cardiology Flashcards
cardiac electrophysiology
Main Leads?
I
II
III
other leads
AVL
AVR
AVF
electrical conduction pathway
SA node
-> AV node
-> bundle of His
-> Left and right bundle
-> Purkinje fibres.
inferior leads + corresponding vessel ?
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.
anterolateral leads + vessel ?
I, aVL, V5 + V6
left circumflex or LAD
anteroseptal leads + vessel ?
V1-V4
LAD vessel
ECG analysis components
rate
rhythm
axis
P waves
QRS
PR interval
QT
ST segment
T waves
rate
300/no of large squares OR add number of QRS and x 6.
rhythm
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.
causes of a RAD (>+90)
- anterolateral MI (busting this shifts activity to right)
- RVH, PE
- L post hemiblock WPW
- ASD secundum
causes of a LAD
- inferior MI (busting this shifts activity to the left)
- LVH
- L ant. Hemiblock WPW
- ASD primum
P waves
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.
QRS complex
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.
PR Interval
(120-200ms)
start of P wave to start of QRS.
- prolonged: ♡ block
- short: WPW, accessory conduction, nodal rhythm, HOCM
- depressed: pericarditis
QTc
(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)
ST segment
Elevated (limbs: >1mm, chest >2mm)
- Acute MI
- Prinzmetal’s angina
- Pericarditis: saddle-shaped
- Aneurysm: ventricular
Depressed (>0.5mm)
- Ischaemia: flat
- Digoxin: down-sloping
T waves
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+
Extra waves in ECG?
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
Conduction Defects - Heart Blocks.
1st Degree?
PR > 200ms. (5 little poke boxes)
2nd degree heart block - Wenckebach/Mobitz I?
- Progressive lengthening of PR interval
- One non-conducted P wave
- Next conducted beat has shorter PR interval
2nd Degree heart block - Mobitz II
Constant PR
Occasional non-conducted P wave
- Often wide QRS
- Block is usually in bundle branches of Purkinje fibres.
2nd Degree Heart Block - 2:1 Block
Two P waves per QRS
Normal consistent PR intervals.
3rd Degree Heart Block
P waves and QRS @ different rates
- Dissociation
Abnormally shaped QRS
- Ventricular origin (40bpm)
Right BBB ECG findings?
MaRRoW
Wide QRS
RSR pattern in V1.
qRs in V6.
Right BBB Aetiology?
Infarct - inferior MI Normal Variant Congenital - ASD, VSD, Fallot's Hypertrophy - RVH (PE, Cor Pulmonale). PE
Left BBB ECG findings
WiLLiaM
Wide QRS with Notched at top
T wave inversion in Lateral leads.
Left BBB aetiology?
Fibrosis
LVH - AS, HTN
Infarct - Inferior MI
Coronary HD
Bifascicular Block
RBBB + Left anterior fascicular block (RBBB + left anterior hemiblock)
Trifascicular block
RBBB + LAFB + 1st Degree AV block.
Escape Rhythms: appear late (after antipated beat)
- Atrial Escape
SAN fails to depolarise
Abnormal P wave
Normal QRS
60-80bpm
Junctional Escape?
Usually no P waves (occasionally after QRS)
Normal QRS
40-60bpm.
Ventricular Escape
Usually result of complete AV Block therefore regular P waves seen.
May be SAN Failure –> No P waves.
Wide QRS
20bpm
Extrasystoles: appear early (before anticipated beat)
- Atrial Extrasystole
Abnormal P wave
Normal QRS
Nodal Extrasystole
P wave buried in QRS or sometimes immediately before/after QRS. May be negative.
Normal QRS
Ventricular extrasystole
No P waves
Wide QRS and abnormal T waves.
Narrow Complex Tachycardia Types?
AV Nodal Re-entrant tachycardia AVRT Atrial Tachycardia Atrial Flutter Atrial Fibrillation
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.
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.
Atrial Tachycardia?
- Abnormally shaped P waves.
- Normal QRS complexes
- Rate > 150bpm
- May be associated with AV block.
