Cardiology Mbchb4

ACUTE CORONARY SYNDROMES (ACS)

Defintions and Pathophysiology

1. Collective term for –

  • a. STEMI
  • b. Non-STEMI
  • c. Unstable Angina

2. Common mechanism to all ACS is rupture or erosion of the fibrous cap of a coronary artery plaque with subsequent formation of a platelet rich clot + vasoconstriction produced by platelet release of serotonin/thromboxane A2
3. Unstable angina – ischemia caused by dynamic obstruction of a coronary artery
4. NSTEMI – ischemia is severe enough to cause sufficient myocardial damage to cause elevation of serum markers of myocardial injury (Troponin, Creatinine kinase) – a neg troponin at 6 and 12 hs post onset of CP suggests unstable angina
5. Both Unstable angina and NSTEMI may be complicated by myocardial infarction with ST segment elevation if tx inadequate

Presentation

Symptoms
1. Chest pain/discomfort

  • a. tight, pressure, squeezing, crushing
  • b. midline chest, retrosternal, radiation to jaw/down L arm

2. Dyspnoea

  • a. ↑ filling LV → ↑ pulmonary sys pres → impaired gas exchange

3. N/V
4. Syncope
5. Palpitations

Signs

1. General – sweating, pallor, cool peripheries, cyanosis
2. Pulse – tachycardia, weak
3. BP – usually hypotension (high BP contra for thrombolysis due to risk of cerebral hemorrhage)
4. Auscultatory crackles

Differential Dx

1. Cardiac

  • a. Pericarditis – worse on inspiration, radiation to shoulders
  • b. AD – severe tearing pain, radiation to back

2. Pulmonary

  • a. PE
  • b. Pneumonia
  • c. Pneumothorax

3. GI

  • a. Reflux – burning, can radiate to jaw/down L arm
  • b. Peptic ulcer dis – deep, gnawing

4. MS

  • a. Chest wall injuries
  • b. Costochondritis
  • c. Herpes zoster

Ixs

1. Bloods

  • a. FBC – Hb, wcc
  • b. U&E – BUN ↑ in renal failure ie pre-renal azotemia
  • c. Cardiac markers
  • i. Tropinin T/I – markers of myocyte necrosis (>8 hrs post onset of sxs, slow to rise)
  • ii. Creatinine kinase, CK-MB, myoglobin – less sensitive but appear earlier
  • d. CRP – inflammatory marker
  • e. BNP
  • f. Glucose
  • g. Lipids – risk markers
  • h. a

2. ECG

  • a. Repeat every 15 mins if non-diagnostic + persistent CP
  • b. ST segment elevation + q waves = acute MI (total ischemia)
  • c. ST segment depression + t wave inversion + NSTEMI (partial ischemia)
  • d. Bundle branch blocks

3. Coronary angiogram

  • a. Assessment of coronary artery dis
  • b. Soft catheters introduced percutaneously into femoral artery
  • c. Advanced to coronary ostia, dye injected into vessels → outline of stenoses and occlusions, cine XRs record info

4. a

Risk Stratification – TIMI Score

1. TIMI risk score – simple prognostication scheme categorising a patient’s risk of death and ischemic events
2. Provides a basis for therapeutic decision making
3. Early coronary angiography with a view to surgery or angioplasty is recommended in pts at high risk and some who are at intermediate risk
4. Coronary stenting may stabilise the disrupted coronary plaque + ↓ angioplastic restonisis rates compared to angioplasty alone
5. Low risk pts → exercise ECG prior to hospital discharge if they remain pain free + no evidence of ischemia, HF or arrhythmias

TIMI Risk Score in ACS
1. Age >65 y
2. >3 CAD risk factors – HTN, hyperlipidaemia, F.hx, DM, smoking
3. Prior coronary artery stenosis of >50% on angiography
4. Aspirin use in last 7 days
5. At least 2x episodes of rest pain in last 24 hrs
6. ST deviation on admission ECG – depr or elev >1mm
7. Elev cardiac markers – CK-MB or tropinin

One point per RF –
1. 0-2 = low risk
2. 3-4 = intermediate risk
3. 5-7 = high risk

Emergency Treatment

1. IV access
2. Bloods
3. ECG
4. Aspirin 300mg chewed + Clopidogrel 300mg
5. Pain relief
a. Sublingual GTN
b. Morphine 2.5-5mg IV + Metoclopramide
6. a

Immediate Management of ACS

1. Antiplatelet therapy
a. Aspirin 300mg stat, then 75mg OD
i. ↓ risk of subsequent vascular events + deaths
ii.
b. Clopidogrel 75mg OD – to pts where aspirin is not tolerated or contraindicated
c. Platelet glycoprotein 11b/111a rececptor inhbitiors (eg abciximab) are sometimes added for high risk pts
2. Heparin 1mg/kg BD – interferes w thrombosus formation at site of ruptured plaque → ↓ risk of ischemic events + death
3. Anti-ischemia agents
a. Nitrates sublingually – 0.4mg Q5min for 3x doses or by IV infusion
b. Long acting nitrates – useful for recurrent ischemia
c. B-blockers
4. Plaque stabilisation
a. Statins
b. ACEI

Myocardial Infarction

1. Most common COD in developed countries
2. Sxs
a. CP similar to that of angina
i. Occurs at rest
ii. Lasts for some hours
iii. 20% of pts have no pain (silent infarctions; go unnoticed or present with hypotension, arrhythmias or p.edema)
b. Sweating
c. Dyspnea
d. N/V
e. Restlessness
3. Signs
a. May be no physical signs unless complications develop
b. Pale
c. Sweaty
d. Grey
4. Investigations
a. ECG
i. Normal ECG in early stages does not exclude dx
ii. ST segment elevation
1. >1mm in 2 or more continguous leads
iii. T wave inversion or flattening
iv. Pathological q waves (negative deflections that start the qrs complex)
1. broad >1mm
2. deep >2mm or >25% of amplitude of following r wave
3. Seen once full thickness infarction has occurred
v. New LBBB
vi. Typically changes are confined to the leads that face the infarct
1. 11, 111, AVF → inferior infarcts
2. 1, 11, AVL → lateral infarcts
3. V2-6 → anterior infarcts
b. Cardiac markers
i. Trop T/I – highly specific and sensitive to cardiac mus damage
1. released <8hrs of event onset
2. persist for several days
ii. CK – less sensitive for myocardial damage
1. Myocardial-bound (MB) isoenzyme of CK is specific for heart mus damage and the size of the enzyme rise is broadly proportional to infarct size
c. CXR
d. FBC, U&E, Glucose, Lipids (if within 12 hrs, represent pre-infarct levels but after this time, altered for up to 6 wks)
5. Management
a. Immediate
i. Ixs and Tx as per ischemic CP (above)
ii. Thrombolysis - Streptokinase IV
1. indicated in pts w CP consistent w MI and ST segment elev
2. Reperfusion rates in 50-70% of pts (vs 30% of pts with spontaneous reperfusion)
3. Benefit <12 hrs from sx onset – earlier is better
4. Commonly used – streptokinase or tissue-type plasmin activator (tPA)
5. tPA preferred in pts <50yrs w anterior MIs, in pts previously treated w streptokinease or when sys BP <100 mmHg
6. tPA must be followed by LMWH
7. Not appropriate for NSTEMI as only full clot justifies the risk of thrombolysis
8. Contraindications - ↑ bleeding risk (cereberal hemorrhage, minor head trauma), dementia, recent stroke, active peptic ulcer disease, recent surgery
iii. Metoprolol IV if HR >100 bpm – do not give if hypotension, HF, bradycardia or asthma
1. B-blockers ↓ the infarct size + ↓ incidence of sudden death
2. Should be given esp if HR >100 or persistent pain
iv. Insulin infusion if BG >11 mmol/L
1. DM pts have ↑ mortality from MI
v. Treat complications
vi. Treat persistent pain w GTN infusion
vii. Consider angiography and possible angioplasty
b. Subsequent management of uncomplicated infarction
i. Repeat ECG, cardiac markers, electrolytes 24-48hrs post admission
ii. Initiate 2ndry prevention therapy – aspirin, statin, metoprolol, ACEI, modification of CAD RFs (continued indefinitely)
1. ACEI → ↓ mortality + prevent devt of HF – start 1st day post MI
iii. Transfer from CCU to medical ward within 48hrs
iv. Gradual mobilisation if pain free (after 24-48hrs)
v. D/C at 6 days
vi. Submaximal exercise ECG prior to D/C → consider angiography if ischemic ECG changes or CP in early stages
vii. Return to work ~2 months

Post MI Complications

1. Arrhythmias
2. HF
3. Mitral regurgitation
4. Heart block
5. Rupture of free wall of infracted ventricle – usu fatal
6. Rupture of interventricular septum
7. Thromboembolism
8. Pericarditis

ATRIAL FIBRILLATION

1. Def – atrial activity chaotic and ineffective, irreg atrial rhythm 300-600 bpm, AV node conducts some of these beats → irreg ventri rhythm
2. Epidem – common, 5-10% of >65 yrs
3. Classification
a. Paroxysmal (ie self terminating) – if spontaneously terminates in <7 days (usu <24 hrs)
b. Persistent AF – fails to terminate <7 days
c. Permanent AF - >1 year and cardioversion not attempted or failed
d. Lone AF – paroxysmal, persistent or permenant AF in individuals w/o structural heart dis
4. Complications of AF – main risk → embolic stroke
5. Etiology
a. Lone AF – no obvious cause
b. HF / Ischemia
c. HTN
d. MI
e. PE
f. Mitral valve disease
g. Pneumonia
h. Hyperthyroidism
i. Alcohol
j. Post-operative
k. ↓ K
l. ↓ Mg
6. Presentation
a. Asx
b. CP
c. Palpitations
d. Dyspnea
e. Fatigue
f. Faintness, Dizziness
7. ECG – no clear p waves, fine oscillation of baseline
8. Management
a. AF emergency - acute onset and very unwell, hemodymanically unstable → emergency cardioversion
i. If unavailable → IV amiadorone
ii. Ø delay to start anti-coag
b. Acute AF
i. Tx any precipitating events – eg MI, thyrotoxicosis etc
ii. Immediate heparinisation + cardioversion with synchronised DC shock
iii. If cardioversion fails or AF recurs → amioadorone + further cardioversion attempt
c. Chr AF
i. Rate control + anticoagulation (majority of AF pts)
1. B-blockers – metoprolol, atenolol
2. CCBs – verapamil, diltiazem
3. Anti-coagulation – warfarin (↓ risk of embolic stroke from 4 to 1%)
a. Warfarin INR 2-3 (aspirin if warfarin contraindicated or v low risk of embolic stroke)
b. Contraindications – bleeding diathesis, platelets <50, compliance issues, freq falls, NSAIDs, past intracranial bleed, >80 yrs age
4. Digoxin – only if concomitant HF
d. Rate control
i. >65 yrs
ii. Contra to antiarrhythmics
iii. Unsuitable for cardioversion (eg anticoagulants contraindicated)
iv. AF > 1yr duration
v. Failed cardioversion
e. Rhythm control
i. Cardioversion – DC electrocardioversion or pharmacologic
1. Indications - symptomatic AF, CHF, younger, 1st presentation lone AR
2. Synchronised DC cardioversion – short duration AF, hemodynamically stable pts, greater efficacy
3. Pharmacologic cardioversion
a. AF <7 days → flecainide
b. AF >7 days → dofetilide, amiodarone
4. AF duration >48 hrs → Warfarin 4 wks (to prevent dislodgement of pre-existing thrombi)
a. Unless TEE (transesophageal echo demonstrates no L atrial thrombi)
5. Anti-coag continued for >1 month post cardioversion – atrial stunning may lead to de novo thrombus formation
6. Anti-arrhythmic drugs recommended if persistent sxs despite adequate rate control
a. Flecainide – for pts w no or minimal HD, Ø structural HD
7. Amiodarone – for pts in HF, structural HD
8. ~50% relapse rate within 1 yr either method
f. Rate vs Rhythm control
i. No difference in stroke risk betw pts who have converted to NSR with ant-arrhythmic tx cf to tx w rate cotnrol
g. Radiofrequency ablation (RFA)
i. Indications – cardioversion unsuccessful and rate control drugs are ineffective
ii. Method – ablation of a grp of cells near pulmonary veins where AF thought to originate

ARRHYTHMIAS

1. Symptoms
a. Asx
b. Syncope
c. Dizziness
d. Palpitations
e. Sudden death
2. Types
a. Bradycardia
i. <60 bpm
ii. More likely to cause sxs
b. Tachycardia
i. >100 bpm
ii. More likely to be symptomatic when fast + sustained
iii. Types
1. Supraventricular tachycardias (SVT)
a. Arise from atrium or AV junction
2. Ventricular tachycardias
a. Arise from the ventricles
3. General principles of management
a. Pts w adverse s/s require urgent tx of their arrhythmias
i. Ongoing CP
ii. Low CO
iii. Cold clammy extremities
iv. Hypotension
v. Impaired consciousness
vi. Pulmonary edema
b. O2 given to all pts
c. IV access
d. Serum electrolytes (K, Mg, Calcium) → corrected

Sinus Rhythms

1. Sinus arrhythmia
a. Fluctuations of autonomic tone result in phasic changes in sinus d/c rate
b. Inspiration → parasymp tone ↓ + HR ↑
c. Expiration → ↓ HR
d. Variation is normal esp children + young adults
e. Regularly irregular pulse

