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IPE > CVS > Flashcards

CVS Flashcards

1
Q

Causes of Hypertension

A 
Primary
Renal - PKD, RVD, PAN, GN
Endo - Conns, Cushings, Pheo, Acro, Hyperthyroidism
Drugs - Cocaine, OCP, NSAIDS
ICP raised
Coarction aorta
Toxaemia of pregnancy
Increased viscosity
Overload of fluid
Neurogenic
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2
Q

Signs of end-organ damage in HTN

A 
Cardiac - IHD, LVF - CCF, AR/MR
Aorta - aneurysm/ dissection
Neuro - CVA (ishaemic/haemorrhagic); encephalopathy ( malignant HTN - headaches, seizure, coma)
Eyes - HTN retinopathy 
Renal - Proteinuria, CRF
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3
Q

Classification of hypertensive retinopathy

A

Keith - Wagener classification

1) Tortous A and silver wiring
2) AV nipping
3) flame haemorrhages and cotton wool spots
4) Papilloedema

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4
Q

Investigations for hypertension

A

1) 24h ABPM
2) Bloods - FBC, UE, Glucose, Fasting lipids, eGFR
3) 12-lead ECG
4) Urine - haematuria; alb:Cr
5) Calculate 10 year CV risk –> QRisk2 (+ Atorvastatin 20mg if >10% )

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5
Q

Management for hypertension

A

LIFESTYLE
- educate; stop smoking; reduce alcohol; reduce salt; reduce caffiene; increase exercise
PHARMACOLOGICAL
- treat if >140/90 and end organ damage/ CV risk >20% or if >160/100
- 1st line –> <55/DM - ACEi; >55/black - CaCB/ thiazide
- 2nd line –> ACEi +CCB
- 3rd line –> +thiazide
- 4th line —> + spironolactone / a/b blocker

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6
Q

Target BP for hypertensive

A

<140/90
<130/80 if DM
<150/90 if >80

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7
Q

Name and give SE of ACEi

- And name of ARB

A

Lisinopril , Ramipril
ARB - candesartan

SE: renal impairment; persistent dry cough; angioedema; rash; hypotension; pancreatitis; hyperkalaemia; GI effects.

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8
Q

Name and give SE of dihydropyridine calcium channel blocker

A

Nifedipine

SE–> abdominal pain; nausea;
palpitations, flushing, oedema; headache;
dizziness; sleep disturbances; fatigue

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9
Q

Name and give SE of Thiazide

A

Bendroflumethiazide.

SE–> postural hypotension; hypokalaemia;
hypomagnesaemia; hyponatraemia; hypercalcaemia; metabolic alkalosis; hyperuricaemia; impotence; hyperglycaemia.

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10
Q

Treatment of

a) malignant hypertension
b) malignant hypertension + encephalopathy

A

a)

1) reduce BP over a few days to avoid stroke
2) Atenolol / Long-acting CaCB

b)
1) sodium nitroprusside infusion- monitor BP intra- A  
OR
IV labetalol 
2) Reduce BP to <110 over 4 hours
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11
Q

NYHA Heart Failure Classification

A

Class I- No limitation of physical activity
Class II- Slight limitation of physical activity (symptomatically mild heart failure)
Class III - Marked limitation of physical activity (symptomatically moderate heart failure)
Class IV- Symptoms at rest
(symptomatically severe heart failure)

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12
Q

Which murmur has increased intensity on inspiration and why

A

Right - Inspiration ↑ venous blood return to the right

side of the heart.

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13
Q

Grading of murmurs

A

Grade 1: Very faint.
Grade 2: Soft.
Grade 3: Heard easily.
Grade 4: Loud, with a palpable thrill
Grade 5:Very loud, with thrill. May be heard when stethoscope is partly off the chest.
Grade 6:Very loud, with thrill. May be heard with stethoscope entirely off the chest

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14
Q

Causes of Mitral Stenosis

A
  • Rheumatic fever or
    chorea
  • Old Age and calcification
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15
Q

Effects of Mitral Stenosis

A 
High LA pressure
↓
Pulmonary venous hypertension
↓
Pulmonary arterial hypertension
↓
Right ventricular hypertrophy
↓
Tricuspid regurgitation
↓
Right heart failure
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16
Q

Signs of MS

A
  • Atrial Fibrillation
  • Malar flush
  • Tapping apex beat due to palpable 1st heart sound

Auscultation

  • Loud S1
  • Opening snap
  • Rumbling MDM best heard with BELL at APEX lying on LEFT
  • Signs of RHF -
    ↑ JVP, Oedema, Ascites
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17
Q

Signs of Pulmonary Oedema on CXR

A 
Airspace shadowing
B lines (Kerley
Cardiomegaly
Diversion to upper lobes
Effusion
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18
Q

ECG changes in MS

A

o Atrial Fibrillation
o Bifid P wave if SR (Left atrial delay)
o RVH - right axis deviation and tall R waves in
leads V1 and V2

