cardiology Flashcards
1
Q
cardiac electrophysiology
Main Leads?
A
I
II
III
2
Q
other leads
A
AVL
AVR
AVF
3
Q
electrical conduction pathway
A
SA node
-> AV node
-> bundle of His
-> Left and right bundle
-> Purkinje fibres.
4
Q
inferior leads + corresponding vessel ?
A
II, III, AVF
RCA
The RCA supplies the AV node therefore patient will have 1st degree heart block and is in the inferior leads.
Also presents with third degree heart block in an MI.
5
Q
anterolateral leads + vessel ?
A
I, aVL, V5 + V6
left circumflex or LAD
6
Q
anteroseptal leads + vessel ?
A
V1-V4
LAD vessel
7
Q
ECG analysis components
A
rate
rhythm
axis
P waves
QRS
PR interval
QT
ST segment
T waves
8
Q
rate
A
300/no of large squares OR add number of QRS and x 6.
9
Q
rhythm
A
look for P waves followed by QRS complexes.
- AF: no discernable P waves; irregularly irregular QRS
- Atrial Flutter: saw-toothed baseline
- Nodal rhythm: regular QRS but no P Waves.
10
Q
causes of a RAD (>+90)
A
- anterolateral MI (busting this shifts activity to right)
- RVH, PE
- L post hemiblock WPW
- ASD secundum
11
Q
causes of a LAD
A
- inferior MI (busting this shifts activity to the left)
- LVH
- L ant. Hemiblock WPW
- ASD primum
12
Q
P waves
A
absent: AF, SAN block, nodal rhythm
dissociated: complete heart block
P mitrale: bifid P waves = LA hypertrophy: HTN, AS, MR, MS.
P pulmonale:
peaked: RA hypertrophy from pulmonary HTN, COPD.
13
Q
QRS complex
A
Width (~120ms / 3 small boxes)
wide: ventricular initiation, conduction defect, WPW
- pathological Q wave (>1mm wide and >2 mm deep)
- full thickness MI (associated with previous MI) - Hole in conduction of myocardium.
- RVH: Dominant R wave in V1 + deep S wave in V6.
- LVH: R wave in V5/V6 + S wave in V1 >35mm.
14
Q
PR Interval
A
(120-200ms)
start of P wave to start of QRS.
- prolonged: ♡ block
- short: WPW, accessory conduction, nodal rhythm, HOCM
- depressed: pericarditis
15
Q
QTc
A
(380-420 ms)
start of QRS to end of T wave
long
- macrolide
- anti-arrhythmics (quinidine, amiodarone)
- TCAs
- anti-histamines
- citalopram
- inherited (Romano-Ward)
- ischaemia
- myocarditis
- mitral valve prolapse
- electrolytes: decreased magnesium, decreased potassium, decreased calcium, decreased temp.
short (<380)
- digoxin
- betablockers
- phenytoin
- hypercalcaemia (stones, bones, groans, moans)
16
Q
ST segment
A
Elevated (limbs: >1mm, chest >2mm)
- Acute MI
- Prinzmetal’s angina
- Pericarditis: saddle-shaped
- Aneurysm: ventricular
Depressed (>0.5mm)
- Ischaemia: flat
- Digoxin: down-sloping
17
Q
T waves
A
Normally inverted in aVR and V1 (+ V2-V3) in blacks.
- Abnormal if inverted in I, II, V4-6.
- Suggests: Strain, ischaemia, ventricular hypertrophy, BBB, Digoxin.
- Peaked in increased K+
- flattened in decreased K+
18
Q
Extra waves in ECG?
A
U waves
- Occurs after T waves
- Seen in decreased K+
J waves/Osborne Waves - Occur between QRS and ST segment - Causes Hypothermia <32 C SAH Hypercalcaemia
19
Q
Conduction Defects - Heart Blocks.
1st Degree?
A
PR > 200ms. (5 little poke boxes)
20
Q
2nd degree heart block - Wenckebach/Mobitz I?
A
- Progressive lengthening of PR interval
- One non-conducted P wave
- Next conducted beat has shorter PR interval
21
Q
2nd Degree heart block - Mobitz II
A
Constant PR
Occasional non-conducted P wave
- Often wide QRS
- Block is usually in bundle branches of Purkinje fibres.
22
Q
2nd Degree Heart Block - 2:1 Block
A
Two P waves per QRS
Normal consistent PR intervals.
23
Q
3rd Degree Heart Block
A
P waves and QRS @ different rates
- Dissociation
Abnormally shaped QRS
- Ventricular origin (40bpm)
24
Q
Right BBB ECG findings?
A
MaRRoW
Wide QRS
RSR pattern in V1.
qRs in V6.
25
Right BBB Aetiology?
```
Infarct - inferior MI
Normal Variant
Congenital - ASD, VSD, Fallot's
Hypertrophy - RVH (PE, Cor Pulmonale).
PE
```
26
Left BBB ECG findings
WiLLiaM
Wide QRS with Notched at top
T wave inversion in Lateral leads.
27
Left BBB aetiology?
Fibrosis
LVH - AS, HTN
Infarct - Inferior MI
Coronary HD
28
Bifascicular Block
RBBB + Left anterior fascicular block (RBBB + left anterior hemiblock)
29
Trifascicular block
RBBB + LAFB + 1st Degree AV block.
30
Escape Rhythms: appear late (after antipated beat)
| - Atrial Escape
SAN fails to depolarise
Abnormal P wave
Normal QRS
60-80bpm
31
Junctional Escape?
Usually no P waves (occasionally after QRS)
Normal QRS
40-60bpm.
32
Ventricular Escape
Usually result of complete AV Block therefore regular P waves seen.
May be SAN Failure --> No P waves.
Wide QRS
20bpm
33
Extrasystoles: appear early (before anticipated beat)
- Atrial Extrasystole
Abnormal P wave
| Normal QRS
34
Nodal Extrasystole
P wave buried in QRS or sometimes immediately before/after QRS. May be negative.
Normal QRS
35
Ventricular extrasystole
No P waves
| Wide QRS and abnormal T waves.
36
Narrow Complex Tachycardia Types?
```
AV Nodal Re-entrant tachycardia
AVRT
Atrial Tachycardia
Atrial Flutter
Atrial Fibrillation
```
37
AV Nodal Re-entrant Tachycardia?
P wave absent or immediately before/after QRS. Normal QRS
Episodic tachycardia with abrupt onset and termination; can be associated with symptoms of chest discomfort, dyspnoea, dizziness, or anxiety.
Sensation of regular rapid pounding in the neck is suggestive of AV node re-tenrty.
38
AVRT? (part of WPW)
P waves usually visible between QRS complexes. QRS may be narrow or wide. Accessory conduction bundle.
May have suggestions of secondary cardiomyopathy - S3 gallop, RV heave, laterally displaced point of maximal impulse.
ECG: Delta wave.
WPW = Congenital accessory conduction pathways between atria and ventricles leading to AVRT. Can lead to LAD if right sided accessory pathway + vice versa.
Type A = left sided pathway with dominant R in V1.
- Medical management = sotalol (avoid if AF).
- Definitive management = radiofrequency ablation of accessory pathway.
39
Atrial Tachycardia?
- Abnormally shaped P waves.
- Normal QRS complexes
- Rate > 150bpm
- May be associated with AV block.
40
Atrial Flutter
'Saw-toothed' baseline as atria contract @ 300 bpm.
```
AVN can't conducted >200.
therefore AV block occurs.
- 2:1 (150), 3:1 (100), 4:1 (75).
Normal QRS.
- Flutter waves may be visible following carotid sinus massage or adenosine
```
41
Atrial Fibrillation
No P waves - irregular line
| Irregularly irregular QRS.
42
Examples of Broad Complex Tachycardias?
VT
Torsades
VF
43
What is ventricular tachycardia?
No P waves
Regular, wide QRS
No T waves
Non-sustained VT is an ectopic ventricular rhythm with wide QRS complex, rate faster than 120 bpm, lasting for 3 beats and spontaneously resolving.
44
Torsades
Torsades de pointes (twisting of the points) is a form of polymorphic VT associated with long QT interval. It may deteriorate into VF.
Causes of Long QT (normal QT = 430ms in males and 450ms in males)
- Congenital (Romano-Ward)
Drugs
- Antiarrhythmics: amiodarone, sotalol, class 1a
- Tricyclic antidepressants
- Antipsychotics
- Chloroquine
- Terfenadine
- Erythromycin
- Myocarditis
Electrolyte abnormalities
- hypocalcaemia,
- hypokalaemia,
- hypomagnesaemia
- Hypothermia
- Sub Haemorrhage
Management with MgSO4 IV. if Torsades
```
Otherwise management = Avoid drugs that prolong QT or other precipitants.
Beta blockers (sotalol may exacerbate QT syndrome).
```
45
VF
Shapeless, rapid oscillations and no organised complexes.
46
Ventricular tachycardia vs SVT with bundle branch block?
VT more likely if
- Hx - recent infarction
- Atrioventricular dissociation
- Broad QRS complexes (>140ms)
- Concordant QRS direction in V1-V6
- Fusion and capture beats.
47
P wave abnormalities?
P mitrale
| P pulmonale
48
P pulmonale
Peaked P wave.
Due to RAH
(Pulmonary HTN, Tricuspid stenosis)
49
P mitrale
Broad, bifid P waves
| - LAH (Mitral stenosis)
50
QRS Abnormalities?
RVH
LVH
Narrow
Broad
51
Features of RVH?
```
Tall R wave in V1 (Right for R1)
Deep S wave in V6
RAD
Normal QRS width
May be T wave inversion in V1-V3
```
- Aetiology from Cor pulmonale
52
Features of LVH?
- S wave in V1 and
- R wave in V6 > 35mm
- May be LAD
- May be T wave inversion in II, aVL, V5, V6.
```
- Aetiology?
HTN
AS
COA
H(o)CM
```
53
Other ECG Features:
| WPW
Accessory conducting bundle Short PR interval
Slurred upstroke of QRS called a Delta wave (V3/V4)
Can establish re-entrant circuit --> SVT (antidromic AVRT)
AF + WPW --> irregularly irregular broad QRS complex.
54
Brugada Syndrome
Brugada syndrome is a form of inherited cardiovascular disease with may present with sudden cardiac death.
Presents with a RBBB block.
Coved ST elevation in V1-V3
MAnagement: implantable cardioverter-defibrillator
55
Digoxin signs on ECG?
Reverse Tick Sign
- Down-sloping ST depression
- T wave inversion
56
PE Signs on ECG?
SI QIII TIII (rare).
- Deep S wave in Lead 1 (RAD)
- Pathological Q wave in III inverted T wave in III. (a hole in myocardium)
- T wave inversion in III.
Right ventricular strain
- RAD (S wave in I)
- Dominant R wave and T wave inversion in V1-V3
57
Hyperkalaemia signs on ECG
Tall Tented T waves
Widened QRS
Absent P waves
58
Hypokalaemia signs on ECG?
In Hypokalaemia U have no Pot and no T, but a long PR and a long QT.
```
Small T waves
ST Depression
Prolonged QT interval >600ms
Prominent U wave
Sine wave present
```
Due to furosemide therapy?
59
Causes of Bradycardias (<60bpm)
DIVISIONS
- Drugs (ABCD) = Antiarrhythmias (Amiodarone), B-blockers
Ca-channel blockers (verapamil)
Digoxin
- Ishaemia/Infarction
Inferior MI
- Vagal Hypertonia
Athletes, Vasovagal syncope, Carotid sinus syndrome
- Infection
Viral myocarditis
Rheumatic fever
Infective endocarditis
- Sick sinus syndrome
Structural damage or fibrosis of SAN, AVN or conducting tissue.
PC - SVT alternating with either sinus f ± arrest or SA/AV block.
Rx; bradyarrhythmia: pace
Tachyarrhythmias: amiodarone.
```
- Infiltration: restrictive/dilated cardiomyopathy.
Autoimmune
Sarcoid
Haemochromatosis
Amyloid
Muscular dystrophy
```
- O
Hypothyroidism
Hypokalaemia
Hypothermia
- Neuro: increased ICP
- Septal defects: primum ASD
- Surgery or catheterisation
60
Classification of bradycardia?
- Sinus Bradycardia
- 1st degree heart block: PR >200ms
- Second degree heart block
Wenkebach/Mobitz I
Mobitz II
- Complete Heart block
Junctional: narrow QRS @ 50bpm
Ventricular: broad QRS @ 40bpm
Complete = Syncope, heart failure, bradycardia, wide pulse pressure, JVP: cannon waves.
Bizarre wide inverted T waves seen in Stokes-Adams attack.
(Syncope due to bradycardia)
61
Management of Bradycardia?
If asymptomatic and rate >40: no management needed.
Urgent/rate <40bpm (hemodynamically unstable, pale, sweating cold), syncope, heart failure MI.
- Medical
Atropine 0.6-1.2g (max 3g) IV
Isoprenaline IVI. Can give up to 6 doses.
Then use
- Pacing: External
If haemodynamically stable
- Look for MI
- Check TSH/infection
- Check medications
Elective
- Permanent Pacing
:Mobitz II, Complete AV block, Sick Sinus, AF, Drug-resistant tachyarrhythmias
First degree heart block
- PR >0.2. Asympomatic doesnt need treatment
Second degree
- Type 1 Mobitz Wenckebach - progressive prolongation of PR until dropped beat.
- Type 2 - PR interval constant bu P wave is not followed by QRS.
62
Narrow Complex Tachycardias = SVT. Definition?
Rate >100bpm, QRS width <120ms.
63
Differential for Narrow complex tachy/SVT?
- Sinus Tachycardia
- Atrial (AF, Atrial Flutter, Atrial Tachy)
- AVRT
- AVNRT
64
Principles of management of narrow complex SVT?
- If patient is compromised --> sedate + DC cardioversion
= Shock, syncope, myocardial ischaemia, heart failure. = 3 shocks.
- Otherwise ID rhythm and Rx according (if irregular rhythm = AF = Different Rx)
- Vagal manoeuvres (carotid sinus massage, valsalva (supine + exhale forcefully against a closed glottis after normal inspiratory effort) transiently increased AV block and may unmask underlying atrial rhythm.
- If manoeuvres unsuccessful, give adenosine while recording rhythm strip 6mg, then repeat again 12mg, then again 12 mg.
Half-life of adenosine is 10s.
Contraindicated in asthmatics - verapamil
- -> Transient AV block, unmasking atrial rhythm
- -> Cardioverts AVNRT/AVRT to sinus rhythm
65
Adult Tachycardia with pulse alogrithm?
- Assess with ABCDE
- Give oxygen
- Monitor ECG, BP, SpO2, record ECG
- Treat reversible causes
If patient is unstable/MI/shock --> DC shock. Then consider amiodarone 300mg IV over 10-20 mins + repeat shock.
If stable and QRS narrow, is rhythm regular?
Yes - Use vagal manoeuvres, then 6mg adenosine IV bolus if unsucessful, give 12mg, then a further 12mg, continuous ECG monitoring. Consider lidocaine but use with caution in severe left ventricular impairment. Can also use procainamide.
No - Irregular narrow complex tachy - AF - Control rate with B-blocker, consider digoxin/amiodarone.
if sinus rhythm restored probs Re-entry paroxysmal SVT.
If not restored - Possible atrial flutter - Control rate with B-blocker + Seek expert help.
66
MOA of Adenosine?
MOA: temporary AVN block
SEs: Transient chest tightness, dyspnoea, flushing, headache, bronchospasm
Relative CIs: asthma, 2nd/3rd degree heart block.
Interactions
- fx of drug increased by dipyridimole
- fx decreased by theophylline.
Adenosine half-life is less than 10 sec, central route or large-calibre vein needed.
Insert large-bore 16G cannula.
Patients with SVT are treated with IV Adenosine
67
Prophylaxis of Narrow Complex Tachy?
1st line: B-B
- AVRT: flecainide
- AVNRT: verapamil
68
If AF treat as AF?
Control rate with B-blockers (metoprolol) or digoxin
- If onset <48hrs cardioversion with amiodarone or DC shock
- Consider anticoagulation with heparin and or warfarin.
69
Avoid adenosine, CCB, B-blocker in which patients?
- AF/fduke with WPW or Hx of WPW. --> VF.
| - Use Amiodarone or flecainide.
70
Broad Complex Tachycardia definition?
Definition: Rate >100bpm, QRS width >120ms.
71
Differential for Broad Complex Tachycardia?
VT
Torsades de Pointes
SVT with BBB
VT can be monomorphic - caused by MI
Polymorphic: TdP.
72
Causes of a VT?
Most important cause - Hypokalaemia
Then Hypomagnesaemia
I'M QVICK
- Infarction (esp with ventricular aneurysm)
- Myocarditis
- QT interval increased
- Valve abnormality: mitral prolapse, AS
- Iatrogenic: Digoxin, antiarrhythmics, catheter
- Cardiomyopathy (dilated)
- Potassium decreased, Mg decreased, Oxygen decreased, acidosis
73
Management of a Broad Complex Tachycardia?
- Check the pulse? If no pulse start CPR (30:2)
- Then get O2 and IV Access
- Check for adverse signs (BP <90, HF, Chest Pain, decreased consciousness, HR >150)
- If there are adverse signs
- Must consider cardioversion!
(sedation --> synchronised cardioversion:
1. 200
2. 300
3. 360
Then give Amiodarone (300mg over 20-60m, then 900mg over next 23hr. Give adrenaline at the same time. at the 3rd shock. Then every 3-5 mins.
If no adverse signs
- Correct electrolyte problems
- Decreased K?: max 60mM KCL @ 20mmol/h
- Decreased Mg: 4ml 50% MgSO4 in 30mins
```
Then assess the rhythm
- Regular (ie VT)
Amiodarone
or lignocaine 50mg over 2mins
- Irregular Dx is usually:
AF with BBB
Pre-excited AF: flec/amio
Torsades de pointes: MgSO4 2g IV over 10mins
```
- Failure - Synchronised Cardioversion
If in Asystole/PEA: give adrenaline 1mg. Treat with 2 mins of CPR.
74
What is the pathology behind atrial fibrillation?
LA Loses refractoriness before the end of atrial systole -->
recurrent, uncoordinated contractions @300-600bpm. Promotes atrial re-entry.
- Atrial contraction responsible for 25% of Cardiac output, therefore often triggers heart failure.
- General guide - offer rate control as first-line for AF except in those with reversible causes of AF, though with HF and AF, New onset AF.
75
Causes of AF?
Common
- IHD
- Rheumatic Heart Disease
- Thyrotoxicosis
- HTN
Others
- Alcohol
- Pneumonia
- PE
- Post-op
- Hypokalaemia
- RA
76
Symptoms of AF?
- Asymptomatic
- Chest pain
- Palpitations
- Dyspnoea
- Faintness
77
Signs of AF?
- Irregularly irregular pulse
- Pulse deficit: difference between pulse and HS
Fast AF --> Loss of diastolic filling --> no palpable pulse
- Signs of LVF
78
Investigations for Atrial Fibrillation?
- ECG
- Holter Monitor - records ECG for 24,48,72hrs.
- If this doesn't work can use an external loop recorder
- FBC, U+E, TFTs, Trop
- Consider TTE: structural abnormalities
79
- Management of acute onset AF (<48hrs)
Patient's symptoms are from rapid ventricular response, therefore dramatic improvement when ventricular rate is slowed.
1) Aim to prevent systemic embolisation
2) choose rate or rhythm
- Haemo unstable --> Emergency cardioversion. IV Amiodarone 2nd line.
- Treat underlying cause.
When stable
- 1) Control Ventricular Rate
1st line - BB or CCB (Bisoprolol, Dilitiazem or verapamil or metoprolol). (slow AVN conduction and reduce rate).
2nd line - Digoxin or amiodarone.
-2) Embolisation prevention with antithrombolitic therapy - anticoagulate with LMWH or DOAC - dabigatran/apixaban
-3) Cardioversion: only if acute AF <48hrs
Only attempted once patient is anticoagulated with INR of 2-3 for 3-4 weeks following a repeat TOE to confirm left atrial thrombus.
Electrical cardioversion or pharmacological
1st: Flecainide (if no structural heart disease) - 200-300mg
2nd: Amiodarone -150mg IV over 10 mins, 1mg/min infusion for 6hrs. If structural heart disease present.
