Cardiology Flashcards
HFrEF definition
- Symptoms and signs of HF
- AND LVEF <50%
HFpEF Definition
- Symptoms and signs of HF
- AND LVEF >/=50%
- AND obejective evidence of:
- -Relevant structural heart disease (LV Hypertrophy, LA enlargement)
- -OR Diastolic dysfunction w/ high filling pressure shown by cath, TTE, elevated BNP, or exercise
SGLT2 evidence in CCF
Shown to reduce hospitalisation and CCF in patients with CCF and diabetes or without diabetes
Indications for CRT
- NSR, LVEF <35%, and QRS >150 ms despite optimal medical Mx
- Maybe in NSR, LVEF <35% and QRS 130-149 ms
- Maybe in LVEF <50% with high grade AV block requiring pacing to decrease hospitalisation with HF
Benefits of CRT
Decreases mortality
Decreased HF related hospitalisation
Improved QoL
Contraindication to CRT
QRS <130 ms due to possible harm
Which type of BBB has the best benefit from CRT
LBBB >RBBB
When can there be an acheived benefit with CRT when a patient has AF
Only if they are essentially pacing dependent, at least 92% of the time, otherwise no benefit in AF
Who benefits from an ICD insertion for primary prevention
Strongest evidence:
-HFrEF due to IHD and an LVEF <35% to decrease mortality
Can be considered in dilated cardiomyopathy with an LVEF <35%, but not as much benefit as IHD
What does evidence show in regards to when catheter ablation for AF should be considered
HFrEF with LVEF <35% with recurrent admissions for symptomatic AF to decrease mortality and hospitalisation
Evidence for iron transfusions in CCF for anemia
Transfuse if Tsat <20% and Ferritin <300 OR if Ferritin <100
Shown to improve QoL and hospitalisations
BNP cut off
Good test for ruling ot CCF
BNP <100 pg/ml = 83% accuracy
Why can’t BNP be used for testing when on an ARNI
Increased levels due to blockade
Use NT Pro BNP instead
Red flags for Advanced HF
- Hypotension: persistent SBP <90
- Persistent NYHA 3+ Sx
- Hospitalisations 2+ in 12 months
- Recurrent 2+ ICD shocks
Early cause of heart transplant failure
Rejection
Late cause of heart transplant failure
CAD
Evidence of stenting non culprit lesion as well as culprit lesion during AMI
Reduced mortality in stenting non culprit lesions, but timing is unclear and concern for possible complications during index procedure
Usually manage bystander disease with staged PCI
Evidence for Thromboaspiration in STEMI
Does not improve mortality or reduce infarct size
Increased risk of strokes
Evidence for radial vs femoral access for PCI
Radial Access:
-Reduced mortality, reduced bleeding, reduced vascular complications
Particularly for STEMI patients
What is a significant FFR
<0.8
DES vs BMS
DES less instent restenosis
Evidence for Aspirin in primary prevention
No clear benefit of aspirin as primary prevention
Evidence for supplemental O2 in STEMI
A/W larger infarct size, more recurrent MI and more major arrhythmia
Pharmaco-Invasive Approach for STEMI
Thrombolysis then PCI 3-24 hours post thrombolysis
STEMI: PCI time for PCI capable centre
Ideally <60 min door to PCI time
STEMI: PCI time for NOT PCI capable centre
If PCI possible <120 mins, then transfer for PCI
If not possible to have PCI <120 min, then thrombolysis within 30 mins
- If successful - PCI in 3-24 hrs
- If unsuccessful immediate Rescue PCI
High Sensitivity Troponin T
Higher negative predictive value
Reduces troponin blind period
Elevation of 13 fold limited positive predictive value
Done at 0 and 2 hours
Contraindications for prasugrel
Previous stroke/TIA
Age > 75
Weight <60 kg
Increased bleeding risk
Benefits of Stress echo vs nuclear
Nuclear has higher sensitivity and Stress echo has higher specificity
Current TGA indications for loop monitors
Syncope F.I Cryptogenic stroke (?AF)
Familial hypercholesterolaemia
AD
Very elevated LDL usually >4.9
Xanthomata highly suggestive