2. Sinus bradycardia
a. Normal during sleep + athletes
b. During acute phase of MI → often reflects ischemia of sinus node
c. Other causes → hypothermia, hypothyroidism, cholestatic jaundice, ↑ ICP, b-blocker drug therapy + other anti-arrhythmic drugs
d. Pts w persistent symptomatic bradycardia treated with a permanent cardiac pm
e. Acute situation → Atropine IV

3. Sinus tachycardia
a. Physiological response during exercise and excitement
b. Other causes → fever, anemia, HF, thyrotoxicosis, drugs (eg catecholamines, atropine)
c. Tx aimed at correcting underlying cause
d. B-blockers can be used to slow the sinus rate eg hyperthyroidism

Pathological Bradycardias

Etiology
• Sinus node dysfunction – failure of impulse formation
• AV block – failure of impulse conduction
• Also occurs during a vasovagal attack (fainting)

1. Sinus Node Dysfunction
a. Etiology – most cases caused by sick sinus syndrome → idiopathic fibrosis occurring in elderly people
b. Bradycardia is caused by –
i. intermittent failure of sinus depol (sinus arrest)
ii. failure of sinus node impulse to propoagate through the perinodal tis to atria (sinoatrial block)
c. ECG → intermittent long pauses betw consecutive p waves (>2s)
d. Slow HR predisposes to ectopic pm activity and tachyarrhythmias are common (tachy-brady syndrome)
e. Management
i. Insertion of a permanent pm is only indicated in symptomatic pts to prevent dizzy spells + blackouts
ii. Antiarrhythmic drugs are used to treat tachycardias
iii. Thromboembolism is common in sinus node dysfunction → anti-coagulation unless contraindicated
2. AV Block
a. Common causes
i. CAD
ii. Cardiomyopathy
iii. Fibrosis of conducting tissue – esp elderly
b. 1st degree
i. Result of delayed AV conduction
ii. ECG - Prolonged PR interval (>0.22s)
iii. No ∆ in HR
iv. Tx unnecessary
c. 2nd degree (partial)
i. Some atrial impulses fail to reach ventricles
ii. Mobitz type 1 (wenkebach)
1. Progressive PR interval prolongation until a p wave fails to conduct (absent qrs)
2. PR int then returns to normal + cycle repeats
iii. Mobitz type 2
1. Dropped qrs not preceded by progressive PR prolongation
iv. 2:1 or 3:1 block occurs when only every 2nd or 3rd p wave conducts to the ventricles (4:1 and 5:1 also possible)
v. Management
1. Progression to complete heart block occurs more frequently following anterior MI + in type 2 mobitz → tx with pacing is usually indicated
2. Pts w wenkebach AB block or with 2nd degree block following acute inferior infarction are usually monitored
d. 3rd degree (complete)
i. No assoc betw atrial and ventr activity
ii. Ventricular contractions maintained by a spontaneous escape rhythm (usu ~40/min) from an autonomic centre below the site of the block
iii. ECG → regular p waves and regular qrs complexes, but these occur independently of each other
iv. Sxs
1. Dizziness, blackouts (stokes-adams attacks)
2. HF may occur if ventr rate v slow
v. Management
1. Sustained complete heart block → Insertion of a permanent pm always reqd
2. In acute situation (eg MI) – recovery may be expected
a. temporarly transvenous pacing wire is only necessary for pts w adverse s/s or who are at risk of asystole (wide qrs complex, ventr pauses >3s)
b. Interim measures before placement of wire → Atropine or transcutaneous external pacing
3. Intraventricular conduction disturbances - BBB
a. Complete bundle branch block → wide QRS (>0.12s) with an abnormal pattern
b. Usu asx
c. William Marrow = LBBB →↑ W in V1 / RBBB → M in V1
d. RBBB
i. R bundle branch no longer conducts an impulse and the two ventricles do not receive an impulse simultaneously
ii. Sequential spread of an impulse – first to LV then to the RV resulting in a 2ndry R wave (RSR’) in V1 (M shaped QRS in V1-2)
iii. Occurs in normal healthy individuals
iv. Other causes – Congenital HD (ASD, VSD), Pulmonary dis (PE, Cor pulmonale), Myocardial dis (acute MI, cardiomyopathy)
e. LBBB
i. Opposite of RBBB → RSR’ pattern in the LV leads (1, AVL, V4-6) – ie M shaped QRS V5-6 (W in V1-2)
ii. Indicates important underlying cardiac pathology
iii. Causes – LV outflow obstruction (HTN, aortic stenosis), CAD (acute MI, coronary artery dis)

Pathological Tachycardias

A. SVT → narrow complex (QRS <0.12s) or broad complex if couple with BBB
B. VT → broad complex tachycardia (QRS >0.12s)

Mechanisms of tachycardia/arrhythmia production
1. ↑ automaticity
a. Arises if there is enhanced automaticity of normal conducting tissues
b. Or automaticity is acqd by damaged cells of the atria or ventricles
c. → ectopic beats and if sustained causes tachyarrhythmias
2. AV nodal Re-entry
a. May occur if there are 2 separate pathways for impulse conduction
b. Eg. impulse conducted normally through AV node and intitiates ventr depol; in certain circumstances the accessory pway is able to transmit the impulse retrogradely back into atria, thus completing a circuit and initiating a self-sustaining re-entry tachycardia
c. Often initiated by ectopic beat + then sustained by re-entrant circuit
3. Triggered activity
a. Can cause ventr arrhythmias in pts w coronary HD – incompletely repolarised cell membr

A. Supraventricular Tachycardia
1. Atrial tachyarrhythmias – AF, Atr flutter, Atrial ectopic beats
a. All arise from atrial myocardium
b. Share common etiologies – eg IHD, rheum HD, thyrotox, cardiomyopathy, WPW etc
2. Atrial fibrillation (AF)
a. Common - 5-10% of pts >65y age
b. Younger pts – tend to have paroxysmal form
c. Atrial activity is chaotic and mechanically ineffective – irregular atrial rhythm 300-600 bpm
d. AV node conducts a proportion of atrial impulses to produce an irregular ventr response
e. Main risk → embolic stroke
i. Warfarin - ↓ this risk from 4 to 1% pa
ii. Any person with an irregular pulse → ECG (+/- 24h ECG if dizzy, faint, palpitations
f. Etiology
i. HF / Ischemia
ii. HTN
iii. MI
iv. PE
v. Mitral valve disease
vi. Pneumonia
vii. Hyperthyroidism
viii. Alcohol
ix. Post-operative
x. ↓ K
xi. ↓ Mg
xii. Lone AF – no obvious cause
g. Sxs
i. Asx
ii. CP
iii. Palpitations
iv. Dyspnea
v. Fatigue
vi. Faintness, Dizziness
h. ECG
i. No clear P waves
ii. Fine oscillation of baseline
i. Management
i. Acute onset + very unwell + hemodynamically unstable → emergency cardioversion
1. if unavailable →IV amidoarone
2. Ø delay to start anti-coag
ii. Rate control if –
1. >65y
2. CAD
3. Contras to antiarrhythmics
4. Unsuitable for cardioversion (ie anticoagulants contraindicated)
5. AF lasted >1 yr
6. Past attempts failed
7. Ongoing reversible cause
8. Pharmacology for acute/paroxysmal AF
a. Diltiazem or Verapamil or Metaprolol
b. Digoxin or Amiodarone (2nd line)
9. Pharmacology for chr AF
a. B-blocker or rate limiting CCB
iii. Rhythm control if –
1. Symptomatic or CCF
2. Younger
3. Presenting first time with lone AF
4. AF 2ndry to corrected precipitant
5. Pre-cardioversion echo reqd
6. Pre-treat with sotalol or amiodarone for >4wks if ↑ risk of cardioversion failure (past failure, past AF recurrence)
7. Pharmalogical conversion → flecainide 1st choice, amiodarone if structural HD
iv. Acute AF
1. Tx any precipitating events (eg alcohol toxicity, chest infection, thyrotoxicosis, MI, pneumonia)
2. Pt s w adverse s/s require immediate heparinization + cardioversion with synchronised DC shock
3. If cardioversion fails or AF recurs → amiadorone 300mg over 1 hr given, then further attempt at cardioversion (2nd dose of amiadorone can be given)
v. Chr AF
1. Rate control
2. Consider rhythm control if – 1st episode or younger pt
3. Anticoagulation
a. Warfarin INR 2-3
b. Aspirin if warfarin contraindicated or low risk of emboli (<65y, Ø HD)
c. Contraindications of warfarin
i. Bleeding diathesis
ii. Platelets <50
iii. Compliance issues around dosing or INR monitoring
iv. Freq falls
v. On NSAIDs
vi. Past intracranial bleeds
vii. >80y age
4. Maintenance of sinus rhythm with antiarrhythmic drugs after cardioversion
5. Rate control + anticoagulation → b-blockers/verapamil + warfarin
j. AF and Thromboembolism
i. ↑ risk of thromboembolism (chr AF INR warfarinised goal 2-3)
ii. In young pts with lone AF (Ø demonstrable HD), ØDM, ØHTN → low risk and tx with aspirin alone
3. Atrial flutter
a. Often assoc w AF and usu assoc w organic dis of the heart
b. Atrial rate usu 300 bpm
c. AV node conducts every 2nd flutter beat → 150 bpm ventricular rate
d. ECG
i. Sawtooth pattern
ii. Most clearly seen when AV conduction is transiently impaired by carotid sinus massage or IV adenosine
e. Tx
i. Acute paroxysm → electr synchronised cardioversion
ii. Prophylaxis → class 1c or 111 drugs
iii. Chr arrhythmia → rate control with b-blockers
iv. Recurrent atr flutter → radiofrequency catheter ablation of focal arrhythmogenic sites
f. A
g. a
4. Atrial ectopic beats
a. Caused by premature d/c of an ectopic atrial focus
b. ECG → early + abnormal p wave, usu followed by normal QRS
c. Tx → not usu reqd unless they cause troublesome palpitations or provoke more significant arrhythmias where b-blockage may be effective
5. Atrioventricular Junctional Tachycardias – AVNRT and AVRT
6. AVNRT (atrioventricular nodal reciprocating tachycardia)
a. Most common type of SVT
b. Due to presence of 2 functioning and anatomically distinct conducting pways in the AV node
i. 1x fast conducting, 1x slow conducting
ii. During an SVT episode – one of these pways acts as the anterograde limb of a re-entry circuit while the other acts the retrograde limb
c. Hx → Sudden onset of fast regular palpitations (140-280 bpm)
d. ECG
i. p waves may be seen close to the qrs complex or not seen at all
ii. QRS complex normal shape bec ventricles activated in normal way
iii. Occasionally – qrs complex may be wide due to reat-related bbb making it difficult to distinguish from VT
7. AVRT (atrioventricular reciprocating tachycardia)
a. Due to presence of an accessory pway that connects atria and ventricles, but that lies outside the AV node
b. Accessory pways may be capable fo antegrade or retrograde conduction or both
c. Eg. WPW → accessory bundle of kent betw atr and ventr
d. Resting ECG
i. Evidence of pway if path allows some of the atr depol to pass quickly to the ventricle before it gets through the AV node
ii. Early depol of part of the ventr → shortened PR int + slurred start to QRS (delta wave)
iii. QRS is narrow`
8. Acute Management of Junctional Tachycardias
a. Emergency cardioversion reqd in pts whose arrhythmia is accompanied by adverse s/s
b. Hemodynamically stable pt → attempt manoeuvres that ↑ vagal stimulation of the sinus node
i. Valsalva manoeuvre – pt blows into 20 ml syringe w enough force to push back the plunger
ii. Carotid sinus massage – CI in presence of carotid bruit
iii. Occular pressure
c. Drug Tx – if physical manoeuvres ineffective
i. Adenosine 3mg bolus IV – v short acting AV nodal blocking drug → will terminate most junctional tachycardias
ii. If no response after 1-2 mins → 6mg bolus adenosine IV
iii. Up to 3 more 12mg boluses may be given at 1-2 min intervals if no response
iv. Transient side effects → complete heart block, hypotension, bronchospasm, nausea, flushing, chest discomfort
v. Alternative → Verapamil IV
d. LT mgt
i. Radiofrequency ablation of accessory pway via cardiac catheter 95% successful
ii. Flecainide, amiodarone, b-blockers drugs most commonly used