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19
Q

Causes of Mitral Regurgitation

A 
o Prolapsing mitral valve
o Rheumatic mitral regurgitation (the cusps are
shrunken and fibrotic)
o Papillary muscle rupture post MI 
o Cardiomyopathy of any sort
o Connective tissue disorders
􏰀Marfan's syndrome 
􏰀Ehlers Danlos 
􏰀Osteogenesis imperfecta
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20
Q

Signs of MR

A
  • Pulse in sinus rhythm
  • Malar flush
  • Displaced, volume loaded apex beat
  • Palpable thrill
  • Auscultation - Panstyolic murmur radiating to the axilla
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21
Q

Signs of MR on CXR and ECG

A

CXR - cardiomegaly

ECG - Bifid p wave and LVH

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22
Q

Causes of Aortic Stenosis

A

Bicuspid Aortic Valve (under 65)
Age related Calcification (over 65)
Rheumatic Fever

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23
Q

Symptoms of AS

A

Exercise-induced syncope, angina and dyspnoea develop

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24
Q

Signs of AS

A

o Pulse
– Character = slow rising
– Volume = low volume with narrow pulse pressure

oForceful apex beat
Auscultation:
o Ejection systolic murmur radiating to carotids

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25
Q

Findings on CXR and ECG in AS

A

CXR
o Relatively small heart with a prominent, dilated,
ascending aorta. → ‘post-stenotic dilatation’
ECG:
o LVH
o left ventricular ‘strain’ pattern (depressed ST
segments and T wave inversion in leads orientated towards the left ventricle)

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26
Q

Causes of Aortic Regurgitation

A 
oRheumatic fever (commonest) 
o Bicuspid valve
o Infective Endocarditis
o Others:
􏰀 Marfan’s syndrome
􏰀 Tertiary Syphilis
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27
Q

Pathology of AR

A

Reflux of blood from aorta to LV in diastole.
For cardiac output to be maintained, total
volume to be pumped into aorta must ↑, therefore LV size must increase.

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28
Q

Signs of AR

A

– Collapsing pulse(wide pulse pressure)

􏰀 Quincke’s sign - capillary pulsation in the nail
beds.
􏰀 De Musset’s sign - head nodding with each
heartbeat.
􏰀 Pistol shot femorals - a sharp bang heard on
auscultation over the femoral arteries in time with
each heartbeat.
– Displaced apex beat
uscultation:
o High-pitched early diastolic murmur best heard at the left sternal edge in the fourth ICS with the patient leaning forward and their breath held in expiration

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29
Q

ECG changes in AR

A

LVH

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30
Q

How to calculate a regular and irregular rate on ECG

A

Regular
300 divided by the number of big squares
between the R-R interval.

Irregular
Count the total number of QRS complexes in a
10 second rhythm strip (50 large squares) and
multiply by 6.

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31
Q

ECG changes in Atrial flutter and why

A

Sawtooth” P waves - usually most prominent in lead II.

The atria depolarize in an organized circular movement due to re-entry. The atria contract at around 300 bpm, which results in a fast sequence of p-waves in a sawtooth pattern.
For most AVN 300 bpm is too fast to conduct the signal to the ventricles.
2:1 conduction = rate of 150 3:1 conduction = rate of 100 4:1 conduction = rate of 75

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32
Q

What is the normal PR interval

A

0.12 - 0.2 milliseconds (3-5 small squares)

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33
Q

What is 1st degree Heart Block and causes

A

P-R interval prolonged by constant amount (> 5 small squares)

causes
- AVN disease; acute MI; myocarditis; CCB; BB

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34
Q

What are the types of second degree Heart block

A

•Mobitz I (Wenckebach)
o Progressive lengthening of P-R until one QRS is dropped

• Mobitz II
o Intermittent failure of AV node to conduct atrial
depolarisations to the ventricles
o May be fixed i.e. 2:1 / 3:1 P-R interval

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35
Q

Describe 3rd degree Heart Block and the causes

A

Complete HB
• No relationship between P waves and QRS complexes
• Rate usually 30-50bpm
• Stoke-Adams attacks

Causes:
o CAD
o Fibrosis of AVN/ Bundle of His
o Drugs e.g. Digoxin toxicity, Diltiazem

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36
Q

Describe the criteria is used to measure LVH on an ECG

A

Sokolow-Lyon Voltage criteria
o S wave in V1 + R wave in V5 or V6 =>35mm
or 3.5 large ECG squares
o If severe T wave inversion may also be seen in
V5, V6
+/- LAD

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37
Q

How would you assess RVH on on ECG

A

R wave >5mm in Right ventricular leads + RAD

(R1S6) +/- RAD

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38
Q

How is the QRS affected in BBB and causes

A 
Widened in BBB -->  WiLLiaM and MaRRoW
o LBBB: WinV1 and MinV6
- LVH; Inf MI; Coronary HD
o RBBB:MinV1 and WinV6
- Inf MI; ASD/VSD; RVH
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39
Q