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
Atrial Fibrillation
No P waves - irregular line
Irregularly irregular QRS.
Examples of Broad Complex Tachycardias?
VT
Torsades
VF
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.
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).
VF
Shapeless, rapid oscillations and no organised complexes.
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.
P wave abnormalities?
P mitrale
P pulmonale
P pulmonale
Peaked P wave.
Due to RAH
(Pulmonary HTN, Tricuspid stenosis)
P mitrale
Broad, bifid P waves
- LAH (Mitral stenosis)
QRS Abnormalities?
RVH
LVH
Narrow
Broad
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
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
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.
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
Digoxin signs on ECG?
Reverse Tick Sign
- Down-sloping ST depression
- T wave inversion
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
Hyperkalaemia signs on ECG
Tall Tented T waves
Widened QRS
Absent P waves
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?
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
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)
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.
Narrow Complex Tachycardias = SVT. Definition?
Rate >100bpm, QRS width <120ms.
Differential for Narrow complex tachy/SVT?
- Sinus Tachycardia
- Atrial (AF, Atrial Flutter, Atrial Tachy)
- AVRT
- AVNRT
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
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.
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
Prophylaxis of Narrow Complex Tachy?
1st line: B-B
- AVRT: flecainide
- AVNRT: verapamil
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.
Avoid adenosine, CCB, B-blocker in which patients?
- AF/fduke with WPW or Hx of WPW. –> VF.
- Use Amiodarone or flecainide.
Broad Complex Tachycardia definition?
Definition: Rate >100bpm, QRS width >120ms.
Differential for Broad Complex Tachycardia?
VT
Torsades de Pointes
SVT with BBB
VT can be monomorphic - caused by MI
Polymorphic: TdP.
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
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:
- 200
- 300
- 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.
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.
Causes of AF?
Common
- IHD
- Rheumatic Heart Disease
- Thyrotoxicosis
- HTN
Others
- Alcohol
- Pneumonia
- PE
- Post-op
- Hypokalaemia
- RA
Symptoms of AF?
- Asymptomatic
- Chest pain
- Palpitations
- Dyspnoea
- Faintness
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
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
- 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.
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).
Persistent AF definition?
> 7 days, may recur even after cardioversion.
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
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
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
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.
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)
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)
What is the HAS-BLED score?
Likelihood of haemorrhage and anticoagulation bleeding risk.
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
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)
Epidemiology of ACS?
Incidence 5/1000 for STEMI
Pathophysiology of ACS?
Plaque rupture, thrombosis and inflammation.
Rarely due to coronary spasm
Risk factors of ACS? Modifiable
HTN DM Smoking Increased cholesterol Obesity
Risk factors for ACS? Non-modifiable?
Age
Male
FH (MI <55yrs)
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
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)
Differentials for ACS?
- Angina
- Peri/endo/myocarditis
- Dissection
- PE, pneumothorax, pneumonia
- Costochondritis
- GI e.g GORD, spasm
- Anxiety
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).
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.
What do no Q waves mean?
A subendocardial infarct (below the endocardium)
Inferior view, RCA vessel? Which leads?
II, III, AVF
Anterolateral view, LCx vessel? Which leads?
I, aVL, V4-V6
Anteroseptal view, LAD vessel? Which leads?
V2-V4
Anterior view LMS?
V2-V6
Posterior view, RCA?
V1,2,3 reciprocal.
Changes to see are
- ST depression
- Tall, broad R-waves
- Upright T-wave
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.
Investigations - Chest X-ray ACS
Cardiomegaly
Pulmonary Oedema
Widened mediastinum: aortic rupture.
Don’t forget CCTA (coronary angiogram)
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
How to diagnose NSTEMI on ?
- Typical symptoms
- no ST elevation
- +VE) trop
How to diagnose UA on ECG?
- Typical symptoms
- no ST elevation
- ve trop.
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
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.
Prognosis of ACS?
