Cardiology Flashcards
Where are alpha 1 receptors found and what are their effects?
- Smooth muscle of blood vessels - incr. peripheral vasoconstriction -> incr. preload and afterload
- smooth muscle of GIT - GI sphincter contraction
- bladder neck - urinary retention
- iris dilator muscle - mydriasis
- increase in glycogenolysos
Where are beta 1 receptors found and what are the effects of beta 1 stimulation?
- heart: SA node, AV node and atrial and ventricular muscle -> increase contractility, HR, conduction velocity
- kidneys - increase renin release
Where are alpha 2 receptors located and what are effects of alpha 2 stimulation?
- CNS (hypothalamus -> prejunctional nerve terminalis) -> decrease noradrenaline synthesis and release via negative feedback
- pancreas - decrease insulin release
- platelet - platelet aggregation
- eye (ciliary body) -> decrease aqueous humor production
- glands - decrease lipopysis
Where are beta 2 receptors located and what are the effects of beta 2 stimulation?
- smooth muscle of bronchioles- bronchidilation, blood vessels -> vasodilation, uterus -> uterine relaxation
- liver -> increase glycogenolysis
- skeletal muscle -> increase contractility
- pancreas -> increase insulin release
Where are beta 3 receptors located and what are their effects?
- bladder -> bladder relaxation
- adipose tissue -> lipolysis
- thermogenesis
What is the role of exercise training / cardiac rehab in heart failure?
In compensated HFrEF -> reduces total and HF related hospitalisation, improves exercise tolerance, decreases symptoms of depression, improves health related quality of life
In HFpEF and HFmrEF - improves exercise tolerance and health related quality of life but benefits are small
What are the causes of pulmonary hypertension?
- Group 1 = pulmonary arterial hypertension (e.g. idiopathic, connective tissue disease, congenital heart disease)
- Group 2 = due to left heart disease
- Group 3 = due to chronic lung disease
- Group 4 = due to chronic VTE
- Group 5 = multifactorial (e.g. sickle cell)
What are the risk factors for sudden cardiac death in Brugada syndrome?
High risk factors
- history of sudden cardiac arrest (highest risk)
- arrhythmic syncope (second highest risk)
- sustained ventricular tachycardia
- spontaneous type 1 ECG pattern
Intermediate risk factors
- AF
- family history of sudden cardiac death and/or Brugada syndrome
- syncope (non-arrhythmic)
- drug induced type 1 ECG pattern
Possible risk factors
- male sex
- inferolateral ECG changes
What are the complications of R) heart catheterisation?
Ventricular arrhythmia or RBBB (usually transient)
CHB in patients with prior LBBB
Pulmonary artery rupture
Air embolism
What is the equation for cardiac index?
CI = CO/body surface area
What is the equation for stroke volume index?
SVI = CI/heart rate
What is the equation for systemic vascular resistance?
SVR = 80 x (mean artery pressure - CVP)/CO
What is the equation for pulmonary vascular resistance?
PVR = 80 x (mean pulmonary artery pressure - PCWP / CO)
Normal JVP waveform
Causes of elevated RA pressure
Restriction of RA and RV filling (constrictive pericarditis, restrictive cardiomyopathy, cardiac tamponade)
RV failure
Fluid overload due to renal disease
TR or TS
What does S3 indicate?
- Abnormal heart sound in early diastole, in >40 yrs.
- May represent tensing of chordae tendinae and AV ring
- suggestive of ventricular enlargement
-associated with LA pressure >20mmHg and LVEDP >15mmHg - almost always present in severe MR
What is Kussmaul’s sign? When does it occur?
Kussmaul sign = JVP increases with inspiration (NORMALLY decreases)
During inspiration => decr. intrathoracic pressure => incr. venous return to RA / RV
If pericardium or myocardium are non-compliant, venous return to R heart during inspiration is restricted
Most commonly associated with constrictive pericarditis or restrictive cardiomyopathy
Other conditions with Kussmaul sign
- RV infarct (inferior STEMI with Kussmaul sign almost always means predominant RV infarct)
- Severe TR
- Severe RV dysfunction
- Massive PE
- Rarely seen in cardiac tamponade
What is pulsus paradoxus and what are it’s causes?