AMI <45 usually
FH Genetics
ApoB/E receptor mutation
Gain of PSCK9 function
Highest points for criteria of FH
LDL >8.5 (8points) Tendon Xanthomata (6 points)
Mx of FH
Screen al first degree relatives
Statins first line
If LDL >3.3 then PSCK9 inhibitors next
Familial combined hyperlipidaemia profile
High chol
High TG/LDL
Low HDL
LDL to apo-B ratio <1.2
Dyslipidamia profile in T2DM
High Tg
High LDL
Low HDL
Dyslipidamia profile in cholestatic liver/PBC
Marked chol increase - accumulation of lipoprotein X
Dyslipidamia profile in nephrotic syndrome
Marked total chol and LDL increase
Dyslipidamia profile in CKD
Less prominent increase in LDL and Tg
Low HDL
Dyslipidamia profile in hypothyroidism
Raised LDL predominantly
Sometimes high Tg
Dyslipidamia profile in obesity
High chol High LDL High VLDL High Tg Low HDL
Dyslipidamia profile in smoking
Low HDL
Dyslipidamia profile in ETOH
Raised Tg
PCSK9
This protein mainly expressed in the liver and intestines but also present in plasma binds to and degrades LDL-R
Statins increase PCSK9 expression and hence combination therapy should have a synergistic effect
PBS indication for PCSK9 inhibitor
Familial homozygous hypercholesterolemia
AND
LDL >3.3
Meds that can be used in a hypertensive crisis
Hydralazine
SNP
GTN
Labetalol
Target BP for control
<130/80
Urinary Gopamine is elevated in what condition
essential HTN
B1 adrenergic effect
chronotropy/inotropy/lusitropy (relaxation)/dromotropy (increased conduction)
B2 adrenergic effect
bronchodilation, vascular smooth muscle relaxation (vasodilation)
B3 adrenergic effect
sympathetic mediation of lipolysis and thermogenesis
Reversible causes in Arrest - 4 H’s
Hypoxia
Hypovolemia
Hypo/Hyperkalemia/metabolic
Hypothermia/Hyperthermia
Reversible causes in Arrest - 4 T’s
Thrombosis
Tension pneumothorax
Tamponade
Toxins
Drugs in shockable rhythm
- Adrenaline 1mg after 2nd shock (then every 2nd)
- Amiodarone 300mg after 3rd shock (then every 2nd)
Drugs in nonshockable rhythm
-Adrenaline 1mg immediately (then every 2nd)
Amount of shock given in CPR
200J biphasic
360J monophasic
Targeted temp post cardiac arrest
33-36 celsius
Indications for PPM
- SND
- Only if symptomatic - AV block
- Pace even if symptomatic in Type 2 AV block, high degree AV block, CHB
- Otherwise only if symptomatic
Indication for HIS bundle pacing
Consider if EF 35-50% and will need >40% pacing
Mx of inferior infarct with new CHB
Reversible CHB
Monitor and temporarily pace, but likely will not need PPM
Genetic disorders at risk of SCD that benefit from ICD
Long QT syndrome Brugada HOCM ARVC (Arrhythmogenic right ventricular cardiomyopathy) Catecholaminergic polymorphic VT
RHC Waveforms in order
RA>RV>PA>PCW
PCWP =?
PCWP = LA = LVEDP
Atrial pressure waveform: A wave
Atrial systole
Atrial pressure waveform: X descent
Atrial Contraction
Atrial pressure waveform: V wave
Ventricular contraction
(<a>A in LA)</a>
Atrial pressure waveform: Y descent
Atrial emptying
Large V wave and prominent y descent
TR
Prominent X and y descent
Constrictive pericarditis
Large A wave
TS
Which atrial waveforms are not seen in AF
A and v wave
Kussmaul’s sign: Inspiratory rise or lack of decline in RA pressure: ?Cause
Cosntriction or RV ischemia
Causes of Constrictive pericarditis
TB pericarditis REcurrent pericarditis PRevious mediastinal RTx Uraemia CTD
Causes of Restrictive cardiomyopathy
Idiopathic Infiltrative -Amyloidosis -Sarcoidosis -Haemochromatosis Post radiation Endocardial fibroelastosis
Mx of Constrictive pericariditis
Pericardial stripping
Mx of restrictive cardiomyopathy
Medical therapy
Transplant
Differentiating Constrictive pericariditis and Restrictive cardiomyopathy on Ix
TTE:
- Both have diastolic function
- Eprime low in restriction (if >8, then constriction)