Causes of ST elevation

A

Acute MI

Pericarditis: Concave and widespread over many leads

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40
Q

Causes of ST depression

A

Ischaemia
> 1mm in 2 consecutive limb leads or
> 2mm in 2 consecutive chest leads

+ Level or Downsloping

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41
Q

Features of MI on ECG

A

Acute infarct: ST elevation

Recent infarct: T wave inversion+ Pathological Q
waves (> 1/4 height QRS)
• Old infarct: Q waves remain
• Also new onset LBBB

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42
Q

Location of MI and correlating Blood vessels

A

> V1-V2: Septal and V3-V4: Anterior - LAD
V5-V6: Lateral and I, aVL: High Lateral -L circumflex
V2-6 - L mainstem
II, III, aVF: Inferior -RCA

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43
Q

ECG changes in PE

A

S1, Q3, T3
􏰀 Large S wave in lead I
􏰀 Q wave inversion in lead III
􏰀 T wave inversion in lead III

o RAD
o Tachycardia (the most common finding on ECG!)
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44
Q

ECG changes in Hyperkalaemia

A

Low flat P waves
Broad bizarre QRS
Slurring into the ST segment
Tell tented T waves

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45
Q

Causes of Heart Failure

A

Ischaemic heart disease (70%)

Non-Ischaemic Dilated Cardiomyopathy (25%)

Hypertension (5%)

Other:
Valve disease; CHD; AF; HB; Anaemia; Pericardial disease; Pul HTN; PE; Alcohol

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46
Q

Pathophysiology of Heart failure

A 
INITIALLY 
Reduced CO - compensation 
o Starling effect dilates heart to enhance contractility 
oRemodelling- Hypertrophy
oRAS and ANP/BNP release
oSympathetic activation

PROGRESSIVE
- ↓ CO - decompensation
o Progressive dilatation –> impaired contractility + functional valve regurgitation
o Hypertrophy –> Relative myocardial iscaemia
o RAAS activation –> Na+ and fluid retention –> ↑ Venous P –> oedema
o Sympathetic excess –> increase afterload –> ↓ CO

Severe HF - ↓ CO even at rest despite ↑ venous pressure and sinus
tachycardia

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47
Q

Causes of LHF

A
  1. Ischaemic Heart Disease
  2. Non Ischaemic Dilated Cardiomyopathy
  3. Hypertension
  4. Mitral / Aortic Valve Disease
    Also:
    o MS - LA HTN and signs LHF
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48
Q

Symptoms of LHF

A

o Fatigue (common)
o Exertional dyspnoea
o Orthopnoea / PND

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49
Q

Signs of LHF

A

o Displaced Apex Beat –> Cardiomegaly
o Gallop Rhythm and tachycardia on Auscultation - S3
o Features of MR - Dilatation of the mitral annulus
o Pulmonary oedema
o Dependent Pitting Oedema
o Cold peripheries

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50
Q

Causes of RHF

A

LHF
Chronic Lung Disease (Cor pulmonale)
PE or Pulmonary Hypertension
Tricuspid / Pulmonary Valve Disease

Causes of pulmonary hypertension

  • LH disease (MS/MR/LVF/ L–> R shunt)
  • Lung (hypoxic vasoconstriction increased P)- COPD; asthma; ILD; CF: bronchiectasis
  • Pulmonary vasc disease - SLE; Wegners; SCD; PE; Portal HTN; idiopathic
  • Hypoventilation - OSA; obesity; kyphosis/scoliosis; NM (MND, MG, polio)
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51
Q

Symptoms of RHF

A

Fatigue
Dyspnoea
Anorexia / Nausea

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52
Q

Signs of RHF

A

↑ JVP ± V waves of tricuspid regurgitation
Cardiomegaly - Dilatation of the RV +- TR
Hepatic Enlargement = Tender and smooth
Ascites
Dependent Pitting Oedema

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53
Q

Management of HF

A 
General 
• Low level exercise
• Low salt diet
• Stop smoking
• Education
• Vaccination
Medical 
1) ACEi/ARB + β-Blockers + Furosemide 
2nd line - Spironolactone; GTN
3rd line - Digoxin 
- Cardioresynchronisation therapy ± implaented cardioverter defribillator

Consider Anticoagulation

Further

  • LV Assist Device and Artificial Heart
  • Revascularisation
  • Cardiac transplant
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54
Q

Pathophysiology of atherosclerosis and in ACS

A

• Triggered by injury
• Lipoproteins oxidised - taken up by macrophages =
foam cells
• Release of cytokines → accumulation fat and smooth
muscle proliferation
• Plaque formation

ACS

  • Rupture of a coronary artery plaque
  • Platelet aggregation and adhesion
  • Localised thrombus, vasoconstriction
  • Myocardial ischaemia
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55
Q