Pulsus paradoxus - decrease in SBP > 10mmHg during inspiration
NORMALLY - during inspiration, venous return to RA/RV increases due to decreased intrathoracic pressure. Free wall of RV expands into unoccupied pericardial space with little impact on LV volume. Also incr. compliance of pulmonary vasculature during inspiration => decr. pulmonary venous return to LV
Important causes - cardiac tamponade, obstructive pulmonary disease (asthma, COPD), hypovolemic shock
Infrequently seen in constrictive pericarditis & restrictive cardiomyopathy
Rarely seen in PE, marked obesity, pregnancy and partial obstruction of SVC
Which conditions have a prominent Y descent in JVP? In which conditions is Y descent in JVP absent?
Prominent Y descent - tricuspid regurg, constrictive pericarditis
Y descent is absent in cardiac tamponade and tricuspid stenosis
What causes a prominent v wave in JVP?
V wave = filling of RA against closed tricuspid valve
TR
R) heart failure
Features of JVP in TR
Prominent v wave, combined c-v wave, prominent Y descent
Features of JVP in TS
Large a wave, absent Y descent
Features of JVP in cardiac tamponade
Elevated, x descent preserved, y descent absent, Kussmaul sign only very rarely
Features of JVP in constrictive pericarditis
Elevated, prominent y descent
BNP / NT-pro BNP cut off
Pulsus paradoxus mechanisms
BNP in renal failure
What are the benefits of CRT for patients with HFrEF on OMT with LBBB and duration 150msec or longer?
Normal pressure/volume relatioship
Effect of noradrenaline on PV loop
- Increased inotropy/contractility (high pressures)
- Higher systolic blood pressure (higher peak)
- Increased stroke volume (wider loop)
Effect of metaraminol on PV loop
- Vasopressor
- SBP and DBP have increased but SV is lower
- ESV is higher as aortic valve closes earlier due to higher afterload which results in EDV increasing as more blood left in ventricle after systole. No change in inotropy
Effect of GTN on PV loop
- Decreased preload/EDV (shifted left)
- Decreased stroke volume (narrower loop)
- Reduced systolic blood pressure (lower peak)
Effect of beta blockers on PV loop
- Negative inotropy
- SBP, SV and LVESP have decreased
- ESV has increased (less blood pumped) (shifted right)
- EDV has increased (because more time to fill) (shifted right)
EF has decreased (SV lower and EDV higher)
What are the indications for revascularisation in stable coronary artery disease?
- Activity limiting symptoms despite OMT
- Active patients who prefer PCI over OMT for QoL
- Anatomy for which revascularisation has a proven survival benefit (e.g. proximal LAD lesion with LVEF <30% or evidence of a large area of potentially ischaemic myocardium)
What are the indications for revascularisation in stable coronary artery disease?
Revascularisation for TVD / LM disease
Timing of angiography in NSTEMI
Timing of angiography depends on RISK:
(1) Very high risk criteria - immediate invasive strategy within 2 hours
(2) High risk criteria - early invasive strategy within 24 hours
(3) Intermediate risk criteria => angio within 72 hours of admission
(4) Low risk
Contraindications to fibrinolysis
- BP >180/110mmHg
- Recent trauma / surgery
- GI or GU bleeding within last 2-4 weeks
- Stroke / TIA in last 12 months
- Prior ICH at any time
- Current anticoagulation or coagulopathy (relative contraindication with Warfarin)
Mechanism of action of PCSK9 inhibitors
SA node action potential
Phases
- Phase 4 spontaneous depolarisation (pacemaker potential)
- Phase 0 depolarisation
- Phase 3 repolarisation
1. When membrane potential is very negative (about -60mV) => depolarisation of pacemaker cells is initiated by slow inward Na current = funny current Phase 4 (spontaneous depolarisation) 2. As the membrane potential reaches -50mV => transient or T-type calcium channels open Phase 4 3. As membrane depolarises to -40mV => long-lasting L-type calcium channels open Phase 0 depolarisation 4. With further influx of Ca ions, action potential threshold is reached (between -30mV and -40mV) 5. During phase 0 - funny Na channels and T-type calcium channels close 6. Repolarisation occurs due to opening of K channels => K efflux ; concurrently L-type Ca channels close Phase 3