CT chest - thickened pericardium suggestive of constrictive
HOCM inheritance and pathophysiology
AD
Proteins encoding proteins of thick and thin myofilament contractile components of the cardiac sarcomere or Z-disk
Most commonly involves beta-myosin heavy chain (40%) and myosin-binding protein C (40%)
Diagnosis of HOCM
Wall thickness > 15mm in one or more LV myocardial segments
Not explained by other conditions
Mx HOCM
Treatment of Symptomatic LVOTO
- BB (reduce LVOTO and Ventricular arrhythmia)
- Central CCB (2nd line)
- Disopyramide (Class 1 A antiarrhthymic
- Amiodarone for AF
- Myoectomy in some cases
- ICD in medium to high risk
- ICD if previous VT/VF arrest
ARVC
Dilation and myocardial thinning of the RV, particularly inflow, outflow and posterolateral LV
Replacement of myocardium with fibrofatty tissue
Genetic mutations predominantly of desmosomal proteins (intercellular adhesion complexes that provide connections between myocytes)
-Desmoplakin, Plakoglobin
ARVC ECG
Prolonged S-wave upstroke
Epsilon wave
Twave inversion V1-V3
ARVC Mx
Activity restriction (risk of arrhthymia and CCF)
BB
ICD if high risk
Drugs causing Long QT
Psychotropics Class 2 antiarrhythmics (amiodarone, sotalol) TCAs SSRIs/SNRIs Macrolides HCQ
LQT Genes
LQT1: KCNQ1 (K+Channel)
LQT2: KCNH2 (K+ Channel)
LQT3: SCN5A (Na Channel)
LQT1
Most common form
Loss of function mutation of KCNQ1
Associated with sensorineural hearing loss
Triggered by exercise
LQT2
Loss of function mutation of KCNH2
Triggered by sleep and emotion, post partum, auditory triggers
LQT3
Gain of function mutation of SCN5A - sodium channel
Triggered by sleep
Tx of Long QT
- BB (Propanolol is best)
- Left cardiac sympathetic denervation
- ICD
Tx of Torsades
MgSO4 2g (20ml of 10%) up to 6 g Correct K Isoprenaline Temporary pacing DCR
Brugada
More common in males
Associated with SCZ
Due to loss of function mutation in SCN5A and SCN10A
Fever can be a precipitant
Brugada Mx
Antipyretics
ICD if previous arrest
Quinidine/amiodarone
Catheter ablation to reduce freq of arrhythmia
Best way to differentiate constrictive pericarditis from restrictive cardiomyopathy
Systolic area of index
(Ratio of RV pressure: LV pressure in inspiration vs expiration)
> 1.1 = Constrictive pericarditis
Constrictive pericarditis = Increase in RV pressure with inspiration
Elevated RVSP
= Pulmonary HTN or RVOTO
What Mx will have the most improvement in 6MWT in Pulm HTN
Exercise training
Oximetry sampling in shunts: ASD
Step up in RA
Oximetry sampling in shunts: VSD
Step up in RV
Oximetry sampling in shunts: PDA
Step up in PA
Types of ASD
Ostium Primum
- More common in Down syndrome
- Partial AVSD
Osteium Secundum
- Most common
- Amenable to percutaenous closure
ASD associated with right ventricular volume overload
Sinus Venosus
SVC more common than IVC
Associated with anomalous pulmonary venous return
When to close an ASD?
Symptoms RV enlargement Qp:Qs >1.5 Paradoxical embolism Playpnea-orthodeoxia syndrome
When not to close an ASD
Eisenmenger
VSD presentation
Murmur
CCF (dilated LV)
Endocarditis
Cyanosis (PHTN)
When to close VSD
Symptoms LV enlargement Qp:Qs >2:1 PHT with net L to R shunt Endocarditis AR RVOTO
PDA presentation
Continuous murmur
If large CCF
When to close PDA
Left chamber enlargement
PHTN (net left to right shunt)
Previous endarteritis
Audible murmur
Most common cause of eisenmenger in order
PDA>VSD>ASD
Coarctation presentation
HTN in upper limbs
-Reduced femoral pulses, femoral-femoral delay, Arm-leg BP gradient
Exercise intolerance
-Angina, claudication
Coarctation associations
Bicuspid Aortic valve +Aortopathy
Cengenital heart disease (VSD, PDA, etc)
Berry aneursyms
Mx Coarcatation
Stenting
Monitor afterwards for residual HTN and risk of wall complication (aneurysm)
Causes of pulmonary stenosis
Noonans Syndrome
