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Flashcards in CVS Deck (133):
1

Causes of Hypertension

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

2

Signs of end-organ damage in HTN

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

3

Classification of hypertensive retinopathy

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

4

Investigations for hypertension

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

5

Management for hypertension

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

6

Target BP for hypertensive

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

7

Name and give SE of ACEi
- And name of ARB

Lisinopril , Ramipril
ARB - Canaesartan

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

8

Name and give SE of dihydropyridine calcium channel blocker

Nifedipine

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

9

Name and give SE of Thiazide

Bendroflumethiazide.

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

10

Treatment of
a) malignant hypertension
b) malignant hypertension + encephalopathy

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

11

NYHA Heart Failure Classification

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)

12

Which murmur has increased intensity on inspiration and why

Right - Inspiration ↑ venous blood return to the right
side of the heart.

13

Grading of murmurs

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

14

Causes of Mitral Stenosis

- Rheumatic fever or
chorea
- Old Age and calcification

15

Effects of Mitral Stenosis

High LA pressure

Pulmonary venous hypertension

Pulmonary arterial hypertension

Right ventricular hypertrophy

Tricuspid regurgitation

Right heart failure

16

Signs of MS

- 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

17

Signs of Pulmonary Oedema on CXR

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

18

ECG changes in MS

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

19

Causes of Mitral Regurgitation

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

20

Signs of MR

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

21

Signs of MR on CXR and ECG

CXR - cardiomegaly
ECG - Bifid p wave and LVH

22

Causes of Aortic Stenosis

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

23

Symptoms of AS

Exercise-induced syncope, angina and dyspnoea develop

24

Signs of AS

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

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

25

Findings on CXR and ECG in AS

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)

26

Causes of Aortic Regurgitation

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

27

Pathology of AR

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.

28

Signs of AR

– 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

29

ECG changes in AR

LVH

30

How to calculate a regular and irregular rate on ECG

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.

31

ECG changes in Atrial flutter and why

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

32

What is the normal PR interval

0.12 - 0.2 milliseconds (3-5 small squares)

33

What is 1st degree Heart Block

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

34

What are the types of second degree Heart block

•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

35

Describe 3rd degree Heart Block and the causes

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

36

Describe the criteria is used to measure LVH on an ECG

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

37

How would you assess RVH on on ECG

wave >5mm in Right ventricular leads + RAD

38

How is the QRS affected in BBB

Widened in BBB
WiLLiaM and MaRRoW
o LBBB: WinV1andaMinV6
o RBBB:MinleadV1andaWinleadV6

39

Causes of ST elevation

Acute MI

Pericarditis: Concave and widespread over many leads

40

Causes of ST depression

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

+ Level or Downsloping

41

Features of MI on ECG

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

42

Location of MI and correlating Blood vessels

> 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


43

ECG changes in PE

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!)

44

ECG changes in Hyperkalaemia

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

45

Causes of Heart Failure

Ischaemic heart disease (70%)

Non-Ischaemic Dilated Cardiomyopathy (25%)

Hypertension (5%)

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

46

Pathophysiology of Heart failure

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

47

Causes of LHF

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

48

Symptoms of LHF

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

49

Signs of LHF

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

50

Causes of RHF

LHF

Chronic Lung Disease (Cor pulmonale)

PE or Pulmonary Hypertension

Tricuspid / Pulmonary Valve Disease

51

Symptoms of RHF

Fatigue
Dyspnoea
Anorexia / Nausea

52

Signs of RHF

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

53

Management of HF

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

54

Pathophysiology of atherosclerosis and in ACS

• 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

55

Risk factors for ACS

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

56

Initial management of ACS

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)

57

Investigations for ACS

- ECG
- Bloods - FBC, LFT, UE, Glucose, Lipids, CK, Troponin I
- Portable CXR

58

Presentation of STEMI

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

ECG findings in STEMI

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

60

Management of STEMI

Thrombolysis
or
PCI (Percutaneous Coronary Intervention)

61

Indications for Thrombolysis and PCI in STEMI

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

Contraindications for Thrombolysis

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

Complications of thrombolysis

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

64

Complications of STEMI

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

65

Drugs to discharge with pt after STEMI and risk prevention

• 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

Presentation of NSTEMI and unstable angina

• Rest angina / Increasing angina
• New-onset severe angina

67

ECG changes for NSTEMI and unstable angina

• T wave inversion
• ST depression

68

How to differentiate between NSTEMI and unstable angina

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

Management of NSTEMI/UA

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

Pathophysiology of LV failure

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

Presentation of LV failure

• 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
o Fine crepitations bilaterally
o Gallop rhythm: S-3

72

Causes of LVF

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

73

Management of LVF

• 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

Investigations for LVF

• ECG: Arrhythmia, tachycardia, MI, LVH
• Bloods: FBC, U&E, CK, Troponin I
• CXR
• ABG
• Echo