Risk factors for ACS

A 
• Non - modifiable 
o ↑Age
o Male gender 
o Family History 
o Ethnic origin
• Modifiable
o Smoking
o Diabetes
o Hypertension
o Hypercholesterolaemia
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56
Q

Initial management of ACS

A

Airway, Breathing, Circulation IV access
12-lead ECG

Give:
Morphine (2.5-10mg IV, plus antiemetic)
Oxygen
Nitrates (GTN spray 2 puffs sublingually) 
Aspirin (300mg)
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57
Q

Investigations for ACS

A
  • ECG
  • Bloods - FBC, LFT, UE, Glucose, Lipids, CK, Troponin I
  • Portable CXR
58
Q

Presentation of STEMI

A 
o Chest pain - not relieved by GTN
o N+V, sweating
o May be painless +/- atypical (diabetics)
o May present as acute pulmonary oedema,
SOB, syncope, cardiogenic shock etc.
59
Q

ECG findings in STEMI

A

o ST elevation
o New LBBB
o +/- T wave inversion
o +/- Pathological Q waves

60
Q

Definitive management of STEMI

A

Thrombolysis
or
PCI (Percutaneous Coronary Intervention)

61
Q

Indications for Thrombolysis and PCI in STEMI

A

Thrombolysis
o < 12 hours onset pain + any 1 of the following:
o ST elevation >1mm in 2+ consecutive limb leads
o ST elevation >2mm in 2+ consecutive chest leads
o Posterior infarct o New onset LBBB

PCI
If can undergo <90 min from onset
- Same as thrombolysis and if doesn’t fulfil criteria or thrombolysis CI

62
Q

Contraindications for Thrombolysis

A 
Absolute:
Haemorrhagic stroke or Ischaemic stroke < 6 months CNS neoplasia
Recent trauma or surgery
GI bleed < 1 month
Bleeding disorder
Aortic Dissection

Relative:
Warfarin
Pregnancy
Advanced Liver Disease Infective Endocarditis

63
Q

Complications of thrombolysis

A
  • Bleeding
  • Hypotension
  • Intracranial haemorrhage
  • Reperfusion arrhythmias
  • Systemic embolisation of thrombus
  • Allergic reaction (especially if Streptokinase)
64
Q

Complications of STEMI

A 
S - Sudden death
P - Pump failure / Pericarditis
R - Rupture papillary muscles or septum 
E - Embolism
A - Aneurysm / Arrhythmias
D - Dressler’s syndrome
65
Q

Drugs to discharge with pt after STEMI and risk prevention

A
  • Aspirin
  • Clopidogrel
  • ACE inhibitor
  • β-blocker
  • Statin
  • Address modifiable risk factors
  • 1 month off work
  • Need to inform DVLA – no driving for 4 weeks.
66
Q

Presentation of NSTEMI and unstable angina

A
  • Rest angina / Increasing angina

* New-onset severe angina

67
Q

ECG changes for NSTEMI and unstable angina

A
  • T wave inversion

* ST depression

68
Q

How to differentiate between NSTEMI and unstable angina

A

Check Troponin I 12 hours after onset of pain to
distinguish between NSTEMI and UA. NSTEMI will have a positive Troponin I and Unstable Angina will have a negative troponin.

69
Q

Management of NSTEMI/UA

A 
1. Analgesia
   o Morphine
2. Anti-ischaemic
   o Nitrates (GTN infusion)
   o ACE inhibitors
   o β-blockers
   o Calcium channel antagonists
   o Statins
3. Antiplatelet o Aspirin
   o Clopidogrel 
4. Antithrombotic
   o LMWH
Consider PCI if: 
↑ Troponin I
Recurrent angina / ischaemic ECG changes despite optimal medical therapy
Features of heart failure
Poor LV function
Haemodynamic instability
PCI < 6 months / previous CABG
70
Q

Pathophysiology of LV failure

A

The heart is unable to maintain sufficient cardiac output to meet the demands of the body.
• Compensatory mechanisms are not yet operative in acute LVF.
• The cardiac output is reduced. Failure of the ventricles to eject blood results in increased intracardiac pressures and pulmonary capillary pressure.

71
Q

Presentation of LV failure

A 
Presents as acute pulmonary oedema: 
o Acute breathlessness
o Cough; frothy pink sputum
o Orthopnoea, paroxysmal nocturnal dyspnoea 
o Collapse, arrest, cardiogenic shock
Signs
o Distressed, pale and sweaty
o Tachycardic and tachypnoea 
o Fine crepitations bilaterally
o Gallop rhythm: S-3
o Pulsus alternans
72
Q

Causes of LVF

A

o Myocardial ischaemia
o Hypertension
o Aortic stenosis or aortic incompetence o Mitral incompetence

73
Q

Management of LVF

A
  • Airway, Breathing, Circulation
  • Sit upright
  • 100 % O2 via non rebreather mask
  • IV access and monitor ECG
  • Morphine 2.5-5mg IV (with antiemetic)

Other:
• If SBP >100mmHg – Nitrate (GTN) IV infusion
• Furosemide 40-80mg IV
• CPAP

