Cardiology Flashcards
S1 HS ??
MV & TV closure
Causes of Loud S1
- MS
- Left to Right shunt
- Short PR interval, Atrial Premature beat
- Hyperdynamic states
Causes of Quiet S1
- Long PR
- MR
S2 HS
Closure of AV (A2) very closely followed by PV (P2)
Causes of Loud S2
- HTN: Systemic (A2) or Pulm. (P2)
- Hyperdynamic states
- ASD without Pulm. HTN
Causes of Soft S2 : AS
Causes of FIXED Split : ASD
Causes of-
- Widely split S2 ??
- Reverse Split or Paradoxical Split S2 (P2 before A2) ??
Deep Inspiration
RBBB
Pulmonary Stenosis
Severe MR
LBBB
Severe AS
RV Pacing
WPW Type B (causes early P2)
PDA
S3 HS
Diastolic filling of Ventricles
- Normal if < 30 yr (may persist in women in upto 50 yrs)
Heard in Left Ventricular Failure
- CDM
- Constrictive Pericarditid
- MR
S4 HS
Atrial Contraction against stiff ventricles
- Coincides with P wave
- Occurs just before S1
Causes
- AS, HOCM, HTN
Causes of
- Ejection Systolic Murmur ??
- Late Systolic Murmur
“RILE”
Ejection Systolic Murmur
Louder on Inspiration
- PS, - ASD, - ToF
Louder on Expiration
- AS, - HOCM
Late Systolic
- MVP
- Coarctation of Aorta
Causes of
- Holosystolic murmur ??
TR (becomes louder during Inspiration)
MR (louder on Expiration)
MR/TR: High pitched & blowing in character
VSD : Harsh in character
Causes of
- Mid-late Diastolic murmur ??
- Early Diastolic ??
- Continuous Machinery murmur ??
MS & Austin-Flint (Severe AR)
- Rumbling in character
AR & Graham-Steel (PR)
- High pitched & Blowing character
PDA
What is Pulsus paradoxus ??
Greater than the normal (10 mmHg) fall in SBP during Inspiration => Faint or absent pulse on Inspiration
-Severe Asthma
- Cardiac Tamponade
Causes of
- Slow rising/ Plateau pulse ??
- Collapsing Pulse ??
- AS
- AR, - PDA
- Hyperkinetic states (Anaemia, Thyrotoxic, Fever, Exercise/Pregnancy)
Causes of
- Pulsus alternans ??
- Bisferiens pulse ??
- Jerky pulse ??
Regular alternation of the force of the arterial pulse
- Severe LVF
Double pulse- 2 systolic peaks
Mixed Aortic Valve disease
HOCM
- Bisferiens pulse may be seen
Bisfereins pulse ??
MIXED AV Disease
2 distinct peaks during Systole, involves Both Stenosis & Regurgitation of AV. The double peak occurs because of
- Initial upstroke (V ejection)
- 2nd Peak: regurgitant flow when V relaxes
1st line investigations of Palpitations ??
12-Lead ECG
TFT
U&E
FBC
How to Ix. Episodic Arrhythmias ??
Holter Monitoring
- Battery operated
- Continuously records ECG from 2- 3 leads
- Done for >= 24 hrs
- Pt. is asked to keep a dairy to record any symptomatic episodes
If Holter Monitor is (-)ve
- External loop recorder
- Implantable loop recorder
Reasons for Inaccurate BP values ??
Wrong Cuff size
- Bladder too small: Overestimation
- Bladder too large: Underestimation
The arm should be Horizontal at the level of Heart
- Below Heart level: Overestimation
- Above Heart level: Underestimation
Sitting Posture is considered std.
Arm Support
- If unsupported, may raise DBP (as arm will be performing Isometric exercise)
Valsalva Maneuver Stages ??
Forced expiation against a closed glottis
- Leads to increased Intrathoracic pressure
STAGES:
- Increased Intrathoracic pressure
- Resultant increase in Venous & RA pressure, reduces venous return
- Reduced Preload => fall in CO (Frank-Starling mechanism)
- When pressure released, there is a further slight fall in CO due to increased Aortic volume
- Return to normal CO
Coronary Circulation ??
LCA or Left Main
- LCX
- Obtuse Marginal Artery
- LAD (supplies Ante. 2/3rd of IV Septum, Anterolateral Papillary muscle & Ante. surface of LV
RIGHT CORONARY Artery
- PDA (supplies Posterior 1/3rd of IV septum, Poste. 2/3rd wall of ventricle & Posteromedial Papillary Muscle
- Acute Marginal Artery (supplies RV)
RCA supplies AVN (in 90%) & SAN (in 60%)
How is Dominance in the Coronary Artery decided ??
Right Dominant Circulation (MC)
- PDA arises from RCA
Left Dominant Circulation
- PDA arises from LCX
CoDominant Circulation
- PDA arises from both LCX & RCA
Venous drainage of Heart ??
Coronary Sinus runs in the Left AV groove & drains into RA
Coronary Blood flow to LV & IV Septum peaks at
- EARLY Diastole
Pericardial layers ??
Out => In
- Fibrous P
- Parietal P
Pericardial Space
- Epicardium (Visceral P)
Coronary vessels lies here
- Myocardium
Pericardium is innervated by PHRENIC Nerve
ECG localization
Anteroseptal (LAD)
- V1- V2
Antero-apical (Distal LAD)
- V3- V4
Antero-lataral (LAD or LCX)
- V5- V6, aVL
Lateral (LCX)
- I, aVL +/- V5, V6
Inferior (RCA)
- II, III, aVF
Posterior (PDA)- LCX & also RCA
- V7- V8,
- ST depression in V1-V2 + Tall R waves
Posterior Territory ECG changes ??
Changes seen in V1- V3
Reciprocal changes of STEMI are typically seen:
- Horizontal ST depression
- Tall, Broad R wave
- Upright T wave
- Dominant R wave in V2
Posterior Infarction is confirmed by
- ST Elevation &
- Q wave in posterior leads (V7- V9)
New onset LBBB ??
can be ACS
Normal variants of ECG ??
The following are considered normal in an Athlete
- Sinus Bradycardia
- Junctional Rhythm
- 1st degree heart block
- Mobitz type-1 (Wenckebach phenomenon)
Causes of LAD ??
Left Anterior Hemiblock
LBBB
IWMI
Hyperkalaemia
Congenital: Ostium primum ASD, Tricuspid atresia
Minor LAD in OBESE people
Causes of RAD ??
Right Ventricular Hypertrophy
Left Posterior HEmiblock
Lateral MI
Chr. Lung disease => Cor Pulmonale
Pulm. Embolism
Ostium Secundum ASD
Normal in infants < 1 yr old
Minor RAD in Tall people
Axis deviation seen in WPW syndrome ??
LAD
- RIGHT Sided Accessory Pathway
- More common
RAD
- LEFT Sided Accessory Pathway
- Less common
Dextrocardia ECG changes ??
Inverted P wave in Lead 1
RAD
Loss of R wave progression
P wave changes ??
Increased P wave amplitude
- Cor Pulmonale
Broad, notched (Bifid) P wave
- Sign of LA enlargement classically seen in MS
- Often most pronounced in Lead 2
Absent P wave
- AF
PR interval Changes ??
Start of P wave to start of QRS
- 0.12 to 0.20 sec
Causes of Prolonged PR interval
- Idiopathic
- IHD, - Rheumatic Fever
- Digoxin toxicity
- Aortic Root pathology eg.- Abscess secondary to Endocarditis
- Lyme’s disease
- Sarcoidosis, - Myotonic Dystrophy
- Hypo[K+]
- Hyper[K+] (very Rare)
- Normal in Athletes
SHORT PR Interval
- WPW syndrome
T wave changes
Peaked T waves
- Hyper[K+]
- Myocardial Ischaemia
Inverted P wave
- Myocardial Ischaemia
- Digoxin Toxicity
- SAH
- Arrhythmogenic RV Cardiomyopathy
- Pulmonary Embolism [S1Q3T3]
- Brugada syndrome
ST Depression causes ??
ST Depression
- Secondary to abnormal QRS (LVH, LBBB, RBBB)
- Ischaemia
- Digoxin
- Hypo[K+]
- Syndrome X
ST Elevation changes ??
Myocardial Infarction
Pericarditis/ Myocarditis
Normal variant- ‘High Take-off’
LV Aneurysm
Prinzmetal Angina (CA Spasm)
Takotsubo Cardiomyopathy
Rare: SAH
Hypo[K+] ECG features ??
U wave
Small or Absent T waves (Occasional inversion)
Prolong PR Interval
ST depression
Long QT
“U have no Pot. & no T, but a long PR & a long QT”
Hypothermia ECG changes ??
Bradycardia
J wave (Osborne waves)- Small hump at the end of QRS complex
1st degree Heart Block
Long QT interval
Atrial & Ventricular Arrhythmias
What are the features suggesting VT rather than SVT with aberrant conduction ??
- AV Dissociation
- Fusion or Capture beat
- (+)ve QRS concordance in Chest leads
- Marked LAD
- H/o IHD
- Lack of response to Adenosine or Carotid sinus massage
- QRS > 160 ms
AV Blocks ??
FIRST Degree HB
- PR interval > 0.2 ms
- Asymptomatic HB: NO Rx.
SECOND Degree HB
Mobitz-1, Wenckebach
- Progressive prolongation of PR interval until a dropped beat occurs
Mobitz-2
- PT interval is constant
- P wave is often NOT followed by QRS complex
2nd degree AV block (2:1 block)
THIRD Degree HB
- No association b/w P wave & QRS complex
Complete HB features ??
Syncope
Heart Failure
Regular Bradycardia (30- 50 bpm)
Wide Pulse Pressure
JVP: Cannon wave in neck
Variable Intensity of S1
LBBB & RBBB ECG features ??
“WiLLiaM MaRRoW”
LBBB
- ‘W’ in V1 & a ‘M’ in V6
RBBB
- ‘M’ in V1 & a ‘W’ in V6
Causes of LBBB ??
New LBBB is ALWAYS Pathological
- M Infarction
- HTN
- AS
- Cardiomyopathy
- Rare: Idiopathic Fibrosis, Digoxin toxicity, Hyper[K+]
Original Sgarbossa Criteria ??
Used to Dx. Infarction in pts. with LBBB
- Concordant ST elevation >= 1 mm in >= 1 leads with a (+)ve QRS complex (score 5)
- Concordant ST depression >= 1 mm in >= 1 lead of V1- V3 (Score 3)
- Excessively discordant ST elevation > 5 mm in leads with (-)ve QRS complex (Score 2)
These criteria are SPECIFIC but not Sensitive (36%)
Smith-Modified Sgarbossa Criteria ??