Long-term anticoagulation not needed if sinus restored no RFs (0 CHADSVAS) + low recurrence risk.
80
What is paroxysmal AF?
- Self-limiting, <7 days, recurs.
- Anticoagulate: use CHADSVAS
- Management: pill in pocket 'Flecainide, propafenone'
- Prevention: B-Blocker, Sotalol (rhythm control) , amiodarone, or CCB (diltiazem, verapamil).
81
Persistent AF definition?
>7 days, may recur even after cardioversion.
82
Management of AF - when to try rhythm control first line? When is it rate control
Try rhythm control first-line if
- Symptomatic or CCF
- Younger (<65)
- Presenting first time with lone AF
- Secondary to treated precipitant. Has a reversible cause.
Rate control favour
- Older than 65
- History of IHD
83
Management of persistent AF - Rhythm control
TTE first: structural abnormalities
- Anticoagulate with warfarin for >3weeks
- Pre-Rx >4 weeks with sotalol or amiodarone if increased risk of failure
- Electrical or pharmacological cardioversion.
- >4 weeks anticoagulation afterwards (target INR 2.5)
Maintenance antiarrhythmic
- Not needed if successfully treated precipitant
- 1st line - B-Blocker (bisoprolol, metoprolol)
- 2nd line: amiodarone
Other options for rhythm control
- Radiofrequency ablation of AV node
- Maze procedure
- Pacing
Rate control (target <90)
- 1st line: B-Blocker or rate limiting CCB (not both)
- 2nd line: add digoxin (don;t use as monotherapy)
- 3rd line: consider amiodarone
84
What is the management of Permanent AF?
- Failed cardioversion/unlikely to succeed
- AF > 1yr, valve disease, poor LV function
- Patient doesnt want cardioversion
- -> Rate control
85
Assessment of stroke in AF?
CHA2-DS2-VAS score determines the necessity of anticoagulation in AF?
Do remember that if a patient with AF has a stroke or TIA - anticoagulant of choice should be warfarin or direct thrombin or factor Xa inhibitor such as Apixaban. Most times it is rivaroxaban
A patient with an acute stroke should have anticoagulation started 2 weeks after the event. This is due to the haemorrhagic transformation.
They should then be on lifelong anticoagulation to prevent risk of stroke.
86
Algorithm for AF?
Assess haemodynamic stability + need for emergent cardioversion .
Then evaluation?
Cardioversion? --> Yes or No depending on haemodynamic stability. If AF <48hr cardiovert, if unknown, anticoagulate for 4 weeks before DC current. Pre-cardioversion anticoag not required if transoesophageal echo shows no thrombus in left atrial.
Rate control --> use beta blockers or CCB as fast line (<80bpm). Consider digoxin or diltiazem
Anticoagulation - Use CHAD2DS2-VASc score and risk of bleeding with HAS-BLED score
- >2 is anticoagulate.
If anticoagulating - Consider Warfarin, or DOACs (Dabigatran, Rivaroxaban, Apixaban).
If no - offer no treatment (previously offered aspirin)
87
What does CHA2-DS2-VAS Score stand for?
```
CCF
HTN
Age >75 (2 points)
DM
Stroke or TIA (2 points)
```
VAS
- Vascular
- Age (65-75)
- Sex: female
Warfarin CI in AF (Bleeding diathesis, decreased platelets, BP >160/90, poor compliance.
Dabigatran may be cost-effective alternative.
0: aspirin 300mg
> or equal 1: Warfarin (target INR = 2-3)
88
What is the HAS-BLED score?
Likelihood of haemorrhage and anticoagulation bleeding risk.
89
What does HAS-BLED stand for?
```
HTN
Abnormal Renal Function + liver Function
Stroke
Bleeding
Labile INR
Elderly (Older than 65)
Drugs + alcohol.
```
>3 or more indicates patient has a high likelihood of haemorrhage
90
Acute Coronary Syndrome definition?
ACS = Unstable angina + evolving MI
Divided into
- ST Elevation or New Onset LBBB (STEMI)
- NSTEMI (myocardial damage)
- Unstable angina (no presence of myocardial damage)
91
Epidemiology of ACS?
Incidence 5/1000 for STEMI
92
Pathophysiology of ACS?
Plaque rupture, thrombosis and inflammation.
| Rarely due to coronary spasm
93
Risk factors of ACS? Modifiable
```
HTN
DM
Smoking
Increased cholesterol
Obesity
```
94
Risk factors for ACS? Non-modifiable?
Age
Male
FH (MI <55yrs)
95
Symptoms of ACS?
- Acute central/left chest pain > 20mins
- Radiates to left jaw or arm
- Nausea
- Sweating
- Dyspnoea
- Palpitations
Can also get silent MIs in elderly/diabetics
- Syncope
- Delirium
- Post-op oliguria/hypotension
Patient presenting with chest pain
- Give GTN, Aspirin and do ECG.
Refer patient with current chest pain or chest pain in last 12 hrs with abnormal ECG (emergency).
Chest pain 12-72hrs ago, refer to hospital for same day assessment.
chest pain > 72 hours ago: perform full assessment with ECG and troponin measurement before deciding upon further action
96
Signs of ACS?
- Anxiety
- Pallor swearing
- Pulse tachy/brady
- BP Hyper/hypo
- 4th heart sound
- Signs of LVF (basal creps, increased JVP, 3rd HS)
- PSM: Papillary muscle dysfunction/rupture (MR)
97
Differentials for ACS?
- Angina
- Peri/endo/myocarditis
- Dissection
- PE, pneumothorax, pneumonia
- Costochondritis
- GI e.g GORD, spasm
- Anxiety
98
Investigations ECG for STEMI?
ECG STEMI sequence
- Normal
- ST Elevation + hyperacute (tall) T waves (often first sign)
- Q waves, full-thickness infarct
- Normalisation of ST segment
- T wave inversion
- New onset LBBB also = STEMI
New ST elevation at the J point in two contiguous leads with cut off points: >0.2mV in men or >=0.15mV in women in leads V2-3.
ST elevation of >2mm in 2 or more anterior leads
ST elevation of greater than 1mm in greater than 2 consecutive inferior leads (II, III, aVF, avL).
99
Investigations ECG NSTEMI?
- ST depression
- T wave inversion
- Deep arrowhead T wave inversion in the anterior leads is a sign of Wellen's Syndrome.
Trop is raised at this stage + no ischaemic damage yet.
100
What do no Q waves mean?
A subendocardial infarct (below the endocardium)
101
Inferior view, RCA vessel? Which leads?
II, III, AVF
102
Anterolateral view, LCx vessel? Which leads?
I, aVL, V4-V6
103
Anteroseptal view, LAD vessel? Which leads?
V2-V4
104
Anterior view LMS?
V2-V6
105
Posterior view, RCA?
V1,2,3 reciprocal.
Changes to see are
- ST depression
- Tall, broad R-waves
- Upright T-wave
106
Bloods on ACS?
```
Troponin T/1
- Myofibrillar protein linking actin and myosin
- Elevated from 3-12hr
therefore need 12hr trop to exclude MI
- Peak at 24hrs
- Baseline from 5-14 d
FBC, U+E, glucose, lipids, clotting
```
Creatinine Kinase remained elevated for 3-4 days.
Troponin remains elevated for 10days. CK-MB can the be used to find a re-infarction of 4-10 days.
107
Investigations - Chest X-ray ACS
Cardiomegaly
Pulmonary Oedema
Widened mediastinum: aortic rupture.
Don't forget CCTA (coronary angiogram)
108
How to diagnose STEMI/LBBB ?
- Typical symptoms + ST elevation (?LBBB)
- Typical rise of biomarkers of myocardial necrosis with at least (ischaemic symptoms, pathological Q waves, ECG Changes indicative of ischaemia
- coronary angio
109
How to diagnose NSTEMI on ?
- Typical symptoms
- no ST elevation
- +VE) trop
110
How to diagnose UA on ECG?
- Typical symptoms
- no ST elevation
- ve trop.
111
Management of STEMI?
- Oxygen?
- Morphine
- Aspirin 300mg (limit platelet activation)
- clopidogrel/ticagrelor and
- unfractionated heparin.
PCI is gold-standard treatment for STEMI. If you can't do that, use thrombolysis with tPA or tenecteplase.
Repeat ECG 90 mins later.
(if no access to PCI within 90 mins, within 12 hr of symptoms and no contraindications to thrombolysis = alteplase/reteplase
Contraindications - active internal bleeding, intracranial neoplasm, aortic dissection, pregnancy, head injury, coagulation disorders.
Secondary Prevention:
- ACE
- B-blocker
- Statin
- Dual antiplatelet (aspirin + (clopi or ticagrelor or prasugrel))
consider continuing for up to 12 months. Post ACS = add ticagrelor to aspirin + stop ticagrelor after 12 months.
Post PCI = add prasugrel or ticagrelor to aspirin, stop the second antiplatelet after 12 months
112
Management of NSTEMI/UA
(M)OGA
- Oxygen,
- GTN (nitrates - avoid in hypotension) ,
- Aspirin (300mg)
+ clopidogrel/Ticagrelor (antiplatelet ADP binding)
In some patients:
- Fondaparinux (activates antithrombin III) offered to patients who are not at a high risk of bleeding + who are not having angiography within next 24hrs.
- IV glycoprotein IIb/IIIa receptor antagonist (eptibibatide or tirofiban) - those with intermediate or higher risk of adverse cardiovascular events).
Assess need for invasive or conservative approach
- Consider PCI/CABG in patients who have a predicted 6 month mortality above 3%
- Give it in 96 hrs.
MI: secondary prevention
All patients should be on dual antiplatelet therapy (aspirin + ticagrelor or prasugrel) , ACEi, B-Blocker and Statin.
Lifestyle Suggestions: Diet, exercise, sexual activity may resume 4 weeks after an uncomplicated MI.
NICE: Add ticagrelor to aspirin, stop ticagrelor after 12 months
Post PCI: add prasulgrel or ticagrelor to aspirin, stop second antiplatelet after 12 months.
Aldosterone antagonist: patients who have had an acute MI and who have symptoms and/or signs of heart failure and left ventricular systolic dysfunction. Treatment with aldosterone antagonist eplerenone.
113
Prognosis of ACS?
STEMI: 30 day mortality ~15%
NSTEMI: overall mortality ~ 1-2%
114
MI complications mnemonic?
Ventricular fibrillation is the most common cause of death in patients with MI.
Post PCI experiencing pain - or haemodynamically unstable - urgent coronary artery bypass = continuing MI.
Death Passing PRAED St
Death: VF, LVF, CVA
Pericarditis
Rupture: myomalacia cordis/cardiac tamponade, papillary muscle (MR) - Can lead to a flash pulmonary oedema
Septum - VSD
Arrhythmias
= (Tachy = AF, flutter, ventricular (premature ventricular contractions common after acute MI - no management)
- sustained VT, consider cardioversion or amiodarone/lignocaine),
(VT, VF))
- Brady (AV block, ventricular brady)
Aneurysm
Embolism
Dressler's Syndrome
115
What is presentation/management of pericarditis?
- Occurs Early
- Mild fever
- Central chest pain/change in pain
- Relieved by sitting forward
- Pericardial friction rub
ECG
- Saddle-shaped ST elevation
- ± PR depression
Rx
- NSAIDs: Ibuprofen
- Echo to exclude effusion
116
Cardiac Rupture Complications?
Cardiac Tamponade:
- Left ventricular free wall rupture
Beck's triad (low BP, High JVP, muffled heart sounds)
Pulsus paradoxus (BP drop greater than 10mmHg on inspiration)
- Need emergency pericardiocentesis + thoracotomy.
Papillary muscle/chordae rupture --> Leads to mitral regurg
- PSM
- Pulmonary oedema
Septum
- PSM
- increased JVP
- Heart failure
117
Ventricular Aneurysm presentation + management?
- 4-6 weeks
- LVF
- Angina
- Recurrent VT
- Systemic emboli
ECG: Shows persistent ST elevation
Management: Anticoagulate + consider excision
Embolisms arise from LV mural thrombus, consider warfarin for 3 months after large anterior MI.
118
Dressler's Syndrome?
Pleuro-pericarditis
- Due to auto-antibodies vs myocyte sarcolemma.
Presentation
- 2-6 weeks
- Fever
- Pleural pain
- Recurrent pericarditis
- Pleural effusion
- Anaemia
- Increased ESR
Management
- NSAIDs
- Steroids if severe
119
Acute Management of a STEMI - Immediate
- 12 lead ECG
- O2 - 2-4L for 94-98%
- IV access (bloods for FBC, U+E, Glucose + lipids)
- Brief assessment of Hx of CVD + risk factors. Thrombolysis CIs, CV exam.
- Management
1) Antiplatelet
Aspirin 300mg PO (then 75mg/d) +
Clopidogrel/ 300mg PO (then 75mg/d) or Prasugrel/Ticagrelor
2) Unfractionated heparin: enoxaparin IV then SC or LMWH
Add on:
3) Analgesia
- Morphine 5-10mg IV
- Metoclopramide 10mg IV
4) Anti-ischaemia
- GTN 2 puffs or 1 tablet SL
- B-B atenolol 5mg IV (CI asthma, LVF)
Admit to CCU for monitoring
- Arrhythmias
- Continue meds except CCBs
Aim for Primary PCI or Thrombolysis
120
What is PCI?
Primary Percutaneous Coronary Intervention
- Rx of choice if <12hr
- angioplasty and stenting
- + GP IIb/IIIa antagonist (tirofiban) if high risk
Delayed PCI, DM, Complex procedure
Complications
- Bleeding
- Emboli
- Arrhythmia
121
What is thrombolysis when do you used it in a STEMI?
- Without access to PCI
- Contraindicated beyond 24hr from pain onset
- ECG criteria- ST elevation >1mm in 2+ limbs OR >2mm in 2+ chest leads. New LBBB. Posterior: Deep ST 'depression' and tall 'R' waves in V1-V3.
122
Contraindications to thrombolysis?
AGAINST
- Aortic dissection
- GI bleeding
- Allergic reaction previously
- Iatrogenic: recent surgery
- Neuro: cerebral neoplasm or CVA hx
- Severe HTN
- Trauma inc CPR
123
Agents used for thrombolysis?
Streptokinase
Alteplase
Tenecteplase
Activate plasminogen to form plasmin. This in turn degrades fibrin and helps breakup thrombi.
124
Complications of Thrombolysis
Bleeding
Stroke
Arrhythmia
Allergic reaction
125
Continuing Therapy for STEMI?
- ACEi: Start w/i 24hrs (lisinopril 2.5mg)
- B-blocker: e.g bisoprolol 10mg OD (or CCB)
- Cardiac rehabilitation (group exercise)
- DVT prophylaxis until fully mobile (continue for 3 mont if large MI)
- Statin: regarless of basal lipids (atorvastatin)
Give advice
- Stop smoking
- Diet: oil fish, fruit, veg, decreased sat fats
- Exercise: 30 mins OD
- Work: return in 2m
- Sex: avoid for 1 month
- Driving: avoid for 1 mon
Continue clopidogrel for 1 year following STEMI, continue aspirin indefinitely.
126
NSTEMI + UA Management?
- 12 lead ECG + Admit to CCU
- O2 2-4L + SPO2 of 94-98
- IV access + FBC bloods
- Brief assessment (Hx of CVD/Risk factors) + CV exam.
- Antiplatelet (aspirin 300mg PO then 75/d) and Clopidogrel (300mg PO)
- Anticoagulate (Fondaparinux 2.5mg SC)
- Analgesia (morphine 5-10mg IV) + metaclopramide (10mg IV)
- Anti-ischaemia (GTN: 2 puffs or 1 tablet, B-blocker atenolol (CI in asthma and LVF), IV GTN if pain continues.
Assess the CVS risk: using the GRACE/TIMI score (Estimates admission-6 month mortality for patients with acute coronary syndrome)
Intermediate-High Risk
- Persistent/recurrent ischaemia, ST depression, DM, POSITIVE trop
- GPIIb/IIIa antagonist (tirofiban) should be given to patients who have high/intermediate risk + who are scheduled to undergo angiography.
- Angiography (±PCI) w/i 96hs
- Clopidogrel 75mg/d for one yr
Low Risk
- No further pain, flat or inverted T wave or normal ECG (negative trop)
- May discharge if 12hr trop is negative
- Outpatient test: angio, perfusion scan, stress echo.
Continuing Therapy: address risk factors
- ACEi (lisinopril 2.5mg)
- B-blocker (bisoprolol 10mg OD) or CCB
- Cardiac Rehabilitation (physio)
- Stop antithrombotic therapy when pain free (but give 3-5d)
- Statin (atorvastatin 80mg).
Continue clopidogrel for 1yr following NSTEMI.
Continue aspirin indefinitely.
127
angina pectoris
atherosclerosis --> myocardial ischaemia
NICE defines anginal pain
1. constricting discomfort: front chest, neck, shoulders, jaw or arms
2. precipitated by physical exertion
3. relieved by rest or GTN in about 5 minutes
all three = typical angina
two = atypical angina
one or none = non anginal chest pain
128
angina pectoris aetiology
- atheroma
- anaemia
- AS
- tachyarrhythmias
- arteritis
129
angina pectoris risk factors
modifiable
- smoking
- DM
- high cholesterol
- HTN
- obesity
130
angina pectoris symptoms
- central chest tightness/ heaviness
- brought on by exertion, relieved by rest
- radiate to one/both arms, neck, jaw, teeth
- other ppt: emotion, cold weather, heavy meals.
131
angina classification
stable: induced by effort
unstable: at rest/minimal exertion
decubitus: induced by lying down
132
angina differentials
- AS
- aortic aneurysm
- GI: GORD, spasm
- musculoskeletal
133
angina investigations
bloods: FBC, U+E, lipids, glucose, ESR, TFTs
ECG
perfusion scan
CT contrast coronary angiography
134
angina management
lifestyle: smoking/weight loss
medical:
secondary prevention
- aspirin 75mg OD
- ACEi: ramipril, captopril
- statins, simvastatin
- beta-blockers: propranolol, atenolol
anti-anginals: prevents angina episodes
- sublingual glyceryl trinitrate
- beta blocker: atenolol
- CCB:
long-acting dihydropyridine
non-dihydropyridine: verapamil, diltiazem
- both BB + CCB
(use nifedipine instead of verapamil)
- ISMN (isosorbate mononitrate): ivabradine, nicorandil (potassium channel activator with vasodilatory effect), ranolazine
patients develop tolerance to ISMN - take a second dose after 8hrs, rather than 12 hrs. Modified release doesn't lead to tolerance.
```
Interventional: PCI
- Poor response to medical Rx
- Refractory angina but not suitable for CABG
- Complications
Re-stenosis (20-30% at 6 mo)
Emergency CABG
MI (<2%)
Death (
```
135
Surgical Management of angina pectoris?
Indications
- LMS disease
- Triple Vessel Disease
- Refractory Angina
- Unsuccessful angioplasty
Complications
- MI
- Stroke
- Pericardial tamponade or haemothorax
- Postperfusion syndrome
- Post-op AF
- Non-union of sternum
- Graft Stenosis
136
Heart failure definition
CO is inadequate for the body's requirements despite adequate filling pressures.
137
Epidemiology of Heart failure?
Prevalence: 2% @ 50yrs --> 10% @ 80yrs
138
Pathophysiology of heart failure?
Reduced CO initially --> Compensation
- Starling effect dilates heart to enhance contractility.
- Remodelling --> Hypertrophy
- RAS and ANP/BNP release
- Sympathetic activation
Progressive decreased in CO --> decompensation
- Progressive dilatation --> impaired contractility + functional valve regurgitation.
- Hypertrophy --> relative MI
- RAS activation --> Na and fluid retention --> increased venous pressure --> oedema
- Sympathetic excess --> increased afterload --> decreased CO.
139
Types of pump failure in Low output Heart failure?
Due to this low output: the cardiac output decreased and fails to increase with exertion.
- The pump failures:
Systolic failure --> impaired contraction (mainly due to ischaemia/MI), or a dilated cardiomyopathy, HTN, Myocarditis.
Diastolic Failure --> Impaired filling (due to pericardial effusion/tamponade/constriction. But also cardiomyopathy: restrictive, hypertrophic).
Arrhythmias --> Bradycardia, heart block, tachycardias, or anti-arrhythmics (beta-blockers or verapamil).