STEMI: 30 day mortality ~15%
NSTEMI: overall mortality ~ 1-2%
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
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
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
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.
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
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
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
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.
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
Agents used for thrombolysis?
Streptokinase
Alteplase
Tenecteplase
Activate plasminogen to form plasmin. This in turn degrades fibrin and helps breakup thrombi.
Complications of Thrombolysis
Bleeding
Stroke
Arrhythmia
Allergic reaction
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.
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.
angina pectoris
atherosclerosis –> myocardial ischaemia
NICE defines anginal pain
- constricting discomfort: front chest, neck, shoulders, jaw or arms
- precipitated by physical exertion
- relieved by rest or GTN in about 5 minutes
all three = typical angina
two = atypical angina
one or none = non anginal chest pain
angina pectoris aetiology
- atheroma
- anaemia
- AS
- tachyarrhythmias
- arteritis
angina pectoris risk factors
modifiable
- smoking
- DM
- high cholesterol
- HTN
- obesity
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.
angina classification
stable: induced by effort
unstable: at rest/minimal exertion
decubitus: induced by lying down
angina differentials
- AS
- aortic aneurysm
- GI: GORD, spasm
- musculoskeletal
angina investigations
bloods: FBC, U+E, lipids, glucose, ESR, TFTs
ECG
perfusion scan
CT contrast coronary angiography
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 (
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
Heart failure definition
CO is inadequate for the body’s requirements despite adequate filling pressures.
Epidemiology of Heart failure?
Prevalence: 2% @ 50yrs –> 10% @ 80yrs
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.
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).
Low output HF: Causes of Excessive pre-load?
AR, MR, fluid overload. Initial stretching of the myocytes before contraction.
Low output HF: Causes of excessive afterload?
The pressure the heart must work against once contracting?
- AS
- HTN
- HOCM
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.
Causes of RVF?
- LVF
- Cor pulmonale
- Tricuspid and pulmonary valve disease
Symptoms of RVF?
Anorexia and Nausea
Signs of RVF?
Increased JVP + jugular venous distension
Tender smooth hepatomegaly
Pitting Oedema
Ascites
Causes of LVF?
1st: IHD
2nd: Idiopathic dilated cardiomyopathy
3rd: Systemic HTN
4th: Mitral and aortic valve disease
Specific Cardiomyopathies
Symptoms of LVF?
Fatigue Extertional dyspnoea Orthopnoea + PND Nocturnal cough (± pink, frothy sputum) Wt loss and muscle wasting
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.
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
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
Investigations of Chronic Heart Failure?
Suspected HF?
1. ECG + Tests to consider (CXr, Lipid, Renal, Thyroid, HbA1c, peak flow etc)
Still suspected HF?
- NT-proBNP (regardless of previous MI)
- 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
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
What are the actions of BNP?
- Increased GFR, and decreased renal Na reabsorption
- Decreased preload by relaxing smooth muscle
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.
What is the New York Association Classification?
- No limitation of activity
- Comfortable @ rest, dyspnoea on ordinary activity
- Marked limitation of ordinary activity
- Dyspnoea @ rest, all activity –> discomfort.
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
Management of precipitants/Cause of CCF?
- Underlying causes
Valve disease
Arrhythmias
Ischaemia - Exacerbating factors
Anaemia
Infection
Increased BP.
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.
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)
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.
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)
Invasive therapies for CCF?
- Cardiac resynchronisation ± ICD
- Heart transplant
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.
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.
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
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
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
What are the symptoms of Severe Pulmonary Oedema?
- Dyspnoea
- Orthopnoea
- Pink Frothy Sputum
Signs of severe pulmonary oedema
- Distressed, sweaty, cyanosed
- Increased HR/ Increased RR
- Increased JVP
- S3/ gallop rhythm
- Bibasal creps
- Pleural effusions
- Wheeze (cardiac asthma)
Differentials for severe pulmonary oedema?
- Asthma/COPD
- Pneumonia
- PE
How would you monitor the progress of severe pulmonary oedema?
- RR
- HR
- BP
- JVP
- urine output
- ABG
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).