Concordant ST elevation >= 1 mm in >= 1 lead
Concordant ST depression >= 1 mm in >= 1 lead of V1 to V3
Proportionally excessive discordant ST elevation in >= 1 lead anywhere with >= 1 mm STE, as defined by >= 25% of the depth of preceding S wave
Causes of RBBB ??
Normal Variant (MC with Aging)
RV Hypertrophy
Chr. increased RV Pressure
- eg.- Cor Pulmonale
Pulmonary Embolism
Myocardial Infarction
ASD (Ostium Secundum)
Cadiomyopathy or Myocarditis
JVP waves ??
A wave : Atrial Contraction
C wave : TV closure (cusps bulging into RA)
X descent: RA relaxation (Fall in Atrial pressure during Ventricular Systole)
V wave : Passive rapid filling of blood into RA against a closed TV (during late Systole)
Y descent: TV opening
- Early V filling (during Early diastole)
A wave pathology ??
Absent in AF or A Flutter
Increase in TS or PS & RV Failure (due to increase resistance to forward flow)
Cannon A waves
- Junctional Rhythm
- VT & Third degree HB
- RA contracts against closed TV => Large reflection wave back into RA
C wave pathology ??
TR causes fusion of ‘C’ & ‘V’ waves with blunting of ‘X’ descent
X wave pathologies ??
Increase in ‘X’ descent
- Constrictive Pericarditis
Decrease or Absent ‘X’ descent
- TR (as this jet increase RA pressure)
- Suggests RV dysfunction due to decreased apical motion
V wave Pathologies ??
Increase ‘V’ wave
- TR (from regurgitation jet => increases RA pressure)
Y descent pathologies ??
Increase ‘Y’ descent
- Constrictive Pericardotis
- RV Failure
Decreased or Absent ‘Y’ descent
- Cardiac Tamponade (Pericardial fluid pressure impairing caval inflow to RA)
Non-Pulsatile JVP is seen in ??
What is Kussmaul’s Sign ??
- Superior Vena Caval Obstruction
- Paradoxical rise in JVP during inspiration seen in Constrictive Pericarditis
Cardiac catheterisation & O2 sats. ??
Normal O2 Sats. in Heart
- RA & RV & PA : 70%
- LA & LV & Aorta : 100%
Mixing of Deoxygenated blood with Oxygenated blood : 85%
Types of Cannon ‘A’ waves ??
Caused by Atrial contraction against a closed TV
2 types
REGULAR Cannon waves
- VT (with 1:1 Ventricular-Atrial conduction)
- AV Nodal Re-entry Tachycardia
- Single-chamber Ventricular Pacing
IRREGULAR Cannon Waves
- Complete H B
Hallmarks of Cardiac MRI ??
aka CMR is the Gold std. for providing
- STRUCTURAL Images of Heart
Particularly useful when assessing
- Congenital Heart disease
- Determining RV & LV masses
- Differentiating forms of Cardiomyopathy
Myocardial Perfusion can also be assessed following administration of GADOLINIUM
Hallmarks of Cardiac CT ??
Useful for assessing suspected IHD using 2 main methods
[Ca2+] Score:
- There is correlation b/w the amount of Atherosclerotic plaque Ca2+ & risk of future Ischaemic events
CECT:
- Allows visualization of CA Lumen
When these 2 technique when combined, Cardiac CT has a very high (-)ve predictive value for IHD
Nuclear Imaging of Heart ??
These technique use Radiotracers which are extracted by normal myocardium; Eg. are
- Thallium
- Fluorodeoxyglucose (FDG): PET scan
- (99m)Tc Sestamibi: A complex of Radioisotope Tc-99m + Methoxyiso-butyl Isonitrile (MIBI) used in ‘MIBI’ or Cardiac SPECT scans
Cardiac Imaging uses ??
1) Cardiac CT : IHD
- Atherosclerotic plaque Ca2+
- CA Lumen visualization
2) CMR:
- Str. Imaging of heart
- Myocardial Perfusion (with Gadolinium use)
3) SPECT :
- Myocardial Perfusion & Viability (Ischaemic tissue can be identified)
4) MUGA Scan
- Used before & after Cardiotoxic drug usage
- Accurately measure LVEF
SPECT scan of Heart ??
To assess Myocardial Perfusion & Myocardial Viability
Two sets of images are acquired
- 1st Myocardium at Rest
- 2nd Myocardium during Stress (Exercise or following Adenosine/ Dipyridamole)
By comparing the 2 images, site of Ischaemia can be identified & classified as Reversible or Irreversible
MUGA scan of Heart ??
Multi Gated Acquisition Scan aka Radionucleotide Angiography
- Tc-99m is injected as IV
- Then placed under Gamma Camera
- Can be performed as Stress test
- Can accurately measure LVEF
- Typically used Before & After Cardiotoxic drug use
Name the murmurs heard at
- Aortic area ??
- Pulmonary area ??
Aortic area
Systolic Murmurs
- AS
- AV Sclerosis
- Flow Murmur (eg.- Physiological)
Pulmonary area
Systolic Ejection Murmurs
- PS.
- ASD
- Flow Murmur
Name the Murmurs heard at
- Mitral area (Apex) ??
- Tricuspid area ??
Mitral area
Systolic Murmur
- MR
- MVP
Diastolic Murmur : MS
Tricuspid area
Holosystolic Murmur
- TR
- VSD
Diastolic Murmur : TS
Which murmurs are heard at Left Sternal Border ??
Systolic Murmur
- HOCM
Diastolic Murmur
- AR
- PR
CVS changes a/w the following
- Standing, Valsalva (Strain phase) ??
- Passive Leg raise ??
- Squatting
- Hand Grip
- Inspiration
- Decrease Preload (decrease LV vol.)
- Increase Preload (Increase LV vol.)
- Increase Preload, Afterload (Increase LV volume)
- Increase Afterload => increase reverse flow across AV (increase LV volume)
- Increase Venous return to Rt. Heart, Decrease V return to left heart
Name the murmurs that INCREASE with
- Standing, Valsalva ??
- Passive Leg raise & Squatting ??
- Hand grip ??
- Inspiration ??
- MVP (decrease LV vol.) with Earlier Midsystolic Click & HCM (decrease LV vol.)
- Most murmurs (Increase flow through Stenotic/ Regurgitant valve)
- Most other Lt. sided Murmurs (AR, MR, VSD)
- Most Rt. sided murmurs
Name the murmurs that DECREASE with
- Standing, Valsalva ??
- Passive Leg raise & Squatting ??
- Hand grip ??
- Inspiration ??
- Most murmurs (decrease flow through Stenotic/Regurgitant valves)
- MVP (increase LV vol.) with later Midsystolic click & HCM (increase LV vol.)
- AS (decrease transaortic valve pressure gradient) & HCM (increase LV vol.)
- Most Lt. sided murmur
Indications of Implantable Cardiac Defibrillators ??
Long QT syndrome
HOCM
Previous Cardiac arrest due to VT/VF
Previous MI with
- Non-Sustained VT on 24hr monitoring
- Inducible VT on Elecrtrophysiology testing & Ef < 35%
Brugada Syndrome
Indications of Temporary Pacemaker ??
1) Symptomatic/ Haemodynamically unstable Bradycardia
2) Post- ANTERIOR wall MI induced
- Type 2 or Complete HB
3) Post- InFERIOR wall MI Complete HB + Asymptomatic & Stable Haemodynamically
4) Tri-Fascicular Block prior to Sx.
Hallmarks of MR ??
aka Mitral Insufficiency (seen when blood leaks back through MV at systole)
- As MR becomes more severe, the body’s O2 demands may exceed the heart’s capacity to pump => Thickened Myocardium
RFs
- Female, - Age, - Low BMI
- Renal dysfunction
- Prior MI
- Prior MS or MVP
- Marfan’s or Ehlers-Danlos
Causes of Mitral Insufficiency ??
CAD or Post-MI: If Papillary muscle or C tendinae are affected by insult
MVP:
- MV Leaflets are deformed => valve does’t close properly
INFECTIVE Endocarditis
- Vegetation prevents valve from closing properly
RHEUMATIC Fever
- Inflammation of valve => MR
CONGENITAL
Signs & Symptoms of Mitral Insufficiency ??
Asymptomatic (Mild to mederate MR)
LV Failure, Arrhythmias or Pulm. HTN
- This may present as Fatigue, SoB & Oedema
Pansystolic ‘Blowing’ murmur
Best heard: Apex & Radiates to Axilla
S1 may be quiet (due to incomplete closure)
Severe MR: Widely Split S2
Ix. & Rx. of Mitral Insufficiency ??
ECG: Broad P wave (Atria enlarged)
CXR: Cardiomegaly (enlarged LA & LV)
2D-Echo: imp. for Dx. & to assess severity
Rx.-
- Drugs: Nitrates, Diuretics, (+)ve Inotropes & Intra-aortic balloon pump to increase CO
- HF: ACEi/ ARBs, Beta Blockers, Spironolactone
Acute Severe MR: Surgery
- Repair preferred over Replacement
- When repair not possible Replacement with an Artificial or Pig valve is considered
Why is valve Repair preferred over Replacement ??
Repair has a lower rates of
- Degenerative regurgitation
- Lower Mortality
- Higher Survival rates
MR Rx. ??
ACUTE MR
- Immediate Sx: Repair preferred over replacement
- Replacement is done with Artificial valve or pig valve
- Post-Op. after load reduction (Diuretics, Na nitroprusside, &/or Intra-aortic Balloon Counterpulsation
CHRONIC MR
Primary: Symptomatic/Asymptomatic
Secondary
- Medical Rx of HF (ACEi/ARBs, Beta B, Spironolactone) => Failed + Low Sx. Risk => Transcath. MV Intervention
Rx. of Primary Chronic MR ??
SYMPTOMATIC
- If acceptable Sx. Risk: MR Sx.
- Inoperable/ High Sx. risk: Transcath. MV Intervention or HF Rx.
ASYMPTOMATIC
Preserved LVSF
- [LVEF > 60% + LVESD < 40 mm] + No other indications for Sx. => TTE 6- 12 monthly
MV Sx (if one of the 7 indications)
Indications to perform MV Sx. in an Asymptomatic pt. ??
Low LVSF: LVEF< 60% + LVSD> 40mm
2) New onset AF
3) Increase Systolic PAH
4) Left Atrial Dilatation
- LA vol. >= 60 ml/m3 or Diameter >= 55 mm
5) Progressive increase in LV size on > 3 serial imaging studies
6) Progressive decrease in LVEF on >= 3 serial imaging studies
7) High likelihood of durable repair + Low risk of Sx.
Hallmarks of MS ??
Increases pressure in LA, Pulm. vasculature & Rt. side of Heart
Causes:
- RHEUMATIC FEVER (most imp.)
- Rare : Mucopolysaccharidoses, Carcinoid & Endothelial fibroelastosis
Features of MS ??
Dyspnoea
- Increase LA pressure => Pulm. Venous HTN.