74
Q

Investigations for LVF

A
  • ECG: Arrhythmia, tachycardia, MI, LVH
  • Bloods: FBC, U+E, CK, Troponin I
  • CXR
  • ABG
  • Echo
75
Q

Mechanisms of tachycardias

A
  1. Accelerated automaticity
    o An area of myocardial cells depolarises faster
    than the SA node
  2. Triggered activity
    o Myocardial damage
  3. Re-entry
    o Propagating action potential
    keeps meeting excitable myocardium.
    o There must be 2 pathways around an area of conduction block.
76
Q

Precipitating factors for VT

A
  • Metabolic
  • IHD
  • Cocaine
  • Cardiomyopathy
  • MI
77
Q

Precipitating factors for SVT

A
  • IHD
  • Thyrotoxicosis
  • Caffeine
  • Alcohol
  • Smoking
78
Q

Precipitating factors for AF

A 
Pericardial and lung disease
IHD
Regurg/stenosis -mitral
Anaemia, Alcohol, Age
Thyrotoxicosis
Elevated BP
Smoking, surgery

Caffeine and Cardiomyopathy

79
Q

Types of SVT (narrow)

A 
• Regular
o Sinus tachycardia
o Atrial flutter (some)
o Atrial tachycardia
o Junctional tachycardia
o AV node re-entry
o Accessory patheay e.g. WPW

• Irregular
o Atrial fibrillation (AF)
o Atrial flutter (some)
o Multifocal atrial tachycardia

80
Q

Management of regular SVT

A
  • ABC+O2+IV access –> Seek help
  • Vagal Manoeuvres
  • Adenosine 6mg rapid IV bolus; +12 +12 - monitor ECG continuously
  • if rhythm restored probably re-entry PSVT –> 12 lead ECG and adenosin if recurs
    • Haemodynamically unstable (Low BP; HF; reduced consciousness; HR>200)
    –> sedate - DC cardiovert —> amiodarone 300mg over 20-60 mins
81
Q

Management of AF

A

Control rate with b-blockers or digoxin IV

If onset <48h consider amiodarone 300mg IV 20-60 min; then 900mg over 24g

Anticoagulate

82
Q

Types of broad complex tachycardias

A

oVT
- Including Torsades de pointes

o SVT with BBB

83
Q

Differences between SVT and VT

A

• SVT
o Is slowed or terminated by vagal manoeuvres /
adenosine
o Atrial and ventricular coupling
• VT
o QRS >160ms
o Independent atrial activity o Fusion / Capture beats

84
Q

Management of VT

A

ABC (if pulseless = arrest protocol)
Oxygen and IV access

No adverse signs
o Amiodarone / Lidocaine
o K+/Mg2+ if needed
o Sedation and DC cardioversion

Adverse signs (↓ BP, HF, ↓ GCS; Chest pain, HR>150)
Sedation --> DC cardioversion --> Amiodarone 300mg over 20-60 mins
85
Q

Causative organisms of infective endocarditis

A

Streptococcus viridians

S.Aurues (IVDU)

86
Q

Pathophysiology of IE

A

Endothelial damage/ damaged valve

platelet and fibrin deposited

Bacteriaeia

Adherence and colonisation of bacteria

Fibrin aggregates protect the bacteria vegetation from host defence mechanisms

87
Q

Consequences of IE

A

o Disruption of the valve cusps, commonly
leading to mitral or aortic regurgitation.
o Vegetations embolise.
o Deposition of immune complexes.

88
Q

Clinical presentation of IE

A

• HEART MURMUR + FEVER

1. Systemic infection
o Malaise
o Pyrexia
o Myalgia
o Weight loss 
o Fatigue
  1. Valvular / Cardiac damage
    o Changing Murmur- AR/MR
    o Heart failure
    o Conduction Abnormalities
3. Embolisation
o Cerebral
o Pulmonary
o Coronary
o Renal (haematuria)
4. Immune Vasculitis
o Roth spots (Retinal infarcts with surrounding haemorrhage)
o Oslers nodes
o Janeway lesions
o Clubbing
o Splinter haemorrhages 
o Glomerulonephritis
89
Q

DUKES CRITERIA FOR IE

A

BE FIVE PM

MAJOR
Blood culture +ve
o Typical organism in 2 separate cultures. OR
o Persistently positive cultures (3 sets, at different times, from different places, at peak temperature).

Endocardium involvement - o Positive echocardiogram (Vegetation, abscess, prosthetic valve damage).
OR
o New valvular regurgitation.

