40% = systolic HF, over 50%=HF w preserved EF
CXR

87
Q

What are the features of HF on a CXR?

A 
Alveolar oedema ('bat wing' appearance)
B-lines (Kerley) (interstitial oedema)
Cardiomegaly (CTR>50%)
Dilated upper lobe vessels (pulmonary venous HTN)
Effusion (pleural)
88
Q

How is chronic HF managed?

A

Treat underlying cause

Conservative:
Smoking cessation
Weight management - exercise
Diet - reduce salt intake

Medical:

  1. ACE-Is: enalapril, perindopril, ramipril
    - can use ARB if cough
    - must monitor K
  2. B blockers: bisoprolol, carvedilol
  3. Diuretics
    - aldosterone antagonist - spironolactone
    - loop diurectics - furosemide
    - thiazide - hydrochlorthiazide
89
Q

How is acute HF managed?

A
  1. Sit patient up
  2. Oxygen - SpO2 target 94-98% - 15L via non rebreathe mask
  3. IV access and ECG (arrhythmia?)
  4. Furosemide IV
  5. GTN spray 2 puffs sublingual
  6. Morphine 2.5mg (but do not give routinely)
90
Q

What are the possible complications of HF?

A

Pleural effusion
Renal failure
Acute exacerbations
Death

91
Q

What is the prognosis for HF?

A

50% severe HF patients die within 2 years

92
Q

What are the different types of valvular heart disease?

A 
Tricuspid regurgitation
Mitral regurgitation
Mitral stenosis
Aortic regurgitation
Aortic stenosis
93
Q

What does S1 signify?

A

Closure of AV valves: tricuspid and mitral

94
Q

What does S2 signify?

A

Closure of aortic and pulmonary valves

95
Q

What does valvular heart diseases often produce on examination?

A

Murmurs

Heart sounds produced when blood flows over the valves

96
Q

Which valvular heart diseases cause systolic murmurs?

A

Aortic stenosis
Mitral regurg
Tricuspid regurg

A systolic murmur, really tiring respiration

97
Q

Which valvular disease cause diastolic murmurs?

A

Aortic regurg

Mitral stenosis

98
Q

What is tricuspid regurgitation?

A

Backflow of blood from RV to RA

99
Q

What is aortic stenosis?

A

Narrowing of LV outflow at aortic valve

100
Q

What is mitral regurgitation?

A

Backflow of blood from LV to LA

101
Q

What are the symptoms of AS, MR and TR?

A 
Dyspnoea - SOB
Syncope on exertion
Angina
HF signs
Palpitations

Also may be asymptomatic

102
Q

What are the signs of aortic stenosis?

A

Ejection systolic murmur (aortic area = 2nd-3rd right ICS)
Radiating to carotids and apex
Ask pt to hold breath on expiration

BP - narrow pulse pressure

Pulse - slow-rising

Palpation - thrill (palpable heart murmur)

103
Q

What are the signs of mitral regurgitation?

A

Pan-systolic murmur at apex
Radiates to axilla

Pulse - normal/irregularly irregular

Palpation - laterally displaced apex beat

104
Q

What are the signs of tricuspid regurgitation?

A

Pan-systolic murmur
Ask pt to hold breath on inspiration
Tricuspid area - L lower sternal border

Inspection - raised JVP

Palpation - parasternal heave

Signs of RHF - pleural effusion, hepatomegaly, ascites, pitting oedema

105
Q

How are AS, MR and TR investigated?

A

ECG:
AS - signs of LV hypertrophy - enlarged R waves, inverted T waves, L axis deviation
TR - signs of LVH - tall p-wave

CXR:

  • enlargement of ascending aorta
  • aortic valve calcification (AS)
  • right-sided enlargement (TR)
  • cardiomegaly (MR)
106
Q

How can valvular disease be classified?

A

Systolic - AS, MR, TR

Diastolic - AR, MS

107
Q

What is aortic regurgitation?

A

Reflux of blood from aorta to LV during diastole

108
Q

What is mitral stenosis?

A

Narrowing of mitral valve, obstructing blood flow from LA to LV

109
Q

What causes diastolic murmurs - AR and MS?

A

Infection - rheumatic HD (MS), infective endocarditis

Congenital - bicuspid aortic valve

Dilation of aorta - HTN, aortitis

CTD

110
Q

When do people usually get diastolic murmurs?

A

late 50s-80s

111
Q

What percentage of mitral stenosis if caused by rheumatic heart disease?

A

90%

112
Q

What are the symptoms of AR and MS?

A 
Dyspnoea - SOB
Syncope on exertion
Angina
HF signs
Palpitations
Orthopnoea

May be asymptomatic

113
Q

What are the signs of AR?

A

Early diastolic murmur (2nd to 3rd R ICS) - lub pssssh
Radiates to carotids and apex
Ask pt to sit forward and hold breath on expiration
Wide pulse pressure
Collapsing pulse
Displaced apex beat

114
Q

What are the signs of MS?

A

Mid-diastolic murmur
Loud S1 with opening snap
Bell of stethoscope
Apex

Malar flush
Thready or irregularly irregular pulse
Tapping apex
Parasternal heave

115
Q

How are AR and MS investigated?