Haemoptysis
- Due to pulm. pressures & vascular congestion
- Pink frothy to sudden haemorrhage Mid-Late Diastolic murmur
Loud S1, Opening Snap
Low Vol. Pulse, Malar Flush
AF (2ndary to LA enlargement)
Features of Severe MS ??
Is the Haemoptysis in MS an arterial or Venous bleed ??
Length of Murmur INCREASES
Opening Snap becomes closer to S2
Secondary to rupture of thin-walled & Dilated Bronchial VEIN
Dx. & Rx. of MS ??
CXR: LA Enlargement
2D-Echo: Normal area of MV is 4-6 cm2; ‘Tight’ MS < 1 cm2
Rx.-
Pts. a/w AF: require AntiCoagulation
- Moderate/Severe MS: Warfarin
- Mild AS: DOACs may be suitable
Asymptomatic Pts.
- Regular 2D-Echo
- Percutaneous/ Sx. Rx. NOT advised
Symptomatic Pts.
- Percutaneous Mitral Balloon Valvotomy
- MV Sx. (Commissurotomy or Valve replacement)
CXR features of MS ??
LA Enlargement
- Splaying of Carina
- Elevation of Left Main Bronchus: Double Rt. Heart Border
- Cardiomegaly
Hallmarks of MVP ??
IDIOPATHIC but may be a/w wide variety of CVS diseases
- Congenital HD: PDA, ASD
- Cardiomyopathy
- Turner’s Syndrome
- Marfan’s, - Fragile X
- Osteogenesis imperfecta
- Pseudoxanthoma Elasticum
- WPW, - Long-QT syndrome
- Ehlers-Danlos Syndrome
- PCKD
Features of MVP ??
- Atypical Chest pain or Palpitations
- Mid-Systolic click (occurs later if Squatting)
- Late Systolic murmur (longer if pt. Standing)
Complications - MR
- Arrhythmias (including Long-QT)
- Emboli
- Sudden Death
Hallmarks of TR ??
Signs-
- Pan Systolic Murmur
- Prominent V wave on JVP
- Pulsatile Hepatomegaly
-Left Parasternal Heave
Enlarged RV
Causes
- RV Infarction
- Pulm. HTH eg.- COPD
- RHD
- Infective E (specially IVDU)
- Ebstein’s Anomaly
- Carcinoid Syndrome
Hallmarks of AR ??
Causes blood to flow in Reverse direction during V Diastole
Features
- Early Diastolic Murmur (intensity increased by handgrip maneuvre)
- Collapsing Pulse
- Wide Pulse Pressure
- QUINCKE’s Sign: Nail Pulsations
- DE MUSSET’s Sign: Head Bobbing
Ix.- 2D-Echo
Severe AR features ??
Mid-Diastolic AUSTIN- FLINT murmur
- AR: due to partial closure of Anterior MV cusps caused by Regurgitation stream
Causes of AR ??
AR due to VALVE Disease
- Rheu. F (MCC in developing nations)
- Calcific Valve disease
- Infective Endocarditis
- Connective Tissue disease (RA/ SLE)
- Bicuspid Aortic Valve (affects BOTH valve & aortic root)
AR due to AORTIC ROOT Disease
- Bicuspid Aortic Valve
- Aortic Dissection
- HTN, - SYPHILIS
- Marfan’s & Ehlers-Danlos
- Spondyloarthropathies (eg- Ank. Spon.)
Rx. of AR ??
Ix.- 2D-Echocardiography
Rx.-
Medical Rx. if a/w HF
Surgery: AV indications includes
- Symptomatic pts. with Severe AR
- Asymptomatic pts. with Severe AR + LV Systolic Dysfunction
Hallmarks of AS ??
Causes
- Degenerative Calcification
- Bicuspid AV, - William Synd.
- Post-Rheumatic disease, - HOCM
C/F
- Chest pain, Dyspnoea
- Syncope/ Presyncope (eg.- Exertional dizziness)
ESM; radiates to Carotids; decreased following Valsalva
Features of Severe AS ??
- Narrow Pulse Pressure
- Slow Rising Pulse
- Delayed ESM
- Soft/ Absent S2
- S4
- Thrill, - Duration of Murmur
- LVH or LVF
MCC of AS in
- Older pts. > 65 yrs
- Younger pts. < 65 yrs
Supravalvular cause of AS
Subvalvular cause of AS
- Degenerative Calcification
- Bicuspid AV
Supravalvular AS: William Synd.
Subvalvular AS: HOCM
Rx. of AS ??
1) Asymptomatic: Observe
2) Symptomatic: Valve Replacement
3) Asymptomatic + Valvular gradient > 40 mmHg + LVSD features
- Surgery
4) Options for AV replacement (AVR)–
- Sx. AVR: ToC for Young, Low/ Medium operative risk pts. => Do Angiogram prior to Sx. (can be done together)
- Transcatheter AVR: High operative risk pts.
5) Balloon Valvuloplasty (Indications)
- Children + No AV Calcification
- Adults: Critical AS + Not fit for Sx.
Which Murmur
- Radiates to Axilla ??
- Radiates to Carotids ??
- Mitral Insufficiency (MR)
- AS (ESM)
Hallmarks of Bicuspid AV ??
Asymptomatic in Childhood
- Maj. develop AS or AR
A/W
- Left Dominant Coronary Circulation (PDA arises from LCX instead of RCA)
- Turner’s Syndrome
5% pts. have Coarctation of Aorta
Complications
- AS or AR
- High risk of Aortic Dissection & Aneurysm formation of Ascending aorta
Which is the MC valve that needs replacement ??
AV & MV
What are the 2 main types of Prosthetic Heart Valves ??
Bioprosthetic or Mechanical HV
Biological (Bioprosthetic)
- Bovine or Porcine in origin
- Disadv.- Str. deterioration & Calcification over time
- Indications: Older pts.- > 65 yrs for AV & > 70 yrs for MV
Long Term AntiCoagulation NOT usually needed
- Warfarin given for first 3 months
- Low-dose Aspirin: Long term
Mechanical HV ??
BiLeaflet valve (MC type now used)
Have LOW Failure rate
Disadv.- Higher risk of THROMBOSIS
- Long Term AntiCoagulation needed
- Warfarin preferred to DOACs
- Aspirin is only given IF there is additional indication eg.- IHD
Target INR
- Aortic: 3.0
- Mitral: 3.5
ACS Hallmarks ??
Is an umbrella term covering a no. of Acute presentations of IHD
Presentations
STEMI
NSTEMI
Unstable Angina: Ischaemic C/F suggestive of ACS + NO elevation in Troponins +/- ECG changes indicative of Ischaemia
- Rise in Troponins may take some hrs., it may be indistinguishable for NSTEMI initially & is hence treated the same until Trops. result is known
Pathophysiology of IHD ??
1) Initial Endothelial Dysfunction
- Smoking, HTN, Hyperglycaemia
- Results in Proinflammatory, Pro-oxidant, Proliferative & Reduced Nitric Oxide bioavailability
2) Fatty Infiltration of SubEndothelial space with LDL particles
- Monocytes migrate from blood => become Macrophages => These Phagocytose Oxidized LDL => Large Foam Cells
- As these Macrophages die => Propagates Inflam. process
3) SMOOTH Muscle Proliferation & Migration from T media into intima
- Results in the formation of Fibrous capsule covering Fatty plaque
Symptoms & Signs of ACS ??
CHEST Pain
- Central/ Left sided
- May radiate to Jaw/ Left arm
- ‘Heavy’ or ‘Crushing’, like an elephant on my chest
DM & Elderly may NOT experience any chest pain
Dyspnoea, Sweating, N & V
Signs:
- HR, BP, Temp., O2 sats. are often normal or mildly altered- Tachycardia
- ACS Complications: HF
- Pale & Clammy
Common Rx. of all pts. with ACS ??
Initial: MONA
Morphine (Only if in severe pain)
O2 (only if sats, < 94% on RA)
Nitrates
- Sublingually or IV
- Useful if ongoing Chest pain or HTN
- Used in Caution if pt. Hypotensive
Aspirin 300mg
Next step is to determine with ECG if its STEMI or NSTEMI/ Unstable Angina
STEMI ECG Criteria ??
C/F of ACS (for >= 20 min) + Persistent (> 20 min) ECG features in >= 2 contiguous leads of V2- V3:
- Men < 40 yrs: >= 2.5 mm (0.25mV)
- Men >= 40yrs: >=2.0 mm (0.2 mV)
- Women: >= 1.5 mm (0.15 mV)
- In other Leads: >= 1mm (0.1 mV)
New LBBB (considered new unless there is evidence otherwise)
PCI ??
1) Further Anti-platelet prior to PCI
- Aspirin + another drug
- If the pt. NOT on Oral AC: Prasugrel
- If pt. is on Oral AC: Clopidogrel
2) Drug Therapy during PCI
PCI with Radial access
- UfH + Bailout GP2b/3a inhibitor
PCI with Femoral access
- Bivalirudin + Bailout GP2b/3a
3) Other procedure during PCI
- Thrombus Aspiration (NOT mechanical thrombus extraction) should be considered
- Complete Revascularisation: in pts. with Multi-vessel CAD without Cardiogenic shock
Rx. of STEMI ??
STEMI confirmed => MONA => Assess eligibility for Coronary Reperfusion Therapy
TWO Types of C Reperfusion T
1) PCI
- If pt. presents in < 12hrs of C/F + PCI can be delivered in 120 min
- If pt. presents > 12hrs of C/F + still has evidence of ongoing Ischaemia, consider PCI
- Drug-Eluting stents are used
- RADIAL preferred over Femoral (Give UfH + Bailout GP2b/3a i)
- Consider Fibrinolysis IF there is a significant delay in providing PCI
2) FIBRINOLYSIS
- Given < 12hrs of C/F + PCI can’t be delivered in 120 min.
- Give Anti-Thrombin
- After procedure give Ticagrelor
- If ongoing MIschaemia, consider PCI
NSTEMI/ Unstable Angina Criteria ??
1) MONA
2) Anti-Thrombin Rx
- FONDAPARINUX offered if pt. not at high risk of bleeding + not having Angiography immediately (OR)
- UfH offered if Immediate Angio. planned or Cr. > 265 umol/L
3) Estimate 6 m Mortality (GRACE)
Low Risk <= 3% :
- Ticagrelor (Not high risk of bleeding)
- Clopidogrel if High risk of bleeding
Intermediate/High risk > 3% : PCI
- Offer asap if clinically unstable OR ELSE offer in <= 72 hrs
PCI: UfH given regardless of Fondaparinux is given or not.
Aspirin + another drug prior to PCI
- If pt. NOT on Oral AC: Prasugrel/Ticagrelor
- If on Oral AC: Clopidogrel
GRACE scoring components ??