MINOR
Fever
Immune Phenomenon
Vascular Signs/emboli
ECHO +ve
Predisposition
Microbiology +Ve

2 Major OR 1 Major, 3 Minor OR 5 Minor

90
Q

Management of IE

A

ABC
Involve microbiologist and cardiologist
Benzylpenicillin and Gentamycin 4 weeks IV

91
Q

Investigations for IE

A 
Bloods: FBC (anaemia), U+E, LFT, CRP ↑, Blood Cultures x 3 
CXR
ECG
Echocardiogram
Urinalysis (microhaematuria)
92
Q

Risk factors for IE

A

o Structural congenital heart disease
o Acquired valve disease
o Prosthetic valves
o Previous endocarditis

93
Q

Presentation of acute pericarditis

A 
o Chest pain
1. Sharp
2. Worse on inspiration 
3. Central chest pain
4. Radiating to left shoulder
5. Eased sitting forward
o Pericardial friction rub 
o Serial ECG changes
o Tachycardia and Tachypnoemia
o +/- Dyspnoea, Fever

If Constrictive pericarditis:
- signs RHF
􏰀 ↑JVP, severe ascites, hepatomegaly, Kussmaul’s sign (JVP ↑ with inspiration)

  • Hypotension, Pulsus Paradoxus (↓ in palpable pulse and ↓ in systolic BP on inspiration)
  • Loud high-pitched S3 (pericardial knock)
94
Q

Pathophysiology of pericarditis

A 
• Pericardium is acutely inflamed.
• Infiltration of polymorphonuclear (PMN) leukocytes
and pericardial vascularisation.
o May develop constrictive pericarditis
􏰀 Exudates + adhesions encase the heart within a non expansile pericardium.
o May develop a pericardial effusion
􏰀 Serous or haemorrhagic.
􏰀 May lead to cardiac tamponade.
95
Q

Causes of Pericarditis

A 
Viral -  Coxsackie; EBV; HIV
Bacterial - pneumonia, TB, staph 
- ABx for at least 4 weeks and drainage of pericardial fluid
Develops from:
􏰀 Direct pulmonary extension
􏰀 Haematogenous spread
􏰀 Myocardial abscess
􏰀 Endocarditis
􏰀 Penetrating injury to chest wall (trauma or surgery)
􏰀 Subdiaphragmatic suppurative lesion
MI/ Dresslers
Drugs - penicillinm, isoniazid 
Other - RA/SLE; Lung tumour, uraemia
96
Q

Investigations of pericarditis

A 
• Bloods: FBC, U+E, LFT, CRP, CK, Troponin I
• Further investigations:
o Virology screen
o Blood cultures
o Antistreptolysin titre
o Rheumatoid factor
o Antinuclear antibodies (ANA) 
o Anti-DNA antibodies
o Tuberculin testing
o Sputum for acid-fast bacilli

Imaging
• Echocardiography (ECHO)
o If pericardial effusion or tamponade is suspected.
o If there is a pericardial effusion, you may see
right ventricle compression as this is compromised first.

• CT / MRI

97
Q

ECG changes in Pericarditis

A

o Stage 1: Saddle shaped ST elevation (Diffuse
concave upward ST elevation, except aVR and V1 (usually
depressed).

o Stage 2: Occurs several days later. ST
segment returns to baseline, followed by T
wave flattening.

o Stage 3: T wave inversion.

o Stage 4: ECG returns to the pre-pericarditis
baseline weeks to months after onset.

98
Q

Treatment of pericarditis

A

If a cause is found, this should be treated!

Bed rest and oral NSAIDs
o High-dose aspirin, indometacin or ibuprofen.
o But NOT post-MI: NSAID associated with
myocardial rupture.
o Corticosteroids have been used when the
disease does not subside rapidly.

Further Treatment:
o Pericardial window
o Pericardiectomy

99
Q

What is a pericardial effusion

A

Abnormal accumulation of fluid in the pericardial cavity.

100
Q

What is Cardiac Tamponade

A

Pericardial effusion causing haemodynamically significant cardiac compression.
􏰀 Pericardial pressure increases inhibiting venous return to the heart.
􏰀 This results in reduced cardiac output, hypotension and shock.

101
Q

Causes of Pericardial effusion/ cardiac tamponade

A

• ‘Acute’
o Trauma
o Iatrogenic (cardiac surgery / catheterisation / anticoagulation)
o Aortic dissection
o Spontaneous bleed (uraemia / thrombocytopenia) o Cardiac rupture post-MI

• ‘Subacute’
o Malignancy
o Idiopathic pericarditis 
o Uraemia
o Infection (including TB) 
o Radiation
102
Q

Presentation of Pericardial effusion/ cardiac tamponade

A

o Cardiac arrest
o Hypotension
o Confusion
o Shock

Slowly developing tamponade
o SOB
o Cough, hiccups, dysphagia

103
Q

Signs of Pericardial effusion/ cardiac tamponade

A

• Beck’s triad: o ↑JVP o ↓BP o Muffled heart sounds
• Tachycardia
• Kussmaul’s sign (JVP ↑ with inspiration)
• Pulsus paradoxus (↓ in palpable pulse and ↓ in sBP on
inspiration)

104
Q

Management of Pericardial effusion/ cardiac tamponade

A 
EMERGENCY 
• Get senior help
• ABC, IV Access and fluids, ECG, Bloods
• USS guided Pericardiocentesis
o Needle inserted at level of Xiphisternum, aim for tip of left scapula, aspirating continuously.

o Send the pericardial fluid for microbiology and
cytology.
• A drain may be left in temporarily to allow sufficient
release of fluid

105
Q

Example of β - Blockers and Action

A

Bisoprolol; Atenolol; Propanolol.