B. Ventricular Arrhythmias
1. Ventricular ectopic beats (extrasystoles, premature beats)
a. May be axs or pts may complain of extra beats, missed beats or heavy beats
b. Ectopic electr activity not conducted through normal conducting tissues
c. ECG – wide QRS with bizarre configuration
d. In normal individuals – ectopic beats are of no significance; tx sometimes given for sxs
e. In pts w HD – assoc w ↑ risk of sudden death → prophylaxis w amiodarone may ↓ mortality by preventing arrhythmias
2. Ventricular tachycardia (VT)
a. Both VT and VF are usu assoc w underlying HD eg Ischemia, cardiomyopathy, HTN HD
b. VT defined as 3 or more consecutive ventr beats occurring at 120 /min or faster
c. ECG → rapid ventr rhythm w broad abnormal QRS complexes (can sometimes be confused w broad complex junctional tachycardia)
d. Mgt
i. Adverse s/s w arrhythmia → urgent DC cardioversion
ii. If no hemodynamic compromise → lidocaine IV
iii. Prophylaxis → mexiletine, disopyramide, flecainide, amiodarone
iv. Pts refractory to all med tx → implantable cardioverter-defibrillator (ICD)
1. small device implanted behind rectus abdominus + connected to the heart
2. recognises VT or VF and automatically delivers a defibrillation shock
3. Ventricular fibrillation (VF)
a. Rapid + irregular ventr activation
b. No mechanical effect and thus no CO
c. Pt is pulseless + rapidly unconscious + respiration ceases (cardiac arrest)
d. VF rarely reverts spontaneously + mgt is immediate cardioversion
e. Survivors of VF are (in the absence of identifiable reversible causes eg MI, severe metab disturbance) are at high risk of sudden death
f. Tx → ICD 1st line mgt of these pts
4. Tosades de pointes
a. Uncommon
b. Characterised by rapid irregular sharp QRS complexes that continuously change from upright to inverted postion on ECG
c. Arises when ventr repolarisation (QT interval) is greatly prolonged (ie long QT syndr)
d. Causes palpitations and syncope
e. Usu terminates spontaneously but can degenerate to VF and cause sudden death
5. Cardiac arrests
a. Unconscious
b. Apnoeic
c. Absent arterial pulses – best felt in carotid artery
d. Irreversible brain damage – within 3 mins if adequate circ not established
e. Emergency mgt
i. Call for help
ii. Thump the chest firmly over sternum → will occasionally revert VT/VF to sinus rhythm
iii. Airway
1. pl pt on back on firm surface
2. Remove obstructing material eg blood, vomit
3. Open airway by flexing neck back + extending head
iv. Breathing
1. ?4x quick breaths in rapid succession mouth-to-mouth
2. watch for rise + fall of chest indicating adequate ventilation
v. Circulation
1. external chest compression
2. fingers interlocked, straight arms, sternum depressed 1-2 inches
3. Compression:Respiration ratio 30:2 @ 100 compressions/min
vi. Advanced life support
1. Continue cardiac massage throughout except during defib
2. Defib immediately (VF = most common arrhythmia in cardiac arrest)
3. 100% O2 via ambu-bag, intubate asap and initiate pos pres vent
4. IV access + ECG
5. Drugs followed by saline flush
6. IF IV access not possible → drugs via endotracheal tube (3x iV dose + diluted with 0.9% saline)
f. Prognosis of cardiac arrest
i. In many pts – resus unsuccessful (esp those who collapse outside of hosp)
ii. In pts successfully resus – prognosis is often poor due to severe underlying HD
iii. Exception is those pts who are successfully resus from VF arrest in early stages of MI where prognosis is much the same as for other pts w an infarct

Classification of antiarrhythmic drugs

1. Membrane stabilising
a. 1a – Disopyramide, procainamide, quinidine
b. 1b – lidocaine, mexiletine
c. 1c – flecainide propafenone
2. B-adrenergic blockers
a. metaprolol, atenolol, propranolol
3. Prolong AP
a. amiadorone, sotalol
4. CC blocking agents
a. Verapamil, diltiazem
5. Other
a. Adenosine, digoxin
Note – these drugs all have proarrhythmic side effects and should be used with caution, all except amiodarone are negatively ionotropic and may exarcerbate HF

Therapeutic Procedures

1. External defibrillation and cardioversion
a. Synchronised cardioversion – process by which a tachycardia or arrhythmia is terminated by therapeutic dose of electrical current to heart at specific moment in cardiac cycle
i. Used to tx hemodynamically sig SVTs incl AF, A.flutter, wide complex VTs when pulse present
b. Pulseless VT and VF → unsynchronised shocks referred to as defibrillation
2. ICD – implantable cardioverter-defibrillator
a. Automatically sense + terminate life threatening ventr arrhythmias
b. ICDs have all the functionof a pm (ie tx of bradycardia) but can also treat tachyarrhythmias using overdrive pacing, synchronised cardioversion or defib
c. Implant surgery subject to same compications as pacemakers – eg infection, erosion etc
d. Key indications for ICD therapy
i. Primary prevention – a. post MI (if LV ej fraction <30%), b. mild to mod symptomatic HF w optimal drug tx + ej fraction <35%
ii. 2ndry prevention – a. survivors of VT or VF cardiac arrest not due to transient/reversible cause, b. VT w hemodynamic compromise or sig LV impairment (ej fraction <35%)
3. Catheter ablation
a. Tx of choice for pts w recurrent arrhythmias
b. Esp – AVNRT, AVRT, atrial tachycardias, atrial flutter, AF, some forms of VT
c. Series of electrodes inserted into venous sys, then used to record activation of heart in sinus rhythm/tachycardia etc
d. Once an arrhythmia focus/circuit identified → catheter placed into this zone and culprit tis is selectively ablated using heat (radiofreq current)
e. Eliminates LT drug therapy
f. Serious side effects rare
4. Temporary or permanent pacemakers
a. Temporary
i. Transcutaneous pacing – administered via electr stimulus through 2x large adhesive gel pads
ii. Transvenous pacing
iii. Indications – mgt of transient heart block and other arrhythmias complicating acute MI, or to maintain adequate rhythm in situations of transient/reversible bradycardia (eg drug overdose, metabolic disturbance)
b. Permanent – indications;
i. Atrial pacing – SA node dis w/o AV block
ii. Ventr pacing – continuous AF, bradycardia
iii. Dual chamber – atrial electrode detects spontaneous atrial activity and triggers ventr pacing (preservation of ventr/atr rate during exercise)

CARDIAC SURGERY

wikipedia

Heart Lung (H-L) Machine

Pump, oxygenator, resoivoir, filters to remove particules (eg platelets, activated wbcs), heat exchanger (warm/cool bld), accessory pumps (for brain/hrt)

↓ temp → ↓ BMR → ↓ O2 demand → ↓ blood flow reqd

Organs differ in susceptibility to ischaemia
Brain/spine > heart > gut/kidney > limbs

Function of H-L Machine
Isolate heart to enable bloodless field to operate on outside/inside of heart
Perfuse isolated heart w preservative solution
Augment pump and lung function
Change body temp (eg hypothermia)
Filter to remove excess fluid

Cardioplegia

Cold 4-10’
↑ K
blood buffer
substrate enriched citric acid cycle intermediatries - ↑ ATP stores
Stop heart + add preserves (stops/reverses ischaemic injury)
Delivered anterograde (into aorta normal blood flow) or retrograde (not blocked by a coronary blockage)

CABG

Indics L main or 3VD or 2VD + LAD
Failure of med tx – stent, drugs
Concomitant op
Any vessel >50% diameter loss (equiv to 75% cross sectional area (CSA) loss)
Grafts LIMA (L internal mammary art), RIMA, Radial artery, SVG
Outcome 1-2% CVA mortality, <10% reop at 10 yrs
Advantages of CABG over PCI
Survival advantage, ↓ need for reintervention, chr

Valvular Surgery

Indics Severe dis +/- sxs
Limited options for medical tx
Concomitant moderate dis
Valve replacement – autograft (pulmonary valve), homograft (donor), pig/bovine
Mechanical
Animal valves – easily inserted, freely available, avoidance of LT warfarin tx, silent, durable
Mechanical valves – permanent (less degen) but requires LT anti-coag tx

Aortic dissection

Glue, sutures

CARDIOMYOPATHIES

Cardiomopathies → Myocardial disorders that are not 2ndry to CAD, HTN, congenital, valvular or pericardial abnormalities
• Abnormalities of heart muscle; many different causes
Four main types
1. Dilated
2. Hypertrophic
3. Restrictive
4. Arrhythmogenic right ventricular

Dilated Cardiomyopathy (DCM)

1. Definition
a. Characterised by a dilated L ventr which contracts poorly
b. ~25% familial
2. Clinical Features
a. SOB (usu the first complaint)
b. Embolism (from mural thrombus) – less common
c. Arrhythmia – less common
d. Subsequently → progressive HF with s/s of biventricular failure
3. Ixs
a. CXR → cardiac enlargement
b. ECG → often abnormal, non-specific changes, may include arrhythmias and t-wave flattening
c. Echo → dilated ventricles, global hypokinesis (cf ischaemia – regional contractile impairment)
d. Other tests such as coronary arteriography, viral and autoimm screen, endomyocardial biopsy – may be reqd to excl other dis that presents with the same clinical feats of DCM
i. Ischaemia
ii. HTN
iii. Congenital HD
iv. Infections
4. Mgt
a. HF and AF treated conventionally
b. Dis progression slowed by ACEI, Ang11 R blockers, Spironolactone → indicated in most cases with b-blockers
c. Ventr tachycardia not prevented with antiarrhtyhmic drugs and best treated with an internal cardioverter-defibrillator
d. A hx of embolisation or AF → anticoagulation
e. Severe cardiomyopathy → cardiac transplant

Hypertrophic Cardiomyopathy

1. Definition
a. Characterised by marked ventricular hypertrophy of unknown cause
b. Often disproportionate involvement of interventricular septum
c. The hypertrophic non-compliant ventricles impair diastolic filling → ↓ SV
d. Most cases familial, AD – caused by mutations in genes coding for proteins that regulate contraction eg troponin T, B-myosin
2. Clinical features
a. Asx
b. Dyspnea, angina or syncope
c. Atr and ventr arrhythmias are common → ventricular tachyarrhythmias are major cause of sudden death (most common in adolescence and young adulthood)
d. Carotid pulse jerky – due to rapid ejection and sudden obstruction to ventr outflow during systole
e. Ejection systolic murmur occur bec of L ventr outflow obstr
f. Pan-systolic murmur of functional m.regurg may also be heard
3. Ixs
a. ECG → usu abnormal, pattern of LV hypertrophy with no discernible cause is diagnostic
b. Echo → ventr hypertrophy w disproportionate involvement of septum
4. Mgt
a. Risk of arrhythmias and sudden death ↓ by amiadorone
b. Cardiac arrest survivors require internal defibrillator
c. CP and dyspnea tx with b-blockers and verapamil
d. Selected cases – outflow tract gradients are reduced by surgical resection or alcohol ablation of the septum or by dual chamber pacing
e. Family members screened for dis by ECG and Echo

Restrictive Cardiopmyopathy

• Rigid myocardium restricts diastolic filling
• Clinical feats resemble those of constrictive pericarditis + RH failure
o JVP elev
o Edema
o Ascites
o Hepatomegaly
o Kussmauls sign (JVP rises paradoxically w inspiration)
o Pulsus paradoxus
o AF
o Pericardial knock on ausc caused by rapid ventr filling
• Most common cause amyloidosis
• ECG, CXR, Echo are often abnormal but findings non-specific
• Dx by cardiac cathertisation which shows characteristic pres changes
• Endomyocardial biopsy may be taken during the catheter procedure thus providing histological dx
• No specific tx and prognosis poor
• Most pts dye <1 yr after dx
• Cardiac transplantation may be performed in selected cases

Cardiomyopathies 2ndry to other causes

Ischaemic Cardiomyopathy
• Myocardium has incurred damage from underlying CAD
• Damage typically occurs due to one or more MIs
• Remained one of the most common causes of HF in developed countries

Hypertensive Cardiomyopathy
• Myocardial adaptation to long standing HTN is initially hypertrophy
• Subsequently sustained HTN can lead to the syndr of HF

Alcoholic Cardiomyopathy
• Alcohol and other drugs may result in damage to the myocardium and result in HF

CARDIOVASCULAR CASES

Cases – Valvular Disease

Case 1 – Aortic Stenosis

78 M Farmer
Exertional chest tightness and dyspnea 2/12
Blackout when chasing sheep
O/E
• Slow rising pulse
• Bp 140/85
• JVP normal
• Ejection systolic murmur at base, no aortic closure sound (calcified, non-rigid, non-mobile valve)
Ixs
• LVH – L axis deviation, ↑ ventr voltage (R waves)
• CXR – normal heart size (hypertrophy does not cause ↑ heart size shadow on CXR unless other pathology), lung fields clear, but calcified aortic valve present
Management
• Surgical valve replacement – mechanical or tissue (no anti-coag reqd, ↓ resis to flow, degeration is a disadvantage)

?Primary Dx → aortic stenosis + subsequent CAD
?2ndry Dx → arrhythmia (triggered by ischemia)

Case 2 – Aortic Regurgitation

36 M Construction worker
Well, murmur noted on routine medical
O/E
• PR 80, BP 145/65, JVP N
• Murmur – decrescendo diastolic murmur L sternal edge (high pitch moving to low pitch)
• Apex beat prominent and displaced → dilation due to vol load on ventricles (due to regurgitant flow)
• Chest clear
Dx
• Aortic regurgitation
Ixs
• CXR – large heart, dilated asc aorta
• ECG – N
• Echo – dilated aortic root, moderate aortic regurg
• CT – aortic root aneurysm 6.5cm
Mgt
• Feels well
• Observation
• Operation – valve replacement, aortic root replacement
o Severity of leak → regurg causing irreversible harm to heart that will not allow normality after valve replacement
 If ej fraction <50% → SOB, tiredness, LT risk of sudden death
o Aneurysm growing – risk of rupture if >5.5cm
Other dx
• Bacterial endocarditis → valve damage

Case 3 – SBE + Mitral Regurg

40 F
Heart murmur 10 yrs ago, usually well
PC – tired, night sweats 4/52, tooth extraction 6/52 ago
Dx – bacterial endocarditis (SBE) → non-specific sxs
Heart murmur = predisposition due to high velocity blood flow
O/E
• Pale (chr illness anemia), 38.5 temp, pulse 90, BP N
• Splinter hemorrhages in nails
• Palpable spleen (chr low grade infection)
• Loud systolic murmur at apex radiating to axilla → mitral regurg
Ixs
• Blood cultures → Strep sanguis?
• Echo
• FBC, RF
• ECG
Management
• A/Bs – prolonged 6 wk course IV – to rid infection of vegetations
• Mitral valve surgery – for persistent inf, hemodynamically sig regurg or with high embolic risk of vegetations

Case 4 – Mitral Stenosis (Rheumatic HD)

25 F Samoan
Usually well, PC sudden onset racing heart + SOB (suggestive of arrhythmia)
Age 12 – polyarthralgia, rash, unwell 2/12
O/E
• Pulse 120 irreg
• BP 105/70
• Malar flush
• Early diastolic snap, low pitched diastolic murmur at apex, loud S1
• Chest wheezy
Ixs
• ECG – AF, wavy baseline, irregular R waves
• CXR – LA enlargement, pulm vein congestion
• Echo – Mitral stenosis with fusion of ant and post leaflets at commissures, LA moderate enlargement, pulmonary HTN (RV pres 50 mmHg)
Management
• Mitral valve stenosis with no leak → balloon valvatomy
• Rate control

Cases – Various Cardiovascular Cases

Case 1 – Cardiomyopathy?