-AD, skeletal abnormalities, learning difficulties
William’s syndrome
“Double chamber RV”
Ebstein anomaly
Tricuspid valve regurg
Accessory pathway
80% have ASD or PFO as well
Tx: Closure of ASD/PFO and repair of TVR
Tetralogy of Fallot
VSD
Overriding Aorta
RVH
RVOTO (Pulmonary stenosis or pulmonary atresia)
High risk cardio conditions in pregnancy
Severe PHTN Eisenmenger Syn Cardiomyopathy (NYHA2+, EF <40%) Severe obstructive cardiac lesion (AS, PS, MS) Marfan Syn with aortic root >40 mm Previous severe peripartum CM
Which patient groups get endocarditis prophylaxis
Prosthetic cardiac valve
Congenital heart disease (unrepaired cyanotic, repaired with residual disease)
PRevious endocarditis
Cardiac transplant patients with valvular disease
Procedure that will need endocarditis prophylaxis in high risk groups
Dental with manipulation of gingival tissue
Invasive resp tract procedures
Procedure within infected skin, tissue
Tx:
Single dose Amoxy or Clinda 30-60 mins pre op
AF ablation in patients with HF
Evidence shows reduced mortality and HF hospitalisations
2 Most common genes in HOCM
MYBPC3 (cardiac myosin binding protein C)
MYH7 (Beta-myosin heavy chain)
Catecholaminergic polymorphic VT gene
RYR2
Causes of MS
- Rheumatic heart disease
- Mitral annular calcification
Radiation
Carcionid
SLE/RA
Fabrys, Whipple’s
MS severity based on area
Mild: >1.5 cm2
Mod: 1.0-1.5 cm2
Severe: <1.0 cm2
MS severity based on Gradient (mmHg)
Mild <5
Mod 5-10
Severe >10
Effect on gradient in MS with exercise
Gradient increases with HR and exercise, so can get APO
Mx of MS
MEdical therapy
-BB, diuretics if overloaded
Balloon valvuloplasty
Indications for Balloon valvuloplasty in MS
Mod to severe MS (<1.5 cm2 area)
Symptomatic
Asymptomatic +
- New AF
- PASP >50mmHg at rest
Contraindications for balloon valvuloplasty in MS
> mild MR
LA thrombus
Heavy calcification
Predominant subvalvular involvement
Wellen’s Syndrome Definition and ECG
Severe proximal stenosis of LAD, usually with a rich collateral supply
Usually no chest pain but recent severe angina in the last 24-48hrs
• Classic ECG: Deep and symmetric T wave inversion in V1-V6, aVL and I (at least V2-V5), no ST changes. *highest risk if aVL and I are involved
Mx: Urgent Angio
Acute instent thrombosis
<24 hours
Subacute instent thrombosis
<30 days
Late instent thrombosis
1-12 months
Very late instent thrombosis
> 12 months
Stent restenosis
• Gradual renarrowing of the stented segment (usually after 3-12 months)
Greatest predictor of death post MI
REduced LVEF
Evidence for PCI of occluded vessels when asymptomatic
Even if post AMI
Shown to increase mortality and worsen LV function if PCI performed
Only PCI if symptomatic
Geneticsi n MArfan’s Syndrome
AD
FBN1 gene for protein fibrillin-1
Diagnostic Criteria for Marfan’s Syndrome
W/O FHx:
-Aortic cteria +one other major criteria or FBN1 mutation
W/ FHx
-Any one of the major criteria
Major:
- Aortic diameter Z >2 if above 20 yo, Z>3 if below 20 yr old, or aortic root dissection
- Ectopia Lentis
- Systemic score >7 based on smaller clinical findings
Features suggesting successful thrombolyisis
Improvement/relief of chest pain
reduction by 50% of the initial ST-segment elevation within 60–90 minutes
reperfusion arrhythmias (e.g. accelerated idioventricular rhythm)
restoration of haemodynamic and/or electrical stability
ECG Changes suggestive Right ventricular infarct
ST elevation in the right-sided leads (V3R-V6R)
• ST elevation in V1 – the only standard ECG lead that looks directly at the right ventricle.
• ST elevation in lead III > lead II – because lead III is more “rightward facing” than lead II and hence more sensitive to the injury current produced by the right ventricle.
• ST elevation in V1 + ST depression in V2 (= highly specific for RV MI).