75

Mechanisms of tachycardias

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

Precipitating factors for VT

• Metabolic
• IHD
• Cocaine
• Cardiomyopathy
• MI

77

Precipitating factors for SVT

• IHD
• Thyrotoxicosis
• Caffeine
• Alcohol
• Smoking

78

Precipitating factors for AF

• IHD
• Thyrotoxicosis
• Caffeine
• Alcohol
• Smoking
• Mitral valve disease
• Hypertension
• Lung disease
• Post op
• Pericardial disease
• Cardiomyopathy

79

Types of SVT (narrow)

• 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

Management of regular SVT

• ABC+O2+IV access
• Vagal Manoeuvres
• Adenosine 6mg rapid IV bolus; +12 +12 - monitor ECG continuously
• SEEK HELP
• Antiarrhythmic
• DC cardioversion if haemodynamically unstable

81

Management of AF

Control rate with b-blockers or digoxin IV

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

82

Types of broad complex tachycardias

oVT
- Including Torsades de pointes

o SVT with BBB

83

Differences between SVT and VT

• 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

Management of VT

ABC (if pulseless = arrest protocol)

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

Adverse signs (↓ BP, HF, ↓ GCS; Chest pain, ↑HR)
Sedation
DC cardioversion Amiodarone / Lidocaine

85

Causative organisms of infective endocarditis

Streptococcus viridians

S.Aurues (IVDU)

86

Pathophysiology of IE

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

Consequences of IE

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

88

Clinical presentation of IE

• HEART MURMUR + FEVER

1. Systemic infection
o Malaise
o Pyrexia
o Myalgia
o Weight loss
o Fatigue

2. 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

DUKES CRITERIA FOR IE

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

2 Major OR 1 Major, 3 Minor OR 5 Minor

90

Management of IE

ABC
Involve microbiologist and cardiologist
Benzylpenicillin and Gentamycin 4 weeks IV

91

Investigations for IE

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

92

Risk factors for IE

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

93

Presentation of acute pericarditis

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

Pathophysiology of pericarditis

• 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

Causes of Pericarditis

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

Investigations of pericarditis

• 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

ECG changes in Pericarditis

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

Treatment of pericarditis


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

What is a pericardial effusion

Abnormal accumulation of fluid in the pericardial cavity.

100

What is Cardiac Tamponade

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

Aetiology of Pericardial effusion/ cardiac tamponade

• ‘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

Presentation of Pericardial effusion/ cardiac tamponade

o Cardiac arrest
o Hypotension
o Confusion
o Shock

Slowly developing tamponade
o SOB
o Cough, hiccups, dysphagia

103

Signs of Pericardial effusion/ cardiac tamponade

• 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 systolic BP on
inspiration)

104

Management of Pericardial effusion/ cardiac tamponade

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

Example of β - Blockers and Action

Bisoprolol; Atenolol; Propanolol.

Action: Negatively inotrophic & chronotrophic.

106

SE of β - Blockers

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

107

CI of β - Blockers

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

108

Example of Non-dihydropyridines calcium channel blocker and action

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

109

Example of Dihydropyridines calcium channel blocker and action

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

110

SE of calcium channel blocker

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

111

CI of calcium channel blocker

o Verapamil & Diltiazem: HF, 2nd or 3rd degree
heart block, cardiogenic shock.

o Dihydropyridines: Unstable angina, significant
AS.

112

Example of nitrates and SE

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

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

113

CI of nitrates

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

114

Action of ACEi

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

CI of ACEi

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

116

Example of loop diuretic and action

Furosemide, Bumetanide.

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

117

SE of Loop diuretics

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

118

Action of Thiazides

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

119

CI of thiazides

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

120

Example and actino of K+ sparing diuretics

Act on collecting tubules.

Spironolactone is an aldosterone antagonist.

Amiloride directly inhibiting sodium channels

121

SE of K+ sparing diuretics

GI disturbances; impotence;
gynaecomastia; menstrual irregularities; lethargy; headache; confusion; hyperkalaemia; hyponatraemia; hepatotoxicity.

122

Example and action of statins

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

SE of statins

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

124

CI of statins

active liver disease; pregnancy; breast-feeding.

125

Action of aspirin

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

Action of Clopidogrel

Inhibits ADP-induced aggregation through an active metabolite.

127

LMWH v UFH

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

SE and CI of herparin

SE - haemorrhage; UFH (Heparin induced thrombocytopenia)

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

129

Action of warfarin

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

SE and CI of warfarin

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

131

What to do in Warfarin Overdose and in major bleed

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

Causes of bradycardia

DIVISIONS
Drugs - Amiodarone, b-b, CaCB, Digoxin
Infarction
Vagal hypertonia (athletes)
Infection (myocarditis; rheumatic; IE)
Sick sinus syndrome
Infiltration (AI/Sarcoid)
O - Low T3/4; K; Temp
Neuro - ↑ ICP
Septal defect
Surgery

133

name 2 scoring systems used in AF

CHAD2VASC and HASBLED