43 F, Obese
PC – SOB, palpitations, ↓ exercise capacity 1/12, light headed/fainting 2/52, worried
Ixs
• ECG – polymorphic VT + showers of ectopic beats
• O2 sat 85%
• ABGs – no Aa gradient
• Normal D-dimers
• CXR – pulm.edema
• Echo

Dx – RV cardiomyopathy

Case 2 – Junctional tachycardia

44 M
Fit and well 3/12 ago
Florridly unwell now – O2 sat <85%, SBP 85, HR 120, RR 28, grey, sweaty, cool peripheries
Ixs
• ECG → ST depr, T wave inversion, tachycardia 150bpm
• CXR → fluid
• Echo – 20% ejection fraction
• Coronary angiogram – Normal
• Pt given adenosine (see below) → atrial tachycardia is unmasked (ECG now shows heart block)

Adenosine IV
• Causes transient heart block at AV node
• Useful when a pt is suspected of having a junctional tachycardia (type of SVT); ie AVNRT, AVNT

Case 3 – long QTc syndrome

26 F
Recurrent fainter – triggers; swimming, exercise, vasovagal
F.hx fainting, fit and healthy
Ixs
• ECG - normal
• Exercise stress test - provocative
QT prolongation → long repol phase (QTc)
• Fam hx of cardiac death and syncope
Management
• Avoid exacerbations that provoke dangerous situations
• Potential for torsades de pontes

Case 4 – Aortic Dissection

35 M
Acute CP – crushing, central, radiation to back , autonomic features, no prior hx
Background – Ø → CP, IHD, CAD risk factors
F.hx – father died suddenly in 30’s
O/E
• Pigeon chest → Marfans and ↑ risk of AD
• ↓ breath sounds (base)
• ↓ pulses but BP disparity (?↑BP)
• aortic regurg murmur
CXR – blunting of costophrenic angle
Management
• Analgesia
• Aggressive ↓ in BP reqd

Case 5

65 F
Normally fit and well, daughter committed suicide
PC – severe ant CP then SOB
Stress → trigger for MI (or AD due to ↑ BP)
Ixs
• ECG → T wave inversion
• Bloods → Trop T elev
• CXR → pulmonary venous congestion
• Coronary angiogram → N
Dx
• Apical ballooning Syndrome (broken heart syndr)
• Occurs w stressful event → huge outpouring of catecholamines → ventricles balloon out, recovers over 5 days but high risk of VF

CONGENITAL HEART DISEASE

• Most lethal and complex forms of congenital HD present <1 yr age
• Next most common presentation is later with a murmur in a child who is otherwise well or suffers mild exercise restriction or current chest infections

Topics
1. Innocent Murmurs
2. Atrial septal defects
3. Ventricular septal defects
4. Pulmonary valve stenosis
5. Aortic coarctation
6. Patent ductus arteriosus

Innocent Murmurs

• Heard in 40% of 4yr olds
• 2ndry to high SV + thin chest
• Exacerabeted during fever
• ECG + CXR normal
• Dx of exclusion
• Stills murmur – midsystolic, low pitched vibratory charater, heard all over precordium but best at lower sternal edge, varies w posture + disappears w neck hyper-extension
• Continuous venous hum – heard below the clavicles, differentiated from a ductal murmur by change in murmur w posture + disappearance on pressing on the side of the neck

Atrial Septal Defects (ASD)

1. Normal development of atria
a. Foramen ovale remains open during fetal devt to allow venous blood to bypass the lungs
b. After birth, the foramen ovale closes
c. In 10-20% of adults, the foarmen ovale does not entirely seal causing ↑ pulm pres (pulm HTN) – PTO (patent foramen ovale); usu asx + therefore undx
2. Defintion and Pathophysiology
a. Common – 1/1500 live births (30-40% of congenital HD in adults)
b. Blood flow LA→RA via interatrial septum
c. Large ASD (>9mm) – LA→RA shunt → vol overload of RA and RV → if left untx → HF
d. Any process the causes ↑ LV pres will worsen the L→R shunt - eg HTN
e. R heart overload of pulm vasculature → pulmonary HTN → RV failure
f. When RA pres > LA pres → reverse pres gradient across ASD + subseq R→L shunt (Eisenmengers syndr) → cyanosis
g. Types
i. Ostium secundum ASD – most common type, usu arises from enlarged foramen ovale + inadequate growth of septum secundum or excessive absorption of septum primum
1. 20% will also have mitral valve prolapse
2. Most will have no sig sxs through adulthood → 70% develop sxs by their 40’s
3. Sxs incl ↓ exercise tol, easy fatigueability, palpitation, syncope
4. Complications if untx → pulm HTN, RH failure, AF or flutter, stroke, Eisenmengers
ii. Naming of ASD
1. According to position not underlying cause
2. Ostium primum defects – close to AV valves
3. Ostium secondum defects – occur higher in the inter-atrial wall
4.
3. Presentation
a. Often asx until adulthood, although large defects may result in ↑ number of chest infections
b. Pulmonary systolic murmur due to ↑ flow across pulm valve
c. Fixed splitting of S2 and RV lift due to ↑ RV vol
d. In large shunts – diastolic murmur due to ↑ flow across tricuspid valve
4. Ixs
a. ECG
i. secundum defects have an incomplete RBBB + normal or R axis
ii. Primum defects (partial AV canal defects; common in downs) → incomplete RBBB but a superior or left axis
b. CXR – cardiomegaly and pulm.plethora
5. Tx
a. secundum defects can usu be closed via cardiac catheter around the age of 4-6 y, other defects require surgery

Ventricular Septal Defects (VSD)

1. Defintion
a. Defect in ventricular septum
b. Collectively – the most common congenital heart defects
c. Ventricular septum - inferior muscular and superior membranous portion
d. Membranous portion close to AV node is most commonly affected
e. L→R shunt → continuous refluxing of blood causes vol overload and ↑ RV pres/vol → pulm HTN
2. Presentation
a. Sxs
i. Asx – small defect
ii. SOB
iii. Poor feeding + FTT in infancy
iv. Recurrent chest infections (large defect)
b. Exmn
i. Overactive precordium
ii. Ausc – pathognomonic holsystolic murmur
3. Ixs
a. ECG – LVH, RVH
b. CXR – cardiomegaly, pulmonary plethora
c. Echo
d. Cardiac catherization – more accurately measures ventr pressures

4. Tx
a. Surgical
i. Open procedures require heart-lung machine + median sternotomy
ii. Percutaneous endovascular procedures – less invasive and done on beating heart but not suitable for all pts
b. Non-surgical
i. Smaller VSDs often close on their own as the heart grows

Pulmonary Valve Stenosis

• Common – 7% of all congenital HD
• Most cases are mild
• May be an ejection systolic murmur (+/- click) in the pulmonary area, radiating to back
• Severe → present with cyanosis in newborn period (R→L shunting via PFO (patent foramen ovale)), severe RVH + strain on the ECG; mild-moderate forms just have murmur + usu asx
• ECG – post-stenotic dilation of MPA and LPA
• CXR – may show strain if severe
• Tx – catheter balloon dilation necessary

Aortic Co-arctation

1. Defintion
a. Narrowing of aorta in the area where the ductus arteriosus - diagr 2 point 3 - (ligamentum arteriosum after regression) inserts (diagr 1 – point A)
b. Types
i. Preductal coarctation – narrowing prox to ductus arteriosus (if severe, blood flow to aortal distal of narrowing dependent on patent ductus arteriosus, hence its closure can be life threatening) – diagr 2 point B
ii. Ductal coarctation – narrowing occurs at insertion of the ductus arteriosus, usu appears when the ductus arteriosus closes - diagr 2 point A
iii. Postductal coarctation – distal narrowing (even with open ductus arteriosus, blood flow to lower body can be impaired; newborn are often critically sick from birth) - diagr 2 point C
c. A
d. a
2. Clinical features
a. Arterial HTN in R arm w normal to low BP in lower extremities (classical sign)
b. Poor peripheral pulses in femoral arteries (severe cases)
c. Coarctation prox to left subclavian artery → asynchronous radial pulses, radial-femoral delay betw R arm and femoral art while no delay with left arm radial-femoral palpation
d. Coarctation distal to left subclavian artery → synchronous radial pulses, radial-femoral delay both arms
3. Ixs
a. XR - Post-stenotic dilation of aorta results in classical ‘reverse 3 sign’ – characteristic bulging of the sign is caused by dilation of the aorta due to an indrawing of the aortic wall at site of cervical rib obstruction with consequent post-stenotic dilation
b. Echo – may not be conclusive in adults and teenagers
c. MR angiography – accurate dx; in adults with untreated coarcation, blood often reaches the lower body through collaterals eg internal throracic arteries via subclavian arteries – can be seen on MR or angiography
d. ECG – LVH (due to arterial HTN)
4. Mgt
a. Conservative if asx, but may require resection of narrow segment if arterial HTN present
b. Angioplasty – in some cases to dilate the narrowed artery
c. If coarctation left untreated → arterial HTN may become permanent due to irreversible changes in some organs eg kidney

Patent Ductus Arteriosus (PDA)

1. Normal ductus arteriosus closure
a. Fetus – ductus arteriosus (DA) = shunt connecting pulmonary artery to aortic arch
b. Allows blood to flow from RV to bypass fluid filled lungs (high resistance)
c. When the newborn takes first breath → lungs open and pulmonary pres ↓ below that of the L heart
d. At the same time, lungs release bradykinin to constrict the smooth mus wall of the DA and reduce bloodflow
e. In addition, more blood flow from pulmonary arteries to lungs → ↑ delivery of oxygenated blood to L heart further ↑ aortic pres so that blood no longer flows via the DA
f. In newborns, the DA closed within 15 hrs of birth and is completely sealed at 3 wks (due to fall in circ maternal PGs)
g. Ligamentum arteriosum = non-functional vestige of the DA remains in adult heart
2. Defintion
a. PDA is normal but reverses soon after birth
b. If PDA is persistent, there is an irregular transmission of blood between the pulmonary arteries and aortic arch
c. DA does not close but remains patent
d. Common in infants with persistent respiratory problems such as hypoxia
i. Hypoxic newborns – too little O2 reaches the lungs to produce sufficient levels of bradykinin and subseq closure of DA
ii. High occurrence in premature children (more likely to be hypoxic and thus have PDA due to underdeveloped heart/lungs)
e. In other babies – the DA remains open allowing oxygenated blood flow from aorta to pulmonary arteries → SOB, ↑ HR
f. Left untreated – infant will likely experience CHF (heart unable to meet metabolic demands of body)
3. Pres
a. Tachycardia or other arrhythmia
b. SOB or repiratory problems
c. Continuous machine like murmur upper L sternal edge due to continuous L→R flow
d. Enlarged heart
4. Ixs
a. ECG → arrhythmias, LVH
b. CXR → may reveal a patent DA, cardiomegaly
c. Echo
5. Mgt
a. Infants w/o adverse sxs may be monitored
b. Symptomatic PDA
i. Surgical – DA closed by ligation; manually tied shut or with intravascular coils/plugs leading to DA thrombus
ii. Non-surgical closure – fluid restr + PG inhibitors such as indomethacin also used successfully

Tetralogy of Fallot

Most common cyanotic heart defect and most common cause of blue baby syndr
Four classical heart malformations that present together
1. VSD
2. Pulmonic stenosis
a. RV outflow obstr valvular stenosis
b. Stenosis result fo hypertrophy of septoparietal trabeculae
3. Over-riding aorta
a. Aortic valve not restricted to the LV – thus biventricular connections
4. RVH
a. 2ndry to incr obstruction of R outflow tr
Pathophysiology
1. TOF → low oxygenation of blood (due to mixing of oxy and deoxygenated blood in LV through VSD and preferential flow through aorta (R→L shunt)
2. Children w TOF may develop acute severe cyanosis
Symptoms
1. Low blood oxygen saturation +/- cyanosis from birth or developing first year of life
2. W/o Cyanosis → baby referred to as a pink tet
3. Other sxs → heart murmur (variable), difficulty feeding, FTT, dyspnea on exertion, clubbing, polycythemia
4. Tet spells – marked by sudden incr in cyanosis, syncope and may result in hypoxic brain injury and death
Dx
1. CXR → boot like appearance
Mgt
1. Emergency mgt of tet spells
a. Acute hypoxia treated with b-blockers
b. Morphine - ↓ ventilatory drive
c. Phenylephrine - ↑ BP
d. O2 ineffective – alveolar O2 not the problem
e. Knee-chest position → ↑ aortic wave reflection → ↑ pres on L side of heart thus ↓ R→L shunt
2. Total Surgical Repair
a. Infants 1 yr of age or younger
b. <5% peri-operative mortality
c. Relief of R outflow tract stenosis
d. Repair of VSD
e. Other reconstructive work as reqd
Prognosis
1. Untreated → progressive RVH and dilation – dilated cardiomyopathy progresses to RHF then LHF
a. Survival rates 75% after 1 yr of life, 60% by 4 yrs, 30% by 10 yrs, 5% by 40 yrs
2. Repaired TOF → potential to lead normal lives with excellent cardiac function
a. Ø lifetime correction – leaky pulmonary valve, continued R outflow stenosis, arrhythmias