140
Low output HF: Causes of Excessive pre-load?
AR, MR, fluid overload. Initial stretching of the myocytes before contraction.
141
Low output HF: Causes of excessive afterload?
The pressure the heart must work against once contracting?
- AS
- HTN
- HOCM
142
High output HF? Define and main causes?
- Increased needs - the heart needs to pump harder to meet the needs of the body.
--> RVF initially, then LVF
Anaemia, AVM, Thyrotoxicosis, Thiamine Deficiency (beri beri), Pregnancy, Paget's.
143
Causes of RVF?
- LVF
- Cor pulmonale
- Tricuspid and pulmonary valve disease
144
Symptoms of RVF?
Anorexia and Nausea
145
Signs of RVF?
Increased JVP + jugular venous distension
Tender smooth hepatomegaly
Pitting Oedema
Ascites
146
Causes of LVF?
1st: IHD
2nd: Idiopathic dilated cardiomyopathy
3rd: Systemic HTN
4th: Mitral and aortic valve disease
Specific Cardiomyopathies
147
Symptoms of LVF?
```
Fatigue
Extertional dyspnoea
Orthopnoea + PND
Nocturnal cough (± pink, frothy sputum)
Wt loss and muscle wasting
```
148
Signs of LVF?
- Cold peripheries ± cyanosis
- Often in AF
- Cardiomegaly with displaced apex
- S3 + tachycardia = gallop rhythm (blood back and forth through atria + ventricles)
- Wheeze (cardiac asthma)
Bibasal creps
- Cardiac cachexia
- Venous congestion of GI organs leading to early satiety.
-
149
Acute vs Chronic Heart Failure?
```
Acute
- New onset or decompensation of chronic
- Peripheral/pulmonary oedema
- ± evidence of peripheral hypoperfusion
= Give Furosemide. GTN IV.
```
Chronic
- Develops/progresses slowly
- Venous congestion common
- Arterial pressure maintained until v.late
150
Diagnosis of CCF?
Framingham Criteria for CCF
- 2 major or 1 major + 2 minor.
Major
- PND (paroxysmal nocturnal dyspnoea)
- + ve abdominojugular reflux
- Neck Vein Distension
- S3
- Basal Creps
- Cardiomegaly
- Acute Pulmonary Oedema
- increased CVP (>16cmH20) (central venous pressure)
- Weight loss > 4.5kg in 5d sndry to management.
Minor
- Bilateral ankle oedema
- SOBOE
- Increased HR > 120
- Nocturnal cough
- Hepatomegaly
- Pleural effusion
- 30% decrease in vital capacity
151
Investigations of Chronic Heart Failure?
Suspected HF?
1. ECG + Tests to consider (CXr, Lipid, Renal, Thyroid, HbA1c, peak flow etc)
Still suspected HF?
2. NT-proBNP (regardless of previous MI)
3. Echo
Bloods: FBC, U+E, BNP (raised but not specific), TFTs, glucose, lipids.
```
CXR
- ABCDE
Alveolar shadowing
Kerley B lines (demonstrate expansion of the interstitial space by fluid)
Cardiomegaly (Cardiothoracic ratio >50%)
Diversion (upper lobe)
Effusion
Fluid in the Fissures
```
ECG
- Ischaemia
- Hypertrophy
- AF
Echo
- the key investigation
- Global systolic and diastolic function.
Systolic failure echo shows dilated left and/or right ventricle with LOW ejection fraction. With pure diastolic heart failure LVEF is normal, but evidence of LVH and of abnormal diastolic filling patterns.
- Ejection fraction normally ~60%. Low EF = 40%.
- Focal/global hypokinesia
- Hypertrophy
- Valve Lesions
- Intracardiac shunts
152
When is B-type Natriuretic Peptide: BNP or NTproBNP secreted in response to?
Secreted from ventricles in response to
- Increased pressure --> Stretch
- Tachycardia
- Glucocorticoids
- Thyroid
- RV overload
- Hypoxaemia
- Renal dysfunction
- Sepsis
- COPD
- Diabetes
- Cirrhosis
153
What are the actions of BNP?
- Increased GFR, and decreased renal Na reabsorption
| - Decreased preload by relaxing smooth muscle
154
What is BNP a biomarker of?
Heart failure
- >2000 = 2WW
- Increased BNP (>400) supports a diagnosis of abnormal ventricular function. = 6WW.
- Intermediate value (100-400) is grey zone, may be due to COPD etc.
- Low (<100) can rule out decompensated heart failure.
- BNP also increased in RHF: cor pulmonale/PE.
Causes of falsely low BNP
- Aldosterone antagonist, ACEi, ARB, Beta-blockers, Diuretics.
155
What is the New York Association Classification?
- 1. No limitation of activity
- 2. Comfortable @ rest, dyspnoea on ordinary activity
- 3. Marked limitation of ordinary activity
- 4. Dyspnoea @ rest, all activity --> discomfort.
156
General management of CCF?
- Manage primary risk factors + treat precipitants/causes.
- Specific management
- Offer annual influenza vaccine
- Offer pneumococcal vaccine
Primary and Secondary CVS risk factors
- Stop smoking
- Decreased salt intake
- Optimise weight: increased or decreased (dietician)
- Supervised group exercised based rehab programme
- Aspirin
- Statins
157
Management of precipitants/Cause of CCF?
- Underlying causes
Valve disease
Arrhythmias
Ischaemia
- Exacerbating factors
Anaemia
Infection
Increased BP.
158
Specific Management of CCF - First Line
- General principles
Newly diagnosed patient need congestion and volume overload control
- If patient is anxious or distress consider morphine. (also has vasodilator properties).
- Those with low LVEF (add ACEi, B-Blockers, Aldosterone Antagonist (spironolactone)
Therefore
- ACEi, B-B --> decrease mortality.)
1st line: ACEi/ARB + B-B (watch K on ACEi)
ACEi/ARB: lisinopril/captopril 2.5-40mg OD/6.25-50mg TDS. ARB in Class II-IV if tolerated?
```
B-B: Carvedilol (3.125mg BDS)
/Bisoprolol 1.25mg orally)
Start low, go slow
Wait >2 weeks between increments
Switch stable pt taking B-Blocker for a comorbidity to a B-B licensed for heart failure.
B-B is good therapy for COPD.
```
Consider diuretics for fluid overload - Furosemide in Acute HF.
159
2nd line management of CCF?
Get advise
- Spironolactone (watch K carefully (also on ACEi) (recommended in those with II-IV with LVEF <35%. Can cause hyperkalaemia.
- ACEi + ARB (if cannot tolerate ACEi, use ARB).
- Vasodilators: hydralazine + ISDN nitrate (for those who cannot be given ACE/ARB-II)
160
3rd line management CCF?
- Digoxin (especially in those with AF. Used with ACEi, B-B, Diuretics.
- Consider ivabradine (already on ACEi, B-B, Aldosterone antagonist), HR >75 + LVEF <35%
- Consider ICD:
1) Prevention of sudden cardiac death in patients with non-ischaemic + ischaemic heart failure.
2) Secondary prevention to prolong survival in patients with current or prior symptoms of heart failure with history of cardiac arrest/VF.
3) Asymptomatic patients with an LVEF less than 30% NYHA class I.
- Cardiac Resynchronisation therapy ± ICD. - When refractory to optimal medical treatment. Used where LVEF <30% with a LBBB. Involves simultaneous activation of both right and left ventricles. Enhances ventricular contraction + reduced degree of functional mitral regurg.
161
Other considerations in CCF?
Monitoring
- BP: may be V low
- Renal function
- Plasma K
- Daily weight
Use amlodipine for comorbid HTN or angina
- Avoid verapamil, dilitiazem, nifedipine (short acting)
162
Invasive therapies for CCF?
- Cardiac resynchronisation ± ICD
| - Heart transplant
163
What is an Acute Exacerbation of congestive heart failure?
- Reduced CO, Tissue Hypoperfusion, increased pulmonary pressure.
- Presents with dyspnoea, decreased exercise tolerance, swelling or legs + generalised fatigue.
164
Immediate management of Severe Pulmonary Oedema?
- Sit up
- Oxygen (15L/min via reservoir mask)
- Target SpO2: 94-98%
- IV access + monitor ECG (bloods for FBC, U+E, trop, BNP, ABG) + check for arrhythmias.
- Diamorphine 2.5-5mg IV/Metoclopramide 10mg (makes patient more comfortable + pulm venodilators --> decrease preload --> optimise position on starling curve).
- Treat fluid overload - Loop diuretics (Furosemide/Bumetanide (40-160mg).
- Treat with vasodilators (lower left ventricular filling pressure + symptomatic improvement.
GTN (5mg - 2 puffs unless SBP <90) OR 5micrograms/min IV and increase by 5-20 every 3-5 mins.
- If worsening CPAP, more furosemide or increase infusion.
- BiPAP is not used in acute pulmonary oedema (matches person's respiration)
- Haemofiltration/dialysis.
165
History, Examination, Invx in severe pulmonary oedema?
- CXR: Looking for ABCDE
- ECG: MI, Arrhythmias, pulsus alternans (upstroke of pulses is weak then strong) - shows in heart failure.
- Consider Echo
166
What to consider if SBP <100mmHg in severe pulmonary oedema?
Consider Inotropes or vasopressor
- Milrinone (25-50micro IV) or Dobutamine (5-15 micro)
If in shock.
2nd/3rd line: Can also consider Intra-aortic balloon pump and left ventricular assist device
167
What are the causes of severe pulmonary oedema?
```
Cardiogenic and Non-cardiogenic:
- Cardiogenic
MI, Arrythmias, fluid overload: renal/iatrogenic
- Non-cardiogenic
- ARDS: sepsis, post-op, trauma
- Upper airway obstruction
- Neurogenic: head injury
```
168
What are the symptoms of Severe Pulmonary Oedema?
- Dyspnoea
- Orthopnoea
- Pink Frothy Sputum
169
Signs of severe pulmonary oedema
- Distressed, sweaty, cyanosed
- Increased HR/ Increased RR
- Increased JVP
- S3/ gallop rhythm
- Bibasal creps
- Pleural effusions
- Wheeze (cardiac asthma)
170
Differentials for severe pulmonary oedema?
- Asthma/COPD
- Pneumonia
- PE
171
How would you monitor the progress of severe pulmonary oedema?
- RR
- HR
- BP
- JVP
- urine output
- ABG
172
Continuing Therapy for Pulmonary Oedema?
- Daily Weights
- DVT prophylaxis
- Repeat CXR
- Change to oral furosemide or bumetanide
- ACEi + B-B if heart failure
- Consider Spiro
- Consider digoxin + warfarin (esp if in AF).
173
What is the definition of Cardiogenic shock?
Inadequate tissue perfusion primarily due to cardiac dysfunction.
In Cardiogenic shock - PAOP high, Cardiac Output Low, SVR high.
In Hypovolaemia - PAOP low, cardiac output low, SVR high.
174
Causes of cardiogenic shock?
MI HEART
- MI
- Hyperkalaemia (inc electrolytes)
- Endocarditis (valve destruction)
- Aortic Dissection
- Rhythm disturbance
- Tamponade
Obstruction
- Tension pneumothorax
- Massive PE
175
Presentation of cardiogenic shock?
- unwell: pale, sweaty, cyanosed, distressed.
- Cold clammy peripheries
- Increased RR + increased HR
- Pulmonary oedema
176
Management of cardiogenic shock
- O2 15L/min on a reservoir mask with a target SpO2 of 94-98%.
- IV access + ECG (need an ABG + standard bloods)
- Diamorphine + metoclopramide 10mg IV
- Correct any arrhythmias, Electrolyte disturbances, acid-base abnormalities (MI needs angioplasty or CABG, tamponade needs drainage, PE needs thrombolysis)
- Ix (CXR, Echo, CT Thorax (dissection/PE))
- Consider need for dobutamine (in hypotension + No MI) Used to treat reversible heart failure related to shock.
177
What is cardiac tamponade?
Accumulation of pericardial fluid within the pericardial space increasing intra-pericardial pressure, restricting cardiac filling and decreasing cardiac output.
178
Causes of Tamponade?
- Trauma (presents with classic Beck triad signs).
- Lung/breast Ca (Subacute - most common).
- Pericarditis (scarred pericardium)
- MI (regional/local effusion)
- Bacteria (TB) (subacute)
179
Signs of Tamponade?
- Beck triad: Hypotension, raised JVP and muffled heart sounds.
- Kussmaul's sign: Increased JVP on inspiration (inspiration increases venous return to right heart) and volume of right side decreased). When the pericardium is stretched, this is greater exaggerated leading to pulsus paradoxus. Rare sign in cardiac tamponade. (inspiratory drop systemic bp of >10).
Difference between Cardiac Tamponade + Constrictive Pericarditis?
- CP = X+Y JVP, no Pulsus paradoxus, and pericardial calcification.
180
Investigations of Tamponade?
Echo: Diagnostic
ECG - Electrical alternans
CXR: Globular heart
181
Mx of Tamponade?
- ABCs
- give fluid. Do NOT dry these patient.
- Pericardiocentesis (under echo guidance (if effusion present less than 1 month, echo shows effusion larger than 20mm).
- Paraxiphoid - 15 degree angle
182
Definition of Hypertension?
Essential HTN is over >140/90 with no secondary cause.
ACC Guidelines: Average of 2 or more seated measurements:
Normal BP: Systolic BP 120-129 mmHg and diastolic BP <80
Grade 1 HTN: Systolic BP 140-159 or Diastolic BP 90-99. ABPM of 135/85
Grade 2 HTN: systolic BP 160-179 or diastolic BP 100-109 mmHG. ABPM of 150/95
Grade 3 HTN: Systolic BP >180 or Diastolic BP >110
Malignant HTN: BP >180/110 + papilloedema and/or retinal haemorrhage. Chest pain due to increased workload on the heart. Nosebleeds, haematuria due to kidney failure.
Isolated SHT: SBP >140, DBP <90.
183
Aetiology of HTN?
```
PREDICTION
- Primary: 95%
- Renal (RAS System): RAS, GN, APKD, PAN
- Endo: increased T4, Cushing's, Phaeo, Acromegaly, Conns (5-10%)
Congenital adrenal hyperplasia
- Drugs: cocaine, NSAIDS, OCP, MOAi,
- ICP increased
- CoA
- Toxaemia of Pregnancy
- Increased Viscosity
- Overload with fluid
- Neurogenic: Diffuse axonal injury, spinal section
```
184
Aetiological clues for source of HTN?
Increased HR: Thyrotoxicosis
Radio-femoral delay: CoA
Renal Bruits: RAS
Palpable Kidneys: APKD
Paroxysmal Headache, tachycardia, sweating, palpitations, labile or postural hypotension: phaeo
Conns: Excess aldosterone therefore retaining salt HTN and losing K.
Acromegaly: Coarse facial appearance, spade hands, large tongue, excess sweating.
185
What are the end-organs that are damaged by HTN?
CANER
- Cardiac: (IHD, LVH --> CCF, AR, MR)
- Aortic: (aneurysm, dissection)
- Neuro: (CVA: ischaemic, haemorrhagic). Encephalopathy (malignant HTN).
- Eyes: (hypertensive retinopathy)
- Renal (proteinuria, CRF)
186
What is the Keith- Wagener Classification?
hypertensive retinopathy
- 1. Tortuosity and silver wiring
- 2. AV nipping (tight constrictions)
- 3. Flame (retinal) haemorrhages (copper wiring) and cotton wool spots (ischaemic changes) , exudates
- 4. Papilloedema
3 + 4 = malignant hypertension
187
Investigations for HTN
- 24hr ABPM - confirm HTN in those found with elevated clinic reading.
NICE recommends taking two readings during the consultations. If both at >140/90 then offer ABPM or HBPM. Use HBPM if ABPM declined.
If at ABPM/HBPM >= 135/85 (stage 1). treat if <80 + any of the following - target end organ damage, CVS, Renal disease, diabetes.
If ABPM/HBPM >150/95 offer drug treatment regardless of age.
- Urine: Haematuria, Alb:cr ratio (end organ damage)
- Bloods:
FBC,
U+E, (renal insufficiency, hypokalaemia suggesting Conn's (Hyperaldosteronism)
eGFR (end organ damage)
Glucose (metabolic syndrome)
Fasting lipids (high LDL, Low HDL)
- 12 lead ECG: LVH, old infarct (rule out CAD)
- Calculate 10yr CV risk
188
Management for HTN - Lifestyle
Do ABPM to confirm Dx before management
- Lifestyle
Increase exercise, decrease smoking/ETOH, salt, decrease caffeine.
189
Indications for pharmacological management HTN?
<80 yr, Stage 1 HTN (>135/90) - via ABP and one of the following:
- Target organ damage (LVH/retinopathy)
- 10yr CV risk >20%
- Established CVD
- DM
- Renal Disease
Anyone with Stage 2 HTN (>160/100)
Severe/malignant HTN (specialist referral)
Consider specialist opinion if <40yr with stage 1 HTN and no end organ damage.
190
BP targets for with HTN?
Age <80
- Clinic = 140/90.
- ABPM/HBPM = 135/85
Age >80
- Clinic = 150/90
- ABPM/HBPM = 145/85
If end-organ damage <130/80.
Otherwise <140/90.
191
Management of HTN 1st line if <55?
patients < 55-years-old or a background of type 2 diabetes mellitus: ACE inhibitor or a Angiotension receptor blocker (ACE-i or ARB): (A) because renoprotective.
If <55 or T2DM
1st Line <55 = ACEi or ARBs
- lisinopril 10mg OD (increase to 30-40mg).
- Candesartan 4mg OD (max 32 mg OD)
- Captopril, losartan. NOT recommended in pregnancy.
Avoid all ACEi ARBS in pregnanc
192
Management of HTN 1st Line if black or >55?
patients >= 55-years-old or of Afro-Caribbean origin: Calcium channel blocker (C)
1st line >55/Black
- CCB or Thiazide-like diuretics.
CCB =
Nifedipine MR 30-60, Amlodipine 2.5mg orally once daily initially.
Diltiazem: 120-180mg orally.
Peripheral vasodilators. May also be helpful in Raynaud's, coronary artery spasm
If diabetic - use ACEi (ramipril).
Thiazide-Like Diuretics:
- Hydrochorothiazide (12.5 to 25mg.
- Chlortalidone - 12.5mg,
- indapamide 1.25mg orally.
Thiazide diuretics work by inhibiting sodium reabsorption at the beginning of the distal convoluted tubule. Blocking Na Cl symptoms.
Use this instead of traditional Diuretics
Adverse effects - Dehydration, postural hypotension, gout, impaired glucose tolerance, impotence. can also cause agranulocytosis, photosensitivity rash, pancreatitis.
193
Management of HTN for <55 or >55/Black if first monotherapy doesn't work.
if already taking an ACE-i or ARB add a Calcium channel blocker or a thiazide-like Diuretic.
if already taking a Calcium channel blocker add an ACE-i or ARB
A+C or A+ D
- ACEi or ARB
- !!use ARBs over ACEi in blacks!! + Either CCB or Diuretics.
- Can also be used as a low-dose 1st line therapy.
Remember ACEi is ok in CKD, just not AKI.
A potassium above 6mmol should prompt cessation of ACEi in a patient with CKD.
194
Management of HTN for <55 or>55/Black if A + C/D doesnt work?
A + C +D
195
Management of resistant HTN?
A + C + D + consider Spiron or a/b blocker (hydralazine = a or labetalol (b).
Consider adding Spiro if the K was below 4.5
Consider adding alpha or beta blocker if above 4.5 e.g carvedilol (beta-blocker)
196
HTN + Coronary Artery disease without heart failure?
Consider Beta-blockers
- Cardioprotective effects in patients with CAD. Decreases myocardial wall stress and lessens myocardial oxygen demand.
Then consider CCB
Then B-B + CCB
Then B-B + ACE/ARB
197
Management of Malignant HTN?
HTN emergency Systolic is usually >180 and diastolic >120 + risk factors. May have dizziness/headache, cardiac symptoms (SOB, palpitations), oliguria (end organ renal damage), fundoscopy abnormal
- Controlled decreased in BP over days to avoid stroke
- 1st line Labetalol IV 20mg.
- 2nd line = nicardipine long acting CCB
If LV failure or Pulmonary oedema
- GTN + Furosemide (peripheral dilator IV) OR Clevidipine (CCB that increases stroke volume and coronary vasodilatory activity).