Cardiac myocyte action potential
- Resting membrane potential is very negative (approx. -90mV) due to efflux of potassium ions (fast sodium channels and L-type slow calcium channels are closed) Phase 4
- Threshold voltage for depolarisation is -70mV => triggers opening of fast sodium channels
- Rapid depolarisation due to Na influx through fast sodium channels ; at the same time potassium channels close (so outward directed K conductance ceases) Phase 0 (rapid early depolarisation)
- Brief repolarisation due to transient outward K current Phase 1 (early depolarisation)
- L-type calcium channels open up when membrane potential depolarised to approx. -40mV => plateau phase that prolongs the action potential Phase 2 (plateau)
- Repolarisation occurs when L-type calcium channels become inactivated and K efflux increases Phase 3 (repolarisation)
Effective refractory period occurs because sodium channels remain inactivated after they close till membrane is repolarised
Sympathetic affects on heart
Parasympathetic affects on heart
TTE & ECG features in cardiomyopathy
Work up of cardiac amyloidosis
ECG, TTE and CMR features of cardiac amyloidosis
ECG: associated with AF, AV conduction disease, low QRS voltages in limb leads
TTE: non-dilated, marked wall thickening, “granular sparking” of myocardium, bi-atrial enlargement, normal systolic function, impaired longitudinal contraction with apical sparing
CMR - global subendocardial / transmural LGE
Clinical / radiological features of cardiac amyloidosis
Types of amyloidosis
What are the family screening recommendations in HCM?
Clinical screening for 1st degree relatives of patient with HCM (clinical exam, ECG, TTE)
- LVH typically occurs during adolescence (hence screen annually in 1st degree relatives between 12-18 yrs.)
- BUT there is a possibility for delayed-onset hypertrophy - therefore screen every 5 years for >18 yrs.
What are the genes associated with HCM? Who should have genetic testing for HCM?
Two most commonly associated genes:
(1) Beta myosin heavy chain (MYH7)
(2) Myosin binding protein C (MYBPC)
Only 50% patients have an identifiable mutation
Absence of an identified sarcomeric mutation does not exclude diagnosis of HCM
Perform genetic testing if:
- suspicion of a genetic condition known to cause LVH (Fabry’s disease, lysosomal storage diseases)
- 1st degree relatives of patient with HCM where a specific mutation has been identified
What are the clinical findings (including characteristics of murmur) in HCM?
- Ejection systolic murmur (harsh, crescendo-descrescendo)
- caused by LVOT obstruction (due to a combination of LV septal hypertrophy and SAM of the MV)
- radiates to axilla and base (BUT not to neck)
- becomes more intense with Valsalva (AS murmur either does not change or becomes less intense) & sitting upright - as both of these manouevres worsen LVOT obstruction
- becomes less intense with squatting/sitting, with handgrip and passive leg elevation - Mid-late systolic murmur at apex
- due to MR with posteriorly directed jet - JVP with prominent A wave
- S4 heart sound (in late diastole due to blood entering a hypertrophied ventricle)
- Paradoxical splitting of S2 (occurs during expiration, disappears during inspiration)
Caused by delayed closure of AV - Double carotid pulse - brisk upstroke and bifid (due to sudden deceleration of blood due to mid-systolic obstruction)
- Laterally displaced and forceful apex beat
- Systolic thrill at apex or left lower sternal border
- Parasternal lift suggests significant MR or pulm HTN
Predictors for exertional syncope in HCM
Syncope during exertion or immediately after exertion occurs in 15% patients with HCM
- risk factors including NSVT on ambulatory ECG monitor, small LV cavity size, age <30
Predictors for SCD in HCM
Resuscitated cardiac arrest
Age <30 yrs.
Early age at symptom onset
Family history of SCD
NSVT
Syncope
Exertional ischaemia or hypotension
Septal thickness >30mm
LVOT
LA enlargement
CMR - LGE
Indications for ICD in HCM
Medical management of LVOT obstruction in HCM
What are the clinical and echocardiographic signs of severity in AR?