Global Registry of Acute Coronary Event is the most widely used risk assessment tool
The following factors are considered
- Age
- HR, BG
- Cardiac (Killip Class) & RFT (S. Cr)
- Cardiac arrest on presentation
- ECG Findings & - Trops level
Risk stratification of GRACE ??
Predicted 6 m Mortality : Risk of further adverse CV Events
- <= 1.5% = Lowest
- 1.5 to 3.0% = Low
- 3.0 to 6.0% = Intermediate
- 6.0 to 9.0% = High
- > 9.0% = Highest
Which pts. with NSTEMI/Unstable Angina should have Coronary Angiogram (with follow-on PCI if necessary) ??
1) Immediate PCI
- If clinically unstable (eg. Hypotensive)
2) Within 72 hrs
- Pts. with a GRACE score > 3% ie. hose at Intermediate/High or Highest risk
3) Coronary Angiography
- Considered for pts. if Ischaemia is subsequently experienced after admission
Prognostic Factors of ACS ??
Poor Prognostic Factor
- Age
- Development (or History) of HF
- Peripheral Vascular Disease
- Reduced SBP
- KILLIP Class: used to stratify risk Post-MI
- Initial S Cr. conc.
- Elevated initial Cardiac markers
- Cardiac arrest on admission
- ST segment deviation
Killip Class ??
Class-1 : No C/F of HF : 6% (30-day mortality)
Class 2 : Lung Crackles, S3 : 17%
Class 3 : Frank Pulm. Oedema : 38%
Class 4 : Cardiogenic Shock : 81%
Secondary Prevention in ACS ??
ACS pts. require Lifelong Drug therapy to help reduce the risk of further events
Std. therapy comprises the following
- Aspirin
- Second Anti-platelet if appropriate
- Beta-Blockes
- ACE i or ARBs
- Statin
Hallmark of Acute Pericarditis ??
Causes
- Viral infection (Coxsackie)
- TB, - Trauma
- Uraemia (Fibrinous Pericarditis)
- Post- MI, Dressler’s
- Connective Tissue Disorder
- Hypothyroidism, - Malignancy
Rx.-
- Treat the Underlying cause
- 1st line for Acute Idiopathic or Viral pericarditis : NSAIDs + Colchicine
Features of Pericarditis ??
Chest pain: may be Pleuritic
- Relieved by Siting & Leaning forward
Dyspnoea, Flu-like C/F, Non-Productive Cough
Peri-cardial Rub
Tachyponea & Tachycardia
Ix. done in Acute Pericarditis ??
1) ECG changes
- Global/ Widespread
- PR depression: Most specific
- Saddle shaped ST elevation
2) TTE (all pts. must undergo)
Most specific ECG marker for Pericarditis ??
PR Depression
Rx. of Angina Pectoris or Stable Angina ??
Lifestyle changes, Medications, PCI, Surgery
MEDICATIONS
1) Aspirin & Statin (All pts must receive in the absence of CI)
2) Sublingual GTN (for acute attacks)
3) BETA_Blockers or CCBs (based on co-morbidities)
4) If CCBs used as monotherapy
- Rate-limiting CCBs (Verapamil or D is used)
5) If CCBs is used in combination with Beta-Blockers
- Long-acting Dihydropyridine CCBs are used eg.-Mod. Release Nifedipine
6) If poor response to initial Rx., drug should be increased to max. tolerated dose
7) If still has C/F add a 2nd drug (Beta-blocker or CCBs)
8) 3rd line: Long-acting Nitrates, Ivabradine, Nicorandil or Ranolazine
What is Nitrate tolerance ??
When Nitrates are taken for a long time, reduced efficacy is noted
Pts. on Std. release Isosorbide Mononitrate should use Asymmetric dosing interval ie.
- Maintain a daily Nitrite-free time of 10- 14 hrs
This effect is NOT sen if Once daily Mod. Release Isosorbide Mononitrate used
Why should Beta-blockers NOT be coprescribed with Rate-limiting or Non-Dihydropyridine CCBs ??
Risk of Complete Heart Block
Complications of PCI ??
Stent Thrombosis (1- 2% cases)
- Due to Platelet aggregation
- MC in FIRST Month after PCI
- Presents with Acute MI
Restenosis (5- 20% cases)
- Due to Excessive Tissue Proliferation around stent
- MC in 3- 6 months after PCI
- Presents with recurrence of Angina
- RFs: DM, Renal impairment & Stents in Venous Bypass grafts
Types of Stents ??
Bare-Metal Stents
Drug-Eluting Stents
- Coated with Paclitaxel or Rapamycin which (-) local tissue growth
- This REDUCES Restenosis.
- Rates of Stent Thrombosis are INCREASED as process of Stent Endothelization is slowed
- S Thrombosis is prevented by Anti-Platelet Therapy
- Aspirin continued for Life long
Hallmarks of Aortic Dissection ??
Tear in Tunica Intima of Aortic Wall
Associations-
- HTN (Most imp. RF)
- Bicuspid Aortic Valve
- Marfan’s & Ehlers-Danlos
- Turner’s & Noonan’s
- Pregnancy & SYPHILIS
Features of Aortic Dissection ??
Chest/ Back pain
- Severe & Sharp, Tearing/Ripping
- Maximal at onset
- Classic C pain is MC in Type-A D
- Upper back pain is MC in Type-B D
- But there is Overlap
PULSE Deficit
- Weak or absent Carotid, Brachial ir Femoral pulse
- Variation (> 20 mmHg) in SBP b/w Arms
AR, HTN
ST Elevations in INFERIOR Leads
Symptoms specific to the arteries involved in Aortic Dissection ??
Angina if Coronary artery involved
Paraplegia: Spinal artery involved
Limb Ischaemia: Distal aorta
Aortic Dissection Classification ??
Stanford Classification
- Type-A: Ascending A [2/3rd cases]
- Type-B: Descending A distal to Lt. Subclavian origin [1/3rd cases]
DeBackey Classification
- Type-1: Originates in Ascending A, propagates to at least aortic arch & possibly beyond it Distally
- Type-2: Originates in & is confined to Ascending A
- Type-3: Originates in Descending A, rarely extends Proximally but will extend Distally
Ix. done in Aortic Dissection ??
Pt. is Haemodynamically stable
- CT Angio of Chest, Abd. & Pelvis
Pt. is Haemodynamically unstable
- TOE
CXR: Widened Mediastinum
IoC: CT Angio of Chest, Abd. & Pelvis
Rx. of Aortic Dissection ??
Type A
- Sx. Rx. & BP should be controlled to 100 to 120 mmHg
Type B
- Conservative Rx.
- Bed Rest
- Reduce BP: IV Labetelol to prevent progression
- Endovascular repair of Type-B A D may have a role in the future
Complications of Aortic Dissection ??
Backward Tear Complication
- Aortic Incompetence or AR
- MI: IWMI (due to RCA involvement)
Forward Tear Complications
- Unequal Arm pulses & BP
- Stroke
- Renal Failure
Coarctation of Aorta ??
Congenital narrowing of DESCENDING Aorta
- MC in MALES (despite a/w Turner’s)
Features
- Infancy: HF
- Adult: HTN
- Radio-Femoral delay
- Mid-Systolic Murmur; Maximal over back
- Apical Click from AV
- Notching of Inferior Border of Ribs (due to Collateral vessels) is NOT seen in Young children
Associations of Co of Aorta ??
Turner’s Syndrome
Bicuspid AV
Berry Aneurysm
Neurofibromatosis
Hallmark of PAH ??
Mean P A Pressure >= 25 mmHg
10% cases is inherited as A D disease
- MC in Females aged 30- 50 yrs old
PAH can develop 2ndary to
- COPD
Increased risk is seen in
- HIV
- Cocaine, Anorexigen (Fenfluramine)
Features of PAH ??
“Progressive Exertional Dysponea”
Exertional syncope
Exertional Chest pain
Peripheral Oedema
Cyanosis
- RV heave, Loud P2, TR, Raised JVP- Prominent ‘A’ wave
Rx. of PAH ??
1) Acute Vasodilator Testing is done
PA pressure is measured after administration of Vasodilator such as IV Epoprostenol/ Inhaled Nitric Oxide
- If PA pressure falls significantly (seen only in a minority of pts.) : Oral CCBs can be used to treat
- If PA Pressure does’t fall significantly (Vast maj. pts.)
— Prostacyclin analogues: Iloprost, Treprostinil
— Endothelin r Antagonist: Bosentan, Ambrisentan
— PDE inhibitor: Sildenafil
Progressive C/F despite Rx. consider Heart-Lung Transplant
Hallmark of Pulm. Capillary Wedge Pressure ??
PCWP is measured using a balloon tipped Swan-Ganz catheter which is inserted into the Pulm. Artery
- Pressure measured is similar to that of the LA (normally 6- 12 mmHg)
Uses-
- Find out if Pulm. Oedema is caused by HF or ARDS
HTN Rx. strategy ??
Clinic BP : >= 140/90 mmHg => Offer ABPM or HBPM
If ABPM/HBPM
- < 135/85 mmHg : No HTN
- >= 135/85 mmHg : Stage 1 HTN (Treat if < 80yrs + any of 5 condition)
- >= 150/95 mmHg : Stage 2 HTN (Treat all pts. regardless of age)
Conditions to treat Stage 1 HTN in a pt. who is < 80 yrs old ??
TREAT Stage 1 HTN if < 80 yrs + Any one of the following
- Target Organ damage
- Established CV disease
- Renal disease
- DM
- 10 yrs CV Risk >= 10% (Drug Rx. is considered in addition to lifestyle advice in adults < 60yrs old + Stage 1 HTN + 10 yrs CV Risk < 10%
BP Classification ??
Stage 1 HTN
- Clinic BP >= 140/90 mmHg
- ABPM/ HBPM average BP >=135/85
Stage 2 HTN
- Clinic BP >= 160/100 mmHg
- ABPM/ HBPM average BP >=150/95
SevereHTN
- Clinic SBP/DBP >= 180/120 mmHg
How to Dx. HTN ??
Measure BP in BOTH arm
- If difference > 20 mmHg, repeat
- If still a difference of > 20 mmHg, subsequent BP readings should be recorded from the arm with higher reading
Pathological conditions is considered in unequal BP readings eg., SUPREVALVULAR Aortic Stenosis
- So, listen to the heart
Also take a 2nd reading if 1st reading is > 140/90 mmHg & lower one of the 2 is considered
How to manage a pt. with BP >= 180/ 120 mmHg ??
1) ADMIT for Specialist assessment
- Retinal Bleed or Papilloedema (or)
- Life threatening C/F like- New onset confusion, Chest pain, HF signs or AKI
2) REFER if Phaeochromocytoma is suspected: Headache,Labile/ Postural Hypotension, Palpitations, Pallor, Diaphoresis
3) If NONE of the Above, do Ix. for End-Organ Damage (Bloods, ACR, ECG)
- If Present: Start Antihypertensives immediately without waiting for ABPM or HBPM results
- If NOT present: Repeat clinic BP within 7 days
How to measure ABPM & HBPM ??