- 2nd line = Nitroprusside + furosemide. (arterial and venous vasodilator reducing afterload and preload.
198
What are the causes of Aortic Stenosis?
- Senile calcification (60yr+) = commonest
- Congenital:
bicuspid valve (40-60yrs), William's syndrome
- Rheumatic fever (Strep autoimmune inflammation reaction triggered by prior Strep infection. leads to inflammation + calcification).
- Subvalvular: HOCM
199
Symptoms of Aortic Stenosis?
- Triad: Angina, dyspnoea, syncope (esp with exercise)
- LVF: PND, orthopnoea, frothy sputum
- Arrhythmias
- Systemic emboli if endocarditis
- Sudden death
200
Signs of Aortic Stenosis?
- Slow rising pulse with narrow PP (taking time to get through the stenosis, pushing harder therefore narrow pressure) - due to reduced stroke volume due to narrow valve
- Aortic thrill (palpable murmur)
- Apex: (forceful, non-displaced) pressure overload.
- Heart Sounds
Quiet A2 (aortic valve closing)
Early systolic ejection click if pliable (young) valve)
S4 (forceful atria contraction vs hypertrophied ventricle)
Murmur
- ESM (crescendo/decrescendo). Loudest in the right upper sternal border.
- Right 2nd ICS
- Sitting forward in end-expiration
- Radiates to carotids
- Gallavardin's phenomenon -
Mimic Mitral Regurg (holosystolic murmur present at apex of heart)
201
Clinical indicators of severe AS?
- Quiet/absent A2
- S4 (indicative of left ventricular hypertrophy)
- Narrow pulse pressure
- Decompensation: LVF
202
Differentials for Aortic stenosis?
Coronary artery disease
MR - Gallavardin's phenomenon
Aortic Sclerosis
- Valve thickening: no pressure gradient
Turbulence --> murmur
- ESM with no radiation and normal pulse.
- HOCM
ESM murmur which increases in intensity with valsalva (AS decreases with valsalva)
203
Difference between Aortic Stenosis and Aortic Sclerosis?
Stenosis
- Valve narrowing due to fusion of the commissures
- Narrow PP, slow rising
- Forceful apex
- ESM radiating --> carotids
- ECG: LVF
Aortic stenosis
- Valve thickening
- ESM with no radiation.
204
Investigations for AS?
- Bloods: FBC, U+E, Lipids, Glucose
- ECG: LVH, LV strain, Tall R, ST depression, T inversion in V4-V6
LBBB or complete AV block (septal calcification)
May need pacing
- CXR
Calcified AV (esp on lateral film)
LVH
Evidence of failure
Post-stenotic aortic dilatation
- Echo + Doppler: Diagnostic
Thickened, calcified, immobile valve cusps
Severe AS (Stage D): Pressure gradient >40mmHg, Jet velocity >4m/s, Valve areas <1cm.
- Cardiac Catheterisation + Angiography
Can assess valve gradient and LV function
Assess coronaries in all pt planned for surgery.
- Exercise Stress Tet
Contraindicated if symptomatic AS
May be useful to assess ex capacity in asymptomatic patient.
205
Management of AS?
If asymptomatic then observe patient
If symptomatic then valve replacement
If asymptomatic but valvular gradient >40mmHg then consider surgery.
Medical
- Optimise RFs: Statins, antihypertensives, DM
- Monitor: regular f/up with echo
- Angina: B-blockers
- Heart failure: ACEi and diuretics
- Avoid nitrates due to profound hypotension
```
Surgical
- Poor prognosis if symptomatic
Angina/syncope: 2-3 yr
LVF: 1-2 yrs
- Indications for valve replacement
Severe symptomatic AS
Severe asymptomatic AS with reduced EF (<40%)
Severe AS undergoing CABG or other valve Op
```
-Valve types
Mechanical valves last longer but need anticoagulation: young patient
Bioprosthetic don't require anticoagulation but fail sooner (10-15yrs)
REMEMBER: needs long-tern antibiotic prophylaxis for endocarditis.
206
Options for unfit patients in AS?
Balloon Valvuloplasty
- Limited use in adults as complication rates is high, and restenosis occurs in 6-12 months.
Transcatheter Aortic Valve Implantation (TAVI)
- Folded Valve deployed in aortic root
- increased perioperative stroke risk cf. replacement
- Decreased major bleeding
- Similar survival @ 1 yr
- Little long-term data
Transfemoral rather than a transthoracic approach.
207
What are the causes of aortic regurgitation?
Acute (18%)
- Infective endocarditis (56%)
- Type A aortic dissection (44%) (ascending part of aorta) - alongside an Inferior MR.
Chronic
- Congenital: bicuspid aortic valve (22%)
- Rheumatic heart disease
- Connective tissue:
Marfan's,
Ehler's Danlos
- Autoimmune: Ank Spond, Ra
208
Symptoms of Aortic Regurg?
LVF: Exertional Dyspnoea, PND, Orthopnoea
Arrhythmias (esp AF) --> palpitations
- Forceful heart beats
Angina
209
Signs of Aortic Regurg?
- Collapsing Pulse (water hammer or Corrigan's pulse) - Arterial pulse shows rapid rise and a quick collapse resulting in widened pulse pressure >50 mmHg.
- Wide Pulse Pressure
- Apex: displaced (volume overload) in order to overcome later volume
- Heart Sounds (Soft/Absent S2) - inadequate closure of aortic valve in severe AR ± S3.
- Thrill (increased stroke volume)
- Murmur
Early diastolic murmur
URSE (Upper Right sternal edge) + 3rd left IC parasternal
Sitting forward in end-expiration
± ejection systolic flow murmur. Murmur occurs after S1 due to flow of increased stroke volume across a non-stenotic aortic valve. Early peaking, crescendo-decrescendo systolic sound, best heard at second right intercostal space.
± Austin-Flint Murmur
Soft, rumbling mid to late diastolic murmur heard best at apex. It produced by the abutment of an aortic regurg jet against the left ventricular endocardium. Different to a mitral stenosis by absence of an opening snap and loud S1.
Underlying cause
- High-arched palate
- Spondyloarthropathy
- Embolic phenomena
210
Eponyms of Aortic Regurg
- Corrigan's Sign: carotid pulsation due to increased stroke volume. For collapsing pulse (feel the forearm)
- De Musset's: Head nodding
- Quincke's: capillary pulsation in nail bed.
- Traube's: pistol-shot sound over femorals
- Austin-Flint Murmur: Rubling MDM @ apex due to regurgitant jet fluttering the anterior mitral valve cusp = severe AR.
- Duroziez's - Systolic murmur over the femoral artery with proximal compression. Diastolic murmur with distal compression.
211
Clinical indicators of Severe AR?
- Wide PP
- Collapsing pulse
- S3
- Long Murmur
- Austin Flint murmur
- Decompensation: LVF
212
Pathophysiology of Aortic regurgitation?
- There is a left ventricular volume and pressure overload
- Increase in left ventricular volume and pressure causes an increase in wall tension
- Therefore wall undergoes hypertrophy.
- Systolic hypertension occurs due to increased stroke volume due to regurgitant and forwards stroke volume.
Volume overload related to severity of leak results in an increase in left ventricular end-diastolic volume.
- Low diastolic volume as less blood is present in diastole.
- Increased in systolic as more blood is being sent out.
- If your diastolic is so low, you're gonna see syncope too
- Diastole also supports the coronary arteries, therefore angina.
213
Investigations for AR?
Bloods: FBC, U+E, Lipids, Glucose
- ECG: LVH (R6 + S1 >35mm)
- CXR - Cardiomegaly, Dilated ascending aorta, pulmonary oedema.
- Echo: Aortic valve structure and morphology (e.g bicuspid)
Evidence of infective endocarditis (e.g vegetations)
Severity Jet width (>65% of outflow tract = severe
Regurgitant jet volume
Premature closing of the mitral valve
LV function: ejection fraction, end-systolic dimension
Cardiac Catheterisation
- Coronary artery disease
- Assess severity, LV function, root size
214
Management of aortic regurgitation?
Medical
- Optimise RF: Statins, anti-hypertensives, DM
- Monitor: regular f/up with echo
- Decreased systolic HTN: ACEi (relax blood vessels + volume to reduce systolic bp), CCB
Decreased afterload --> Decreased regurgitation
```
Surgical
- Definitive therapy
- Indicated in severe AR if:
Symptom of heart failure
Asymptomatic with LV dysfunction, decreased EF/increased ES dimension
Can use TAVI or surgery.
```
215
What are the causes of Mitral stenosis?
- Rheumatic Fever (95%) - receive inflammatory damage. Years later, fusion of the mitral leaflet commissures and thickening of leaflets + sub-valvular apparatus causes mitral stenosis.
- Prosthetic Valve
- Carcinoid Syndrome
- Congenital (rare)
216
What is the pathophysiology of mitral stenosis?
- Valve narrowing --> increased left atrial pressure --> Loud S1 and atrial hypertrophy --> AF.
- -> Pulmonary oedema and PHT --> loud P2, PR.
- -> RVH --> left parasternal heave
- -> Tricuspid regurg --> large v waves (represents filling of the right atrium when the tricuspid is closed) - venous filling.
- -> RHF --> increased JVP, oedema, Ascites.
217
What are the symptoms of Mitral stenosis?
- Dyspnoea (increased left atrial pressure results in pulmonary congestion)
- Fatigue
- Chest pain
- AF --> Palpitations + emboli
- Haemoptysis: rupture of bronchial veins due to sudden increases in pulmonary venous pressure.
218
Signs of mitral stenosis?
- Symptoms manifest when orifice <2cm (normally 4-6)
- AF, low volume pulse due to left atrial enlargement.
- Malar flush (decreased CO -->> backpressure + vasocontrisction). Also due to CO2 retention + vasodilatory effects.
- JVP may be raised late on
Prominent a waves: PHT (right atria contraction) or stenosis of tricuspid valve.
Large v waves: TR
Absent a waves: AF
- Neck vein distension due to pulmonary HTN
- Left parasternal heave (RVH 2ndry to PHT)
- Apex: Tapping (palpable S1), non-displaced. S1 is loud as high gradient holds it open until ventricular systole closes it.
- Heart sound
Loud S1, Loud P2 (if PHT). Early diastolic opening snap.
- Murmur
Rumbling MDM
Apex
Left lateral position in end expiration
Radiates to the axilla
± Graham Steell murmur (EDM 2ndry to pulmonary regurg).
219
Clinical indicators of severe mitral stenosis?
- Mitral facies
- Longer murmur
- Opening snap closer to 2nd heart sound
High LA pressure focing valve open early
- Decompensation: RVF
220
Complications of MS?
Pulmonary HTN
Emboli: TIA, CVA, PVD, Ischaemic colitis
Hoarseness: rec laryngeal N.palsy = Ortner's Syndrome (due to the enlarged left atrium encroaching upon the left recurrent laryngeal nerve.
Dysphagia = Left atria encroaching on oesophagus.
Bronchial obstruction
221
Investigations for Mitral Stenosis?
- Bloods: FBC, U+E, LFTs, glucose, Lipids
- ECG
AF, P mitrale (if in sinus) = left atrial enlargement showing bifid P waves, RVH with strain: ST depression and T wave inversion in V1-V2.
- CXR
LA enlargement
Pulmonary oedema: ABCDE
Mitral valve calcification
- Echo + Doppler
Severe MS
Valve orifice <1.5cm
Pressure gradient >10mmHg
Pulmonary artery systolic pressure >50mmHg.
- Use TOE to look for left atrial thrombus if intervention considered.
May see a hockey stick-shaped mitral deformity.
Cardiac Catherisation
- Assess coronary arteries
222
Management of Mitral Stenosis?
Asymptomatic patients with severe disease usually do not require therapy.
Medical
- Optimise RFs: Statins, Anti-hypertensives, DM
- Monitor: regular f/up with echo
- Consider prophylaxis vs rheumatic fever: e.g Pen V
- AF: rate control + anticoagulate
- Diuretics provide symptom relief (furosemide - 40mg orally.) Reduce left atrial pressure + relieve mild symptoms.
```
Surgery
- indicated in symptomatic severe MS
- Percutaneous Balloon valvuloplasty
Management of choice
Suitability depends on valve characteristics
- Pliable, minimally calcified
- CI if left atrial mural thrombus
```
- More severe MS = valvotomy/commissurotomy: valve repair (open valve repair)
- Valve replacement if repair not possible.
223
Mitral Regurgitation causes?
- Mitral valve prolapse
- LV dilatation: AR, AS, HTN
- Annular calcification --> contraction (elderly)
- Post- MI: papillary muscle dysfunction/rupture
- Rheumatic fever
- Infective endocarditis
- Connective tissue: marfan's, Ehlers-Danlos.
224
Pathophysiology of Mitral regurgitation?
- Chronic MR can be mild with asymptomatic.
- With progression, cardiac hypertrophy occurs, increasing left ventricular end-diastolic volume. Left atrial enlargement.
- Acute MR = Acute disruption of mitral valve leaflets, chordae tendineae, papillary muscle following MI, infective endocarditis, rheumatic fever.
225
Symptoms of Mitral Regurgitations?
- Dyspnoea
- Fatigue
- AF --> palpitations + Emboli
- Pulmonary congestion --> HTN + oedema
226
Signs of MR?
- AF
- Left parasternal heave due to RVH
- Apex: displaced
Volume overload as ventricle has to pump forwards SV and regurgitant volume = Eccentric hypertrophy
- HS
Soft S1
S2 not heard separately from murmur
Loud P2 (if PTH)
- Murmur
Blowing PSM
Apex
Left lateral position in end expiration
Radiates to the axilla
227
Clinical indicators of severe MR?
- Larger LV
- Decompensation: LVF
- AF
228
Differentials of Severe MR?
- AS
- TR
- VSD
229
Investigations for MR?
Bloods: FBC, U+E, glucose, lipids
ECG: AF, P mitrale (unless in AF), LVH
CXR: LA and LV hypertrophy, Mitral valve calcification, pulmonary oedema.
Echo
- Doppler echo to assess MR severity: multiple criteria
Jet width (vena contracta) >0.7 cm = severe
Systolic pulmonary flow reversal
Regurgitant volume >60ml
- TOE to assess severity and suitability of repair cf. replacement.
- First line is Transthoracic echo
Cardiac catheterisation
- Confirm diagnosis
- Assess CAD
230
Management of Mitral Regurg?
- Medical
Optimise RF: statins, Anti-HTN, DM
Monitor: regular f/up with echo
AF: rate control and anticoagulate
Also anticoag if: hx of embolisation, prosthetic valve, additional MS.
Drugs to decrease afterload can help with symptoms
- ACEi or B-B (captopril+ metoprolol/atenolol) (if LVEF >60%) or LVESD <45mm.
If less than 60% use surgery (valvuloplasty, annuloplasty (tighten ring) mechanical valve + anticoag, bioprostheses.
- Diuretics
Surgery
- Valve replacement or repair
- Indications
Severe symptomatic MR (EJ 30% or more) + medical treatment.
Severe asymptomatic MR with diastolic dysfunction: Decreased ejection fraction (<60%)
231
Mitral Valve Prolapse (Barlow Syndrome)
Most common valve problem (5%).
| - Systolic prolapse or billowing of one or both mitral valve leaflets into the left atrium.
232
Mitral Valve Prolapse pathophysiology?
Primary MVP is due to myxomatous degeneration eg Marfans, Ehlers-Danlos, osteogenesis imperfecta.
In MVP, progressive changes result in mitral regurg that worsens over time. Produces volume overload of the left ventricles + atrium.
233
Symptoms of mitral valve prolapse?
- Usually asymptomatic
- Autonomic dysfunction: atypical chest pain, palpitations, anxiety, panic attack
- MR: SOB, fatigue.
234
Signs of mitral valve prolapse?
- Mid-systolic click + late systolic murmur (due to mitral regurg). Decreasing the preload, or afterload, the click and murmur occur earlier in systole. Squatting or increasing afterload with handgrip the click + murmur occur later.
235
Complications of MVP?
MR
Cerebral emboli
Arrhythmias --> sudden death
236
Management of MVP?
- B-B may relieve palpitations + chest pain.
Aspirin + warfarin for severe mitral regurg
- Surgery if severe (commonest reason for MV surgery)
237
Right heart valve disease - Tricuspid regurgitation definition
Occurs when blood flows backwards through tricuspid valve. Mainly during systole.
238
Causes of TR?
- Functional: RV dilatation
- Rheumatic fever
- Infective endocarditis
- Carcinoid Syndrome
Can also be due to rheumatoid arthritis, Marfans, tricuspid valve prolapse.
239
Pathophysiology of TR?
Tricuspid valve develops dysfunction with elevation of right ventricular systolic/diastolic pressure, right ventricular cavity enlargement.
If longstanding leads to reduced cardiac output, elevate right atrial pressure, leading to atrial distension and AF. Present with ascites symptoms of dyspepsia or indigestion.
240
Symptoms of TR?
- Fatigue (right-sided heart failure)
- Hepatic pain on exertion
- Ascites and oedema peripherally.
- Palpitations (AF)
241
Signs of TR?
```
Increased JVP with giant V waves - V regurg together
RV heave
Murmur
- PSM
- LLSE in inspiration (Carvallo's sign)
- Pulsatile hepatomegaly
- Jaundice
```
242
Investigations of TR?
LFTs - Cardiac Cirrhosis
Echo - TOE, TTE assessment of L/R heart EF.
ECG - AF
CXR - Cardiomegaly, pleural effusion, presence of pacemaker.
243
Management of TR?
- treatment of underlying cause (endocarditis, rheumatic valvulitis, carcinoid).
- Close follow up
- Medical treatment (management of HF)
Diuretics, ACEi, digoxin
- Surgical: valve replacement. or annuloplasty.
244
Causes of tricuspid stenosis?
- Rheumatic Fever (with MV and AV disease). Group A streptococcus antigens cross react and lead to an inflammatory response of the host tissue.
Requirement case of group A streptococcal pharyngitis?
- Rare condition defined by an abnormally elevated pressure gradient across the tricuspid valve
- Can be due to Carcinoid heart disease (intestinal tumour mets to liver).
245
Symptoms of tricuspid stenosis?
- Fatigue
- Dyspnoea (Concomitant mitral stenosis present in >95% of cases of rheumatic TS).
- Ascites
- Oedema
246
Signs of tricuspid Stenosis?
- Large A waves (hallmark of TS). Due to a poorly compliant right ventricle (increasing the impedence against which the right atrium has to eject blood)
STANosis.
- Opening Snap
- Murmur
EDM
LLSE in inspiration. Can be similar to MS. If right heart signs involved, must have high index of suspicion. Murmur increases in intensity with inspiration and squatting.
247
Management of TS?
- Medical: diuretics - fluid and sodium restriction + diurectics to treat right heart failure. If carcinoid somatostatin analogues.
- Surgical: repairs, replacement. Percutaneous balloon tricuspid dilatation
For Rheumatic fever - intractable RHF or low CO following initial illness. Surgical Valve here is primary treatment in severe disease.
248
Causes of Pulmonary regurgitation?
- Any cause of pulmonary HTN. (MS, Pulmonary Disease/Pulmonary HTN). Endocarditis. Rheumatic Heart disease, carcinoid heart disease.
- PR 2ndry to MS = Graham-Steell murmur
Signs
- Murmur: Decrescendo EDM @ ULSE.
Inx
- ECG (RV dilation + RBBB + RAD, (tall R wave in R1).
- TTE + Doppler
- CXR
249
Pathophysiology of pulmonary regurg?
- Results in volume overload + dilation of right ventricle and RVH.
LEads to equalisation of pulmonary artery pressure with PV pressure in diastole.
- Further more, right-sided stroke volume decreases, leading to peripheral oedema, dyspnoea and easy fatigability.
250
Management of pulmonary regurg
Non-severe
- Medical management of heart failure
- May need inotropic support
Surgery
- If symptomatic with pulmonary valve replacement ± anticoagulation.
251
Causes of Pulmonary Stenosis ?
- Majority are congenital
- Noonans, Williams,Alagille
- Also Carcinoid, endocarditis.
252
Pathophysiology of Pulmonary Stenosis?
Main pathophysiological consequence of PS is RV strain and increase in RV pressure, there is an increase in hypertrophy.