CARDIOVASCULAR RISK AND ATHEROSCLEROSIS

Cardiovascular Disease
• MI, Stroke, PVD → most common causes mortality + morbidity in developed countries – approx 40%

Primary Cardiovascular Prevention
• LT/lifelong mgt of people a ↑ risk but no w no evidence of CV dis to reduce the chance of vasc events and enhance life expectancy
• Requires clinical assessment (hx, exmn, ixs) + calculation of CV risk

2nd CV Prevention
• Prophylactic mgt (pharm + non-pharm) in pts w established arterial dis (coronary, periph, cerebrovascular) to prevent further arterial events + reduce mortality
• All pts require pharmacological tx

Risk Factors
1. Fixed
a. F.hx
b. Age
c. Male
2. Modifiable
a. Smoking
b. Obesity
c. Sedentary lifestyle
3. +/- Modifiable
a. HTN
b. DM
c. Hyperlipidaemia

Framingham Study
• Data used to quantify an indivdual’s risk of future cardiovascular events
• Expressed as a % over 5 or 10 yrs
• Decision to treat a popn for lifelong primary prevention has implications – financial, adherence with polypharmacy, drug side effects and interactions
• Benefit often expressed as NNT (number needed to treat to prevent one cardiovascular event)

4S – Scandinavian Simvastatin Survival Study
• ARR 6yr mortality 4%
• RRR 6yr mortality 30%
• NNT 150 patients

Both HTN and Hyperlipidaemia are continuous variables
• There is no point at which no further RR occurs

Key message
• For the primary prevention of CV dis – all people >40 yrs require an assessment of their LT CV Risk
• All people require lifestyle modification advice + the need for drug tx depends on the absolute calculated risk

Atherosclerosis

Atherosclerosis is a generalised disease

1. Pathophysiology
a. Development of lipid laden atherosclerotic plaque
i. Coronary, carotid and iliac arteries most vulnerable (cf aneurysm in abdo aorta, popliteal arteries)
ii. Endothelium allows cells, protein, lipids, minerals in + out of lumen artery
iii. LDL in intima of a vessel can become oxidised → Monocytes through endothelial layer to try to clear oxidised LDL → become mphages → large foam cells result and laid down in intima
iv. LDL and inflammatory cells cross endothelium at sites of shear stress and endothel damage
v. In some people, LDL more readily trapped in intima layer + thus more readily oxidised
vi. First macroscopic expression of atheroma = thickening of intima → pushes through media toward adventitia
vii. Expanding lesion pushes into lumen where fibrous cap formed by SM cells (which have migrated from media) along with collagen, elastin, calcium and laid down to abscess of inflammatory area
b. Plaque rupture + thrombosis
i. Rupture at edge of fibrous cap where structurally weaker
ii. Plaques that rupture generally have more inflammatory cells present, high lipid to collagen ratio and thick fibrous cap
iii. Once ruptured → layer of platelets + subseq clotting cascade laying down fibrin
iv. RBCs are caught up in thrombus causing a fibrin rich, red cell rich, platelet rich thrombus → obstruction + ischemia
c. Stable vs unstable flow limiting stenoses
2. Consequences of atherosclerosis
a. Coronary artery disease
i. Stable angina
ii. ACS
iii. Arrhythmia (consequence of MI)
b. Aorta
i. Peripheral emboli
ii. Aneurysm rupture
c. Cerebrovascular disease
i. Stroke
ii. TIA
d. Peripheral vascular disease
i. Claudication
ii. Leg ischemia
iii. Necrosis
iv. Impotence
e. Renal arteries
i. HTN
ii. RF
iii. Fluid retention
f. A
g. a
3. RFs (major)
a. Smoking
b. Dyslipidaemia – High LDL, Low HDL, High TGs
c. HTN
d. DM
e. Physical inactivity
f. Male gender
g. ↑ age
h. Metabolic syndrome
4. Other RFs
a. Obesity
b. Genetic – lipoprotein a, familial hypercholesterolemia, familial combined dyslipidaemia, hyper homocysteinaemia
c. F.Hx
d. Ethnicity
e. SES
f. Diet
g. Psycho-social – depression, stress
h. Drugs – cocaine, HRT, COX2 inhibitors, NSAIDs
5. Population based strategies to ↓ cv diseases
a. Clincially unrecognised atherosclerotic dis is common
b. Lifestyle risk factors often shared by whole popn – eg diet, smoking, physical inactivity
6. ↓ risk in ‘high risk’ individuals
a. High risk strategy targets persons at high risk because of the level and number of cv risk factors and the presence of clinical atherosclerotic dis
7. Strategies to ↓ cv risk
a. Statins (HMG-CoA reductase inhibitors) → ↓ LDL
i. Higher dose or more potent statins which ↓ LDL chol to <2 result in ↑ risk reduction
ii. Myositis – common adverse effect
iii. Less evidence that cholesterol lowering meds other than statins reduce m/m
b. Antiplatelet therapy – Aspirin 100mg OD, Clopidogrel 75mg OD
c. Antihypertensive therapy – ACEI, Ang11R blockers, B-blockers
d. Regular physical activity
e. Smoking cessation
f. Benefits of dietary and psychosocial interventions currently not proven

Ischaemic Heart Disease

IHD Clinical Manifestations
1. Angina
2. MI

ECG PRIMER

Limb leads → vertical plane
• Bipolar limb leads – 1, 11, 111
• Unipolar limb leads – AVR, AVL, AVF
V1-6 → horizontal plane
• V1/2 → RV
• V3/4 → Interventricular septum
• V5/6 → LV

Analysis
1. Rate – big sq = 0.2s, sml sq = 0.04s, calc HR by 300/number of big sqs R-R
2. Rhythm
a. Origin of impulse eg sinus
b. Narrow vs broad complex
3. Regularity
a. Regular - RR interval equal (10% variability acceptable)
b. Essentially regular - <0.16sec betw shortest + longest RR
c. Regularly irregular – RR unequal, longest and shortest RR vary by >0.16s, irregular pattern recurs in a repeating fashion
d. Irregular irregular (AF)
4. Axis
a. L axis deviation (> neg than -30’) –
i. Block of anterior bundle of main L bundle conducting sys
ii. Inferior MI
iii. WPW syndr
b. R axis deviation (> pos than 90’)
i. May be normal
ii. Conditions in which there is RV overload
iii. Dextrocardia
iv. WPW syndr
v. L posterior hemiblock
5. Morphology
a. Voltage
b. Shape
6. Normal vs Abnormal – in context of the pt
7. Identify p waves

Two thumbs-up sign – Pos QRS 1 + aVF means electrical conduction 3pm-6pm → Normal

Normal Parameters

Duration Height
P Wave <0.11 sec <2.5 mm
PR Interval 0.12 - 0.20 sec
Shorter in children / Longer in elderly
↓ as HR ↑
QRS Complex 0.06 – 0.10 sec
Q Wave – always negative - (excl 111 / aVR) <0.04 sec <25% amplitude of R wave
ST Segment >1mm displ at j point in 2+ leads facing same area of heart
T Wave <5mm in any limb lead
<10mm in any precordial lead
not <0.5mm in 1/11
QT Interval

P waves

• First deflection
• Caused by atrial depolarisation
• Abnormalities
o Broad + notched (>0.12s) → L atrial enlargement eg mitral stenosis
o Tall + peaked (>2.5mm) → RA enlargement eg. Pulm HTN
o Replaced by flutter or fibrillation waves
o Absent in sinoatrial block

QRS Complex

• Represents ventricular depolarisation
• Negative (downward) deflection preceding R wave = Q wave
o Normal q waves are small + narrow
o Deep q waves (>2mm), wide (>1mm) → indicate MI (except in AVR, V1)
• Positive deflection (upwards) = R wave (regardless of whether or not it is preceded by a q wave)
• Negative deflection (downwards) following r wave = S wave
• Ventr depol starts in septum and spreads L→R → subsequently the main free walls of the ventricles are depolarised
o Thus - in V1/2 the first deflection is upwards as septal depol spreads towards those leads (see figure below)
o The 2nd deflection is downwards (s wave) as the bigger LV (depol spreading away) outweighs effect of RV
o Opposite pattern seen in the LV leads (V5/6) with an initial downwards deflection (small q wave reflecting septal depol) followed by large R wave caused by LV depol

• LVH
o ↑ voltage induced depol of LV free wall eg systemic HTN
o tall R waves (>25mm) in LV leads V5/6 and/or deep S waves (>30mm) in RV leads V1/2
• RVH
o Eg pulmonary HTN
o R waves in RV leads
• QRS duration
o Time that excitation takes to spread through ventricle
o Wide QRS (>0.10s) → delayed conduction
o Eg RBBB, LBBB or if alternative pway of conduction (ventricular ectopic)
• T waves
o Ventricular repol
o Direction of T wave usu same as QRS complex
o Inverted T waves occur in many conditions and although usu abnormal are a non-specific finding
• PR Interval
o Start of p wave → start of qrs complex (either q wave or r wave)
o Time taken for excitation to pass from sinus node through atrium, AV node and His-purkinje system to the ventricle
o Prolonged PR interval (>0.22s) → Heart block
• ST Setment
o Period betw end of QRS complex and start of T wave
o ST elevation (>1 mm above isoelectric line) occurs in early stages of MI + in acute pericarditis
o ST segment depression (>0.5mm below isoelectric line) indicates myocardial ischemia
• QT Interval
o Extends from start of QRS complex to end of T wave
o Measure of time of repolarisation of myocardium (dependent on HR – shorter at faster HRs)
o QTc = correction of QT interval for HR (QTc = QT interval + sq root of RR interval in secs)
o Normal = <0.45s
o Long QT syndr
 Congenital
 Acquired – a. hypokalemia, b. hypomagnesaemia, c. drugs (eg quinidine, sotalol, chlorpromazine)
 ↑ risk of torsades de pontes ventricular tachycardia + sudden death

Bundle branch block (BBB)
• QRS duration >0.12s (3x sml squares)
• LBBB – R,R’ in V1/2
• RBB – R,R’ in V5/6
• William Marrow – W in LBBB and M in RBBB

Infarction → ST elevation, T wave inversion, Q wave
• Anterior Infarction – V1-4 – Ant descending coronary art (q waves)
• Inferior / Septal Infarction – 11, 111 + aVF – R or L coronary arteries (q waves)
• Lateral Infarction – 1 + aVL – circumflex coronary artery (q waves)
• Posterior Infarction – large R wave w ST depr – R coronary artery

Hyperkalemia → flat p wave, wide QRS, peaked T wave
Hypokalemia → flat t wave, u wave

HEART FAILURE MANAGEMENT

Heart Failure
• Complex syndr that can result from any structural or functional cardiac d/o
• Impaired ability of heart to function as a pump + maintain sufficient CO to meet the demands of the body → congestion + edema
• It is never a final dx → you must find underlying cause

Etiology
1. IHD
2. Dilated cardiomyopathy
3. Systemic HTN
4. Other – restrictive/hypertrophic cardiomyopathy, valvular HD, congenital HD
Note – any factor that ↑ myocardial work may aggravate existing HF or initiate failure eg arrhythmias, anemia, thyrotoxicosis, preg, obesity

Pathophysiology

Initial HF → compensatory mechanisms attempt to maintain CO + peripheral perfusion
As HF progresses → compensatory mechanisms become overwhelmed and become pathophysiological
Mechanisms –
1. SNS – sympathetic activation → improves ventr function
a. ↑ HR
b. ↑ myocardial contractility
c. Constriction venous capacitance vessels → ↑ VR → ↑ preload → Starling mechanism augments ventr function
d. Also leads to arteriolar constr → ↑ AL → will eventually ↓ CO
2. RAS
a. ↓ CO → ↓ renal perfusion → RAS activation → fluid retention
b. Salt + water retention further ↑ venous pres + maintenance of SV by starling mechanism
c. As salt + water retention increases → peripheral and pulmonary congestion cause edema + contribute to dsypnea
d. Ang 11 also causes arteriolar constr → ↑ AL → ↑ work of heart
3. Natriuretic peptides
a. ANP (released from atria)
b. BNP (released from ventricles)
c. C-type peptide (released from vascular endothelium)
d. Diuretic, natriuretic + hypotensive properties
4. Ventricular dilation
a. Myocardial failure → ↓ SV → ↑ blood remaining after systole → ↑ diastolic vol → stretching of myocardial fibres + myocardial contraction conservation via starling mechanism
b. Once HF established however, compensatory effects of cardiac dilation become limited by flattened contour of starling curve
c. Eventually, ↑ venous pres contributes to pulm and peripheral edema
d. In addition, as ventr diameter ↑ → greater tension reqd in myocardium to expel given vol of blood → ↑ O2 requirements

6 Compensatory Mechanisms in HF
1. PL (↑ fluid vol)
2. AL (↑ fluid vol + ↑ TPR via sym)
3. Contractility (sym ionotropy)
4. Salt and water retention (RAAS)
5. Myocardial hypertrophy (response to ↑ pres + contraction force reqd)
6. ANP (the only appropriate compensatory mechanism)