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.
Causes of cardiogenic shock?
MI HEART
- MI
- Hyperkalaemia (inc electrolytes)
- Endocarditis (valve destruction)
- Aortic Dissection
- Rhythm disturbance
- Tamponade
Obstruction
- Tension pneumothorax
- Massive PE
Presentation of cardiogenic shock?
- unwell: pale, sweaty, cyanosed, distressed.
- Cold clammy peripheries
- Increased RR + increased HR
- Pulmonary oedema
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.
What is cardiac tamponade?
Accumulation of pericardial fluid within the pericardial space increasing intra-pericardial pressure, restricting cardiac filling and decreasing cardiac output.
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)
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.
Investigations of Tamponade?
Echo: Diagnostic
ECG - Electrical alternans
CXR: Globular heart
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
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.
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
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.
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)
What is the Keith- Wagener Classification?
hypertensive retinopathy
- Tortuosity and silver wiring
- AV nipping (tight constrictions)
- Flame (retinal) haemorrhages (copper wiring) and cotton wool spots (ischaemic changes) , exudates
- Papilloedema
3 + 4 = malignant hypertension
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
Management for HTN - Lifestyle
Do ABPM to confirm Dx before management
- Lifestyle
Increase exercise, decrease smoking/ETOH, salt, decrease caffeine.
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.
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.
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
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.
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.
Management of HTN for <55 or>55/Black if A + C/D doesnt work?
A + C +D
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)
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
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.
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
Symptoms of Aortic Stenosis?
- Triad: Angina, dyspnoea, syncope (esp with exercise)
- LVF: PND, orthopnoea, frothy sputum
- Arrhythmias
- Systemic emboli if endocarditis
- Sudden death
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)
Clinical indicators of severe AS?
- Quiet/absent A2
- S4 (indicative of left ventricular hypertrophy)
- Narrow pulse pressure
- Decompensation: LVF
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)
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.
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.
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.
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.
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
Symptoms of Aortic Regurg?
LVF: Exertional Dyspnoea, PND, Orthopnoea
Arrhythmias (esp AF) –> palpitations
- Forceful heart beats
Angina
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
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.
Clinical indicators of Severe AR?
- Wide PP
- Collapsing pulse
- S3
- Long Murmur
- Austin Flint murmur
- Decompensation: LVF
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.
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
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.
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)
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.
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.
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).
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
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
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
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.
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.
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.
Symptoms of Mitral Regurgitations?
- Dyspnoea
- Fatigue
- AF –> palpitations + Emboli
- Pulmonary congestion –> HTN + oedema
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
Clinical indicators of severe MR?
- Larger LV
- Decompensation: LVF
- AF
Differentials of Severe MR?
- AS
- TR
- VSD
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
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%)
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.
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.
Symptoms of mitral valve prolapse?
- Usually asymptomatic
- Autonomic dysfunction: atypical chest pain, palpitations, anxiety, panic attack
- MR: SOB, fatigue.
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.
Complications of MVP?
MR
Cerebral emboli
Arrhythmias –> sudden death
Management of MVP?
- B-B may relieve palpitations + chest pain.
Aspirin + warfarin for severe mitral regurg - Surgery if severe (commonest reason for MV surgery)
Right heart valve disease - Tricuspid regurgitation definition
Occurs when blood flows backwards through tricuspid valve. Mainly during systole.
Causes of TR?
- Functional: RV dilatation
- Rheumatic fever
- Infective endocarditis
- Carcinoid Syndrome
Can also be due to rheumatoid arthritis, Marfans, tricuspid valve prolapse.
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.
Symptoms of TR?
- Fatigue (right-sided heart failure)
- Hepatic pain on exertion
- Ascites and oedema peripherally.
- Palpitations (AF)
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
Investigations of TR?
LFTs - Cardiac Cirrhosis
Echo - TOE, TTE assessment of L/R heart EF.
ECG - AF
CXR - Cardiomegaly, pleural effusion, presence of pacemaker.