Mild to moderate obstruction will be tolerated, but can then present with cyanosis, syncope in severe disease.
Eventually, RV cannot cope with stenosis, so patient gets jugular venous distension, peripheral oedema, hepatomegaly, ascites.
253
Symptoms of PS?
Dyspnoea
Fatigue
Ascites
Oedema
254
Signs of PS?
- Dysmorphia of Williams, Noonans etc.
- Large A waves (large
- Rheumatic fever
- Dyspnoea
- Chest pain
- Fatigue
- RV heave
- Ejection click, soft P2 (loudest over left upper sternal border. Long and harsh murmur peaking later in systole.
- Murmur
ESM
ULSE --> L shoulder
- Signs of RHF
255
Investigation of Pulmonary Stenosis?
```
- ECG
P pulmonale (peaked P wve in II and V1 - V3)
RAD
RBBB
- CXR
Prominent pulmonary arteries: post-stenotic dilatation
- Echo with doppler
- Catheterisation: diagnostic
```
256
Management of PS?
MIld disease: Observation
Moderate - Percutaneous balloon pulmonary valvuloplasty, surgical valvuloplasty, endocarditis prophylaxis prior to high risk procedures.
257
Infective Endocarditis definition?
Cardiac valves develop vegetations composed of bacteria and platelet-fibrin thrombus.
258
What are the risk factors of infective endocarditis?
Cardiac disease --> Subacute Normal valves --> acute.
- Prosthetic valves
- Degeneration valvulopathy
- VSD, PDA, CoA
- Rheumatic Fever
- Dental caries
- Post-op wounds
- IVDU (tricuspid valve)
- immunocompromised (inc DM)
259
What are the main organisms involved in infective endocarditis?
Culture +ve
Strep viridans (>20%) second most common. Also strep mitis and strep sanguini. Classically linked to poor dental hygiene.
- S. bovis - linked to colorectal cancer
- Staph aureus (coagulase +ve) = IVDU - most common cause
- S. epidermidis (coagulate negative) - Patients with previous prosthetic valve.
Enterococci
Pseudomonas
S. haemolyticus/capitis both coagu negative but rare
Culture -ve (HACEK) or Right sided
- Haemophillis
- Actinobacillus
- Cardiobacterium
- Eikenella
- Kingella
- Coxiella
- Chlamydia
Non-infective
- SLE
- Marantic
260
What are the clinical systemic features of infective endocarditis?
- Fever, rigors* (really important)
- Night sweats
- Weight loss
- Anaemia
- Splenomegaly*
- Clubbing*
- Embolic phenomena
Abscesses in brain, heart, kidney, spleen, gut and lung (if right sided)
Janeway lesions - painless palmar macules (septic emboli from left-sided valves)
261
Cardiac features of infective endocarditis?
```
- new/changing murmur
(MR: 85%, AR 55%)
(TR murmur often absent) In IVDU it is tricuspid
- AV block
- LVF
```
262
Immune complex deposition in Infective Endocarditis?
- Micro haematuria due to GN
- Vasculitis
- Roth Spots: Boat shaped retinal haemorrhages with pale centre
- Splinter Haemorrhages
- Osler Nodes = painful, purple papules on finger pulps.
263
What criteria do you use to diagnose Infective Endocarditis?
Duke's Criteria?
264
Define Duke's Major Criteria?
Major
- 1. +ve blood culture
Typical organism in 2 separate cultures or
Persistently +ve cultures e.g 3 >12hr apart.
- 2. Endocardium involved
+ve echo (vegetation, abscess, valve dehiscence or
New valvular regurgitation
265
What is Duke's Minor Criteria?
Minor
1. Predisposition: cardiac lesion, IVDU
2. Fever >38
3. Emboli: Septic infarcts, splinters, Janeway lesions
4. Immune phenomenon: GN, Osler nodes, Roth Spots, Rheumatoid Factor
5. +ve blood culture not meeting major criteria
266
How can you make a diagnosis using the Duke's criteria?
```
2 major
OR
1 major + 3 minor
OR
5 minor
```
267
Investigations of IE?
Bloods
- N chromic, Normocytic anaemia
- Increased ESR/CRP
- +ve IgG RF (immune phenomenon) - One of the criteria in the Duke's diagnostic criteria
- Culture x3, >12hr apart
- Serology for unusual organism
Urine: Micro Haematuria
ECG: AV block
Echo:
- TTE detects vegetations >2mm
- TOE is more sensitive (90-100% vs 50-60%)
268
Management for infective endocarditis?
- Supportive care (ABCDE)
- May need other supportive management
- Take blood cultures
- BROAD Empirical Antibiotics
Native valve endocarditis (NVE): amoxicillin + gentamicin
NVE with severe sepsis, penicillin allergy or suspected methicillin-resistent staphylococcus aureus (MRSA): vancomycin + gentamicin
NVE with severe sepsis and risk factors gram negative infection: vancomycin + meropenem
Prosthetic valve endocarditis: vancomycin, gentamicin + rifampacin
When confirmed endocarditis on native valve (Strep)
- Benpen ± gentimicin
Methicillin-sensitive staph
- Consider Nafcillin/oxacillin + Clindamycin
HACEK organisms
- Ceftriaxone ± gentamicin
Fungi: Flucystosine IV + fluconazole PO
- Amphotericin if flucytosine resistance or Aspergillus.
Consider surgery
- Heart failure
- Emboli
- Valve Obstruction
- Prosthetic valve
Prophylaxis
- ABx prophylaxis solely to prevent IE not recommended ie for dental procedures, upper GI and lower GI tract procedures. GU tract.
Mortality
- 30% with Staph
- 14% with bowel flora
- 6% with sensitive streps
Infective endocarditis causing congestive cardiac failure is an indication for emergency valve replacement surgery.
- Other indications = CCF, Overwhelming sepsis, recurrent embolic episodes, pregnancy.
269
What is Rheumatic Fever?
Acute rheumatic fever is an autoimmune disease that may occur following a group A streptococcal throat infection.
If can affect multiple systems, including joints, hearty, brain and skin. Only the effects on the heart can lead to permanent illness.
Chronic changes are referred to chronic rheumatic heart disease and without long-term penicillin secondary prophylaxis, acute rheumatic fever can recur, leading to damage of the cardiac valvular tissue.
270
Aetiology of Rheumatic Fever?
Group A beta-Haemolytic Strep (pyogenes)
271
Epidemiology of rheumatic fever?
5-15 yrs
Rare in west. Common in developing world.
Only 2% of population susceptible.
272
Pathophysiology of rheumatic fever?
- Ab cross reactivity following S.pyogenes infection. T2 hypersensitivity reaction (molecular mimicry)
- Abs vs M protein in cell wall
- Cross reaction with myosin, muscle glucogen and SM cells.
- Pathology: Aschoff bodies and Anitschokow myocytes.
273
Diagnosis of Rheumatic Fever?
Revised Jones Criteria
- Evidence of GAS infection plus
2 major criteria or
1 major + 2 minor
274
Major Jones Criteria?
There is a low and high risk population criteria.
Low risk major:
JONES = Joints, Carditis, Nodules, Erythema marginatum, Syndenam Chorea.
- PanCarditis (clinical and/or subclinical)
- Polyarthritis
- Chorea
- Erythema Marginatum
- Subcutaneous nodules
275
Minor manifestations for jones Criteria?
- Fever (>38.5/38)
- Polyarthralgia
- Elevated inflammatory markers (ESR >60 and/or CRP >28.57
- Prolonged PR interval on ECG.
- Previous rheumatic fever
276
Symptoms of Rheumatic Fever - Cardiac?
Pancarditis (60%)
- Pericarditis: Chest pain, friction pericardial rub (squeaky leather, scratching/rasping). Best heard between apex and sternum
- Myocarditis: sinus tachy, AV block, HF, increased CK, T wave inversion.
- Endocarditis: murmur
MR (most common loudest at apex, radiating to axilla and accentuated when patient is rolled over on their left side), AR, Carey Coombs (pseudo-mitral stenosis because increased flow of regurg volume of blood over mitral valve during diastolic filling of left ventricle)
277
Symptoms of Rheumatic Fever - Arthritis?
- Migratory polyarthritis of large joints (esp. knees)
- Typically asymmetrical but not always migratory.
- Joint swelling, with tenderness, warmth, restricted movement.
278
Symptoms of Rheumatic Fever - Nodules? (2-20%)
- Subcutaneous nodules (2-20%)
| - Small mobile, painless nodules on extensor surfaces
279
Symptoms of Rheumatic Fever - Erythema Marginatum?
- Red, raised edges with central clearing
- Trunk, thighs and arms
- Smoke rings beneath skin
280
Symptoms of Rheumatic Fever - Sydenham's Chorea? (10%)
- Occurs late
| - Grimacing, clumsy, hypotonia (Stops in sleep).
281
Other symptoms of Rheumatic fever
- Recent sore throat or scarlet fever
- Arthralgia
- Pronator sign (turning outwards of arms and palms when held above head)
282
Investigations for rheumatic fever?
Bloods:
- Strep Ag test or ASOT
- Throat culture for Beta-haemolytic group A strep.
- FBC,
- ESR (>60 low risk, >30 high risk)
- CRP (28.57 or >3mg/dL)
- WBC
- Blood cultures (no growth) to exclude bacteraemia
ECG - Prolonged PR interval
CXR - Demonstrate CCF, chamber enlargement
Echo - morphological changes to the mitral/aortic valves and severity of regurgitation, pericardial effusion if pericarditis present
283
Management of Rheumatic fever?
If diagnosis has not established - hold off NSAIDS, give paracetamol.
- Bed rest until CRP normal for 2 weeks
- Benpen 0.6-1.2mg IM for 10 days. OR single injection of benzylpenicillin.
- Analgesia for carditis/arthritis: aspirin/NSAIDs
- Add oral pred if: CCF, cardiomegaly, 3rd degree block (1-2mg/kg/day orally for 7 days).
- Chorea: Carbamazepine or valproic acid.
- AF: add digoxin or amiodarone
LONG TERM
- Secondary prophylaxis
Benzylpenicillin - 900mg IM every 3-4 weeks adults.
284
Prognosis of Rheumatic Fever?
-Attacks last ~3 months
- 60% with carditis develop chronic rheumatic heart disease
- Recurrence ppted by
Further strep infection
Pregnancy
OCP
- Valve disease --> Regurg moves on to stenosis. Leads to rheumatic heart disease.
Mitral (70%)
Aortic (40%)
tricuspid (10%)
Pulmonary (2%)
285
What is acute pericarditis?
Inflammation of the pericardium.
- Acute form - new onset inflammation lasting <4-6 weeks.
- Can be fibrinous (dry) or effusive with a purulent,serous or haemorrhagic exudate.
- Clinical triad of Chest pain, pericardial friction rub and serial electrocardiographic changes.
- Constrictive pericarditis impedes normal diastolic filling and can be late complications of pericarditis. Most common disease of the pericardium encountered.
286
Aetiology of pericarditis?
- Causes
Viral (90%) : Coxsackie, flu, EBV, HIV
Other (also common) : uraemia, RA, SLE, Sarcoid, radiotherapy
Bacterial: pneumonia, rheumatic fever, TB, Staph
Fungi
MI - Dressler's
Drugs: penicillin, isoniazid, procainamide, hydralazine
287
Pathophysiology of pericarditis?
- Pericardium consists of a 2-layer pliable fibroserous sac covering surface of heart.
288
What are the clinical features of pericarditis?
Central/retrosternal chest pain
- Sharp (mimic MI)
- Pleuritic
- Worse lying down
- Relieved by sitting forward
- Radiates to left shoulder
Pericardial friction rub (high pitch squeaky)
Fever
Signs of effusion/tamponade
289
Investigations for pericarditis?
ECG (most useful) : saddle-shaped ST-elevation ± PR depression (very diagnostic feature)
Bloods: FBC (WBC) , ESR/CRP raised, Trop (may be increased), urea elevated in uraemic cause, cultures, virology
Echo - All patients should have an echo. may show pericardial effusion, absence of LV wall motion.
CXR - Normal or water-bottle shaped enlarged cardiac silhouette
May take pericardial fluid/ culture
290
Management of pericarditis?
Triage
- Major risk = high fever, large pericardial effusion, cardiac tamponade, failure to respond to 7 days NSAIDs.
Minor = myocarditis, immunosuppression, trauma, oral anticoagulant.
If tamponade - Urgent pericardiocentesis
If purulent - need pericardiocentesis + Vanc + ceftriaxone + NSAID
If viral = NSAIDS + PPI + Colchicine + exercise restriction
- Consider steroids/immunosuppression
If recurrent
- NSAID + PPI + Colchicine + exercise restriction
291
Constrictive Pericarditis
Heart encased in a rigid pericardium - impedes normal diastolic filling and can be a late complication of acute pericarditis.
Most cases occur 3-12 months after pericardial insult.
TB is the main cause in developing countries.
In developed countries, it is caused by prior cardiac surgery, radiotherapy and idiopathic pericarditis.
292
Clinical features of constrictive pericarditis?
- RHF with increased JVP
- Kussmaul's sign: increased JVP with inspiration, Key sign to distinguish this from cardiac tamponade.
- Quiet HS
- S3 (Pericardial knock) - caused by diastolic filling of ventricle. Heard in left ventricular failure (dilated cardiomyopathy), constrictive pericarditis, mitral regurg
- Hepatosplenomegaly
- Ascites, oedema
293
Investigations for contrictive pericarditis?
CXR: small heart + pericardial calcification
Echo
Cardiac Catheterisation
294
Definitive management of constrictive pericarditis?
Surgical Excision - pericardiectomy is removal or portion or all of the pericardium.
295
What is a pericardial effusion?
- Accumulation of transudate, exudate or blood in the pericardial sac.
- Can be due to pericardial inflammation. Increased intrapericardial pressure from pericardial effusion (especially when fluid fills up quickly) can compress the cardiac chambers leading to cardiac tamponade.
296
Clinical features of pericardial effusion
- Dypnoea
- Increased JVP (prominent x descent)
- Bronchial breathing @ let base
Ewart's sign: large effusion compressing left lower lobe
- Signs of cardiac tamponade may be present
297
Investigations of Pericardial effusion?
```
CXR: enlarged, globular heart
ECG
- Low-voltage QRS complex
- Alternating QRS amplitude (Electrical alterans)
- Echo: Echo free zone around heart.
```
298
Management of pericardial effusion
Treat cause
Pericardiocentesis may be diagnostic or therapeutic
- Culture, ZN stain, cytology
- Fluid analysed for glucose, protein, lactate dehydrogenase. Cell count, micro, bacterial/viral culture + cytology performed.
299
Tamponade - what is it?
Accumulation of pericadial fluid --> increased intra-pericardial pressure --> poor ventricular filling --> decreased CO
300
Causes of tamponade?
- Any cause of pericarditis
- Aortic dissection
- Warfarin
- Trauma
301
Signs of tamponade?
Beck's Triad: decreased BP, increased JVP, quiet heart sounds
Pulsus paradoxus: abnormally large decrease in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration. The normal fall in pressure is less than 10 mmHg. When the drop is more than 10 mmHg, it is referred to as pulsus paradoxus.
Kussmaul's sign
302
Investigations of tamponade?
ECG: low-voltage QRS ± electrical alternans
CXR: Large, globular heart
Echo: Diagnostic, echo-free zone around heart
303
Management of tamponade?
Urgent pericardiocentesis
- 20ml syringe + long 18G cannula
- 45, just left of xiphisternum, aiming for tip of left scapula
- Aspirate continuously and watch ECG
Treat cause
Send fluid for cytology, ZN stain and culture.
304
What are the causes of acute myocarditis?
Causes
- Idiopathic (~50%)
- Viral: coxsackie B, flu, HIV
- Bacterial: S.aureus, syphilis
- Drugs: Cyclophosphamide, Herceptin, CBZ, phenytoin
- Autoimmune: Giant cell myocarditis associated with SLE.
305
What are the symptoms of myocardial disease?
- Flu-like prodrome: fever, sore throat, myalgia.
- Dyspnoea, fatigue
- Chest pain (may coexist with Bornholm Disease)
- Arrhythmia --> palpitations
306
Signs of myocardial disease?
```
Age <50.
Chest pain
Soft S1
S4 gallop (CHF)
Signs of autoimmune disease
Signs of prior viral syndrome
```
307
Ix for Myocardial Disease?
ECG
- ST-elevation or depression
- T wave inversion
- Transient AV block
Bloods: +ve trop, increased CK
308
Management of myocardial disease?
```
Supportive
Rx cause
- If autoimmune - Methylprednisolone
- Giant cell myocarditis
Methylprednisolone
```
309
What is hypertrophic obstructive cardiomyopathy?
- LVOT obstruction from asymmetric septal hypertrophy
- AD inheritance (50% sporadic)
- B-myosin heavy chain mutation commonest
- Ask re family hx of sudden death
Can be associated with Friedreich's ataxia, and WPW
Septal thickening as as well abnormal, thickened collagen. Mostly marked below the aortic valve.
310
Symptoms of HOCM?
- Angina
- Dyspnoea
- Palpitations: AF, WPW, VT
- Exertional syncope or sudden death - proposed mechanism is VT secondary to ischaemia and this typically occurs in the setting of extreme exertion.
- Syncope after exercise due to subaortic hypertrophy og ventricular septum, and functional aortic stenosis.
311
Signs of HOCM?
- Jerky pulse
- Pulsus bisferiens
- Large a waves
- Double Apex beat - This transient interruption in cardiac output occurs when anterior leaflet of the mitral valve is pulled into the left ventricular outflow tract during systole).
- Harsh ESM @ LLSE with systolic thrill increased on Valsalva manoeuvre and decreased on squatting.
- S4 - contracting against a stiff ventricle.
312
Investigations of HOCM
ECG
- HOCM associated with WPW congenital accessory conducting pathway between atria and ventricles leading to AVRT.
- Deep Q waves
- LVH/LAD/L strain
- Abnormal ST waves, T waves. (Non-specific)
- ST depression
- Giant T wave inversion
- Ventricular ectopics, VT, VF
CXR - Cardiomegaly
Echo
- Exercise test ± holter (may be normal or demonstrate ventricular or supraventricular arrhythmia) monitor to quantity risk - LVH,
- Asymmetric septal hypertrophy
MR SAM ASH - Mitral regurg, systolic anterior motion of mitral valve leaflet, ash.
313
Management of HOCM?
ABCDE
- Amiodarone, Beta blockers, Cardioverter defib, Dual chamber pacemaker, endocarditis prophylaxis
Medical - -ve inotropes: 1st - B-B, 2nd verapamil. Negative inotropic and chronotropic agents.
Help alleviate obstruction
- Amiodarone: arrythmias (blocks potassium)
- Anticoagulate: if AF or emboli. Warfarin 2-10mg
Non-medical (symptomatic: predominant non-obstructive with preserved systolic function)
- Consider ICD if at any stage during therapy they are found to be at a higher risk level.
- Sudden cardiac death caused by ventricular arrythmias that can be effectively treated by implantable cardioverter defibs.
314
Cardiac Myxoma - what is it?
- Unknown origin
- Familial myxomas have an autosomal-dominant transmission.
May present as a component of a Carney's complex
(An AD condition comprising myxomas, endocrine tumours, spotty pigmentation of the skin).
- Rare, benign cardiac tumour
- May be familial, e.g Carney Complex - Cutaneous myxoma, skin pigmentation and endocrinopathy (Cushings).
315
Features of cardiac myxoma
- Constitutional symptoms: Clubbing, fever, weight loss, increased ESR.
- Dyspnoea, syncope, dizziness (Mitral valve obstruction).
- Signs similar to mitral stenosis (MDM, systemic emboli, AF) but vary with posture.
Diagnosis: Echo
Management: Excision
316
Restrictive Cardiomyopathy -
- Rigid walls but not thickened.
- Heart restricted from stretching and filling with blood properly.
- Much like Constrictive pericarditis
317
Causes of restrictive cardiomyopathy?
miSSHAPEN
- Sarcoid
- Haemochromatosis
- Amyloidosis
- Primary: endomyocardial fibrosis
- Eosinophilia (Loffler's eosinophilic endocarditis)
- Neoplasia: carcinoid (--> TR and PS)
- Post-radiotherapy
318
Clinical features of constrictive pericarditis?