Clinical signs of chronic severe AR
- widened pulse pressure
- collapsing pulse (water hammer pulse)
- long descrescendo high-pitched diastolic murmur
- S3 (early diastolic filling from AR)
- Low-pitched mid-diastolic rumble - as aortic regurgitant jet impinges on anterior mitral valve leaflet (Austin Flint murmur) - heard at apex
TTE signs of chronic severe AR
- abnormal aortic valve leaflets
- large jets of flow on doppler
- steep jet deceleration rate <200msec
- LV dilatation
- prominent reversal of diastolic flow in the descending aorta (AKA prominent holodiastolic reversal)
Indications for intervention in aortic regurgitation
Options for medical therapy
surgical aortic valve replacement is the main treatment option
If not fit for surgery
-ACEi and dihydropyridine CCBs may help with symptoms in symptomatic chronic severe AR, but do NOT delay progression to surgery
Prosthetic valve endocarditis
- affects metal / bioprosthetic, aortic and mitral valves equally
- early PVE more common (within 1st year) - caused by Staph, gram negative, fungi; typically affects junction between sewing ring and annulus with perivalvular abscess, dehiscence, pseudoaneurysm and fistulae
- late PVE - after 1st year, similar organisms to NVE - staph, strep viridans, strep gallolyticus, enterococcus, typically affects the leaflets
-staph PVE - most severe form of endocarditis, mortality > 48% - TTE less sensitive for PVE than NVE. New periprosthetic leak or valve dehiscence on TTE, perivalvular abscess on CT and abnormal uptake on PET are major criteria for PVE
- staph PVE and complicated PVE have worse prognosis if do not have surgery
Need at least 6 weeks Abx for staph PVE
For MRSA: fluclox + rifampicin + 2 weeks gent
For MSSA: vanc + rifampicin + 2 weeks gent - uncomplicated and non-staph PVE can be managed conservatively
Prosthetic device related infective endocarditis
- most common organism is coagulase negative Staph (60-80%)
50% methicillin resisatnt for empiric Rx is vancomycin - remove hardware in all cases - noting risk of PE when pulling lead
- reconsider need for new device - only insert new device if blood cultures negative for 72 hrs, should implant on contralateral side
Diagnostic criteria for IE
Organisms that cause IE
Empiric therapy for IE
Cultures should be negative within 48 hrs of starting empiric therapy
Indications for surgery for IE
- Complicated and staph PVE always need surgery
- Generally do not do surgery for R) sided IE unless - (1) RV dysfunction 2ndary to severe TR not responding to diuresis (2) large residual tricuspid vegetations >20mm after recurrent septic emboli (3) persistent vegetation with respiratory insufficiency requiring ventilatory support after recurrent pulmonary emboli
Indications for surgery in pts with L) sided NVE
(1) Heart failure - refractory or causing haemodynamic instability; secondary to severe valvular regurgitation or stenosis
(2) Uncontrolled infection
-growing vegetation, perivalvular abscess, fistulae, false aneurysm, new AV block, abscess
- fungal or multi-resistant organism
- Staph PVE or PVE caused by non-HACEK gram negatives
- persistently positive BCs or sepsis > 1 week despite abx
(3) Prevention of embolic phenomenon - persistent vegetations 10mm or larger despite 1 or more embolic phenomenon, despite appropriate Abx
When to suspect FH
· When to suspect FH?
1. CHD in <55 yrs, males OR <60 yrs. females
2. Family members with premature CVD
3. Family members with tendon xanthomas
4. Severely elevated LDL - > 5mmol/L in adults, >4 mmol/L in children
5. First degree relatives of patient’s with FH
· When to suspect homozygous FH? 1. Extensive xanthomas 2. Marked premature and progressive CVD 3. Total cholesterol > 13 mmol/L 4. Most patients develop CAD and aortic stenosis <20 yrs. and die before 30 yrs.