SV determined by VR (PL), AL, sym activation, underlying damage to heart (eg valves)
CO = HR x SV
BP = CO x TPR

Clinical Features

Clinically useful to divide HF into syndromes of R, L and biventricular (congestive) HF, but rare for any one part of heart to fail in isolation
Biventricular HF is the most common manifestation
1. LH Failure
a. Most common cause IHD
i. Other causes - systemic HTN, mitral/aortic valve dis, cardiomyopathies
b. Clinical feats largely due to pulmonary congestion
i. Exertional dyspnea (earliest sign)
ii. Fatigue + Exercise intolerance
iii. Orthopnea
iv. Paroxysmal nocturnal dyspnea
c. Signs
i. Tachypnea
ii. Tachycardia
iii. Displaced apex beat
iv. Basal lung crackles
v. S3 – due to rapid filling of ventricles
vi. In severe failure – dilation of the mitral annulus → functional M.regurg
2. RH Failure
a. Most common cause of chr RH failure is 2ndry to LH failure
b. Non-specific features
i. Fatigue
ii. Anorexia
iii. Nausea
c. Signs
i. JVP elev
ii. Hepatomegaly
iii. Dependent pitting edema (over ankles in ambulant pts, over sacrum in bed-bound pts)
iv. Ascites (less frequent)
v. Pleural effusion (less frequent)
3. Biventricular (congestive) HF
a. Reserved for cases where RH failure the result of pre-existing LH failure
b. Physical signs – combination of LH and RH failure signs
4. Systolic vs Diastolic HF
a. Systolic ventricular dysfunction most commonly due to CAD
i. LV dilation + fails to contract normally
ii.
b. Diastolic ventr dysfunction ~ 1/3 of pts w HF (esp elderly)
i. Impaired myocardial relaxation + LV filling impaired and
ii. L ventricular systolic function is normal (defined by LV ej fraction >50%)
iii. Major causes – CAD, HTN w LV hypertrophy, hypertrophic cardiomyopathy, restrictive cardiomyopathy
iv. Presentation similar to systolic HF but there may be an additional place for CCBs
5. Acute HF
a. Medical emergency (presents as pulmonary edema)
b. LH or RH failure develops over minutes/hrs
c. Most commonly occurs in the setting of an MI (may also follow PE or cardiac tamponade)

NYHA Functional Class
• 1 → Asx
• 11 → No sxs w everyday activities
• 111 → Symptomatic w minimal exertion
• 1V → Symptomatic w any exertion or at rest

Investigations

1. CXR
a. Cardiac enlargement (cardiothoracic ratio >50% on pa film)
b. Apperance of LH failure
i. Kerley b lines
ii. Hilar haziness
iii. Fluid in the R horizontal fissure
iv. Upper lobe venous engorgement
2. ECG
a. Evidence of underling causes
i. Arrhythmias
ii. Ischaemia
iii. LVH in HTN
3. Blood Tests
a. FBC → anemia exacerbates HF
b. LFTs → altered due to hepatic congestion
c. Blood glucose → DM
d. U&Es → baseline for starting diuretics + ACEIs
4. Natriuretic peptide
a. BNP or NTproBNP (N terminal fragment released from pro-BNP) to distinguish HF from other causes of dyspnea
b. Normal plasma level excludes HF
5. Doppler Echo
a. In all pts w new onset HF
b. Assessment of ventr systolic and diastolic function
c. May reveal aetiology of HF
i. Valve dis
ii. Regional wall motion abnormalities in IHD
iii. Cardiomyopathy
iv. Pericardial disease
d. Ej fraction <0.45 usu accepted as systolic dysfunction

Note - Establish underlying cause in all pts

Treatment – Chr HF

Goals of Tx – a. relieve sxs, b. retard dis progression, c. improve survival

1. General Tx
a. Correct aggravating factors – eg arrhythmias, anemia, HTN, pulmonary infections
b. Bed rest during acute exacerbations - ↓ demands on heart + promotes diuresis
c. Low level endurance exercise encouraged in compensated HF – to reverse deconditioning of peripheral muscle metabolism
d. Weight reduction
e. Ø alcohol (negative ionotropic effects)
f. Ø smoking
g. Salt restriction
h. Drugs (NSAIDs, CCBs, Steroids) that worsen HF should be discontinued
i. Flu vaccine
2. Drug Tx
a. Vasodilator therapy – Beneficial effect due to ↓ venous constriction (↓ PL) + ↓ arteriolar constr (↓ AL)
i. ACEI
1. Exs. - Captopril, Enalopril, Quinapril, Acupril
2. Action – inhibit production of ang 11
3. Effects
a. Inhibition of Ang 11 (potent vasoconstrictor)
b. ↑ concentration of bradykinin (vasodilator)
c. Enhance renal salt/water excretion
d. ↑ CO (via ↓ AL)
4. Improvement of sxs, limit devt of progressive HF and prolong survival
5. Should be given to all pts w HF
6. Start with low dose, gradual incremental increases every 1-2 wks, monitor serum K + creatinine
7. Major side effects
a. First dose hypotension (esp if large dose + on diuretic)
b. Hyperkalemia – stop K supplements + omit/reduce diuretic dose 24h prior to first ACEI dose)
c. Pre-renal failure – contraindicated in bilateral renal artery stenosis
d. Rash
e. Angioedema
f. Persistent cough – due to inhibition of bradykinin metabolism
ii. Ang 11 R anatogonists
1. Exs. – losartan, candesartan
2. Action - Block binding of ang 11 to type 1 receptor
3. Effects
a. As per ACEI
b. But Ø effect on kinin metabolism → theoretically no cough
4. Side effects as per ACEI
iii. Other vasodilators
1. ISMN (vasodilator) + hydralazine (arteriolar vasodilator) – used when ACEI/Ang11RBs contraindicated or not tolerated → improves sxs + survival
2. CCBs (eg Nifedipine, diltiazem) → ↓ AL but may have detrimental effect on LV function
a. Amlodipine is safe in HF but not of prognostic benefit!
b. B-blockers
i. Exs. – metaprolol, bisoprolol, carvediolol
ii. Effects
1. Improve sxs and exercise tolerance + survival in pts w chr stable HF
2. Thought to arise through blockade of chronically activated sympathetic system
iii. Initiate in all pts w confirmed HF due to LV systolic dysfunction after ACEI (regardless of whether sxs persist)
iv. Following b-blockade – ej fraction may ↓ but usu returns to baseline within a month and ↑ after 3 months
c. Diuretics
i. Used in pts w signs of na/water retention
ii. Promote renal na excretion + subsequent 2ndry water secretion
iii. Fluid loss → ↓ ventr filling pressures (PL) → ↓ pulmonary/systemic congestion
iv. Types
1. Loop diuretics – eg frusemide
a. Potent diuretics used in moderate/severe HF
b. When given IV → also induce arteriolar vasodilation (benefit indep of diuretic effect)
2. Thiazide diuretics – eg bendrofluazide
a. Mild diuretics that inhibit Na reasborption in distal renal tubule
3. K-sparing diuretics – eg Spironolactone
a. Relatively weak diuretic w K-sparing action
b. Low dose spironolactone (25mg OD) + conventional tx ↓ all-cause mortality by 30% in pts w moderate to severe HF and should be given to all these pts
c. Note – amiloride ↑ renal na loss/↓ K loss but no prognostic benefit identified yet
d. Digoxin
i. Benefit in pts w CHF and AF
ii. Also useful in pts in sinus rhythm who remain in severe HF despite standard tx of vasodilators, b-blockers, diuretics)
e. Anti-arrhythmic Drugs
i. Arrhythmias are freq in HF and implicated in sudden death
ii. Medical tx of complex arrhthymias is conflicting, best option may be ICD (implantable cardioverter-defibrillator)
3. Non-pharmacological Tx
a. Revascularization
i. CAD most common cause of HF
ii. Angioplasty + stenting or surgery can result in improvement of regional abnormalities in wall motion
b. Biventricular pacing
i. Insertion improves sxs and exercise tolerance in pts w severe HF
ii. Should be considered in highly symptomatic pts w systolic HF not responding to conventional medical therapy
c. Cardiac transplantation
i. Tx of choice for younger pts w severe intractable HF
ii. Expected 1 yr survival following transplant over 90% (75% at 5yrs)
iii. Death usu the result of operative mortality, organ rejection and overwhelming inf 2ndry to immunosuppressive tx

Prognosis

• There is usually gradual deterioration necessitating ↑ dose of diuretics + admission to hospital
• Prognosis is poor w severe HF (breathlessness at rest or on minimal exertion) – 1 yr survival rate ~50%

IMAGING AND INTERVENTION IN MAJOR AORTIC AND PERIPHERAL ARTERIAL PATHOLOGIES

1. Acute aortic syndromes
2. Imaging of aortic aneurysms
3. Intervention of aortic aneurysm
4. Other aortic pathologies

Acute Aortic Syndromes (AAS)

1. Defintion
a. Spectrum of acute aortic emergencies characterised by
i. Disruption to normal layers of aortic wall
ii. Assoc pain + HTN
2. Etiology
a. Traumatic aortic injury (TAI)
b. Classical aortic dissection (AD)
c. Acute intramural hematoma (AIH)
d. Penetrating atheromatous ulcer (PAU)
e. Ruptured thoracic aorti aneurysm (TAA)

Non-Traumatic AAS Imaging

1. MD-CT (multi-detector) = imaging modality of choice
a. Advantages
i. Widespread availability
ii. Ease of use in critically ill pts
iii. Rapid exmn time
iv. High sens 83-100%
v. High specificity – 100%
2. MR
a. Common Indications
i. Iodinated contrast allergy
ii. Pts w ARF
iii. Differentiation of AIH from a lo flowing patent false lumen in AD
iv. Inflammatory aortic conditions
v. Complications of type A AD
b. a
3. TEE (transesophogeal echocardiogram)
a. Advantges
i. High sens + specificity – 99% + 98% in dx of AAS in the descending thoracic aorta
ii. Quick
iii. Portable
iv. No ionising radiation
b. Disadvantages
i. Operator dependent
ii. Limited availability in acutely ill pt

Classical AD

1. Defintion
a. Collection of blood within aortic media that communicates with the true lumen by one or more intimal tears
2. Pathophysiology
a. Strong assoc betw AD and HTN
b. Intimal tears occur at sites of greatest hydrolic stress
i. R lateral wallof asc aorta
ii. Descending thoracic aorta near ligamentum arteriosum
c. Re-entrance tears common, esp at distal extent
d. Multiple fenestrations common – esp at site of branch vessel ostia
3. Types
a. Stanford Type A (60%) – involves asc aorta, regardless of site of origin
b. Stanford Type B (40%) – does not involve asc and prox transverse aorta
4. Issues to assess on MD-CT in classicalAD
a. Location of true lumen (TL)
b. Presence of TL collapse
c. Acute aortic dilation
d. Aortic rupture w hemomediastinum, left hemothorax
e. Prox involve of coronary arteries, aortic valve, pericardium
f. Cervical and abdo branch artery supply and compromise
g. Distal extent of dissection
5. Direct signs in AD
a. 2 or more enhancing channels separated by intimal falp (straight, curved or serpiginous)
6. Complications in classical AD
a. Acute aortic dilatation
b. TL collapse
c. Cervical branch artery supply and compromise
d. Abdo branch artery supply and compromise
7. Mgt of acute AD
a. Type A dissections → surgical repair
b. Type B dissections →
i. Medical therapy – aggressive anti-HTN tx
ii. Acute endovascular repair for complicated dissections

Acute Intramural Hematoma (AIH)

1. Presentation
a. Similar to clinical sxs of acute classical AD
b. May produce more pain
c. Branch vessel compromise less common
2. Dx reliant on demonstration of fresh intra-mural hemoatoma on non-contrast CT
3. ~6% of non-traumatic AAS
4. Etiology
a. Acute classical AD w thrombosed false lumen
b. Penetrating atheromatous ulcer with intra-mural hematoma
c. Spontaneous intramural hematoma due to primary vasa vasoral bleed
i. Vasa vasorum (small arteries to middle/outer coats of large blood vessels) penetrate the outer half of the aortic media and arborise (branch) within the media
ii. A bleed may extend longitudinally along aortic wall or axially
d.
5. Issues to assess on MD-CT
a. Crescenteric area of aortic wall thickening
b. Confirmed as hyperdense on non-contrast CT w narrow window settings (may be subtle on contrast enhanced CT)
c. Differentiated from intraluminal thrombus by –
i. Displaced intimal calcification
ii. Hypo/isodense on non-contrast CT
6. Natural Hx
a. Inward axial extension results in disruption of intima
b. May result in classicl AD but more often (~70%) produces well defined ulcer or lakes of mural contrast
c. These ulcers freq progress with time and may rupture
d. Arises in desc thoracic aorta ~60% of cases
e. CT surveillance impt – at least 3/12 over first yr (70% will progress)
f. Outward axial extension assoc w tranadventitial rupture with formation of false aneurysm, hemomediastinum or hemothorax

Penetrating Atheromatous Ulcer (PAU)

1. Defintion
a. Ulcer – lesion through skin or mucus membr resulting from loss of tissue, usu w inflammation
b. Atheromatous ulcer penetrating the aortic internal elastic lamina
c. Results in localised intimo-medial dissection
d. 90% involve desc TA
2. Trans-adventitial rupture in PAU
a. Rupture can result in hemomediastinum, hemothorax, false aneurysm
b. Incidence of rupture ~40% - higher than other forms of AAS
c. Signs suggesting rupture
i. Persistent or recurrent pain
ii. Interval increase in pleural effusion
iii. Ulcers >20mm wide or 10 mm deep
iv. Asc/transverse aortic location
d. Imaging features suggesting rupture
i. Hemomediastinum
ii. Hemothorax
iii. Fissuring of contrast in thrombus
3. Aggressive natural hx → more aggressive tx