```
RVH with raised JVP
Kussmaul's sign: increased JVP with inspiration
Quiet Heart sounds
S3
Hepatosplenomegaly
```
319
Management and treatment of constrictive pericarditis?
- Catheterisation and treat cause.
- Allows for ventriculography to be performed. Ejection fraction, ventricular size, wall motion and left ventricular outflow tract size can be estimated.
- Important to distinguish constrictive pericarditis and restrictive cardiomyopathy - use ECG Cardiac MRI, cardiac catheterisation.
320
What is dilated cardiomyopathy?
- Heart becomes enlarged and cannot pump blood effectively.
321
Causes of dilated cardiomyopathy?
DILATE
- Dystrophy: muscular, myotonic, glycogen storage disease
- Infection: complication of myocarditis, Coxsackie B.
- Late pregnancy: peri-, post-partum
- Autoimmune: SLE
- Toxins: Alcohol (big cause), doxorubicin, cyclophosphamide, DXT
- Endocrine: thyrotoxicosis
322
Presentation of dilated cardiomyopathy?
- LVF and RVF
| - Arrhythmias
323
Signs of dilated cardiomyopathy?
- Increased JVP
- Displaced apex
- S3 gallop
- decreased BP
- MR/TR
324
Investigations of Dilated cardiomyopathy?
- CXR: cardiomegaly, pulmonary oedema
- ECG: T inversion, poor progression, wide QRS/LBBB.
- Echo: globally dilated, normal or decreased wall thickness, hypokinetic heart + decreased EF
- Catheter + biopsy: myocardial fibre disarray. Increased ventricular size on ventriculography - used to form coronary angiogram
325
Management of Dilated Cardiomyopathy?
- Bed Rest
- Medical: diuretics, ACEi, digoxin, anticoagulation
- Non-medical: biventricular pacing, ICD
- Surgical: heart Tx
326
Congenital Heart Disease - Bicuspid Aortic Valve
No problems at birth
- Most eventually develop stenosis ± regurgitation
- Pre-disposed to IE/SBE
327
Atrial septal defect?
- Hole connects the atria
- Secundum defects high in the septum are commonest
- Often asymptomatic until adulthood
- LV compliance decreased with age --> increased L--> R shunt.
- Pressure difference between atria lower than ventricles therefore emboli has travelled through ASD rather than VSD to cause a stroke.
Ostium secundum (70% of ASDs)
- associated with Holt-Oram Syndrome
- ECG: RBBB with RAD
LV compliance increased with age, as LV becomes less compliant and gets more stiff. Therefore the right atrium, ventricle and pulmonary arteries may enlarge due to increased volume load. The Pulmonary and Tricuspid valves may become incompetent due to enlargement of valves annuli.
328
Symptoms of ASD?
- Dyspnoea
- Pulmonary HTN
- Arrhythmia
- Chest pain
329
Signs of ASD?
- AF
- Increased JVP
- Pulmonary ESM (excess volume of blood crossing pulmonary valve)
- Pulmonary HTN --> TR or PR
- Fixed splitting of the second heart sound: does not become single with expiration.
330
Complications of ASD?
- Paradoxical emboli - venous thrombus into a systemic arterial circulation through the ASD and may present as a stroke or TIA.
- Eisenmenger's syndrome.
Long-standing L--> R shunt due to VSD/ASD/PDA leading to reversal due to PHTN and overall cyanosis.
Increased RA pressure: R--> L shunt --> cyanosis
331
Investigations of ASD?
- ECG: Secundum will show Right Axis Deviation (right atrial enlargement where P waves >2.5mm, R waves greater than upper limit for RVH. Crochetage pattern in R wave in inferior limb leads (notch near the apex of R wave)
- Echo: Visualisation of the defect: flow pattern and shunt volume ascertained.
- CXR: Pulmonary plethora - Normal or enlarged heart with increased pulmonary markings.
332
Management of Congenital heart Disease?
- Transcatheter closure - median sternotomy/ or cath lab.
- Recommended in adults if high pulmonary to systemic blood flow ratio (>1.5:1)
- In L--> R shunt acute consider closure. Normally at age 2-4 + prophylaxis for antibiotics for bacteraemia.
In R-->L shunt which is reversible - use corrective closure.
For Eisenmenger's syndrome - irreversible shunt therefore avoid pregnancy, dehydration and high altitude. Give pulmonary vasodilators - bosentan/sildenafil. Monitor + treat hyperviscosity due to erythrocytosis to compensate for hypoxaemia - phlebotomy.
Consider heart/lung transplant.
333
Coarctation of the Aorta - definition?
- Congenital narrowing of the aorta
- Usually occurs just distal to origin of left subclavian
- More common in males
- Most common at the insertion of the ductus arteriosus, distal to the left subclavian.
334
What is CoA associated with?
Bicuspid aortic valve
| Turner's syndrome
335
What are the signs of a CoA?
- Radio-femoral delay + weak femoral pulse
- Hypertension - upper extremity systolic hypertension or murmur.
- Systolic murmur/bruit heard best over left scapula
336
What are the complications of a CoA
- heart failure
| - IE
337
Key diagnostic features?
HTN presenting at young age or resistant to treatment
- Diminshed lower extremity pulse
- Differntial upper + lower extremity BP.
- May have an systolic ejection murmur maximal over back or under left clavicle.
338
Investigations of CoA?
- ECG - infants may show right ventricular hypertrophy.
Children may show LVH.
- Chest X-ray: cardiomegaly or posterior rib notching, 3 sign. (not seen in young children)
- Echo: Discrete narrowing in the thoracic aorta: pressure gradient across narrowing.
CT angiogram
339
Management of CoA?
- Balloon dilatation + Stenting
| - Percutaneous stent implantation in repair of aortic coarctation.
340
Ventricular Septal Defects - Definition?
Hole connecting ventricles
341
Cause of VSD?
Congenital
| Acquired: MI
342
Presentation of VSD?
- Risk factors (Down's Syndrome or maternal use of alcohol during pregnancy)
- Pansystolic murmur left parasternal region. Does not increase with inspiration.
Smaller defect is generally louder.
- Best heard on the lower left sternal border.
- Left parasternal heave
- Larger holes have high pressure PHT.
- Failure to thrive
- SOB
- Recurrent pulmonary infections
343
Signs of VSD?
- Infective endocarditis (high flow rate of VSD). May need prophylaxis
- PHT
- Eisenmenger's
344
Ix for VSD?
ECG
- Small: Normal
- Large: LVH + RVH
This is because of left to right shunting and variable amount of PHT.
CXR
- Small: mild pulmonary plethora
- Large: cardiomegaly + marked pulmonary plethora (also common in Eisenmenger's)
Echo
- Single most important + useful tst. Colour flow Doppler are usually diagnostic.
345
Management of VSD?
- Prophylactic antibiotics: amoxicillin because of IE.
- Surgical closure indicated if symptomatic VSD with large shunt.
- Preoperatively furosemide
Should be corrected to avoid Eisenmenger's Syndrome.
Consider pulmonary vasodilators - bosentan/sildenafil
346
What is Tetralogy of Fallot's?
Congenital Cardiac Malformation
- Anterior + cephalad deviation of outlet of ventricular septum
- 1) Mal-alignment ventricular septal defect
- 2) aorta overriding the VSD
- 3) Right ventricular outflow tract obstruction (Pulmonary Stenosis)
- 4) secondary right ventricular hypertrophy
Due to abnormal separation of truncus arteriosus into aorta and pulmonary arteries.
347
Association with ToF?
Di-George: Catch 22q11 deletion.
Alagille's syndrome: Jagged1
Trisomy: 21, 18, 13
348
Presentation of ToF?
Infants: Hypercyanotic episodes, squatting and clubbing
Adult: Often asymptomatic, unoperated: cyanosis, ESM of PS (left sternal border) across narrowed right ventricular outflow tract.
Repaired: dyspnoea, palitation, RVF
349
Signs of ToF?
O2: baby may be hypoxaemic
ECG: RVH + RBBB
CXR: Coeur en sabot. Boot-shaped heart + normal cardiac silhouette does not rule out cyanotic heart disease.
Echo: anatomy + degree of stenosis. Overriding aorta, non-restrictive VSD, RVH.
350
Management of ToF?
Surgical closure (usually before 1yr) - Blalock-Taussig Shunt.
- Closure of VSD
- Correction of pulmonary stenosis
Management of hypercyanotic spells - Knees to the chest. Supportive care with B-blockers, Phenylephrine.
Profound cyanosis of baby- Alprostadil (Prostaglandin E1) to maintain patency of ductus arteriosus.
351
Marfan's Syndrome epidemiology?
- Autosomal Dominant
- Characterised by loss of elastic tissue, resulting in musculoskeletal deformities, lens subluxation, aortic dissection and root aneurysms.
- Spontaneous mutation in 25%
- M =F
- Prevalence = 1/5000
352
Pathophysiology of Marfan's?
Mutation in FBN1 gene on Chr 5
- Encodes fibrillin=1 glycoprotein
- Fibrillin-1 is essential component of elastin
- Cystic medial necrosis
353
Presentation of Marfan's Syndrome?
```
Cardiac
- Aortic aneurysm and dissection
- Aortic root dilatation --> regurgitation
- MV prolapse ± regurgitation (non-ejection systolic click)
Ocular
- Lens dislocation: superotemporal
MSK
- High-arched palate
- Arachnodactyly (long slender fingers)
- Arm-span > height
- Pectus Excavatum (excavate = dig hole therefore funnel chest)>
- Scoliosis
- Pes planus - flat feet
- Joint hypermobility
```
354
Complications of Marfan's Syndrome?
- Ruptured aortic aneurysm (sudden, stabbing onset chest pain). LOC, signs of abdominal ischaemia.
- Spontaneous pneumothorax
- Diaphragmatic hernia
- Abdominal hernia
355
Diagnosis of Marfans'
```
- 3/4 organ systems must be involved
Family history
Lens subluxation
MSK findings
Aortic dilatation or dissection
```
356
DDx of Marfan's
- MEN-2b
- Homocystinuria
- Ehlers-Danlos
357
Investigations of Marfan's?
- Echo (aortic regurg, aortic root dilation, ascending aortic dissection, mitral valve
prolapse) .
- CT scan - Aortic root dilation or ascending aortic dissection.
- Slit lamp examination: ectopia lentis, visualisation of subluxed dislocated lens). Elevated intra-ocular pressure.
- Consider CXR (widened mediastinum, scoliosis, pneumothorax).
- ECG - Arrhythmias.
- MRI - dural ectasia 9dilation of neural canal)
- Genetic testing - FBN-1 mutation.
358
Management of Marfan's
- Refer to ortho, cardio and ophtho
- Lifestyle alteration: decreased cardiointensive sports
- Beta-blockers slow dilatation of the aortic root (metoprolol, atenolol), then consider ACEi, lorsartan).
- Management lens subluxation (spectacles etc)
- Regular cardiac echo
Surgery when aortic root 4.5cm-5 wide.
- Give endocarditis prophylaxis prior to high-risk procedure.
359
Ehlers-Danlos Syndrome?
```
Rare heterogeneous group of collagen disorders.
6 subtypes with varying severity.
Commonest types (1 and 2) are AD.
```
360
Presentation of ED Syndrome?
- Hyperelastic skin
- Hypermobile joints
- Cardiac: MVP, AR, MR and aneurysms
- Fragile blood vessels --> Easy bruising, GI bleeds. (Tissue fragility)
- Poor healing
361
Differential diagnosis for ED Syndrome
Cutis Laxa: loose skin + hypermobile joints
Pseudoxanthoma elasticum: skin laxity
Marfan's
362
Clinical diagnosis for EDs?
MS and Skin manifestations, then Cardio and GI. Joint hypermobility is the only universal symptom.
363
Management of ED Syndrome?
- Avoid contact sports
- Encourage minimise risk of injury.
- Genetic counselling
- Pain management + physiotherapy.
364
What valvular abnormality is associated with polycystic kidney disease?
Mitral valve prolapse.
Mitral regurg is also common.
365
What is Doxazosin and what is it used to treat?
Selective a1-blocker used to treat hypertension.
366
What is prochlorperzine used to treat?
Vertigo
367
What are isoprenaline and dobutamine used for?
Ionotropic agents for patients in shock.
368
What is the management of orthostatic hypotension?
- Education + lifestyle such as hydration and salt intake.
- Discontinuation of vasoactive drugs e.g nitrates, antihypertensives, neuroleptic agents, dopaminergic drugs
- Medication treatment?
fludrocortisone, midodrine, head-up tilt sleeping.
369
What is fludrocortisone?
Increases renal sodium reabsorption and increase plasma volume.
370
Major points of ALS?
- Ratio of chest compressions to ventilation is 30:2
- Chest compression are now continued while a defib is charged
- Shock at 150J
- during VT/VF cardiac arrest, adrenaline 1mg is given once chest compressions have restarted after the 3rd shock and then every other shock.
- Amiodarone given at same time as adrenaline whilst still performing CPR (300mg). 2nd dose of amiodarone given after total of 5 defib attempts.
- A single shock for VF/Pulseless VT followed by 2 mins of CPR, rather than a series of 3 shocks followed by 1 min CPR.
- asystole/pulseless-electrical activity: adrenaline 1mg should be given as soon as possible. Should be treated with 2 minutes of CPR prior to reassessment of the rhythm.
- Atropine no longer recommended for routine use in asystole or PEA
Important to note difference in management in a patient who has a witnessed or monitored shock in CCU, cath lab or crit care. If here VF or pVT identified, patient should be given 3 successive shocks then CPR given.
371
Management of torsades de pointes?
Polymorphic VT
- Acute treatment is IV Magnesium 2g over 10 mins.
- Do not give amiodarone.
- Correct electrolyte abnormalities such as hypokalaemia.
372
Anaphylaxis doses for adrenaline in children?
<6 years = 150micrograms (0.15ml 1 in 1000)
6-12 years = 300 micrograms (0.3ml 1 in 1000)
Adults = 500 micrograms 0.5 1 in 1000, 200mg hydrocortisone, 10mg of chlorphenamine.
Can be repeated every 5 mins.
373
Management of warfarin with patients?
Warfarin is an oral anticoagulant - prevents reduction of Vit K to active form. Affects factors 2, 9, 7, 10.
Overdose of warfarin = increased APTT and PT
- Major bleeding on warfarin - Stop warfarin, give IV vit K 15mg. Prothrombin complex concentrate - if not available then FFP. Used to reverse warfarin
- INR >8.0 minor bleeding
Stop warfarin
Give intravenous vit K 1-3mg
Repeat dose of vit K if INR still too high after 24hr. Restart warfarin when INR <5.0.
INR >8 No bleeding -
Stop warfarin
Give vitamin K 1-5mg by mouth, using the intravenous preparation orally
Repeat dose of vitamin K if INR still too high after 24 hours
Restart when INR < 5.0
INR 5.0-8.0
Minor bleeding
Stop warfarin
Give intravenous vitamin K 1-3mg
Restart when INR < 5.0
INR 5.0-8.0- No bleeding
- Withhold 1 or 2 doses of warfarin
- Reduce subsequent maintenance dose
Indications?
- Venous thromboembolism: target INR = 2.5
- AF, target INR = 2.5
- Mechanical heart valve. Mitral valve requires higher INR than aortic valve.
- Bioprosthestic valve = 2.5 for first 3 months.
- Recurrent PE = 3.5
LMWH is rapid acting, therefore need LMWH.
Factors potentiating warfarin
- Liver disease
- P450 enzyme inhibitors
- Cranberry juice
- Drugs displacing warfarin from albumin (NSAIDS)
- Inhibiting platelet function: NSAIDs.
Side effects
- Haemorrhage
- Teratogenic, although can be used in breastfeeding mothers.
- Skin necrosis
- Purple toes
Patients taking warfarin should avoid food high in vitamin K, such as sprouts, spinach, kale and broccoli.
374
What are normal variants in ECG?
Sinus Brady
Junctional rhythm
First degree heart block
Wenckebach phenomenon
375
For patients of Afro-Caribbean origin taking a CCB for HTN?
Take an ARB over an ACEi.
376
Takayasu's Arteritis
- Large vessel vasculitis.
- Typically occludes the aorta and questions commonly refer to an absent limb pulse.
- More common in females and Asian people.
Features
- Systemic features of a vasculitus e.g malaise, headache.
- Unequal blood pressure in upper limbs
- Carotid bruit
- Intermittent claudication
- Aortic regurg
Associated with renal artery stenosis.
Manage with Steroids
377
Aortic dissection - Associations?
Tear in the tunica intima of the wall of the aorta
Associations
- HTN - most important
- Trauma
- bicuspid aortic valve
- collagens: Marfan's, ED syndome
- Turner's/Noonan's
- pregnancy
- Syphilis
378
Aortic Dissection - Features and symptoms?
- Chest pain: typically severe, radiates through to the back and tearing in nature
- Aortic regurg
- HTN
- Other features may result from the involvement of specific arteries.
Complications of backward tear
- Aortic incompetence/regurgitation
- MI: inferior pattern due to right coronary involvement
Complications of forward tear
- unequal arm pulses and BP
- Stroke
- Renal failure
379
Classification of Aortic Dissection?
Stanford classification
- Type A = ascending aorta, 2/3 of cases.
ascending aorta to at least the aortic arch. Therefore can lead to MI or Neurological symptoms.
- Type B - Descending aorta, distal to left subclavian origin
DeBakey
- Type I - originates in ascending aorta to at least the aortic arch. Therefore can lead to MI or Neurological symptoms.
- Type II - originates in and is confined to the ascending aorta
- Type III - origin in the descending aorta, rarely extends proximally but will extend distally.
Management
- Type A = Surgical management but BP should be controlled at 100-120 SBP whilst waiting. EVAR or Open intervention.
- Type B = conservative management, bed rest + reduce bp with IV labetalol
Analgesia. If uncomplicated (no end-organ involvement).
380
Which drugs have no effect on mortality in heart failure with preserved ejection fraction?
ACE-i
381
Which drug is strongly indicated if there is coexistent atrial fibrillation with heart failure?
Digoxin
382
42 yr old 2day history of anterior chest pain worse on deep inspiration + lying down. Pleuritic in nature
Pericarditis
383
67 yr old female with history of CLL with 3 day history of burning pain right lower chest wall
Shingles - pain + paraesthesia often precede vesicular rash seen
384
Chest pain, history of asthma, marfan's - sudden dysnpnoea + pleuritic chest pain
Pneumothorax
385
Sudden dyspnoea + pleuritic chest pain
Calf pain/swelling
Current combined pill user, malignancy
PE
386
Sharp pain relieved by sitting forwards
| May be pleuritic in nature
Pericarditis
387
Tearing chest pain radiating through to the back
| Unequal upper limb blood pressure
Dissecting aortic aneurysm
388
Burning retrosternal pain
| Regurgiataiton and dysphagia
GORD
389
Aortic Dissection
Flap or filling defect in aortic intima. BLood tracks into medial layer.
Tearing intrascapular pain.
Type A or B.
390
Boerhaaves Syndrome
Mackler's triad of Boerhaave's syndrome: vomiting, thoracic pain and subcutaneous emphysema.
- Spontaneous rupture of oesophagus as a result of repeated episodes of vomiting
- Ruptures is usually distally sited + on the left side.
- Sudden onset of severe chest pain that may complicate severe vomiting.
Treated with thoracotomy + lavage.
391
When should anti-HTN treatment be started?
Aged less than 80 with stage 1 HTN with one or more of target organ damage, established CVS, renal disease, diabetes or a 10yr CVS risk fo 10% or more.
392
What causes an ejection systolic?
```
Aortic stenosis
Pulmonary stenosis
HOCM
Atrial septal defect
Tetralogy of Fallot
```
393
What causes an pansystolic murmur?
Mitral/tricuspid regurg
| Ventricular septal defect
394
What causes a late systolic murmur
Mitral valve prolapse
| Coarctation of aorta
395
What causes a early diastolic murmur?
```
Aortic regurg (high-pitched blowing)
Graham steel (pulmonary regurgitation)
```
396
What causes a mid-late diastolic
```
Mitral stenosis (rumbling)
Austin-Flint murmur (severe aortic regurg)
```
397
Continous machine-like murmur
PDA
398
DVLA: CVS
HTN - Can drive. If 180 or more cannot.
