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
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
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
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% )
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
6
Q
Target BP for hypertensive
A
<140/90
<130/80 if DM
<150/90 if >80
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.
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
9
Q
Name and give SE of Thiazide
A
Bendroflumethiazide.
SE–> postural hypotension; hypokalaemia;
hypomagnesaemia; hyponatraemia; hypercalcaemia; metabolic alkalosis; hyperuricaemia; impotence; hyperglycaemia.
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
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)
12
Q
Which murmur has increased intensity on inspiration and why
A
Right - Inspiration ↑ venous blood return to the right
side of the heart.
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
14
Q
Causes of Mitral Stenosis
A
- Rheumatic fever or
chorea - Old Age and calcification
15
Q
Effects of Mitral Stenosis
A
High LA pressure ↓ Pulmonary venous hypertension ↓ Pulmonary arterial hypertension ↓ Right ventricular hypertrophy ↓ Tricuspid regurgitation ↓ Right heart failure
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
17
Q
Signs of Pulmonary Oedema on CXR
A
Airspace shadowing B lines (Kerley Cardiomegaly Diversion to upper lobes Effusion
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
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
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
21
Q
Signs of MR on CXR and ECG
A
CXR - cardiomegaly
ECG - Bifid p wave and LVH
22
Q
Causes of Aortic Stenosis
A
Bicuspid Aortic Valve (under 65)
Age related Calcification (over 65)
Rheumatic Fever
23
Q
Symptoms of AS
A
Exercise-induced syncope, angina and dyspnoea develop
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
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 and causes
P-R interval prolonged by constant amount (> 5 small squares)
causes
- AVN disease; acute MI; myocarditis; CCB; BB
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
+/- LAD
37
How would you assess RVH on on ECG
R wave >5mm in Right ventricular leads + RAD
| (R1S6) +/- RAD
38
How is the QRS affected in BBB and causes
```
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
```
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
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)
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
Definitive 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 and tachypnoea
o Fine crepitations bilaterally
o Gallop rhythm: S-3
o Pulsus alternans
```
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
```
Pericardial and lung disease
IHD
Regurg/stenosis -mitral
Anaemia, Alcohol, Age
Thyrotoxicosis
Elevated BP
Smoking, surgery
```
Caffeine and 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 --> 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
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)
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
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
Fever
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
Causes 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 sBP 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.
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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
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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!
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Causes of bradycardia
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
name 2 scoring systems used in AF
CHAD2VASC - risk of stroke
HASBLED - for major bleeding risk
134
Causes of long QT
Toxins (Erthyromycin, quinine, TCA, Anti-histamine)
Ishchaemia
Myocarditis
Electrolytes (low mg,K,Ca and temp)
135
Causes of short QT
digoxin (+downsloping); BB, Phenytoin
136
Mx of bradycardia
- Treat underlying cause
- Atropine IV
- Pacing
137
MOA; SE and CI of amiodarone
- Transient AVN block
SE - chest tightness, flushing, headache, dyspnoea
CI - asthma, 2/3 degree HB
138
Signs and symptoms of AF
Sx
- asymptomatic
- chest pain
- palpitations
- dyspnoea
- syncope/ fainting
- fatigue
Signs
- irregularly irregular pulse
- signs LVF
139
Continuing therapy for pulmonary oedema
- 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
Stable Angina sx, ix and mx
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
Causes and Mx of Cardiogenic shock
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
Tricuspid Regurg - causes, sx, signs, Ixand mx
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