Ambulatory BP Monitoring
- At least 2 readings/ hr during wake hrs (eg. b/w 08:00 to 22:00)
- Use Average of >= 14 readings
- If ABPM not tolerated of declined, offer HBPM
Home BP Monitoring
- For each BP recording, 2 consecutive readings is taken at least 1 min apart with pt. seated
- Recorded 2x daily, ideally in the Morning & Evening
- Measured for at least 4 days, ideally for 7 days
- Discard the readings of 1st day & use the average value of ALL Remaining readings
Lifestyle advice given to BP pts. ??
Low Salt: < 6g /day, ideally < 3g /day
- [Average adult daily intake: 8- 12g]
- Reducing salt intake by 6g/day lower SBP by 10mmHg
CAFFEINE intake should be reduced
Stop Smoking, Drink less [-OH],
Eat a balanced diet rich in Fruits & Vegetables, Exercise more, Lose Wt.
If < 40 yrs old consider specialist referral to exclude 2ndary causes
Rx. of High BP ??
STEP 1 Rx.
< 55 yrs or H/o T2DM: ACEi/ ARBs [A]
> 55yrs or Black Africans/ African- Caribbean origin: CCBs [C]
- ARBs preferred over ACEi in Black Africans or African-Caribbean due to reduced efficacy
STEP 2 Rx.
- If on ACEi/ ARBs add a CCBs or Thiazide
- If on CCBs add ACEi/ARBs or Thiazide
- ARBs preferred over ACEi in Blacks
Step 3 & Step 4 Rx. of BP ??
STEP 3 Rx.
Add a 3rd drug ie.,
- If on [ACEi/ARBs + CCBs] add Thiazides
- If on [ACEi/ARBs + Thiazides] add CCBs
STEP 4 Rx
- Step 4 is Resistant HTN & suggests adding a 4th drug or seek Specialist advice
- If K+ < 4.5 mmol/L: add Low dose Spironolactone
- If K+ > 4.5 mmol/L: add Alpha or Beta Blockers
If the BP still remains uncontrolled with optimal or max. tolerated doses of 4 drugs, seek Expert advice if it has not been obtained earlier
What is the target BP for a Hypertensive pts. ??
Age < 80 yrs. old
- Clinic BP: 140/90 mmHg
- ABPM/ HBPM: 135/85 mmHg
Age > 80 yrs. old
- Clinic BP: 150/90 mmHg
- ABPM/ HBPM: 145/85 mmHg
Which BP reading is the most accurate predictor of CV Events ??
ABPM
Novel Anti-Hypertensives ??
Direct Renin Inhibitors
- Aliskiren (branded as Rasilez)
- By (-) Renin, blocks conversion of Angiotensinogen ==> AT-1
S/E: Diarrhoea
Secondary Causes of HTN ??
RENAL Diseases
- GN, - Pyelonephritis
- ADPKD, - Renal Artery Stenosis
ENDOCRINE Disorders (Other than Primary Hyperaldosteronism)
- Phaeaochromocytoma
- Cushing’s Syndrome
- Liddle’s, - Acromagaly
- CAH (11-Beta Hydroxylase def.)
DRUG Causes
- Steroids, - NSAIDs
- MAOi, - COCPs
- Leflunomide
OTHER Causes
- Pregnancy, - Coarctation of Aorta
HTN Rx. in DM ??
BP Target: < 140/90 mmHg
T1DM
- Rx. if BP > 135/85 mmHg (OR)
- Albuminuria or >= 2 Metabolic Synd. features, in which case it should be 130/80 mmHg
1st line Antihypertensives regardless of age: ACEi or ARBs
- ARBs preferred over ACEi in Blacks
Autonomic Neuropathy may result in more Postural C/F in pts. on BP Rx.
Why should Bete-blockers avoided with Thiazides ??
They can cause
- Insulin Resistance
- Impair Insulin Secretion
- Alter Autonomic response to Hypoglycaemia
Hallmarks of Isolated Systolic HTN ??
Common in Elderly, affecting 50% of people > 70 yrs old
Risk Factors
- Aging, - Elastin Calcifications
- Increased Vascular Stiffness
- Increased Endothelial Dysfunc.
- Increased RAAS & Sym. activity
- Ventricular-Arterial Uncoupling
- Increased Salt sensitivity
Rx. is same as the Stepwise strategy used in Std. HTN
Hallmarks of Malignant HTN ??
BP > 200/130 mmHg
Seen in both Essential & 2ndary types
Severe HTN => Exceeding regulation capacity of Arterioles => Capillary Hyperperfusion => Reversible Capillary Leakage
- Fibrinoid necrosis of B vessels => Retinal bleeds, Exudates & Proteinuria, Haematuria (Benign Nephrosclerosis)
Features & Rx. of Malignant HTN
Severe Headache, N & V, Visual probs
Chest pain & Dysponea
Papilloedema
Severe: Encephalopathy (eg. Seizures)
Rx.-
- Reduce DBP no lower than 100 mmHg within 12- 24 hrs
- Bed Rest
- Most pts.- Oral therapy: ATENELOL
- Severe/ Encephalopathy: IV Na Nitroprusside or IV Labetelol
HTN in Pregnancy ??
Women at high risk of developing Pre-Eclampsia should take
- Aspirin 75mg OD from 12 wks POG until delivery
High Risk Group include
- HTN before pregnancy
- CKD, - T1DM & T2DM
- SLE or APLS
BP usually falls in 1st trimester & continues to fall till 20-24 wks POG after which it returns back to Pre-Pregnancy levels by Term
Criteria to Dx. HTN in Pregnancy ??
BP of > 140/90 mmHg (OR)
An increase above Booking readings of > 30 mmHg SBP or > 15 mmHg DBP
Define the following
- Pre-Existing HTN ??
- PIH or Gestational HTN ??
- Pre-Eclampia ??
H/o HTN before Pregnancy (OR) a BP of > 140/90 mmHg before 20wks POG
- No Proteinuria, No Oedema
BP of > 140/90 mmHg after 20 wks POG
- NO Proteinuria & Oedema
- Resolves in 1 months after delivery
PIH + Proteinuria (> 0.3g/ 24 hrs)
- Oedema may occur but now less commonly used as a criteria
Hallmarks of Pre-Eclampsia ??
TRIAD: New-onset HTN + Proteinuria + Oedema
BP >= 140/90 mmHg after 20 wks POG & >= 1 of the following
- Proteinuria
- Other Organ involved (Renal Cr. >= 90 umol/L, Liver, CNS, Utero-Placental dysfunction, Haematological
Consequences of Pre-Eclampsia ??
1) Eclampsia
- Other CNS c/f- Altered mentation, Blindness, Stroke, Clonus, Headaches , Persistent Visual Scotoma
2) Fetal Complications
- IUGR, - Prematurity
3) Liver: Elevated Transaminases
4) Haemorrhage: Abruptio Placenta, Intra-Abd., Intra-Cerebral
5) Cardiac Failure
Features of Severe Pre-Eclampsia ??
HTN > 160/110 mmHg
Proteinuria: Dipstick ++/+++
Headache, Visual disturbance
Papilloedema
RUQ or Epigastric pain
Hyperreflexia
Pit. Count < 100, Abnormal Liver enzymes or HELLP syndrome
Rx. of Pre-Eclampsia ??
Initial Assessment
- Arrange emergency 2ndary care assessment if suspected
- BP >=160/110 : Admit & Observed
Further Rx.
- 1st line: Oral Labetelol
- 2nd line: Nifedipine (if Asthmatic) & Hydralazine
Definitive Mgt: DELIVERY of Baby
Prevention of Pre-Eclampsia ??
HIGH RFs
- HTN in previous pregnancy
- CKD, - SLE, - APLS
- T1DM & T2DM, - Chr. HTN
Moderate RFs
- 1st Pregnancy, - >= 40 yrs old
- Pregnancy interval of > 10 yrs
- BMI >= 35 kg.m2 at 1st visit
- FHx. of Pre-eclampsia
- Multiple Pregnancy
ASPIRIN 75- 150 mg daily from 12 wks POG until birth if
- >= 1 High risk factors
- >= 2 Moderate risk factors
Hallmarks of Eclampsia ??
Seizures + Pre-Eclampsia [(PIH + Proteinuria) seen after 20wks POG]
- Seen upto 6 wks after delivery
Rx.-
- MgSO4 (to Prevent & Treat seizures)
- Given once a decision of Delivery is made
- IV Bolus of 4g over 5-10min followed by an infusion of 1g/hr
- Rx must continue for 24 hrs after last seizure or Delivery
Urine Output, reflexes, RR & O2 sats. should be monitored
MgSO4 induced Resp. Depression can occur: Ca Gluconate
Fluid Restriction
Hallmark of Pulm. Embolism ??
Pleuritic Chest pain, Dyspoenia & Haemoptysis (Triad seen in 10%)
The relative frequency of C/F are-
- Tachypnea (RR > 20/min): 96%
- Crackles - 58%
- Tachycardia (HR > 100/min) - 44%
- Fever (> 37.8 C) - 43%
[Well’s Criteria uses Tachycardia rather than Tachypnoea]
What is the use of
- Pulm. Embolism Rule-Out Criteria ??
- 2-Level PE Wells Score ??
PECR: Rule out PE in pts. known to have a low Pre-test probability (<15%)
What is Pulm. E Rule-out Criteria ??
All criteria must be absent for have a (-)ve PECR result ie. rule out PE
Done when we think there is a low pre-test probability (< 15%) BUT want more reassurance that it isn’t the Dx.
(-)ve PECR reduces PE chances to < 2%
Criteria of PERC ??
Age >= 50 yrs
HR >= 100 bpm
O2 Sats. <= 94%
Previous DVT or PE
Recent Sx. or Trauma in past 4 wks
Haemoptysis
U/L Leg swelling
Oestrogen use (HRTs, COCPs)
If ALL are (-)ve, chances of PE is < 2%
2 level PE Wells Score ??
1) Signs & C/F of DVT (Minimum of Leg swelling & Pain on palpation): 3
2) Alternative Dx. less likely : 3
3) HR > 100 bpm : 1.5
4) Immobile for > 3 days or Sx. in the previous 4 wk : 1.5
5) Previous DVT : 1.5
6) Haemoptysis : 1
7) Malignancy (On Rx./ Treated in last 6m/ Palliative) : 1
PE is likely if > 4 points
PE less likely if <= 4 points
Rx. of PE ??
