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.
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
Diagnostic criteria for IE
Organisms that cause IE
Empiric therapy for IE
Cultures should be negative within 48 hrs of starting empiric therapy
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
Distinguish constrictive vs restrictive cardiomyopathy
Distinguish constrictive vs restrictive cardmiopathy
ALS algorithm
Tachycardia algorithm (ALS)
Bradycardia algorithm (ALS)
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
Approach to rhythm control for AF
Approach to rate control for AF
vasopressors & inotropes
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 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
Estimation of pulmonary artery pressure / RVSP using TR
Clinical signs of TR including murmur characteristics
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
Types of MI
type 4a - PCI; type 4b - in-stent thrombosis
Summary of murmurs
Mechanism of action oral anticoagulants
Echocardiographic criteria for diastolic dysfunction
Compare the features of HCM, Brugada and LQTS