genetics of FH
· Loss of function mutation in LDLR or apoB genes, or gain of function mutation in PCSK9
· 95% cases of FH are caused by mutations in LDLR (>1000 identified mutations)
Mutations can be associated with reduced function or loss of function of LDLR -> loss of function mutations result in more severe hypercholesterolaemia and CVD
How do statins, ezetimibe and PCSK9 work
Statins- competitive inhibition of HMG-CoA reductase -> involved in the rate limiting step of intra-hepatic cholesterol synthesis (conversion of HMG-CoA -> mevalonate)
Reduction in intra-hepatic cholesterol synthesis => upregulated expression of LDLR gene via sterol regulatory element binding protein (SREBP) => reduced LDL, trigs levels, increased HDL level
Pleitropic effects - anti-inflammatory and anti-oxidant -> reduction in CRP, plaque stabilisation, anti-inflammatory effects.
Every 1mmol/L reduction in LDL -> reduces major vascular events by 20%, major coronary events by 20%, CAD death by 20%, total stroke by 17%, total mortality by 10% over 5 years
drugs that interact with statins
Clinical features of MR & clinical signs of severity
Clinical features
· High pitched holosystolic murmur
* Radiates to axilla (anterior leaflet)
* Radiates to sternum (posterior leaflet)
* Increases with handgrip
· Can also sometimes have a diastolic flow murmur
· Sharp upstroke pulse
Parasternal impulse - in second half of systole, suggestive of left atrial enlargement
Clinical signs of chronic severe MR
· Small volume pulse
· Enlarged LV with displaced apex beat
· Apical thrill
· Soft S1, early A2, loud S3, diastolic rumble
· Signs of pulm HTN
· No S4 - either has AF or poorly contractile dilated LA
Acute severe MR
S4 heart sound
Distinguish constrictive vs restrictive cardiomyopathy
Distinguish constrictive vs restrictive cardmiopathy
Echocardiographic features of restrictive cardiomyopathy
· Biatrial enlargement
· Severe diastolic dysfunction
· Increased wall thickness
· Relatively preserved LV cavity size and systolic function
· Tissue imaging parameters indicate sick tissue
Disease specific features on TTE
· Amyloidosis - RV mildly thickened, ‘granular’ myocardium
· Sarcoidosis - myocardial thinning
· Radiation - calcified valves, locally thickened pericardium or FWMA in the same region
Hypereosinophilic syndrome - thrombi
ALS algorithm
Tachycardia algorithm (ALS)
Bradycardia algorithm (ALS)
Indications for left atrial appendage closure
In non-valvular AF - 2/3 stroke is cardioembolic, of which 90% is due to LAA thrombus
LAA closure may be indicated in patients with high stroke risk (CHADSVASC >2) but contraindication to lifelong anticoagulation (e.g. high bleeding risk)
Early trials did not show advantage over Warfarin - however, NOACs now SOC- new trials underway
Approach to anticoagulation for AF
HAS-BLED score
DOAC dosing for AF
**FOR DABIGATARAN (AS PER ETG)
If <75 YRS and CrCl 30-50mL/min OR incr. risk of major bleeding => 110mg BD
If >75 yrs. and CrCl > 30mL/min => 110mg B
DOACs & renal impairment
For CKD stage 4-5 -> apixaban preferred, because less dependent on kidney function for clearance compared with other DOACs in US
High percentage of Dabigatran is renally cleared
- Do not use Dabigatran if CrCl <30 mL/min
- Do not use Apixaban if CrCl <25 mL/min
Do not use Rivaroxaban if CrCl <15 mL/min ; data for use of Rivaroxaban in CrCl 15-29mL/min is limited
DOACs & bleeding risk (compared to Warfarin)
Risk of intracranial bleeding and haemorrhagic stroke is higher with Warfarin
Risk of major bleeding overall - similar with dabigatran and rivaroxaban compared to warfarin
Rate of major bleeding with apixaban was significant lower than Warfarin
In high risk of GI bleeding -> apixaban and dabigatran preferred over Warfarin and rivaroxaban
Rate vs rhythm control for AF - advantages & disadvantages
- Overall, no different in mortality & morbidity
- Early rhythm control in newly diagnosed AF (< 12 months) - is associated with lower risk of adverse CV outcomes, lower risk of death from stroke or CV causes, compared to usual therapy
- in heart failure with LVEF <35%, catheter ablation reduces death and HF hospital
Cather ablation vs anti-arrhythmic drugs for rhythm control of AF
- Cather ablation associated with better QoL outcomes - reduced recurrence of symptomatic AF, improved healthcare usage, improved QoL
- In terms of mortality, thromboembolism, bleeding => similar outcomes
- Reduction in death and HF hospitalisation in CASTLE-AF study with catheter ablation in LVEF <35%
Predictors of failure of catheter ablation of AF
Risks of catheter ablation of AF
○ Older age
○ Longstanding, persistent AF (vs paroxysmal)
○ Increased LA size
○ Female
○ Valvular or structural heart disease
Untreated risk factors for AF e.g. obesity
Risks
- Pulmonary vein stenosis
- Atrial perforation causing atrio-oesophageal fistulas
Approach to rhythm control for AF
Approach to rate control for AF
Pathophysiology of atrial flutter & how to distinguish between typical and atypical flutter
Typical flutter - caused by a macro re-entrant circuit involving the cavo-tricuspid isthmus (RA). Characterised by upright p waves / flutter waves in V1 and negative saw-tooth flutter waves in leads II and III.