If Wells Score > 4
Immediate CTPA (or) Interim Therapeutic AC while awaiting CTPA
- CTPA (+)ve : PE disgnosed
- CTPA (-)ve : Proximal Leg Vein USS if DVT suspected
If Wells Score <= 4 points
Do D-Dimer with results within 4 hrs (or) Interim Therapeutic AC while waiting for D-Dimer
- If D-Dimer (+)ve : Immediate CTPA or Interim T AC (if not given) while awaiting for CTPA)
- If D-Dimer (-)ve : Consider alternative Dx. & Stop AC
CTPA or V/Q scan ??
Non-Massive PE : CTPA (initial Ix.)
V/Q Scan may be used initially if
- Facilities available
- CXR is normal
- No significantC/F concurrent Cardio-Pulmonary disease
- IOC in pts. with RENAL Impairment
Advantages of CTPA over V/Q scan ??
- Faster, Easier to perform out of hr
- Reduced need of further imaging
- Can provide an alternative Dx. if PE excluded
- If CTPA is (-)ve, no need of further Ix. or Rx. for PE
Drawbacks of
- D-Dimers ??
- CXR ??
- V/Q scan ??
- CTPA ??
1) Sensitivity: 95-98%; Poor Specificity
- If > 50 yrs: Age-adjusted D-Dimers must be used
2) CXR is done in all pts. to exclude other pathology
- NORMAL in PE
- Wedge-Shaped Opacification
3) Sensitivity: 75%; Specificity: 97%
4) PERIPHERAL Emboli affecting SUB-SEGMENTAL Arteries may be missed
Causes of Mismatched V/Q ??
Old PEs
AV Malformation
Vasculitis
Previous RT
COPD gives Matched Defect
ECG features of PE ??
1) “S1Q3T3”
- Lead 1: Large S wave
- Lead 3 : Large Q wave & TwI
- These changes are seen in <= 20%
2) RBBB & RAD
3) Sinus Tachycardia
Rx. of PE ??
1) Anti-Coagulation
2) THROMBOLYSIS : Massive PE + Circulatory Failure
3) IVC Filters: Repeat PE despite on AC
- Prevents clots formed in Deep veins of leg from moving to Pulm. Artery
AC in PE ??
1st line : DOACs (Apixaban or Rivaroxaban)
- Instead of LMWH use until Dx. confirmed, DOAC use is advocated in suspected cases as it can be continued if Dx. is confirmed
If DOACs are not suitable, use either-
- LMWH followed by Dabigatran or Edoxaban (OR)
- LMWH followed by Vit. K antagonist (Warfarin)
AC of choice in PE with the following
- Active Cancer ??
- Severe Renal Impairment ??
- APLS [Triple (+)ve] ??
- DOACs (unless CI)
- LMWH followed by UfH (OR) LMWH followed by Warfarin (VKA)
- LMWH followed by Warfarin (Vit.KA)
Length of AC in PE ??
All pts. should have AC for at least 3 months
Provoked VTE:
- Occurs due to an obvious ppt. event
- Stop after Initial 3 months
- 3- 6 months in Active Ca pts.
Unprovoked VTE:
- Occurs in the absence of an obvious ppt. event (unknown factor)
- Continue for 3 more months (6 m in total)
Types of AF ??
FIRST detected episode (irrespective of whether it is symptomatic or self-terminating)
RECURRENT Episodes (>= 2 episodes)
- Paroxysmal AF: If self terminates (< 7 days but typically < 24hrs)
- Persistent AF: If lasts > 7 days
3) PERMANENT AF
- Continuous AF which cannot be Cardioverted (OR) if attempts to do so are deemed inappropriate
- Rx goals: Rate control & AC
Features of AF ??
Palpitations, Dyspnoea, Chest pain
Sign: Irregularly irregular Pulse
Ix.- ECG
Rx.-
- Rate or Rhythm Control
- Reducing Stroke risk
Rate v/s Rhythm Control ??
RATE Control
- Accept pulse is irregular & slow the rate to avoid (-)ve effects on Cardiac function
RHYTHM Control : Try to get the pt. back into & maintain, normal Sinus rhythm Termed as Cardioversion
- Pharmacological CV (Drugs)
- Electrical CV (Synchronised DC shocks)
RATE Control strategy is used in maj. of pts.
Haemodynamically STABLE
- If AF onset < 48hrs : Rate or Rhythm control
If AF onset > 48 hrs or Uncertain : Start Rate control for long-term rhythm control; delay CV & start AC for 3 wks
When is Rhythm Control preferred over Rate control ??
Co-Existent HF
1st onset AF
Obvious Reversible cause
Rate Control in AF ??
Beta-Blocker or a Rate-limiting CCBs (Diltiazem) is used as 1st line
If 1 drug does’t control rate adequately, a combination of 2 of the following can be used
Beta-Blockers (common CI is asthma
CCBs (Diltiazem)
Digoxin (NOT 1st line)
Rhythm Control in AF ??
Pt. must have had C/F for a short duration < 48 hrs (OR) be AC for a period of time prior to attempting CV
- Switch from Rate control to Rhythm control if Symptoms/ HR fails to settle
- The moment a pt., switches from AF to Sinus Rhythm, presents the highest risk for Embolism => Stroke
How to calculate Stroke risk in AF cases ??
CHA2DS2 VASc score
- CHF : 1
- HTN (or HTN on Rx.) : 1
- Age >= 75yrs : 2
- DM : 1
- H/o Stroke, TIA or VTE : 2
- Vascular disease (including IHD & PAD) : 1
- Sex (Female) : 1
Score 0 : NO Rx.
Score 1 :
- Males: Consider AC
- Females: No Rx
Score >= 2 : Offer AC
How to start AC in pts. with previous H/o maj. bleed ??
Assess risk of Stroke & Bleeding
Identify & treat other comorbidities
Identify the cause of Bleeding
- If Treatable cause : Restart OACs (NOACs: Novel Oral ACs)
- If Bleeding cause unknown or Untreatable or Irreversible: No Rx. or Left Atrial Appendage Occlusion
How to assess bleeding risk ??
Use ORBIT or HAS-BLED score
Haemoglobin or Haematocrit
- Males < 130g/L or < 40% : 2
- Females < 120g/L or < 36% : 2
Age > 74 yrs : 1
H/o Bleeding (GI bleed, Intracranial or Haemorrhagic Stroke) : 2
Renal Impairment (GFR < 60ml/min/ 1.73m2 : 1
Rx. with Anti-platelets : 1
ORBIT Score Interpretation ??
There is no formal rules on how we act on ORBIT score & individual pts. factors must be takes into account. But the following table acts as guide-
ORBIT Score = Risk Group = Bleeds/ 100 pt. yrs.
- [0-2] = Low Risk = 2.1
- [3] = Medium = 4.7
- [4-7] = High = 8.1
How to decide whether AC is needed or not ??
1) Ask for H/o AF ie. the following group must be assessed
- Symptomatic or Asymptomatic Paroxysmal/Persistent/Permanent AF
- Atrial Flutter
- Continuing risk of Arrhythmia recurrence after CV back to Sinus rhythm or Catheter Ablation
2) CHA2DS2 VASc used to determine the most appropriate AC strategy.
3) Do TTE (If CHADS VASc suggests no need for AC) to exclude Valvular disease, which in combination with AF is an Absolute indication for AC
AC of choice in AF ??
The following DOACs are promotes by NICE to reduce Stroke risk in AF
- Apixaban
- Dabigatran
- Edoxaban
- Rivaroxaban
2nd line: Warfarin (if DOACs are CI or not tolerated)
Aspirin is NOT recommended
Indication of Cardioversion in AF ??
Electrical CV if Haemodynamically Unstable
Electrical or Pharmacological CV as an Elective procedure where Rhythm control strategy is preferred
E-CV is synchronised to R wave (as it should NOT be delivered during Repolarization as VF can be induced)
CV as Rx. of AF if Onset < 48 hrs ??
Heparinize
Cardioverted using
Electrical: DC Cardioversion
Pharmacology
- Amiodarone [Str. Heart Disease (+)]
- Flecainide or Amiodarone (If NO Str. Heart disease
After DC-CV if the onset was < 48 hrs, further AC is NOT necessary
(Pt. at risk of Ischaemic Stroke should be put on Lifelong AC)
CV as Rx. of AF if Onset > 48 hrs ??
1) AC given for 3 wks prior to CV (OR)
2) Do a TOE to exclude a Left Atrial Appendage (LAA) thrombus => If excluded => Heparinize the pt., => Cardiovert immediately
- E-CV is preferred over Drug-CV
3) If High risk of CV failure (eg. Previous Failure or AF Recurrence): At least 4 wks of Amiodarone or Sotolol prior to E-CV
4) After E-CV : AC continued for 4 wks
Pharmacological CV drugs used ??
Highly Efficacious Drugs
- Amiodarone
- Flecainide (If NO Str. Heart disease)
- Others: Quinidine, Dofetilide, Ibutilide, Propafenone
Less Effective agents
- Beta-Blocker (including Sotalol)
- CCBs, - Digoxin
- Disopyramide, - Procainamide
Post Stroke Rx. of AF ??
After TIA, AC for AF is started immediately once Imaging excludes bleed
- Acute Stroke + No Haemorrhage : AC is started after 2 wks
- Anti-platelet Therapy given in the intervening period
- If imaging shows a very large infarct : AC initiation should be delayed
When should Rate Control NOT be used in AF ??
- AF due to Reversible cause
- HF is the primarily caused by AF
- New-onset AF (< 48 hrs)
- With Atrial Flutter : condition of pt. suitable an Ablation strategy to restore sinus rhythm
- For whom Rhythm Control is more suitable based on clinical judgement
Indication of Digoxin in AF Rx. ??
NOT a 1st line option for AF
- Considered ONLY if the person does NO or Very little Physical exercise (or) other 1st line drugs are CI
- May be used in cases of HF
Rhythm control drugs used to MAINTAIN Sinus rhythm with H/o AF ??
Beta-Blockers
Dronedarone : 2nd line in pts. following CV
Amiodarone : particularly if coexisting HF
Catheter Ablation in AF ??
Indication
- AF who have NOT responded to or wish to AVOID Antiarrhythmic drugs
Aim: Ablate faulty electric pathways that are causing AF
- Site: Aberrant electrical activity b/w the Pulm. Vein & LA
Both Radiofrequency (heat) & Cryotherapy can be used
- Percutaneous procedure (via Groin)
AC for Catheter Ablation ??
AC used 4 wks before & during the procedure
- C Ablation controls rhythm but does NOT reduce Stroke risk (even if the pt. remains in Sinus rhythm)
CHA2DS2 VASc
- Score 0 : 2 months AC
- Score > 1 : Long term AC
Outcomes of Catheter Ablation ??
Complications
- Cardiac Tamponade
- Stroke
- Pulm. Vein Stenosis
Success Rate
- 50% has Early recurrence (in < 3 m) of AF that often resolves spontaneously
- After 3 yrs. + Single procedure : 55% remain in Sinus R
- After 3 yrs. + Multiple Procedures : 80% remain in Sinus R
Hallmark of Atrial Flutter ??