Action: Negatively inotrophic + chronotrophic.

106
Q

SE of β - Blockers

A

GI disturbances; bradycardia; fatigue; cold peripheries; heart failure; hypotension; dizziness; sexual dysfunction; peripheral vasoconstriction; bronchospasm.

107
Q

CI of β - Blockers

A

Asthma; marked bradycardia; heart block; uncontrolled heart failure; PVD; Prinzmetal’s angina; hypotension; cardiogenic shock.

108
Q

Example of Non-dihydropyridines calcium channel blocker and action

A

Verapamil + Diltiazem
􏰀 Negatively inotrophic / chronotrophic but DO NOT
USE IN HEART FAILURE

109
Q

Example of Dihydropyridines calcium channel blocker and action

A

Amlodipine, Felodipine, Nifedipine

􏰀 Dilates peripheral arteries, ↓ after-load, dilates coronary vessels, act on vessels > myocardium

110
Q

SE of calcium channel blocker

A

o Verapamil +Diltiazem: constipation; N+V;
flushing, headache, dizziness; fatigue.
o Dihydropyridines: abdominal pain; nausea;
palpitations, flushing, oedema; headache;
dizziness; sleep disturbances; fatigue.

111
Q

CI of calcium channel blocker

A

o Verapamil + Diltiazem: HF, 2nd or 3rd degree
heart block, cardiogenic shock.
o Dihydropyridines: Unstable angina, significant
AS.

112
Q

Example of nitrates and SE

A

Examples: Isosorbide Mononitrate (PO); GTN infusion (IV); GTN spray (S/L).

Side effects: postural hypotension; tachycardia; throbbing headache; dizziness.
o TOLERANCE

113
Q

CI of nitrates

A

persensitivity to nitrates; hypotensive conditions; hypovolaemia; hypertrophic obstructive cardiomyopathy; AS; MS; cardiac tamponade; constrictive pericarditis; marked anaemia.

114
Q

Action of ACEi

A

Inhibits conversion of angiotensin 1 into angiotensin 2, therefore inhibiting angiotensin 2 having its effects:
o Increasing sympathetic activity.
o Fluid retention by kidney – via Increase in
aldosterone and direct action.
o Arteriolar vasoconstriction.
o Stimulating ADH secretion causing increased
fluid retention.
ACE inhibitors also cause:
o Reversal of left ventricular hypertrophy

115
Q

CI of ACEi

A

hypersensitivity to ACEi (angioedema); renal artery stenosis; pregnancy; aortic stenosis; toxicity.

116
Q

Example of loop diuretic and action

A

Furosemide, Bumetanide.

Action: Blocks Na+/K+/Cl- co-transporter in the apical
membrane of the thick ascending limb of loop of Henle.

117
Q

SE of Loop diuretics

A

Hypokalaemia; metabolic alkalosis; sodium + magnesium depletion; hypovolaemia+ hypotension; deafness; nausea; allergies.

118
Q

Action of Thiazides

A

Inhibits Na+ reabsorption at the beginning of
the distal convoluted tubule. Blocks Na+/Cl- symporter
that is associated with the luminal membrane.

119
Q

CI of thiazides

A

Refractory hypokalaemia; hyponatraemia; hypercalcaemia; symptomatic hyperuricaemia; Addison’s disease.

120
Q

Example and actino of K+ sparing diuretics

A

Act on collecting tubules.

Spironolactone is an aldosterone antagonist.

Amiloride directly inhibiting sodium channels

121
Q

SE of K+ sparing diuretics

A

GI disturbances; impotence;

gynaecomastia; menstrual irregularities; lethargy; headache; confusion; hyperkalaemia; hyponatraemia; hepatotoxicity.

122
Q

Example and action of statins

A

Atorvastatin; Simvastatin.

Lowers cholesterol levels in blood by:
o Blocking liver enzyme hydroxy-methylglutaryl- coenzyme A reductase (HMG-CoA reductase), thereby inhibiting liver synthesis of cholesterol.
o This leads to upregulation of expression of LDL receptors on liver cells causing ↑ absorption of LDL from the circulation.

123
Q

SE of statins

A

myositis; rhabdomyolysis; headache; altered LFTs; paraesthesia; GI effects.

124
Q

CI of statins

A

active liver disease; pregnancy; breast-feeding.

125
Q

Action of aspirin

A

Suppresses production of prostaglandins and thromboxane by irreversibly inactivating the cyclooxygenase (COX) enzyme.
• Irreversibly blocks the formation of thromboxane A2 in platelets, inhibiting platelet aggregation.