Atypical flutter - caused by macro re-entrant circuit involving another part of the atrium. Characterised by upright p waves in all leads. Ablation more challenging in atypical flutter
What could atrial flutter with 1:1 conduction be due to?
- if patient with accessory pathway / WPW is given an AV nodal blocking agent
- patient with AF on flecainide -> atrial flutter with 1:1 conduction (therefore should pair flecainide with AV nodal blocking agent
- sympathetic stimulation
vasopressors & inotropes
Isoprenaline - mechanism of action, contraindications, indications
Non-selective beta 1 and beta 2 agonist
Primarily a chronotropic & inotropic agent, not a vasopressor
Beta 1 stimulation -> predominantly chronotropic effects (increases automaticity, increases AV nodal conduction), also inotropic effects
Beta 2 stimulation -> vasodilation, reduction in peripheral vascular resistance, specifically decreases in DBP
Usually improves coronary blood flow
Indications: heart block, bradycardia with haemodynamic compromise
Contraindications:
- tachycardias / tachy-arrhythmias
- recent MI - may increase infarct size & incr. ventricular ectopic activity
- IHD / angina - may exacerbate symptoms
- HTN - may increase SBP
- Heart block due to digoxin toxicity -> isoprenaline increases risk of ventricular arrhythmias
Management of AF in heart failure
○ Consider catheter ablation for symptomatic AF in select patients with HFrEF
CASTLE-AF study - catheter ablation led to reduced death and HF hospitalisation in patients with LVEF <35%; compared to medical therapy (rate or rhythm control)
Rules for anticoagulation for managing stroke risk peri-cardioversion for AF
What is the mechanism of action of digoxin? What are the common side effects?
- cardiac glycoside
- positive inotrope (weak) and negative chronotrope
-inhibits Na/K ATPase in heart
Increases intracellular Na concentration -> decr. influx of Na and efflux of Ca via the Na/Ca pump p
Increases intracellular Ca which is stored in SR -> more Ca is released with each action potential -> increased inotropy - increases central vagal activity -> decreases HR, decreases AV conduction.
LESS effective at reducing HR during exercise or states of increased sympathetic tone
Common mild side effects - N&V, anoerexia, GI disturbance, bradycardia, rash, headache, drowsiness, dizziness
Serious adverse effects - thrombocytopenia, seizures, confusion, psychosis, ventricular arrhythmias
What can increase the risk of digoxin toxicity?
- hypokalaemia is associated with increased risk of digoxin toxicity at lower concentrations (cautious use of thiazide and loop diuretics - preference K sparing diuretics)
- hypothyroidism may increase dig levels
- renal impairment
Association between K levels and digoxin
In digoxin toxicity -> hyperkalaemia reflects the degree of digoxin toxicity and the risk of death
Hypokalaemia also increases risk of digoxin toxicity at a lower serum digoxin concentration
How does digoxin toxicity present? What is the management of digoxin toxicity?