Thoracic Aortic Injury

1. Aka – rupture, laceration, tear, dissection, transactions, false aneurysm
2. Pathologically – a range of lesions incl –
a. Intimal hemorrhage
b. Intimal laceration
c. Medial laceration
d. Complete laceration with false aneurysm
e. Extrinsic medial an dadventitial laceration
3. Mechanism of Injury
a. Rapid deceleration → shearing injury betw fixed and mobile aorta → intimal split
b. Split usu annular but can be longitudinal
c. 90% of injuries occur at aortic isthmus (prox desc TA betw LSCA and ligamentum arteriosum)
d. 50% fatal at site of trauma
e. 50% reach hospital → 2/3 should survive w appropriate tx
4. CXR Findings
a. Assessment of abnormal mediastinal silhouettes – more impt than reliance on objective measurements
i. Loss of contour posterior aortic arch
ii. Loss of contour desc TA
iii. Loss of aorto-pulmonary window
b. Mediastinum may be widened (>8cm at aortic arch) with normal silouhettes + vice versa
c. Most specific finding = displaced NGT to R of T4 spinous process (proximity of esophagus to aortic isthmus)
5. CT – sens approaches 100%
a. Indirect CT signs of TAI
i. Mediastinal hematoma in continuity with posterior transverse aorta or with aortic br arteries
ii. Isolated anterior mediastinal hematoma w normal aortic contour – low chance of TAI
b. Direct CT signs
i. Intramural hematoma
ii. Localised intimal disruption +/- flap
iii. Abrupt aortic contour change w pseudoaneurysm
iv. AD – uncommon
v. Contrast extravasation
c. a
6. Endoluminal repair in acute TAI
a. Now considered primary tx in most cases
b. Requires – calibrated catheter angiography + rapid availability of graft sys

Imaging of Aortic Aneurysms

Presentation
1. Acute ruptured AAA
2. Acute non-ruptured AAA – abdo pain + tenderness
3. Elective repair of non-ruptured non-acute AAA

Ruptured AAA
1. Sxs
a. Pain – abdo, flank, groin
b. Hypotension
c. Aorto-enteric fistula
d. Aorta-caval fistula
2. Mgt
a. Unstable pts → OT
b. Stable/assisted pts → CT
3. CT signs of ruptured AAA
a. Prior to over rutpure
i. Focal bulge in aneurysm contour
ii. Hazy peri-aneurysmal fat planes
iii. Fissuring of contrast into thrombus
b. Signs of overt rupture
i. Peri-aneurysmal hematoma
ii. More extensive retro-peritoneal and pelvic extra-peritoneal rupture
iii. hemoperitoneum
4. RF for AAA rupture → diameter short axis
a. 85% of existing AAAs grow
b. Larger aneurysms grow faster (>4mm / yr = rapid growth)
5. AAA Screening for high risk pts
a. Males
b. ↑ age
c. Smoking hx
d. F. Hx AAA
e. COPD = ↑ rupture risk
6. U/S
a. Assess long axis of aneurismal aorta
b. Image short axis (not necessarily transverse plane)
c. Measure max short axis diameter
7. Mgt
a. Open surgical repair
i. 30 day mortality 2-3%
ii. ↑ risk for elderly pts, CR impairment, COPD, LF, sig heart dis → consider EAR in this grp
b. EAR – Endoluminal Aneurysm Repair
i. Intial technical success ~97%, acute surgical conversion ~3%
ii. 30 day mortality 1-2%
iii. All elective pts w known AAA assessed with CT
1. CT used to assess aneurysm morphology for possible EAR
iv. CT Technique
1. No oral contrast
2. ~50% of AAAs have suitable morphology for EAR
v. Grafts then customised based on diameter and length measurements from CT
c. Aortic tube grafts – used to treat type A aneurysms
d. Bifurcated grafts – used to treat all type B and most type C aneurysms
e. Surveilance after EAR
i. Modalities – CT, AXR, U/S +/- MRI
ii. Endoleak – a condition assoc w endoluminal vascular grafts – persistence of blood flow outside of graft but within the aneurysm sac or adjacent vascular segment being treated by the graft; may be direct or indirect (retrograde)
iii. Post-EAR CT surveillance – routine initial imaging modality for first 1-2 yrs
1. non-contrast (to differentiate calcium from contrast)
iv. Post-EAR U/S surveillance – can show patent retrograde flowing aortic branch vessels, identification of retrograde endoleaks

Imaging of Lower Limb Arteries

• Non-invasive modalities have replaced invasive angiography as a diagnostic study
• Major modalities are MD-CTA and CE-MRA (mag resonance angiography)
• Catheter angiography largely used as tx modality only
• CTA vs MRA
o Both modalities image arteries during the first pass of contrast
o Similar spatial resolution
o Contrast resolution can be further improved in MRA by image subtraction, fat saturation (10x contrast resolution of CTA)
o But – CTA has better temporal resolution

CTA MRA
• Radiation Yes No
• Allergy/nephrotoxicity Yes No
• Calcium and bone produce signal similar to contrast Yes No

PERICARDIAL AND AORTIC DISEASE

1. Acute pericarditis
2. Pericardial effusion and tamponade
3. Constrictive pericarditis
4. Aortic aneurysm
5. Aortic dissection

Pericardium
• Fibroelastic sac containing a thin layer of fluid (50ml) that surrounds the heart and great vessels
• Fibrous outer layer
• Inner serous membrane (visceral pericardium) – single layer mesothelial cells
• Afferent nerves – pain sens via phrenic nerve C4-5

Acute Pericarditis

1. Defintion – inflammation of the pericardium
2. Etiology
a. Viral – coxsackie b, echovirus, HIV
b. Post MI
c. Other causes – uraemia, CT dis, trauma, inf (bacterial, TB, fungal), malignancy (breast, lung, leukaemia, lymphoma)
3. Clinical Features
a. CP – sharp retrosternal CP relieved by leaning forward, pain may be worse on inspiration, may radiate to neck and shoulders
b. Dyspnea
c. Cardinal Sign = Pericardial friction rub – scratchy, harsh, changeable, may be transient
4. Ixs
a. ECG – concave ST seg elev (saddle shaped); returns to baseline as inflammation subsides
i. Note - infarction produces convex upward ST seg elevation
b. Echo
c. Troponins can be +ve (ie troponins not always for ACS)
5. Mgt
a. Establish dx
b. Tx – underlying dis
c. NSAIDs (pain)
d. +/- steroids (used in resistant cases)
6. Complications
a. Pericardial effusion
b. Chronic pericarditis (>6-12 months)

Pericardial Effusion and Tamponade

1. Defintion
a. Accum of fluid in pericardial sac
b. May result from any of the causes of pericarditis
c. Hypothyroidism also causes pericardial effusion which rarely compromises ventr function
d. Pericardial tamponade is a medical emergency and occurs when large amounts of pericardial fluid (often accumulates rapidly) restricts diastolic ventr filling causing marked reduction in CO
2. Clinical features
a. May be asx ←→ acute collapse
b. Effusion often obscures apex beat
c. Heart sounds are soft
d. Signs of pericardial tamponade
i. Hypotension
ii. Tachycardia
iii. Elevation of JVP which rises paradoxically with inspiration (kussmauls sign)
iv. Pulsus paradoxus – fall in BP of >10 mmHg on inspiration (result of ↑ VR to the R side of the heart during inspire, the R ventr vol thus occupies more space within the rigid pericardium and impairs L ventr filling
3. Ixs
a. CXR → large globular heart
b. ECG → low-voltage complexes
c. Echo → dx tool, echo-free space around heart
d. Invasive tests to est cause of effusion may only be necessary w persistent effusion, if a purulent or tuberculous effusion is suspected or if effusion is not known to be 2ndry to an underlying illness
i. Pericardiocenteis – aspiration of fluid under echocardigraphic guidance
ii. Pericardial biopsy for culture, cytology/histology and PCR (for TB)
4. Mgt
a. Emergency pericardiocentesis
b. Pericardial fluid drained percutaneously by introducing a needle into the pericardial sac
c. If effusion recurs in spite of tx of underlying cause, excision of a pericardial segment may be necessary → fluid then absorbed through the pleural and mediastinal lymphatics

Constrictive Pericarditis

1. Defintion
a. Most cases idiopathic in origin or result from intrapericardial hemorrhage during heart surgery
b. TB inf is no longer a common cause
2. Clinical Features
a. Heart becomes encased within a rigid fibrotic pericardial sac preventing adequate diastolic filling of the ventricles
b. Clinical feats resemble those of R heart failure
i. JVP distension
ii. Dependent edema
iii. Hepatomegaly
iv. Ascites
v. Kussmauls sign (Parodoxical rise in JVP w inspiration)
vi. Pulsus paradoxus
vii. Dyspnea
viii. Pericardial knock on ausc (caused by rapid ventr filling)
c. Clinically cannot be distinguished from restrictive cardiomyopathy
3. Ixs
a. CXR → normal heart size, pericardial calcification (best seen on lateral film)
b. CT/MRI → shows pericardial thickening and calcification (best for dx)
4. Mgt
a. Surgical excision of pericardium

Aortic Aneurysm

1. Definition
a. ↑ in diameter of vessel - >50%
b. Usually abdominal and ?result from atheroma
c. Fusiform vs secular
d. True vs pseudoanurysm
i. True aneurysm – all layers of arteral wall
1. Assoc w CT dis, Marfans, ?NOT due to atherosclerosis
2. M:F 9:1
3. RFs – F.hx, HTN, smoking, Not DM and No change M:F ratio with age like atherosclerosis
4. Theory – MMP (matrix metalloproteins) asisit collagen/elastin formation (MMPase activity destroys MMPs
ii. False aneurysm – not all layers of wall, occur at points of surgical intervention, trauma or infection
2. Abdominal (AAA)
a. May be asx and found as a pulsating mass on abdo exmn or may be found as calcification on a plain x-ray
b. An expanding aneurysm may cause epigastric or back pain
c. A ruptured AAA = surgical emergency presenting w epigastric pain radiating to the back + hypovolaemic shock
d. Dx by U/S or CT
e. Surgical replacement of the aneurismal segment with a prosthetic graft is indicated for symptomatic aneurysm or large asymptomatic aneurysms (>5.5 cm)
f. In pts that are poor surgical risk, endovascular repair with insertion of an aortic stent is being employed
3. Thoracic
a. Cystic medial necrosis and atherosclerosis are the usual causes
b. CV syphilis is no longer a common cause
c. Presentation
i. May be asx
ii. Pres on local structures → back pain, dysphagia, cough
iii. Aortic regurg - if aortic root is involved
4. Presentation
a. Most asx, dx incidental
5. Ixs
a. U/S → presence + size of anerysm
b. CT → more detail, shows complications such as inflammation, rupture, assoc arterial stenosis
c. Angiography → indicated in femoro-poplietal aneurysm to define downstream arterial anatomy

Aortic Dissection – Dissecting aortic aneurysm

1. Results from a tear in the intima
a. Blood under high pres creates a false lumen in the diseased media (cleavage of laminar plane in two)
b. Type A – involves asc aorta
c. Type B – does not involve asc aorta
2. Etiology
a. HTN background
b. CTD – eg Marfans (6-9% of all dissections)
c. Assoc w bicuspid aortic valve and preg
3. Presentation
a. Abrupt onset severe tearing central CP
b. Radiation to back
c. Involvement of branch arteries may produce neurological signs, absent pulses and unequal BP in the arms
d. Syncope, HF, CVA, paraplegia, Cardiac arrests
4. Exmn
a. Hyper or Hypotension
b. Pulse deficits
c. Aortic regurg murmur
d. Neurological sequelae
5. Ixs
a. CXR → widened mediastinum
b. CT, transesophageal echocardiography or MRI → confirmation of dx
6. Mgt
a. Urgent control of BP
b. Surgical repair for proximal aortic dissection
c. Conservative mgt for type B
d. Endoluminal stenting

PULMONARY EDEMA AND ACUTE HEART FAILURE

1. Defintion
a. Edema of the lungs characterised by rapid onset of extreme breathlessness
b. Acute ↑ of LA pres → corresponding ↑ of pulmonary capillary pres → ↑ transudation of fluid into pulmonary interstitium and alveoli (cardiogenic pulmonary edema)
2. Etiology
a. Acute severe LV failure – eg MI
b. Valve disease – eg acute mitral (or aortic) regurg, mitral stenosis
c. Arrhythmias eg AF
d. Severe HTN
e. Non-cardiac causes (non-cardiogenic p.edema)
i. Iatrogenic eg fluid overload
ii. Lung injury
iii. Neurogenic eg subarachnoid hemorrhage
3. Clinical Feats
a. Sxs
i. Acute breathlessness
ii. Wheezing
iii. Anxious
iv. Productive cough of frothy blood tinged (pink) sputum
b. Signs
i. Pt wants to sit up and not lie down
ii. Anxious
iii. Sweating (↑ sympathetic activation)
iv. Tachycardia (“)
v. Tachypnea (“)
vi. Peripheral circulation shutdown (“)
vii. Ausc
1. gallop rhythm
2. wheeze/crackles throughout chest
4. Ixs
a. CXR
i. Distension of upper lobe veins (indicating ↑ pulmonary venous pres)
ii. Bilateral perihilar shadowing (bats wing distribution) – caused by alveolar fluid
iii. Kerley b lines – indicates interstitial pulmonary edema
b. ECG
i. Evidence of MI (precipitating event)
c. Cardiac enzymes
i. Evidence of MI (precipitating event)
d. ABGs
i. Hypoxaemia
ii. Initially PaCO2 falls due to overbreathing but later ↑ due to impaired gas exchange
e. Echo
i. LV function
ii. Valve disease
5. Emergency Management
a. Sit pt up
b. 60% O2 by face mask, ?CPAP
c. Furosemide 40-80 mg IV
i. Immediate vasodilation + ↓ PL
ii. Delayed diuretic response
d. Morphine 2.5-10 mg IV + antiemetic (eg metoclopramide 10 mg IV)
i. Relieves dyspnoea via vasodilation + anxiety relief (beware respiratory depression w large doses, ie >10mg)
e. Consider
i. GTN IV infusion – if pt does not improve and not hypotensive; to ↓ PL
ii. ?ACEI (↓ AL)
f. Treat exacerbating/precipitating factors
i. HTN
ii. Pulmonary infection
iii. Arrhythmias
g. Mechanical ventilation if no response to tx
h. Do not give b-blockers in pulmonary edema!!!