Form of SVT characterised by Rapid Atrial depolarization waves
ECG: (‘Sawtooth appearance’)
Atrial rate is around 300/min
The Ventricular or HR is dependent on the degree of AV block
- 2:1 block = HR is 150/min
Flutter waves may be seen after Carotid sinus massage or Adenosine
Rx. of Atrial Flutter ??
Cure: RF Ablation of TV Isthmus
Drugs: Similar to AF but less effective
More sensitive to CARDIOVERSION
- Lower energy levels are used
[Flutter waves can be seen after Carotid sinus waves or Adenosine]
What is Multifocal Atrial Tachycardia ??
Irregular Cardiac Rhythm caused by at least 3 different sites in Atria
- Morphologically distinctive P waves
MC in Elderly with Chr. Lung disease (COPD)
Rx.-
- Correct Hypoxia & Electrolyte disturbances
- 1st line : Rate-limiting CCBs
- CV & Digoxin NOT useful
What is Supraventricular Tachycardia ??
Tachycardia that is not Ventricular in origin
Sudden onset Narrow complex T
- MC is: AVNRT
- Other causes AVRT (AV Re-entry T) & Junctional T
Rx. of SVT ??
ACUTE Rx.
1) Vagal Maneuvres
- Blow into empty plastic syringe
- Carotid Massage
2) IV Adenosine
- Rapid IV bolus of 6mg => if not successful give 12mg => unsuccessful give further 18mg
- CI in Asthma : Give VERAPAMIL
3) Electrical Cardioversion
Prevention:
- Beta-blocker & RF ablation
What is WPW syndrome ??
Congenital accessory conduction pathway b/w A & V leading to AVRT
- As accessory pathway does not slow the conduction, AF degenerates rapidly to VF
ECG features of WPW Syndrome ??
- Short PR interval
- Wide QRS with Delta wave (Slurred upstroke)
- LAD if Rt. accessory pathway
- RAD if Lt. accessory pathway
In maj. of cases or in questions with qualification, WPW is a/w LAD - Non-Specific ST-T changes are common (do not mistake for Ischaemia)
Types of WPW syndrome ??
Type A (Lt. sided P):
- Dominant R wave in V1
Type B (Rt. sided P):
- NO Dominant R wave in V1
Type C (rare)
- Delta wave are upright in V1- V4 but (-)ve in V5- V6
Rx. of WPW syndrome ??
Cure : RF Ablation of Accessory pathway
Drug Rx.- Sotolol, Amiodarone, Flecainide
[Sotolol is CI in WPW with AF as prolonging Refractory period at AVN increases rate of transmission through Accessory P => Ventricular Rate Increases => VF]
C/F of Bradycardia with Haemodynamic Instability ??
Shock: (SBP < 90mmHg), pallor, sweating, Cold, clammy extremities, Confusion or impaired consciousness
Syncope
M Ischaemia
Heart failure
Rx. of Bradycardia with Haemodynamic Compromise ??
1st line: IV Atropine 500mcg
Unsatisfactory Response
- Atropine upto 3mg
- Transcutaneous Pacing
- Isoprenaline/ Adrenaline infusion titrated to response
RFs for Asystole in Bradycardia ??
- Complete HB with Broad QRS
- Recent asystole
- Mobitz type 2 AV HB
- Ventricular pause > 3 sec.
Transvenous Pacing done even if satisfactory response if seen with Atropine
Peri-arrest Tachycardias ??
Broad-Complex T
Narrow-Complex T
AF
Unified Rx. algorithm has replaced the Separate Rx. algorithm
After basic ABC assessment, pts. are classified as being Stable or Unstable according to the presence of any Adverse Signs-
- Shock: SBP <90mmHg, pallor, Sweating, Cold clammy extremeties, confusion, impaired consciousness
- Syncope, - M Ischaemia, - HF
Rx. of Peri-arrest Tachycardia ??
If ANY of the Adverse signs (+)ve
- Synchronised DC-CV given
- Upto 3 shocks can be given, after this Expert help should be sought
Haemodynamically Stable
Rx. id given based on
- Narrow QRS or Broad QRS ??
- Regular rhythm or Irregular rhythm
Broad Complex T Rx. ??
REGULAR Rhythm
- Assume as VT (unless previously confirmed SVT with BBB)
- Loading dose of AMIODARONE followed by 24hrs infusion
IRREGULAR Rhythm (Expert help)
Possibilities include
- AF with BBB : most likely cause in a Stable pt.
- AF with Ventricular Pre-excitation
- Torsade de pointes
Narrow Complex T Rx. ??
REGULAR Rhythm
- Vagal maneuvres followed by IV Adenosine
- If above Rx. unsuccessful, consider Dx. of Atrial Flutter & Control Rate (eg.- Beta blockers)
IRREGULAR Rhythm
- Probable AF
- If onset < 48 hrs consider E-CV or Chemical CV
- Rate Control: Beta-blockers (1st line) unless CI
What is VT ??
Broad complex Tachycardia originating from a Ventricular Ectopic focus. 2 main types
- Monomorphic VT : MC caused by MI
- Polymorphic VT : A subtype of this is Torsades de pointes which is ppt. by QT interval Prolongation
Causes of Prolonged QT interval ??
Congenital
- Jervell-Lange-Nielsen syndrome (SNHL & is due to abnormal K+ channel)
- Romano-Ward syndrome (No SNHL)
Drugs
- Amiodarone, Sotalol, Class-1a
- TCAs, Fluoxetine
- Chloroquine, - Erythromycin
- Terfenadine
Other
- Hypo[Ca2+], Hypo[K+], Hypo[Mg2+]
- Acute MI
- Myocarditis
- Hypothermia
- SAH
Rx. of VT ??
Broad complex T can result from SVT with aberrant conduction => assume Peri-arrest situation to be Ventricular in origin
Haemodynamically Unstable
- Synchronised DC Shock
Drug Therapy
- Amiodarone: (ideally via central line)
- Lidocaine (use with caution in Severe LV impairment)
- Procainamide
If Drug Therapy FAILS
- Electrophysiology Studies (EPS)
- ICD (particularly in pts. with significantly impaired LV function
Drug CI in VT ??
Verapamil is not used in VT
Hallmarks of Torsades de pointes ??
‘Twisting of the points’ is a form of Polymorphic VT a/w Long QT interval
- Can deteriorate into VF => Death
Rx.-
- IV MgSO4
Hallmarks of Cardiac Tamponade ??
Accumulation of Pericardial Fluid under pressure
Beck’s Triad
Hypotension - Raised JVP - Muffled HS
Other features
- Dysponea, - Tachycardia
1) Absent ‘Y’ descent on JVP (due to limited RV filling)
2) Pulsus Paradoxus: Abnormally large drop in BP on Inspiration
3) ECG: Electrical alternans (alteration of QRS complex amplitude b/w beats)
Rx.- Urgent Pericardiocentesis
Key difference b/w C Tamponade & Constrictive Pericarditis ??
C Tamponade
- JVP: Absent Y descent
- P Paradoxus: Present
- Kussmaul’s Sign: RARE
Constrictive Pericarditis
- JVP: Prominent X + Y descent
- P Paradoxus: Absent
- Pericardial Knock: Loud S3
- Kussmaul’s Sign: PRESENT
- Pericardial Calcification on CXR
Genetic cause of Primary Cardiomyopathy ??
HOCM (A D condition)
- Mutation in gene encoding Beta-Myosin Heavy chain protein
Arrhythmogenic RV Dysplasia (A D)
- RV myocardium is replaced by Fatty & Fibrofatty tissue
ECG features of ARVD ??
A D Condition
- TwI: V1 to V3
- Epsilon wave (50% cases): Terminal notch in QRS complex
Acquired causes of Cardiomyopathy ??
PERIPARTUM CM
- Develops b/w Last month of Pregnancy & 5 months post-partum
- MC in Older women, Greater parity & Multiple gestations
TAKOTSUBO CM
- Stress Induced
- Transient, apical ballooning of Myocardium
- Rx- Supportive
Mixed ( 2ndary + Genetic predisposition) causes of Cardiomyopathy ??
DILATED CM
- Alcohol, - Beri-Beri (Wet)
- Coxasackie B virus, - Doxorubicin
RESTRICTIVE CM
- Amyloidosis
- Post- Radiotherapy
- Loeffler’s Endocarditis
Secondary causes of CM ??
Infective CM
- Chagas & Coxsackie B virus
Infiltrative CM
- Amyloidosis
Storage CM
- Haemochromatosis
Toxicity CM
- Doxorubicin & [-OH] CM
Inflammatory (Granulomatous)
- Sarcoidosis
Endocrine CM
- DM, Thyrotoxicosis, Acromegaly
Neuromuscular CM
- Friedreich’s Ataxia
- Duchenne & Becker’s M D
- Myotonic Dystrophy
Nutritional: Beriberi (thiamine)
Autoimmune: SLE
Hallmarks of DCM ??
MC form of CM (90% cases)
Dilated heart => Systolic Dysfunc.
- All 4 chambers are dilated but LV > RV
- Eccentric Hypertrophy (sarcomeres added in series) is seen
Causes of DCM ??
IDIOPATHIC (MCC)
Myocarditis (Coxsackie B, HIV, Diphtheria, Chagas)
IHD & HTN
Peri-Partum
Iatrogenic (Doxorubicin)
Substance abuse (-OH, Cocaine)
Wet Beriberi (Thiamine deficiency)
Infiltrative (Haemochromatosis, Sarcoidosis) : Can lead to Restrictive CM
Inherited cause of DCM ??
Familial genetic predisposition or a Specific Synd. (Duchenne M D)
- 1/3rd of pts. with DCM are thought to have genetic predisposition
- Maj. are inherited in a A D pattern
Features of DCM ??
Classic finding: HF
Systolic Murmur: MR & TR (Stretching of valves)
S3
CXR: Balloon appearance of Heart
Hallmarks of HOCM ??
A D condition & is the MCC of SCD in the Young adults
Defect in the gene encoding
- Beta-Myosin Heavy chain protein or
- Myosin-binding protein C
DIASTOLIC Dysfunction
- LV Hypertrophy => Decreased Compliance => Decreased CO
Myofibrillar Hypertrophy with Chaotic & Disorganised fashion myocytes (Disarray) & FIBROSIS of Biopsy
Poor prognostic factors of HOCM ??
- Syncope
- FHx of Sudden death
- Young age at presentation
- Non-sustained VT on 24- 48 hrs Holter’s
- Abnormal BP changes on exercise
- Increased Septal wall thickness
Features of HOCM ??