Main clinical manifestations
(1) Cardiac - most dangerous, any type of arrhythmia (except rapidly conducting atrial arrhythmias)
(2) GI disturbance
(3) Neurological changes - including visual disturbance, confusion
Yellow eyes
Downsloping ST depression
Management of dig toxicity
(1) Supportive care A-E
(2) GI contamination - if presents <2 hours of acute intoxication
(3) Digoxin specific antibody fragments (Fab) IF:
-> Life-threatening arrhythmia (e.g. CHB, Mobitz II, VF, VT)
-> End-organ dysfunction (e.g. renal failure, altered mental status)
-> Hyperkalaemia (K>5)
HyperK reflects severity of toxicity and risk of death - but aggressive Rx of hyperK is NOT warranted, as it does NOT reduce mortality, and incr. risk of hypoK after Rx with Fab
Do not measure serum dig concentration after giving dig specific Abs because measures both unbound and bound (inactive) drug. Monitor clinically, if concentration monitoring needed - only free serum dig concentration can be interpreted
Causes of primary TR
> 90% TR is secondary / functional - primarily in association with L) heart disease
Causes of primary TR:
- Infective endocarditis
- Rheumatic heart disease
- Carcinoid syndrome
- Myxomas
- Endomyocardial fibrosis
- Congenital valve dysplasia (Ebstein’s anomaly)
- Thoracic trauma
- Iatrogenic trauma- 30% PPM/ICD leads
In severe TR, how is echocardiographic assessment of pulmonary hypertension affected?
In severe TR, pulmonary pressure are likely to be underestimated
What is the management of TR?
- Preferred intervention if surgical TV repair or replacement
- TV surgery usually occurs in conjunction with left sided valve surgery
- If severe primary or secondary TR OR
- Tricuspid annulus dilatation
- Isolated TV surgery outcomes are not ideal
- Severe primary or secondary TR with:
○ Symptoms OR assoc. RV dilation
○ Otherwise, for medical therapy - If severe secondary TR is associated with severe RV or LV dysfunction or severe pulm HTN -> would be for medical management
In these cases, need to be cautious of pulmonary HTN and RV dysfunction
- Severe primary or secondary TR with:
Indications for ICD in heart failure
Indications for ICD in dilated cardiomyopathy
Causes of dilated cardiomyopathy
20% dilated cardiomyopathy is genetic - most commonly due to mutations in genes encoding sarcomere and desmosomal proteins
- most common mutation is in Titin gene
- lamin A/C (LMNA) and desmin mutations also common
- X-linked mutation in dystrophin uncommon
80% dilated cardiomyopathy acquired
Causes of death in dilated cardiomyopathy
Predictors of SCD in dilated cardiomyopathy
Causes of death in DCM - progressive HF OR SCD due to ventricular arrhythmias (or more uncommonly - bradyarrhythmias)
Predictors of SCD
- LGE on MRI
- QRS fragmentation and T wave alternans on ECG
LGE on MRI predicts risks of all-cause mortality, heart failure hospitalisation and SCD
Estimation of pulmonary artery pressure / RVSP using TR
Clinical signs of TR including murmur characteristics
What are the indications for ICD insertion in Brugada syndrome?
- aborted cardiac arrest
- sustained ventricular arrhythmia
- nocturnal agonal respiration OR arrhythmic syncope with a positive sodium channel blocker test
Factors associated with poor prognosis in acute pericarditis
- fever > 38C
- failure to respond to therapy by 1 week
- subacute onset
- large pericardial effusion
- cardiac tamponade
Diagnostic criteria for acute pericarditis
At least 2 of the following must be present:
- pericarditic pain (sharp, pleuritic, relieved by sitting up & leaning forwards, worse when supine)
- pericardial rub
- new or worsening pericardial effusion
- ECG changes - widespread STE or PR depression
ECG pattern in acute pericarditis
Stage 1 (first few hours to days) - widespread STE. STD in aVR and V1. PR elevation in aVR and PR depression in other leads.