Angioplasty 1 week off driving
CABG - 4 weeks off driving
ACS - 4 weeks off driving 1 week if treated by angioplasty
Angina - Driving must cease if symptoms occur at rest
Pacemaker insertion - 1 week
ICD - if for Ventricular arrhythmia = 6 months.
Successful cathether ablaiton for arrhythmia - 2 days
AAA of 6 cm - notify DVLA
Lorry - Patient must notify the DVLA, may not drive for at least 6 weeks.
399
ECG changes in hypercalcaemia?
Shortening of the QT
J waves (osborne)
Can lead to VT
400
Statins MOA?
Inhibit action of HMG-CoA reductase.
- SE: Myopathy. (more common in simvastatin + atorvastatin than rosuvastatin). This included myalgia, myositis, rhabdomyolisis, asymptomatic raised CK.
- Liver impairment: discontinue if transaminases 3x upper limit of normal
- May increase risk of intracerebral haemorrhage
CI: macrolides + pregnancy
Erythromycin + clarithromycin can induce a statin-induced myopathy
401
Who should receive statins?
All people with CVS
Anyone with a 10 yr CVS risk of 10%
Patient with T2DM to determine if they need it
T1DM more than 10 yrs ago.
Take at night.
- Primary prevention = Atorvastatin 20mg (10 yr risk >10%, most type 1 diabetes, or CKD eGFR <60, older than 40)
- Secondary prevention 80mg
Known IHD or CVD, peripheral artery disease.
When on statins - Check LFTs at baseline, 3 months and 12 months.
402
Which drug can cause erectile dysfunction?
```
Bisoprolol/Beta-blocker
- Side effects
Bronchospasm
Cold peripheries
Fatigue
Sleep disturbance
Erectile dysfunction
```
Contraindications
- Uncontrolled heart failure
- Asthma
- sick sinus
- concurrent verapamil use.
Beta-blockers can theoretically suppress all of the adrenergic mediated symptoms of hypoglycaemia therefore lead to unawareness of hypoglycaemic events.
403
83 yr old recurrent episodes of collapse. 12 lead ECG is normal. What is the most helpful investigation?
Recurrent episodes of collapse + normal resting ECG, 24hr Holter would be pertinent to investigate any underlying arrhythmias.
404
Management of Hypothermia?
- Removing the patient from the cold environment and removing any wet/cold clothing,
- Warming the body with blankets
- Securing the airway and monitoring breathing,
- If the patient is not responding well to passive warming, you may consider maintaining circulation using warm IV fluids or applying forced warm air directly to the patient's body
- Don't put the person into a hot bath.
- Don't massage their limbs.
- Don't use heating lamps.
- Don't give them alcohol to drink.
405
Travel-related thrombosis
Patients with major risk factors should consider wearing anti-embolism stockings. These can either be bought by the patient or prescribed (class I). Clearly if the risk is very high (e.g. a long-haul flight following recent major surgery) then consideration should be given to delaying the flight or specialist advice sought regarding the use of low-molecular weight heparin.
406
Young male smoker with symptoms similar to limb ischaemia
- Buerger's Disease (thromboangiitis obliterans) of small and medium vessel vasculitis that is strongly associated with smoking.
- Features include extremity ischaemia: intermittent claudication, ischaemic ulcer, superficial thrombophlebitis. Raynaud's phenomenon.
407
Why do you not give verapamil with beta-blockers
Verapamil is a highly negatively inotropic calcium channel-blocker; it reduces cardiac output, slows heart rate and may impair atrioventricular conduction.
The BNF recommends that verapamil is not given to patients taking beta-blockers because of the risk of hypotension and asystole.
Do not give it in VT either
408
Action of nitrates
Nitrates are involved in reducing venous return through increased venous capacitance/venous dilatation but also cause large artery dilatation.
As a consequence of the reduced venous return, the diastolic filling time is increased.
Therefore Decreased ejection time, decreased arterial pressure, decreased LV diastolic pressure and decreased ventricular volume.
Avoid in patients with hypotensions
SE: Hypotension, tachycardia, headaches and flushing.
409
Antipsychotic medication monitoring?
Higher probability of causing a prolonged QT interval if administered IV or in combo with other antipsychotic drugs.
410
What to do when comorbidities sugget both antiplatelet and an anticoagulation
```
Antiplatelet = established cardiovascular disease
Anticoag = AF, VTE, Valvular heart disease.
```
Stop Antiplatelet - start anticoag.
In Post-acute coronary syndrome = much stronger indication for antiplatelet = triple therapy (2 antiplatelets + 1 anti-coag) for 4 weeks - 6 months after event and dual therapy (1 antiplatelet + 1 anticoag) to complete 12 months.
VTE
- patient on antiplatelets develops VTE they are likely to be given anticoag for 3-6 months.
411
Features of autonomic neuropathy caused by diabetes?
Postural hypotension
Loss of respiratory arrhythmias
Erectile Dysfunction
T2DM mainly sensory and autonomic neuropathy
412
Postural Hypotension
Defined as fall of SBP >20mmHg after 3 minutes or at least DBP 10mmHg after 3 mins.
Caused by
hypovolaemia (venous pooling)
After meals
autonomic dysfunction: diabetes,
Parkinson's.
Drugs: Diuretics, antihypertensives, L-dopa, Phenothiazines.
413
Choking management
If able to respond - mild airway obstruction:
- Encourage patient to cough
If serious (cannot respond)
- Give up to 5 back-blows
- If unsuccessful give up to 5 abdominal thrust
- If unsuccessful continue the above cycle.
If unconscious
- Call for ambulance
- Start cardiopulmonary resus
414
4 Hs and 4 Ts
Hypoxia
Hypovolaemia
Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders
Hypothermia
Thrombosis (coronary or pulmonary)
Tension pneumothorax
Tamponade – cardiac
Toxins
415
Pulseless + sinus tachycardia. This is pulseless electrical activity.
Organised cardiac electrical activity + lack of a palpable pulse.
Patient is in cardiac arrest so ABCDE aborted and ALS started. They are in PEA/Asystole
Do chest compressions
in PEA asystole 2 mins of 30:2 then reassess
1mg Adrenaline is given IV immediately in PEA. 1
416
Atrial Myxoma?
Pedunculated heterogeneous mass on echo.
Atrial myxoma is a benign tumour most commonly occurring in the left atrium. It can present with the triad of mitral valve obstruction, systemic embolisation and constitutional symptoms such as breathlessness, weight loss and fever.
417
A 30-year-old Asian woman presents with a history of headaches, claudication and having unequal blood pressure in both her arms. Given the most likely diagnosis, which of the following features may develop?
Takayasu's arteritis is a vasculitic disorder generally affecting young Asian women. It affects the aorta and its branches and causes both systemic features and those specific to which vessels coming off of the aorta are affected.
It is associated with renal artery stenosis
- systemic features of a
- vasculitis e.g. malaise, headache
- unequal blood pressure in the upper limbs
- carotid bruit
- intermittent claudication
aortic regurgitation (around 20%)
418
ECG Changes in Hypothermia?
Bradycardia
J wave
1st degree heart block
Long QT
419
Causes of loud S2?
HTN (systemic or pulmonary)
Hyperdynamic states
Atrial septal defects without P HTN
420
Soft S2?
Aortic Stenosis
421
Causes of fixed split s2?
Atrial septal defect
422
Widely split s2
Deep inspiration
RBBB
Pulmonary stenosis
Severe mitral regurg
423
Reversed split s2
```
LBBB
Severe aortic stenosis
Right ventricular pacing
WPW
PDA
```
424
Furosemide side effects?
Loop diuretics
```
hypotensions
hyponatraemia
Hypokalaemia
hypocalcaemia
hyperglycaemia
gout
Ototoxicity
```
425
Types of secondary cardiomyopathies?
Infective = Coxsackie B, Chagas.
Infiltrative = Amyloid
Storage = Haemachromatosis
Toxicity = Doxorubicin, Alcoholic CM
Inflammatory = Sarcoidosis
Endocrine = DM, Thyroxicsis
Neuromuscular = Friedreich's ataxia, Duchenne-Becker muscular dystrophy
426
When to stop warfarin for surgery?
5 days before planned surgery and once the person's INR is less than 1.5
427
What are the side effects of beta-blockers?
Sleep disturbance
```
Bronchospasm
Cold peripheries
Fatigue
Sleep disturbance
Erectile dysfunction
```
428
P450 inhibitors and therefore accumulation of warfarin + raised INR
O-Devices
```
O- Omeprazole
Disulfarim
Erythromycin
Clarithromycin
Ciprofloxacin
Isoniazid
Cimetidine
Allopurinol
SSRI
Ritonavir
Sodium valproate
Fluconazole
```
P450 inducers include - PC BRAS -
- Phenytoin
- Carbamazepine
- Chronic alcohol
- Barbitone
- Rifampicin
- St John's Wort
- Smoking
429
Takotsubo's Cardiomyopathy?
Broken Heart syndrome
- Takotsubo's apical ballooning syndrome -
Described as an octopus trap.
- Bottom of the heart does not contract.
430
What is dipyridamole?
Non-specific phosphodiesterase inhibitor and decreased cellular uptake of adenosine.
Use as an antiplatelet mainly after an ischaemic stroke.
431
ACEi MOA + Side-effects
Inhibits conversation of Angiotensin 1 to II.
SE: Cough, angioedema, hyperkalaemia, first-dose hypotension.
Cautions: Avoid in pregnancy, with aortic stenosis may result in hypotension. ACEi with potassium >5 needs help.
INteractions - pAtients with high-dose diuretics therapy (80mg) - leads to hypotension.
Monitoring - U+E. Rise in creatinine + potassium may be expected after starting ACE. Changes in 30% baseline + increased in potassium up to 5.5mmol.
If there is a rise of creatinine by >100% or to above 310 micromols or if potassium rises to >5.5 mmol ACEi should be stopped.
432
Carotid sinus hypersensitivity test?
Massage carotid artery for 5 seconds. Stimulates baroreceptors + PNS. Increased vagal tone + SA + AV node, leading to decrease in BP and HR>
Cardioinhibitory = ventricular pause of >3 seconds.
Vasodepressive - Fall of SBP >50mmHg.
433
Nuclear imaging in cardiac disease?
These techniques use radiotracers which are extracted by normal myocardium. Examples include:
thallium
technetium (99mTc) sestamibi: a coordination complex of the radioisotope technetium-99m with the ligand methoxyisobutyl isonitrile (MIBI), used in 'MIBI' or cardiac Single Photon Emission Computed Tomography (SPECT) scans
fluorodeoxyglucose (FDG): used in Positron Emission Tomography (PET) scans
The primary role of SPECT is to assess myocardial perfusion and myocardial viability. Two sets of images are usually acquired. First the myocardium at rest followed by images of the myocardium during stress (either exercise or following adenosine / dipyridamole). By comparing the rest with stress images any areas of ischaemia can classified as reversible or fixed (e.g. Following a myocardial infarction). Cardiac PET is predominately a research tool at the current time
434
Causes of eruptive xanthoma
Yellow vesicles on extensor surfaces - elbows, knees.
familial hypertriglyceridaemia
lipoprotein lipase deficiency
435
Causes of Tendon xanthoma, tuberous xanthoma, xanthelasma
familial hypercholesterolaemia
| remnant hyperlipidaemia
436
Management of xanthelasma
surgical excision
topical trichloroacetic acid
laser therapy
electrodesiccation
437
What is amiodarone?
Class 3 antiarrhythmic used to treat atria, nodal and VT.
Blocks potassium channels which inhibit repolarization.
- Long half-life (20-100days)
- Give in central veins
- Lengthens QT
- Interacts with p450 inhibitors.
- Numerous long-term adverse effects.
Monitor TFTs, LFTs, U+E, CXR prior to treatment
TFTs, LFTs every 6 months.
```
Adverse effects
- thyroid dysfunction: both hypothyroidism and hyper-thyroidism
- corneal deposits
- pulmonary fibrosis/pneumonitis
liver fibrosis/hepatitis
- peripheral neuropathy, myopathy
- photosensitivity
- 'slate-grey' appearance
- thrombophlebitis and injection site reactions
bradycardia
lengths QT interval
```
438
What is Ivabradine?
Ivabradine indicated for symptomatic relief of angina in patients with HR of >70.
Deals with mixed sodium and potassium channels. Slows heart rate via SAN.
Most common side effect is the transient luminous phenomenon. Also headaches and Heart block.
Affects by CYP450 inducers or inhibitors.
439
Warfarin and surgery?
If surgery can wait 6-8hr = give 5mg vit K IV.
Ig surgery can't wait - 25-50 units
Stop warfarin before elective or emergency surgery
440
Difference between BiPaP and CPAP
Bipap = Breathing + sucking away excess CO2, therefore used in T2RF or mechanical resp failure.
CPAP is just continous - so mostly in low O2. Pushing more O2 in.
441
LMWH menchanism?
Activates antithrombin III
442
What is the Levine Scale?
- Grade 1 - Very faint murmur, frequently overlooked
- Grade 2 - Slight murmur
- Grade 3 - Moderate murmur without palpable thrill
- Grade 4 - Loud murmur with palpable thrill
- Grade 5 - Very loud murmur with extremely palpable thrill. Can be heard with stethoscope edge
- Grade 6 - Extremely loud murmur - can be heard without stethoscope touching the chest wall
443
Antiplatets vs anticoagulants?
Clotting in arterial system is mainly platelet driven.
Clotting in venous system /AF is blood stasis, not due to damage of endothelium, therefore mostly clotting factor driven.
444
Anteroseptal, inferior, lateral leads and which coronary artery they cover?
Anteroseptal = V1-V4 (LAD)
Inferior = II, III and aVF (RCA)
Lateral = I, aVL, V5, V6 (LCx)
445
Normal P, PR and QRS duration and what they represent?
P = 0.08-0.1 secs (atrial depolarisation)
PR = 0.12-0.2 secs (time between atrial and ventricular depolarisation)
QRS = < 0.1 secs (ventricular depolarisation)
446
Calculating heart rate using the rhythm strip?
Regular = 300 ÷ number of large squares between QRS complexes
Irregular = number of QRS complexes in 6 seconds (30 large squares) x 10
447
ECG features of right axis vs left axis deviation and causes?
Right = lead I + III point to each other
→ RVH, RBB, cor pulmonale, pulmonary embolism, anterolateral MI, left posterior hemiblock
Left axis = lead I + II point away from each other
→ LVH, LBBB, inferior MI, left anterior hemiblock
448
ECG features of RBBB vs LBBB?
WiLLiaM MaRRoW:
RBBB = M in V1, W in V6
LBBB = W in V1, M in V6
449
Bifascicular and trifascicular block?
Bifascicular = RBBB + left anterior or posterior hemiblock
Trifascicular = bifascicular block + 1st degree heart block
450
Outline the sinoatrial (SA) node action potential.
- Slow Na influx (HCN "pacemaker" channel)
- Rapid Ca influx
- K efflux
451
Outline the atrial/ventricular myocyte action potential.
- Rapid Na influx
- K efflux vs Ca influx (plateau phase)
- K efflux exceeds Ca influx
452
Virchow's triad?
Stasis of blood
Endothelial damage
Hyper-coagulability
453
Which coronary artery supplies the atrioventricular (AV) node and significance?
Right coronary artery
RCA infarcts (e.g. inferior MI) can cause arrhythmias
454
Heart attack vs cardiac arrest?
Heart attack = vascular occlusion or ischaemia leads to tissue death
Cardiac arrest = electrical disturbance stops heart beat
455
What does acute coronary syndrome (ACS) cover and ECG/troponin findings?
Unstable angina = abnormal/normal ECG + normal troponin
NSTEMI = abnormal/normal ECG + raised troponin
STEMI = ST-elevation/new LBBB + raised troponin (not required)
456
Patient groups more likely to have an atypical ACS presentation?
Elderly
Diabetics
Women
457
ECG criteria for STEMI diagnosis?
≥ 1mm ST elevation in any 2 contiguous leads except V2 and V3 where these criteria apply:
≥ 2.5mm in men < 40
≥ 2mm in men > 40
≥ 1.5mm in all women
458
ECG feature of posterior MI?
Reciprocal changes in leads V1-V3 (e.g. ST depression)
459
ECG features of a previous MI?
Q waves
Inverted T waves (if recent)
460
Wellen's syndrome and ECG changes?
Severe stenosis of LAD artery
Biphasic or deep T waves in V2-V3
461
Acute management of a STEMI?
Morphine (severe pain)
Oxygen (SaO2 < 94%)
GTN (not if hypotensive)
Aspirin 300mg
Ticagrelor 180mg OR prasugrel 60mg OR clopidogrel 300mg
PCI if < 120 mins = UFH + GPI (radial access) OR bivalirudin + GPI (femoral access)
PCI > 120 mins = thrombolysis + fondaparinux 2.5mg
462
ECG monitoring post-thrombolysis?
ECG after 60-90 mins
Consider PCI if ongoing ischaemia
463
List some contrindications to thrombolysis?
Bleeding/coagulation disorder
Active internal bleeding
Recent bleed, trauma or surgery
Stroke < 3 months ago
Severe hypertension
Intracranial neoplasm
464
First enzyme to be released after skeletal or cardiac muscle damage?
Myoglobin
465
Most sensitive marker of MI, time of elevation, peak levels and how long it remains elevated?
Troponin
4-6 hours
12-24 hours
7-10 days
466
Post-MI persistent ST-elevation and ventricular failure?
Left ventricular aneurysm
467
Post-MI pericarditis classification and management?
< 48 hours = acute pericarditis
2-6 weeks = dressler's syndrome
Management = NSAIDs + colchicine
468
Most common cause of death post-MI?
Ventricular fibrillation (VF)
469
Post-MI cardiac tamponade cause?
Left ventricular free wall rupture
470
Features and management of cardiac tamponade?
Beck's triad: hypotension, raised JVP and muffled heart sounds
Management = pericardiocentesis
471
Post-MI DVLA guidance?
4 weeks off driving OR
1 week if successful angioplasty
472
Statin examples, mechanism of action and side effects?
Examples = atorvastatin, simvastatin
Mechanism of action = inhibits HMG-CoA reductase
Side effects = myalgia, myositis, rhabdomyolysis, deranged LFTs
473
Statin monitoring requirements?
Baseline LFTs
LFTs at 3 months
LFTs at 12 months
474
Acute management of NSETMI and unstable angina?
IV morphine (severe pain)
Oxygen (SaO2 < 94%)
GTN (not if hypotension)
Aspirin 300mg
Fondaparinux 2.5mg
Haemodynamically unstable = immediate angiography +/- PCI
GRACE score > 3% = coronary angiography +/- PCI within 72 hours
GRACE score < 3% = ticagrelor or clopidogrel
475
Drug options for stable angina?
GTN for all then:
1st line = beta-blocker OR non-dihydropyridine CCB
2nd line = beta-blocker + dihydropyridine CCB
3rd line = beta-blocker + isosorbide mononitrate/ivabradine/nicorandil/ranazoline
476
Investigation and surgical management for stable angina?
CT coronary angiogram
PCI or CABG
477
Technique for standard-release isosorbide mononitrate tolerance?
Asymmetric dosing intervals
478
Preferred antiplatelet for patient waiting for PCI vs high bleeding risk?
Waiting for PCI = prasugrel 60mg
High bleeding risk = clopidogrel 300mg
479
Secondary drug prevention of ACS?
Aspirin (lifelong) + ticagrelor or prasugrel or clopidogrel (12 months)
Beta blocker
ACEi
Statin
480
Examples of antiplatelets vs anticoagulants?
Antiplatelets = aspirin, clopidogrel, prasugrel, ticagrelor, dipyridamole
Anticoagulants = warfarin, heparin, rivaroxaban, edoxaban, dibigatran, fondaparinux, apixaban, bivalirudin
481
Route and mechanism of action of warfarin, heparin, rivaroxaban, apixaban, edoxaban, dabigatran, fondaparinux and bivalirudin?
Warfarin (oral) = vitamin K antagonist
Heparin (IV or s/c) = activates antithrombin III
Rivaroxaban (oral) = direct factor Xa inhibitor
Apixaban (oral) = direct factor Xa inhibitor
Edoxaban (oral) = direct factor Xa inhibitor
Dabigatran (oral) = direct thrombin inhibitor
Fondaparinux (s/c) = activates antithrombin III
Bivalirudin (IV) = direct thrombin inhibitor
482
Reversal agent for dabigatran, apixaban and rivaroxaban?