Exam Findings: Hypotension, jugular venous distension, clear lungs
Right ventricular infarct
What medication should be given with thrombolysis
Aspirin and clopidigrel loading
Enoxaparin (IV better than SC)
Absolute contraindications to thrombolysis
- Previous ICH or stroke of unknown origin at anytime
- Ischemic stroke in the last 6 months
- CNS damage/neoplasma/AV malformations
- REcent major trauma/surgery/head injury within last month
- GI bleeding in last month
- Known bleeding disorder
- Aortic dissection
- Non compressible punctures in last 24 hours
Relative contraindications to thrombolysis
TIA in last 6 months -Oral anticoagulant therapy -Pregnancy or within 1 week postpartum -Refractory HTN SBP >180 -Advanced lvier disease IE -Active peptic ulcer -Prolonged or traumatic resus
Indication for CABG
Multivessel disease
Left main disease
Proximal LAD disease
T2DM with multivessel disease
What risk factor has the greatest risk of extension of a pre-existing AAA
Smoking
Mx of CHB
Unstable:
- Atropine
- Transcutaneous pacing
- If unable to pace: isoprenaline
- Low BP: Dopamine
- HF: IV dobutamine
- Normal BP and no HF: Transvenous pacing
Stable:
- Transcutaneous pacing
- Look for reversible causes
- None: PPM
Diagnostic criteria for pericarditis
At leas 2: Typical chest pain Pericardial friction rub Suggestive ECG changes New or worsening pericardial effusion
Mx of Aortic Dissection
Aim SBP <120 and HR <60
IV BB, SNP, or GTN
Biggest risk factor for arrhythmia post CABG
AF most common
Age is greatest risk factor for AF post CABG
Mx of stable VT
IV amiodarone/lignocaine
IF fails can consider retrial or cardioversion
Treat underlying cause too
CHADSVASC
- Congestive heart failure / left ventricular dysfunction
- Hypertension
- Age ≥ 75 (x2)
- Diabetes
- Stroke (x2)
- Vascular disease
- Age 65-74
- Sex (female) (x2)
HASBLED
- Hypertension
- Abnormal renal/liver function
- Stroke
- Bleeding history or predisposition
- Labile INR
- Elderly
- Drugs/alcohol
MAjor risk factors for stroke in AF
- Major: past stroke, age >75, valve disease, mitral stenosis, mechanical valve
- Alone are indications for anticoagulation
Which antihypertensive should not be prescribed in HFrEF
Moxonidine
Benefit of AF ablation in HF
Improves survival
MR and LV dysfunction relationship
Irreversible LV contractile dysfunction may occur despite “normal” EF and without symptoms
Early: Increase in EF because ejecting into low pressure LA (decrease afterload and increase preload)
Late: Increase LV size and interstitial fibrosis (increase afterload) leads to decrease EF into “normal range” (70-60%)
Indications for AR repair
If Symptomatic - Treat
If asymptomatic:
- Resting EF <50%
- Cardiac surgery/CAGS
- Rest EF >50%, but LV Diastolic >70mm or LV systolic >50 mm
Moderate AS
Gradient 20-40
Area 1-1.5
Velocity <0.25
SEvere AS
Gradient >40 mmHg
Area <1 cm2
Velocity <0.25 DI
Flow 4
Indication for TAVI
Symtomatic severe AS
CI to TAVI
Aortic annulus too small LV apical thrombus Peripheral vascular access issues Active endocarditis Life expectancy <1 yr
Tavi Cx
Heart block
AR
Tavi thrombosis
SAVR Cx
AKI
New AF
Major bleeding
Flecainide MOA and CI
Blocks fast inward sodium channels (class 1c) • ECG effects prolonged PR, QRS widening
CI: structural heart disease, CAD
Amiodarone MOA
Multiple sites of action potassium channels,
alpha/beta adrenoceptors, others (sodium and calcium
channels)
Sotalol MOA
Inhibits rapid component of delayed potassium
rectifier Ikr current (class III) and beta receptors
•
ECG effects sinus brady, AV blockade, QT
prolongation (significant TDP risk)
Reduce dose in renal impairment
Digoxin MOA
Inhibits sodium potassium ATPase –> increases
intracellular Ca 2+2+–> positive inotropic effect
•
Increases vagal tone –> slows AV conduction
Sacubitril valsartan MOA
Sacubitril inhibits neprolysin –> raises levels of
endogenous vasoactive peptides (natriuretic
peptides, bradykinin)
Type 1 MI
Spontaneous MI due to primary coronary event
Type 2 MI
MI secondary to ischemia due to either increased O2 demand or decreased supply
Type 3 MI
Sudden unexpected cardiac death
Type 4 MI
4a - assocaiated with PCI
4b - stent thrombosis
Type 5 MI
Associated with cardiac surgery eg. CABG