Stage 2 (within first week) - resolution of ECG changes
Stage 3 - diffuse TWI (after ST changes normalise)
Stage 4 - normal ECG
Management of acute pericarditis
- Treat underlying cause (e.g. dialysis for uraemia, immunosuppression for CTD, antibiotics for purulent pericarditis)
- Mainstay of therapy is - restriction of strenuous exercise + colchicine + NSAIDs; wean NSAIDs by 1 week, continue colchicine for 3 months
Colchicine - improves remission rates and reduces recurrence rates, compared to NSAID therapy alone
When should steroids be used in the treatment of pericarditis?
- recurrent or chronic pericarditis
- contraindications to NSAIDs (e.g. renal failure)
- autoimmune pericarditis
Role of pericardiotomy?
- in recurrent pericarditis with persistent symptoms, after failure of medical therapy (colchicine, NSAIDs, steroids)
Localising ST elevation to coronary arteries
What is Rilonacept?
Rilonacept is an interleukin 1 alpha and interleukin 1 beta trap
In patients with recurrent symptomatic pericarditis and elevated CRP - rilonacept led to rapid resolution and significantly lowered risk of recurrence
Contraindications for percutaneous mitral commissurotomy (PMC) / balloon valvuloplasty, for severe mitral stenosis
- LA thrombus
- more than mild MR
- significant AV disease or severe combined TS and TR
- significant subvalvular involvement
- absense of commissural fusion
- severe calcification of the valve
- MVA > 1.5cm2
- severe concomitant CAD
Types of MI
type 4a - PCI; type 4b - in-stent thrombosis
Summary of murmurs
Revascularisation for LM coronary disease
LM lesions with 50% or more stenosis are considered significant
CAGS has a mortality benefit in LM disease
In patients with low-intermediate complexity anatomy - PCI is a non-inferior option compared to CAGS when it comes to mortality, risk of stroke and MI at 3 years
What are the variables included in the GRACE score?
The GRACE score predicts the risk of in-hospital, 6 month and 3 year mortality and AMI in patients presenting with acute coronary syndrome
- SBP
- HR
- Age
- Creatinine
- Presence of heart failure
- Cardiac arrest on presentation
- STE
- Elevated cardiac enzymes
Oral anticoagulants and risk of bleeding
Risk of intracranial bleeding and haemorrhagic stroke is higher with Warfarin
Risk of major bleeding overall - similar with dabigatran and rivaroxaban compared to warfarin
Rate of major bleeding with apixaban was significant lower than Warfarin
In high risk of GI bleeding -> apixaban and dabigatran preferred over Warfarin and rivaroxaban
Mechanism of action oral anticoagulants
What are the indications for permanent pacemaker insertion for bradycardia?
ANY patient with:
- complete heart block
- high grade AV block
- Mobitz type II 2nd degree AV block
ANY symptomatic patients with:
- sinus node dysfunction
- atrial fibrillation with bradycardia (tachy - brady syndrome)
- bradycardia due to goal directed medical therapy
- 2nd degree AV block Mobitz I or marked PR prolonged (1st degree AV block) with clear correlation with symptoms
Echocardiographic criteria for diastolic dysfunction
Compare the features of HCM, Brugada and LQTS
What is the most commonly identified gene mutation in Brugada syndrome?
SCN5A - cardiac sodium channel protein type 5 subunit alpha
Autosomal dominant, loss of function mutation, with variable expression (M>F)
20-30% patients have mutations in SCN5A
What are the drugs that can unmask the Brugada ECG pattern and predispose to VF?
Anti-arrhythmics
- Procainamide
- Fleicanide
- Ajmaline
Beta blockers
Alpha agonists
Nitrates
Psychotropics
- Lithium
- TCA
Anaesthetics
- propofol
- bupivacaine
- procaine
Other substances
- ETOH
- cocaine
- Cannabis
Who should have a sodium channel blocker test?
Sodium channel blocker tests are NOT recommended in patients with spontaneous Brugada type 1 ECG pattern
if there are ECG changes suspicious for Brugada BUT NOT type 1 pattern, consider a sodium channel blocker test in the following circumstances:
- aborted cardiac arrest or sustained ventricular arrhythmia
- arrhythmic syncope
- history of nocturnal agonal respiration
- family history of Brugada syndrome or family history of sudden arrhythmic death