Dabigatran = idarucizamab
Apixaban/rivaroxaban = andexanet alfa
483
How is INR calculated?
INR = (patient PT ÷ normal PT) x ISI
484
Factors which may potentiate warfarin (e.g. increase INR)?
Liver disease
P450 enzyme inhibitors
Cranberry juice
Drugs with bleeding risk (e.g. NSAIDs)
485
Management of INR 5.0-8.0 (no bleed), INR 5.0-8.0 (mild bleed), INR > 8 (no bleed), INR > 8 (minor bleed) and major haemorrhage?
INR 5.0-8.0 (no bleed) = withhold 1 or 2 doses, reduce maintenance dose
INR 5.0-8.0 (mild bleed) = stop warfarin, IV vitamin K, restart warfarin when INR < 5.0
INR > 8 (no bleed) = stop warfarin, oral vitamin K, restart warfarin when INR < 5.0
INR > 8 (mild bleed) = stop warfarin, IV vitamin K, restart warfarin when INR < 5.0
Major haemorrhage = stop warfarin, IV vitamin K, prothrombin complex OR FFP
486
Mechanism of action of aspirin, clopidogrel, prasugrel and ticagrelor?
Aspirin = COX-1 and COX-2 inhibitor
Clopidogrel/prasugrel/ticagrelor = P2Y12 ADP receptor inhibitor
487
Preferred antiplatelet prophylaxis for ACS, PCI, TIA, ischaemic stroke and PVD?
ACS = aspirin (lifelong) + ticagrelor (12 months)
PCI = aspirin (lifelong) + prasugrel (12 months)
TIA/ischaemic stroke/PVD = clopidogrel (lifelong)
488
Examples of supraventricular tachycardia (SVT)?
Sinus tachycardia
Atrial fibrillation
Atrial flutter
Ectopic beats
Re-entrant pathway e.g. AVRT (WPW)
489
Examples of ventricular tachycardia (VT) and main cause?
Monomorphic = post-MI
Polymorphic = QT prolongation
490
Main mechanism by which drugs prolong QT?
Block delayed-rectifier potassium channels
491
Narrow complex tachycardia vs broad complex tachycardia?
Narrow = SVT
Broad = VT, SVT with BBB
492
Management of REGULAR narrow vs broad complex tachycardia?
If haemodynamically unstable, immediate DC cardioversion
Narrow = vagal manoeuvres, adenosine (6mg → 12mg → 18mg)
Broad = amiodarone or lidocaine
493
Management of torsades de pointes (polymorphic VT)?
IV magnesium sulphate
494
Drug contraindicated in ventricular tachycardia (VT)?
Verapamil
495
Examples of bradycardia?
Sinus bradycardia
Sick sinus syndrome
Heart block
496
Management of bradycardia?
1st line = atropine 500mcg (repeat up to 3mg)
2nd line = transcutaneous pacing
3rd line = transvenous pacing (seek expert guidance)
497
Shockable vs non-shockable cardiac arrest rhythms?
Shockable = VF and pulseless VT
Non-shockable = PEA and asystole
498
4 Hs and 4 Ts of reversible cardiac arrest?
Hs = hypoxia, hypothermia, hyper/hypo and hypovolaemia
Ts = thrombosis, toxins, tamponade and tension pneumothorax
499
Initial defibrillation management of shockable rhythm?
Arrest witnessed = 3 successive shocks then 2 mins of 30:2 CPR
Not witnessed = 1 shock then 2 mins of 30:2 CPR
500
Drug management of non-shockable vs shockable cardiac arrest?
Non-shockable = adrenaline 1mg STAT
Shockable = adrenaline 1mg + amiodarone 300mg after 3 shocks
Repeat adrenaline every 3-5 mins
501
How should drugs be given during cardiac arrest?
1st line = intravenous (IV)
2nd line = intraosseous (IO)
502
ECG feature of hypothermia?
J waves
503
Mild vs moderate to severe hypothermia?
Mild = 32-35°C
Moderate to severe = < 32°C
504
ECG features of hyperkalaemia?
Tall T waves
PR prolongation
ST elevation
Wide QRS
505
ECG features of hypokalaemia?
U waves
Flat or absent T waves
PR prolongation
ST depression
506
Normal ECG variants in athletes?
Sinus bradycardia
Junctional rhythm
1st degree heart block
Mobitz type I (Wenckebach)
507
Antiarrhythmic drug classes and examples?
Class I (Na channel blockers) = lignocaine, lidocaine, flecainide, quinidine, propafenone
Class II (beta blockers) = propanolol, metoprolol, atenolol
Class III = (K channel blockers) = amiodarone, sotalol
Class IV = (Ca channel blocker) = verapamil, diltiazem
Miscellaneous = atropine, adenosine, ivabradine, digoxin
508
Beta-blocker associated with QT prolongation?
Sotalol
509
Monitoring requirements of amiodarone and why?
Prior = TFTs (hyper/hypothyroidism), LFTs (hepatotoxic), U&Es (↑ creatinine) and CXR (pulmonary fibrosis)
6 monthly = TFTs and LFTs
510
Atropine mechanism of action and side effects?
Mechanism of action = muscarinic antagonist
Side effects = anticholinergic (e.g. dry eyes/mouth, urinary retention)
511
Adenosine mechanism of action and side effects?
Mechanism of action = causes transient AVN heart block
Side effects = bronchospasm, chest pain, flushing
512
Ivabradine mechanism of action and side effects?
Mechanism of action = blocks the pacemaker "funny" channel
Side effects = heart block, bradycardia, luminous phenomena
513
Digoxin mechanism of action and side effects?
Mechanism of action = blocks the Na+/K+ ATPase
Side effects = generally unwell, anorexia, yellow-green vision, arrhythmias, gynaecomastia
514
Classic cause of digoxin toxicity and why?
Hypokalaemia
Digoxin binds to the K site on the N+/K+ ATPase so less K means more antagonistic effect
515
ECG change in digoxin use and management of toxicity?
ST "scooped out" or "reverse tick sign"
Management = digibind
516
Features of pericarditis?
Generally unwell (e.g. fever)
Chest pain (relieved sitting forward)
Pericardial rub
517
ECG features of pericarditis?
PR depression (most specific)
Widespread "saddle" ST elevation
518
Investigation and management of pericarditis?
Investigation = transthoracic echo
Management = NSAID + colchicine
519
Conditions associated with a non-pulsatile JVP and Kussmaul's sign (JVP rises on inspiration)?
Non-pulsatile = SVCO
Kussmaul's sign = constrictive pericarditis
520
Features of myocarditis?
Generally unwell (e.g. fever)
Chest pain
Typically young patient
Pulmonary oedema
521
Modified Duke's criteria scores for infective endocarditis diagnosis?
2 major criteria OR
1 major + 3 minor criteria OR
5 minor criteria
522
What are the 2 major and 5 minor Duke's criteria?
Major = positive blood cultures, endocardial involvement
Minor = predisposing heart disease or IVDU, fever > 38 °C, negative microbiology, vascular phenomena, immunological phenomena
523
Most common pathogen and valve affected in infective endocarditis?
Staphylococcus aureus
Mitral valve
524
Pathogen associated with infective endocarditis in IVDUs, poor dental hygiene, prosthetic valves and GI pathology?
IVDUs = staphylococcus aureus
Poor dental hygiene = streptococcus viridans
Prosthetic valves = staphylococcus epidermidis
GI pathology = streptococcus bovis
525
Antibiotic management of infective endocarditis?
Native valve = amoxicillin + gentamicin
Prosthetic valve or MRSA = vancomycin + gentamicin + rifampacin
IVDU or staph aureus = flucloxacillin
526
Stanford classification of aortic dissection?
Type A (most common) = ascending aorta
Type B = descending aorta
527
Features, investigations and management of aortic dissection?
Tearing chest pain (may radiate to back)
Radio-radial delay
Pulse deficit
BP different between arms
Investigations = CT angiography (stable) or TOE (unstable)
Management = manage BP + surgery (type A) OR conservative management (type B)
528
Cause of S1, S2, S3 and S4 heart sounds?
S1 = mitral and tricuspid closure
→ loud in mitral stenosis
S2 = pulmonary and aortic closure
→ soft in aortic stenosis
S3 = diastolic ventricular filling
S4 = atria contracting against stiff ventricle
529
Ejection systolic murmur causes?
Aortic stenosis
Pulmonary stenosis
Atrial septal defect (ASD)
Tetralogy of Fallot
HOCM
530
Pansystolic murmur causes?
Mitral regurgitation
Tricuspid regurgitation
Ventricular septal defect (VSD)
531
Early diastolic murmur causes?
Aortic regurgitation
Pulmonary regurgitation
532
Mid-late diastolic murmur cause?
Mitral stenosis
533
Continuous machine-like murmur?
Patent ductus arteriosus
534
Rule for hearing murmurs best?
RILE:
Right sided on inspiration
Left sided on expiration
535
Murmur associated with AF, wide PP, narrow PP, collapsing pulse, slow rising pulse, large JVP V wave and malar flush?
AF = mitral stenosis
Wide PP = aortic regurgitation
Narrow PP = aortic stenosis
Collapsing pulse = aortic regurgitation
Slow rising pulse = aortic stenosis
Large JVP V wave = tricuspid regurgitation
Malar flush = mitral stenosis
536
Most common cause of aortic and mitral murmurs?
Aortic stenosis = calcification
Aortic regurgitation = infective endocarditis
Mitral stenosis = rheumatic fever
Mitral regurgitation = valve prolapse
537
Management of valve disease?
Asymptomatic = monitor + manage associated heart failure etc.
Symptomatic = valve replacement or balloon valvuloplasty
538
Classification of AF types?
First detected episode
Paroxysmal AF = episodes self-terminate, usually < 24 hours
Persistent AF = episodes do not self-terminate, usually > 7 days
Permanent AF = non-episodic, does not respond to cardioversion
539
Overview of acute AF management?
< 48 hours = rate OR rhythm control
> 48 hours or uncertain = rate control
540
Contraindications for rate control as 1st line management of AF?
AF with reversible cause
Co-existing heart failure
New AF presenting < 48 hours
Co-existing atrial flutter eligible for ablation
541
Rate control management of AF?
1st line = beta-blocker or non-dihydropyridine CCB
2nd line = 2 of either beta-blocker, diltiazem or digoxin
542
Rhythm control management of AF?
DC cardioversion
Pharmacological cardioversion
→ structural heart disease = amiodarone
→ no structural heart disease = flecainide OR amiodarone
543
Cardioversion management of AF?
< 48 hours = DC or pharmacological cardioversion
> 48 hours or uncertain = 3 weeks anticoagulation then DC cardioversion OR TOE to exclude thrombus then immediate DC cardioversion
544
CHADVASC recommendation based on score?
0 = no treatment + arrange echo
1 = consider anticoagulation (male) or no treatment (female) + arrange echo
≥ 2 = anticoagulation
545
Score to assess bleeding risk of AF patients on anticoagulation?
ORBIT
546
Drug options for AF anticoagulation?
1st line = DOAC
2nd line = warfarin
547
Preferred anticoagulant for patients with prosthetic heart valves?
Warfarin
548
Preferred anticoagulant for AF post-ischaemic stroke or TIA and when to start?
Warfarin or DOAC
TIA = immediately
Stroke = after 2 weeks
549
Management of atrial flutter?
Initially the same as atrial fibrillation
Radiofrequency ablation is curative
550
Outline the types of heart block?
1st degree = PR > 0.2, regular
2nd degree (Mobitz type 1) = PR prolongs until a dropped beat
2nd degree (Mobitz type 2) = PR interval constant but beats sometimes dropped
3rd degree = no association between P wave and QRS complex
551
Which types of heart block require a permanent pacemaker?
Mobitz type II
3rd degree (complete) heart block
552
Features of right-sided vs left-sided heart failure?
Right-sided = peripheral oedema, raised JVP, hepatomegaly, anorexia
Left-sided = dyspnoea, orthopnoea, PND, fine bibasal crackles
553
Investigations for chronic heart failure?
NT-proBNP (1st line)
Tranthoracic echocardiogram
554
Raised levels of BNP vs NT-proBNP?
BNP = ≥ 100
NT-proBNP = ≥ 400
555
BNP production?
Made in the left ventriclular myocardium in response to strain
556
NYHA classification of heart failure?
Class I = no symptoms
Class II = mild
Class III = moderate
Class IV = severe (e.g. symptoms at rest)
557
What is ejection fraction and value for heart failure diagnosis?
Percentage of ventricular diastolic volume ejected during ventricular systole
≤ 40% = HFrEF
≥ 40% = HFpEF
558
High-output heart failure and causes?
Normal heart can't meet metabolic demands
Anaemia, pregnancy, thyrotoxicosis
559
Drug options for acute heart failure?
Non-hypotensive = IV loop diuretic
Hypotensive = inotropic agents (e.g. dobutamine), vasopressors (e.g. adrenaline)
560
Drug options for HFrEF?
1st line = ACEi + beta-blocker
2nd line = aldosterone antagonist
3rd line = ivabradine, digoxin, salcubitril-valsartan, hydralazine, hydralazine + nitrate
N.B. loop diuretics for fluid overload
561
Drug which reduce mortality in chronic heart failure?
ACEi/ARB
Beta-blocker
Aldosterone antagonist
Hydralazine + nitrate
562
Vaccination recommendations for heart failure?
Annual influenza vaccine
One-off pneumococcal vaccine
563
Main investigation for hypertension?
Ambulatory BP monitoring (ABPM) or
home BP monitoring (HBPM)
564
Additional investigations for hypertension and why?
ECG = LVH
U&Es = renal disease
Urinalysis = renal disease
HbA1c = co-existing diabetes
Lipid profile = co-existing hyperlipidaemia
Fundoscopy = diabetic retinopathy
565
Classification of hypertension?
Stage 1 = clinic ≥ 140/90 and ABPM/HBPM ≥135/85
Stage 2 = clinic ≥ 160/100 and ABPM/HBPM ≥ 150/95
Stage 3 = clinic systolic ≥ 180 OR diastolic ≥ 120
566
Drug options for hypertension?
1st line = A (< 55 or T2DM) OR C (> 55 or Afro-Caribbean)
2nd line = A+C or A+D (< 55 or T2DM) OR C+A OR C+D (> 55 or Afro-Caribbean)
3rd line = A+C+D
4th line = spironolactone (K < 4.5) OR alpha/beta-blocker (K > 4.5)
567
Blood pressure targets for < 80 years vs > 80 years?
< 80 = clinic 140/90 and ABPM/HBPM 135/85
> 80 = clinic 150/90 and ABPM/HBPM 145/85
568
ACEi/ARB examples, side effects and cautions?
ACEi = ramipril, lisinopril
ARB = losartan, candesartan
Side effects = hyperkalaemia, cough (ACEi), angioedema (ARB)
Cautions = pregnancy, renovascular disease
569
ACEi/ARB renal advice?
Generally considered renoprotective
Contraindicated in bilateral renal artery stenosis
Monitor U&Es regularly
570
Beta-blocker examples, side effects and cautions?
Examples = atenolol, propanolol
Side effects = bronchospasm, cold extremities, erectile dysfunction, sleep issues, fatigue
Cautions = asthma, uncontrolled HF, verapamil use
571
Calcium channel blocker examples and side effects?
Dihydropyridines = amlodipine, nifedipine
Non-dihydropyridines = verapamil, diltiazem
Side effects = peripheral oedema, flushing, headache
572
Thiazide diuretic examples, mechanism of action and side effects?
Thiazide = bendroflumethiazide
Thiazide-like = indapamide
Mechanism of action = blocks NaCl reabsorption via the Na/Cl symporter in the DCT
Side effects = hyponatraemia/hypokalaemia, hypercalcaemia, impaired glucose tolerance, gout, erectile dysfunction
573
Loop diuretic examples, mechanism of action and side effects?
Examples = furosemide, bumetanide
Mechanism of action = blocks Na reabsorption via the Na/Cl/K contransporter in the thick ascending LoH
Side effects = hyponatraemia/hypokalaemia/hypocalcaemia, ototoxicity
574
Potassium sparing diuretic examples and side effects?
Aldosterone antagonists = spironolactone, eplerenone
ENaC inhibitors = amiloride
Side effects = hyperkalaemia, endocrine dysfunction (aldosterone antagonist)
575
Most common cause of secondary hypertension?
Primary hyperaldosteronism
576
Criteria and management of orthostatic hypotension?
Criteria = drop of ≥ 20mmHg systolic +/- ≥ 10mmHg diastolic within 3 mins of standing
Management = midodrine or fludrocortisone
577
Score used to investigate patients with low suspicion of a PE and interpretation?
Pulmonary embolism rule-out criteria (PERC)
All must be absent for negative result
578
Score used to investigate patients with suspected PE and values?
Wells score
> 4 points = PE likely
≤ 4 points = PE unlikely
579
Investigations for a likely PE (Wells > 4)?
Urgent CTPA
DOAC if CTPA delayed
+ve CTPA = PE confirmed
-ve CTPA = consider doppler scan
580
Investigations for an unlikely PE (Wells ≤ 4)?
D-dimer
+ve D-dimer = urgent CTPA
-ve D-Dimer = consider alternative diagnosis
581
Indication for V/Q scan in PE and why?
Renal disease
No contrast required
582
Management of stable PE?
Provoked = 3 months of DOAC
Unprovoked = 6 months of DOAC
583
Management of unstable vs recurrent PE?
Unstable = thromboylsis
Recurrent = IVC filter
584
Advice for patients regarding flights and thrombosis?
Low risk = no measures needed
Moderate-high risk = compression stockings
585
Most common cardiomyopathy?
Dilated cardiomyopathy
586
Most common cause of death in young athletes?
Hypertrophic obstructive cardiomyopathy (HOCM)
587
Medical name for "broken heart" syndrome?
Takotsubo cardiomyopathy
588
ECG feature of Wolff-Parkinson White (WPW) syndrome and management?
Slurred QRS upstroke (delta wave)
Management = radiofrequency ablation
589
ECG feature of Brugada syndrome and management?
ST elevation in V1-V3 followed by inverted T wave
Management = ICD
590
Heart condition associated with DiGeorge vs Turner's syndrome?
DiGeorge = Tetralogy of Fallot
Turner's = coarctation of the aorta
591
Types of atrial septal defect?
Ostium primum
Ostium secundum (most common)
592
Large cell vasculitis associated with occlusion of the aorta and absent limb pulses?
Takayasu's arteritis
593
Small and medium vessel vasculitis with strong link to smoking?
Buerger's disease (thromboangiitis obliterans)
594
Outline the screening programme for AAA?
One-off abdominal US for men age 65
< 3cm = no action
3-4.4cm = re-scan every 12 months
4.5-5.4cm = re-scan every 3 months
≥ 5.5cm = refer for intervention
595
High rupture risk features of AAA?
Symptomatic
≥ 5.5cm
Grown > 1cm/year
596
Management of AAA?
Endovascular repiar (EVAR) OR
Open aneurysm repair
597
Abnormal ABP values?
< 0.9 OR > 1.2
598
Location of venous vs arterial ulcers and management?
Venous = above medial/lateral malleoli
→ compression bandaging
Arterial = toes, shins, pressure points
→ modify risk factors e.g. hypertension
599
Features of lower limb venous insufficiency?
Varicose veins
Venous ulcer
Stasis eczema
Lipodermatosclerosis
Haemosiderin deposition
Superficial thrombophlebitis
600
Management of superficial thrombophlebitis?
Compression stockings + NSAID
601
What does peripheral arterial disease cover?
Intermittent claudication
Critical limb ischaemia
Acute limb-threatening ischaemia
602
Features and management of intermittent claudication?
Pain in leg muscles on exercise
Resolves at rest
Management = statin + clopidogrel + exercise
603
Features and management of critical limb ischaemia?
Rest pain (hang legs out of bed)
Ulceration
Gangrene
Management = endovascular revascularisation (< 10cm) or open surgical revascularisation (> 10cm)
604
Features and management of acute limb-threatening ischaemia?
Pale, pulseless, painful, paralysed, paraesthesis, perishingly cold
Management = analgesia + urgent vascular review
605
Wet vs dry gangrene and management?
Wet = infectious e.g. necrotising fasciitis
→ IV antibiotics + debridement or amputation
Dry = non-infectious e.g. ischaemic
→ amputation