126
Q

Action of Clopidogrel

A

Inhibits ADP-induced aggregation through an active metabolite.

127
Q

LMWH v UFH

A

UHF:
o Binds to Antithrombin III (ATIII).
o ATIII is an endogenous inhibitor of coagulation.
o Increases ATIII ability to inhibit factors IXa, Xa,
XIa, XIIa (serine proteases) and thrombin (unfractionated).
o UHF fully reversible with Protamine.
- Need daily plateleys

LMWH:
o Inhibits factor Xa but not thrombin.
o LMWH not fully reversible with Protamine.

128
Q

SE and CI of herparin

A

SE - haemorrhage; UFH (Heparin induced thrombocytopenia)

CI - uncontrolled bleeding / risk of bleeding e.g. peptic ulcer, recent cerebral
haemorrhage; endocarditis.

129
Q

Action of warfarin

A

Inhibits vitamin K dependent clotting factors
(II, VII, IX, X, protein C + S). Does this through inhibiting the reductase enzyme responsible for the regeneration of the active form of vitamin K.

130
Q

SE and CI of warfarin

A

SE - Haemorrhage
CI - peptic ulcer; severe
hypertension; bacterial endocarditis; pregnancy.

131
Q

What to do in Warfarin Overdose and in major bleed

A

INR <6: Decrease / omit Warfarin

INR 6-8: Stop Warfarin. Restart when INR<5

INR >8: If no bleeding stop warfarin + give 0.5- 2.5mg vitamin K if risk of bleeding.

Major bleed: Stop Warfarin. Give prothrombin complex concentrate (Beriplex) contains factors II, VII, IX, X or FFP. Give 5mg vitamin K. Get HELP!

132
Q

Causes of bradycardia

A

DIVISIONS
Drugs - Amiodarone, b-b, CaCB, Digoxin
Inferior MI
Vagal hypertonia (athletes; vasovagal syncope))
Infection (myocarditis; rheumatic; IE)
Sick sinus syndrome (structural damage SAN/AVN etc)
Infiltration (AI/Sarcoid/ haemochromatosis)
O - Low -T3/4; K; Temp
Neuro - ↑ ICP
Septal defect - primum ASD
Surgery/ Catheter

133
Q

name 2 scoring systems used in AF

A

CHAD2VASC - risk of stroke

HASBLED - for major bleeding risk

134
Q

Causes of long QT

A

Toxins (Erthyromycin, quinine, TCA, Anti-histamine)
Ishchaemia
Myocarditis
Electrolytes (low mg,K,Ca and temp)

135
Q

Causes of short QT

A

digoxin (+downsloping); BB, Phenytoin

136
Q

Mx of bradycardia

A
  • Treat underlying cause
  • Atropine IV
  • Pacing
137
Q

MOA; SE and CI of amiodarone

A
  • Transient AVN block
    SE - chest tightness, flushing, headache, dyspnoea
    CI - asthma, 2/3 degree HB
138
Q

Signs and symptoms of AF

A

Sx

  • asymptomatic
  • chest pain
  • palpitations
  • dyspnoea
  • syncope/ fainting
  • fatigue

Signs

  • irregularly irregular pulse
  • signs LVF
139
Q

Continuing therapy for pulmonary oedema

A
  • daily weights
  • Obs QDS
  • DVT prophylaxis
  • Repeat CXR
  • Change to oral furoesmide +/- thiazide
  • if LVEF <40% - ACEi; if <35% - + Bb and spironolactone
  • Biventricular pacing/ cardiac transplant
140
Q

Stable Angina sx, ix and mx

A

Angina induced by effort
- central chest tightness, relieved by rest, may radiate to arm/neck/jaw

Ix
- Bloods; ECG +/- exercise ECG; ECHO; Angiography

Mx

  • Stop smoking; wt loss and increase exercise; healthy diet
  • refer to rapid access chest pain clinic (if not already under cardiology)
  • Aspirin; ACEI; Statins; Anti-hypertensives
  • GTN spray + BB(?+CBB if doesnt contol)
  • if not responding –> PCI/ CABG
141
Q

Causes and Mx of Cardiogenic shock

A

Causes: MI HEART

MI
Hyperkalaemia
Endocarditis
Aortic Dissection
Rhythm disturbance
Tamponade/ tension pneumo/ PE

Mx

  • ABCDE
  • analgesia
  • correct arhythmias, electrolytes
  • CXR, ECHO, ? CT thorax
  • Monitor
  • treat underlying cause
142
Q

Tricuspid Regurg - causes, sx, signs, Ixand mx

A

Causes - RV dilation; rheumatic fever; IE; carcinoid syn

Sx - fatigue; hepatic pain on exertion; ascites/oedema

Signs - raised JVP; RV heave; PSM; pulsatile hepatomegaly; jaundice

Ix - LFTs and ECHO

MX - Treat cause, diuretics/ACEi, valve replacement

IPE (9 decks)

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