A

ECG:
Signs of LV hypertrophy - enlarged R waves, inverted T waves, L axis deviation
MS - broad bifid p wave, AF

CXR:
Dilation of ascending aorta
Cardiomegaly

116
Q

What do ECG changes in leads II, III and aVF indicate?

A

Inferior (right coronary artery) infarct

117
Q

What do the ECG changes in different leads indicate?

A

Inferior (right coronary artery): II, III, aVF

Anterior (left anterior descending): V1-V5

Lateral (left circumflex): I, aVL, V5/6

Posterior (posterior descending): tall R wave + ST depression in V1-3

118
Q

What do ECG changes in leads V1-V5 indicate?

A

Anterior (left anterior descending) infarct

119
Q

What do ECG changes in leads I, aVL and V5/6 indicate?

A

Lateral (left circumflex) infarct

120
Q

What do ECG changes in leads V1-3 indicate?

A

Posterior (posterior descending) infarct

121
Q

How is ACS managed generally?

A 
Morphine
Oxygen
Nitrates
Antiplatelets (aspirin + clopidogrel)
Beta-blockers
ACE inhibitors
Statins
Heparin
122
Q

What are the complications of ACS?

A

Darth Vader

Death
Arrhythmia
Rupture
Tamponade
Heart failure
Valve disease
Aneurysm
Dressler's syndrome
Embolism
Reinfarction
123
Q

What is atrial fibrillation?

A

Characterised by rapid, chaotic and ineffective atrial electrical conduction

124
Q

What are the causes of AF?

A

Absolutely loads

Pneumonia
PE
Hyperthyroidism
IHD
Alcohol
Pericarditis
125
Q

What are the symptoms and signs of Af?

A

Palpitations
Syncope
Symptoms of underlying causes
Irregularly irregular pulse

126
Q

How do you investigate AF?

A

ECG:
absent P waves
Irregular QRS complexes
Irregularly irregular tachycardia

Bloods: U+E, cardiac enzymes, TFTs

Echo: LA enlargement, mitral valve disease, poor LV function, other structural abnormalities

127
Q

How do you manage AF?

A

If the patient is haemodynamically unstable - DC CARDIOVERSION

Rhythm contol:
<48h since onset of AF:
DC cardioversion
or chemical cardioversion (flecainide (CI if IHD Hx) or amiodarone)
>48h:
anticoagulate for 3-4 weeks before cardioversion

Rate control:
Verapamil
B blockers
Digoxin

Treat the cause

Stroke Risk Stratification
CHADS-Vasc score
Low risk -> aspirin or none
High risk -> warfarin

128
Q

What is in the CHADS-VASc score?

A

Anticoagulate in AF?

Congestive HF - 1
Hypertension - 1
Age 65-74 -1/>74 - 2
Diabetes - 1
Stroke/TIA/Thromboembolism - 2
Vascular disease - 1
Sex Category - female - 1

More than 1 = should be considered

129
Q

What is supraventricular tachycardia?

A

A regular, narrow-complex tachycardia with no p waves and a supraventricular origin

130
Q

What are the symptoms of SVT?

A

Palpitations
Syncope
Dyspnoea
Chest discomfort

131
Q

What are the complications of AF?

A 
Stroke
MI
Congestive HF
Bradycardia
Hypotension
132
Q

What are the types of SVT?

A

Atrioventricular nodal re-entry tachycardia (AVNRT) - local circuit forms around AV node

Atrioventricular re-entry tachycardia (AVRT) - re-entry circuit forms between atria and ventricles due to presence of accessory pathway (Bundle of Kent)

133
Q

How do you investigate SVT?

A

ECG:
Regular
Narrow complex tachycardia
Absent p waves

ECG after termination of SVT:
AVNRT = normal
AVRT = delta wave - slurred upstroke on QRS complex

Test for causes: cardiac enzymes, electrolytes, TFTs, digoxin level

134
Q

What does the presence of an accessory pathway resulting in a delta wave on ECG indicate?

A

Wolff-Parkinson-White Syndrome

135
Q

How do you manage SVT?

A

STEP 1: is the patient haemodynamically stable?
NO –> Synchronised DC cardioversion
YES –> STEP 2

STEP 2: Vagal Manoeuvres (carotid body massage) – did it work?
YES –> Good Job
NO –> STEP 3

STEP 3a: IV Adenosine 6 mg – did it work?
YES –> Good Job
NO –> Step 3b, if that fails, Step 3c, then, Step 4
STEP 3b: IV Adenosine 12 mg
STEP 3c: IV Adenosine 12 mg (again)

STEP 4: Choose from:
IV b-blocker (e.g. metoprolol)
IV amiodarone
IV digoxin
Synchronised DC cardioversion

NOTE: if adenosine is CI eg asthma, use verapamil

136
Q

How does WPW syndrome lead to AVRT?

A

Accessory pathway allows early depolarisation of the ventricles (ie pre-excitation)

Gives rise to slurred QRS upstroke

If a wave of DP travels retrograde back into atria, it can set up a re-entry circuit between atria and ventricles

AVRT

Y3 (20 decks)

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