VALVE DISEASE

Overview
1. Rheumatic heart dis
2. Mitral valve dis
3. Aortic valve dis
4. Tricuspid valve dis
5. Pulmonary valve dis
6. Infective endocarditis

1. RHEUMATIC HEART DISEASE

a. Acute rheumatic fever
Epidemiology
• childr 5-15 yrs
Pathophysiology
• group A strep (GAS) possess antigens that cross react w heart → antibody response against GAS and inflammation of endocardium, myocardium, pericardium and + skin/joints
Presentation
• Typically follows strep pharyngitis by 2-3 wks
• Fever, anorexia, lethargy, joint pains
• Carditis sxs manifesting as dyspnea (HF or pericardial effusion), palpitations and CP
• Jones criteria – 1. carditis, 2. polyarthritis, 3. chorea, 4. erythema marginatum, 5. subcutaneous nodules

b. Chronic rheumatic heart disease
• Chr valvular heart dis develops in >50% of those affected by rheumatic fever w carditis
• Mitral valve (>90%) – fusion of mitral valve commissures + shortening of chordae tendoniae → mitral stenosis w or w/o regurg

2. MITRAL VALVE DISEASE

Mitral stenosis
1. Etiology
a. Rheumatic (almost always)
b. Calcification (elderly)
2. Pathophysiology
a. Mitral valve orifice → progressive fibrosis + calcification of leaflets + cusp fusion
b. Restricted flow from LA to LV → ↑ LA pres → pulm congestion → breathlessness → LA dilation/hypertrophy
c. Exercise poorly tolerated as ↑ HR → ↓ diastolic period → exacerbates LA pres
d. AF – due to progressive dilatation of LA (often precipitates p.edema as tachycardia accompanies AF and loss of LA contraction causes a sudden ↑ in LA pres); note that a gradual ↑ in LA pres is compensated by ↑ pulm vasc resistance and subsequent pulm HTN which is protective against p.edema)
e. All pts w m.stenosis (esp those w AF) - ↑ risk from LA thrombosis and systemic thromboembolism (require anti-coag tx)
3. Sxs
a. Breathlessness (pulmonary congestion)
b. Fatigue (low CO)
c. Edema, Ascites (RHrt failure)
d. Palpitations (AF)
e. Hemoptysis (pulmonary congestion, PE)
f. Cough (pulm congestion)
g. CP (pulm HTN)
h. Sxs of thromboembolic complications (eg stroke, ischemic limb)
4. Signs
a. AF
b. Mitral facies (pink flush cheeks; non-specific mitral valve dis)
c. Ausc – loud S1, opening snap, mid-diastolic murmur
d. Signs of ↑ pulm capillary pres – crepitations, p.edema, effusions)
5. Ixs
a. Doppler echocardiogarphy
6. Mgt
a. Medical
i. Ventricular rate and AF control → Digoxin, B-blockers, CCBs
ii. Diuretics – for pulm congestion
iii. A/B prophylaxis – protection against IE
b. Surgical
i. Mitral balloon valvuloplasty
ii. Mitral valve replacement – indicated if subst mitral reflux or valve rigid and calcified

Mitral regurgitation (Incompetence)
1. Etiology
a. Mitral valve prolapse (floppy mitral valve)
i. Congenital abnormalities or degenerative myxomatous changes
ii. Can be a feature of CT dis eg Marfans
iii. Mild prolapse – valve remains competent but bulges back into atrium during systole → mid-systolic click or Ø murmur
iv. Regurgitant – click followed by late systolic murmur (click not always audible)
v. Sig prolapse – predisposition to IE
b. LV/mitral ring dilation – eg CAD, cardiomyopathy
c. Valve cusp or chordae damage – eg Rheum HD, endocarditis
d. Papillary mus damage
e. MI
2. Pathophysiology
a. Acute mitral regurg → rapid ↑ in LA pres → marked sxs
b. Chr mitral regurg → gradual dilatation of LA w little ↑ in pres → relatively few sxs → gradual LV dilatation → eventual dyspnea + pulm.edema
3. Sxs
a. Dyspnea (pulm venous congestion)
b. Fatigue (low CO)
c. Palpitation (AF, ↑ SV)
d. Edema, Ascites (RHrt failure)
4. Signs
a. AF/Atr.flutter
b. Cardiomegaly – displaced hyperdyamic apex beat
c. Apical pansystolic murmur +/- thrill
d. Signs of pulmonary venous congestion → crepitations, p.edema, p.effusion
e. Signs of pulm HTN + RHrt failure
5. Ixs
a. ECG – LA/LV hypertrophy
b. CXR – enlarged LA/LV, pulmonary venous congestion, p.edema
c. Echo – dilated LA/LV, structural abnormalities of mitral valve (eg prolapse)
d. Doppler – detects and quantifies regurg
6. Mgt
a. Medical
i. ACEI (vasodilating agent) – to tx HTN which worsens degree of regurg
ii. Diuretics – to tx HTN
iii. AB prophylaxis – against IE
b. Surgical
i. Mitral valve repair (preferred)
ii. Mitral valve replacement – artificial (requires lifelong anti-coag tx) or tissue (degeneration over time)

3. AORTIC VALVE DISEASE

Aortic Stenosis
1. Etiology
a. Infants, Children, Adolescents → congenital a.stenosis, congenital subvalvular or supravalvular a.stenosis
b. Young adults, middle age → calcification and fibrosis of congenitally bicuspid aortic valve OR rheumatic
c. Middle age-elderly → senile degenerative a.stenosis, bicuspid valve calcification, rheumatic a.stenosis
2. Pathophysiology
a. LV pres ↑ → LV hypertrophy → coronary blood flow may then become inadequate → angina
b. When LV pres can no longer overcome outflow obstr → p.edema
c. ↓ CO due to outflow obstr → effort related hypotension or syncope w exercise
3. Sxs
a. Asx – mild or moderate a.stenosis
b. Exertional dyspnea
c. Angina
d. Exertional syncope
e. Sudden death
f. Episodes of acute p.edema
4. Signs
a. Slow rising pulse
b. Narrow pulse pres
c. Thrusting apex beat (LV pres overload)
d. Ejection systolic murmur (crescendo-decrescendo), soft S2
e. Sign of p.venous congestion (crepitations)
5. Prognosis
a. Asx for many year, but rapid deterioration when sxs do occur
6. Ixs
a. ECG – LV hypertrophy, LBBB
b. CXR – may be normal, LV enlargement, dilated asc aorta PA view
c. Echo – calcified valve w restricted opening, LV hypertrophy
d. Doppler – measures severity of stenosis
7. Mgt
a. Conservative when pts asx
b. Aortic valve replacement – if severe symptoms
c. Anti-coagulants only reqd in pts w AF or those w artificial valve replacement

Aortic Regurgitation
1. Etiology
a. Congenital
b. Rheumatic heart disease
c. IE
2. Pathophysiology
a. LV dilatation + hypertrophy → ↑ SV → pulsatile arteries
3. Sxs
a. Mild to moderate A.regurg – often asx, awareness of heart beat, palpitations
b. Severe AR – breathlessness, angina
4. Signs
a. Large vol pulse
b. Low diastolic pres
c. ↑ pulse pres
d. Early diastolic murmur, Systolic murmur

4. TRICUSPID VALVE DISEASE

Tricuspid Stenosis
• Usu rheumatic in origin
• Almost always in assoc w mitral and aortic valve dis

Tricuspid Regurg
• Etiology – Primary; 1. Rheumatic HD, 2. Endocarditis (esp IVDU)
• Etiology – 2ndry; 1. RV dilation due to chr LH failure (functional tricuspid regurg), 2. RV infarct, 3. Pulm HTN (eg core pulmonale)
• Sxs – non-specific; 1. tiredness (↓ CO), 2. Edema (venous congestion), 3. Hepatomegaly (venous congestion)

5. PULMONARY VALVE DISEASE

Pulmonary Stenosis - congenital or occurring in carcinoid syndr
Pulmonary Regurg – rarely an isolated phenomenon, usu due to pulmonary artery dilation due to pulmonary HT

6. INFECTIVE ENDOCARDITIS (IE)

Definition
Microbial inf of a heart valve, lining of cardiac chamber or blood vessel (usu bacterial)
Bacterial endocarditis classification
a. Acute bacterial endocarditis (ABE) – typically normal valves
b. Subacute bacterial endocarditis (SBE) – typically abnormal valves

Pathophysiology
• Infection typically occurs at sites of pre-existing endocardial damage (normal hearts are still at risk if virulent organism eg staph.aureus)
• Many acquired and congenital lesions increase vulnerability (esp areas of high pressure jet blood flow eg ventral septal defect, mitr/aor.regurgs)
• Infection tends to occur at sites of endothelial damage because these areas attract platelet and fibrin deposits which are then vulnerable to colonisation
• Infection occurs leading to establishment of vegetations (organisms, fibrin, platelets) that either cause obstruction or break off as emboli
• Adjacent tissues are destroyed, abscesses may form, valve regurgitation may develop/become worse as valve damage occurs, cusp and cordinae disrupted
• LV failure is a common cause of death (vegetations may cause valve destruction, severe regurgitation or valve obstruction)
• Extracardiac manifestions occur due to emboli or immune complex deposition (eg skin lesions, vasculitis)
• Vasculitis may affect any vessel
o Microscopic hematuria (common)
o Glomerulonephritis and acute renal failure may occur
o Roth spots (boat shaped retinal hemorrhages with a pale center)
o Splinter hemorrhages (fingernails or toenails)
o Osler’s nodes (painful pulp infarcts in finger or toes)
o Janeway lesions (painless palmar or plantar macules)
o Emboli may cause abscesses in the relevant organ (eg brain, heart, kidney, spleen, GI tract)

Microbiology
• Staph. Aureus – originating in skin infections, abscesses, vascular access sites – cause ABE
o Highly virulent and invasive, florid vegetations, rapid valve destruction, abscess formation
• Viridans group of Streptococci (Strep. Mitis/sanguis) – these URT commensuals enter blood via chewing, teeth brushing, dental tx etc – cause SBE

Epidemiology
• Underlying conditions (rheumatic HD 25%, congenital HD 20%, other cardiac abnormality 25%, no pre-existing cardiac abnormality 30%)
• > 50% over 60 years age

Presentation ABE
Severe fever, Prominent and changing heart murmurs, petechiae, embolic events
Presentation SBE
Persistent fever, tiredness, night sweats, weight loss, Known congenital or valvular disease, new signs of valve dysfunction/HF

Signs
• Septic signs – fevers, rigors, night sweats, malaise, weight loss
• Anemia
• Petechial rash
• Splinter hemorrhages
• Clubbing
• Splenomegaly
• Cardiac lesions – any new murmur or change in pre-existing murmur
• Hematuria

Dx
Fever + new murmur = Endocarditis until proven otherwise
Duke Criteria
Definitive endocarditis (2 major or 1 maj/3 min or 5 min)
Possible endocarditis (1 maj/1min or 3 min)
Major criteria Pos bld cult (typical org from 2 cultures) or persistent pos bld cultures (>12 hrs apart) or 3 pos cultures (>12 hrs)
Endocardial involvement – positive echo for vegetations/abscesses, new valvular regurg
Minor criteria Predisposing valvular or cardiac abnormality or IV drug user
IV drug misuse
Pyrexia >38
Embolic or vasculitic phenomenon
Blood cultures suggestive but not achieving major criteria
Suggestive echocardiographic findings

Ixs
• Blood cultures
• FBC (normochromic/normocytic anemia, neutrophil leucocytosis, high ESR/CRP)
• Urinalysis (microscopic hematuria)
• CXR (cardiomegaly)
• ECG (prolonged PR interval – AV block due to aortic root abscess)
• Echocardiography (vegetations only visible if >2mm)

Management
Fatality of BE approx 20% (higher if prosthetic valve or AB resis orgs)
• AB Tx Benzylpenicillin + Gentamicin (add Flucloxacillin if acute)
• Surgerical indications – heart failure due to valve damage, failure of AB therapy, valvular obstruction, repeated emboli, persistent bacteraemia, large vegetations (L heart), myocardial abscess, infected prosthetic valve
• AB Prophylaxis prior to dental or URT procedures or at risk pts (prosthetic valve)
• Good dental hygiene

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