Often Asymptomatic
Exertional Dysponea; Angina
Syncope
- Typically after Exercise
- Due to SubAortic Hypertrophy of IV Septum => FUNCTIONAL AS
1) SCD: (MC due to V Arrhythmias), HF
2) Jerky pulse, Large ‘A’ waves
3) Double Apex beat
4) ESM : Increases with Valsalve & decreases with Squatting
- MR (MV impaired closure)
Echo findings of HOCM ??
MR SAM ASH
- MR
- Systolic Anterior Motion of anterior MV leaflet
- Asymmetric Hypertrophy
ECG findings of HOCM ??
- LVH
- Non-Specific ST segment
- T wave abnormalities; Progressive TwI
- Deep Q waves
- AF (occasional)
Rx. of HOCM ??
ABCDE
- Amiodarone
- Beta-blockers or Verapamil
- Cardioverter Defibrillator
- Dual Chamber Pacemaker
- Endocarditis Prophylaxis
Drugs to avoid in HOCM ??
Nitrates
ACEi
Ionotropes
Associations of HOCM ??
Friedreich’s Ataxia
WPW Syndrome
Hallmarks of Restrictive CM ??
Primarily characterised by decreased Compliance of Ventricular Endo-myocardium
- Predominantly DIASTOLIC Dysfunc.
Features
- Similar to Constrictive Pericarditis
- Low voltage ECG
Ix.-
- Echo - Cardiac MRI
What are the features suggesting Restrictive CM over Constrictive Pericarditis ??
Prominent Apical Pulse
ABSENCE of Pericardial Calcification on CXR
Heart may be Enlarged
ECG abnormalities: BBB, Q waves
Causes of Restrictive CM ??
- MCC: Amyloidosis (eg. 2ndary to Myeloma)
- Haemochromatosis
- Post-Radiation Fibrrosis
- Loffler’s Synd.- EndoMyocardial Fibrosis with a prominent Eosinophillic ifiltrate
- Endocardial Fibroelastosis: Thick Fibroelastic tissue forms in Endocardium, MC in CHILDREN
- Sarcoidosis
- Scleroderma
Hallmark of Takotsubo CM ??
Broken Heart Syndrome
Non-Ischaemic CM a/w Transient, Apical ballooning of Myocardium
- Triggered by STRESS
C/F
- Chest pain
-Features of Heart Failure
- ECG: ST elevation
- Normal Coronary Angiogram
Rx.- Supportive (Maj. improve)
ECG feature & Rx. of Myocarditis ??
Tachycardia, Arrhythmias
ST/T wave changes including
- ST segment elevation
- TwI
Rx.-
- Treat the cause, Abx. if bacterial
- Supportive Rx
Pathophysiology of Takotsubo CM ??
Takotsubo is a Japanese word that describes an Octopus Trap
“Transient Apical Ballooning of the Myocardium
Ballooning occurs due to Severe
- Mid & Apical segments: Severe Hypokinesis
- Basal segments: Activity preserved
The bottom (Apex) of the heart does not contract & so appears to balloon out BUT the area closer to the top (Base) continues to contract (Creating the neck of the Octopus trap)
Hallmark of Myocarditis ??
Inflammation of Myocardium
C/F
- Young pt. with an Acute history
- Chest pain, - Dysponea
- Arrhythmias
Ix.-
- Increased inflam. markers (99%)
- Increased Cardiac enzymes
- Increased BNP
Causes of Myocarditis ??
Viral: Caosackie B, HIV
Bacteria: Diphtheria, Clostridia
Spirochetes: Lyme’s
Protozoa: Chaga’s, Toxoplasmosis
Autoimmune
Druga: Doxorubicin
Complications of Myocarditis ??
HF
Arrhythmia => Sudden Death
DCM: late complication
Hallmark of Constrictive Pericarditis ??
Causes: Any cause of Pericarditis; Particularly TB
CXR: Pericardial Calcification
Features
- Dyspnoea
- RV Failure: Elevated JVP, Ascites, Oedema, Hepatomegaly
- Prominent X & Y descent
- Pericardial Knock- Loud S3
- Kussmaul’s sign is (+)ve
Hallmarks of Atrial Myxoma ??
MC Primary Cardiac Tumour
Site: LA (75% cases), MC attached to Fossa ovalis
MC in Females
Features
- Systemic: Dysponea, Fatigue, Wt, loss, Pyrexia of unknown origin, Clubbing
- Emboli
- AF
- Mid-Diastolic murmur, ‘Tumour Plop’
Echo features of Atrial Myxoma ??
Pedunculated Heterogenous mass typically attached to Fossa Ovalis region of Interatrial Septum
Strongest RF foe developing IE ??
Previous episode of Endocarditis
Aetiology of Infective Endocarditis ??
The following types of pts. are affected
- Previous Normal valve (50%, acute presentation)
- Rheumatic V D (30% acses)
- Prosthetic Valves
- Congenital Heart disease
- IVDU (typically TRICUSPID V lesion)
- Others: recent piercing
Organisms causing Infective Endocarditis ??
1) Staph. Aureus (MCC)
- Particularly common in Acute presentation & IVDUs
2) Strepto. Viridans
- MCC in Developing Nations
- MC found in Mouth & in Dental plaques so, is linked with Poor Oral Hygiene or after Dental procedure
- Is a Pseudotaxonomic term & has 2 organism namely-Strep. Mitis & Strep. Sanguinis
3) Staph. Epidermidis-Coagulase (-)ve
- Colonize indwelling lines
- MCC in pats. after Prosthetic valve Sx. (Perioperative contamination)
- After 2 month, it returns back to Stap. aureus
4) Strep. Bovis (a/w Colon Cancer)
- Subtype: Strep. Gallolyticus is most linked with Colorectal Ca
5) Non-infective
- SLE (Libman-Sacks)
- Malignancy: Marantic Endocarditis
Causes of Culture (-)ve I Endocarditis ??
- Prior Antibiotic Therapy
- Coxiella burnetii
- Bartonella
- Brucella
- HACEK: Haemophilus, Actinobacillus , Cardiobacterium, Eikenella, Kingella
Modified Duke’s Criteria ??
PATHOLOGICAL Criteria
- (+)ve Histology/ Microbiology of autopsy or Cardiac Sx. (Valve tissue, vegetations, embolic fragments or Abscess contents)
MAJOR Criteria
POSITIVE Blood Culture (BC)
- 2 (+)ve BC + shows typical bugs (Strep. Viridans or HACEK) [OR]
- Persistent Bacteraemia from 2 B Clutures taken > 12 hrs apart or >= 3 (+)ve BC showing less specific species-Staph. epidermidis or aureus
- (+)ve Serology for C Burnetii/ Bartonella spp./ C Psittaci [OR]
- (+)ve Molecular assays for specific gene targets
Evidence of ENDOCARDIA involved
- (+)ve Echo (Oscillating str./abscess formation/ new valvular involvement/ Dehiscence of prosthetic V) OR New Valvular Regurgitation
What are the Minor Duke’s Criteria ??
1) Predisposing heart condition/ IVDU
2) Microbiological evidence NOT meeting Maj. Criteria
3) Fever > 38 C
4) Vascular Phenomenon
- Major Emboli, Splenomegaly, Clubbing,
- Sphincter Haemorrhages, Janeway Lesions (Non-tender), Petechiae or Purpura
5) Immunological Phenomenon
- Osler’s Node (Tender)
- Roth Spots
- Glomerulonephritis
Poor Prognostic factors in IE ??
Staph. Aureus Infection
Prosthetic H Valve (especially Early, acquired during Sx.)
Culture (-)ve Endocarditis
Low Complement Levels
Indications for Sx. ??
- Severe Valvular Incompetence
- Aortic abscess (indicated by PR interval lengthening)
- Infections resistant to Abx./ Antifungals
- HF refractory to Std. medical Rx
- Recurrent emboli after Abx. Therapy
What is the Mortality rate according to Organisms ??
Staphylococci- 30%
Bowel Organisms: 15%
Streptococci: 5%
Dx. based on Duke’s Criteria ??
Dx. if
- Pathological criteria (+)ve (OR)
- 2 maj. criteria (OR)
- 1 Maj. + 3 Minor (OR)
- 5 Minor
C/F of IE ??
Fever + New onset Murmur
VASCULAR Phenomenon
- Major Emboli
- Splenomegaly
- Clubbing
- Sphincter (Subungual) Haemorrhage (Dark red linear lesions in nail bed)
- Janeway L: Non-Tender macules on palms & soles
- Petechiae or Purpura
IMMUNOLOGICAL Phenomenon
- Osler’s Node: Tender Subcutaneous nodules in PULPS of finger
- Roth Spots: Retinal bleeds with Clear centre
- Glomerulonephritis
Initial Blind Rx. of IE ??
NATIVE Valve
- Amoxicillin + Gentamicin-Low dose
If Penicillin Allergic, MRSA or Severe Sepsis
- Vancomycin + Gentamicin-Low dose
PROSTHETIC Valve
- Vancomycin + Rifampicin + Low dose Gentamicin
Rx. of Staphylococci infection of
- Native Valve IE ??
- Prosthetic Valve IE ??
Flucloxacillin
If Penicillin allergic/ MRSA
- Vancomycin + Rifampicin
Flucloxacillin + Rifampicin + Low dose Gentamicin
If Penicillin allergic or MRSA
- Vancomycin + Rifampicin + Low dose Gentamicin
Rx of Endocarditis caused by
- Fully sensitive Strept. (eg. Viridans)
- Less sensitive Strept.
Benzylpenicillin
If Penicillin allergic
- Vancomycin + Low dose Gentamicin
Benzylpenicillin + L dose Gentamicin
If Penicillin allergic
- Vancomicin + L dose Gentamicin
Prophylaxis of IE ??
The following procedures do NOT require Prophylaxis
- Dental procedures,
- Upper or Lower GI procedures
- Genitourinary tract (Urological, ObGyn procedures, Childbirth)
- URT & LRT (includes ENT procedures & Bronchoscopy)
Condition where Prophylaxis is necessary ??
At risk of IE + Taking Antimicrobial Rx. + Undergoing GI or GU procedure at site where infection is suspected
- give ABX. that covers the bug causing IE
Hallmarks of Rheumatic Fever ??
IMMUNE reaction to recent (2-6 wks ago) Grp. A Strep. (Strept. Pyogenes) infection
- S Pyogenes => Innate immunity activated =>Antigen presented to T-cells => B & T cells produce IgG & IgM antibodies => CD4+ T cells activated
- Cross-reactive immune response (Type 2 HS) mediated by Molecular Mimicry
- Antibodies produced against M protein cross react with Myosin & SM of arteries
Dx. of RF (Jones Criteria) ??
MAJOR Criteria [“JONES”]
- Joint pain (Polyarthritis)
- O Carditis & Valvulitis
- Nodules (Subcutaneous)
- Erythema Marginatum
- Sydenham’s Chorea (Late feature)
- Carditis & Valvulitis
Carditis is NOT based on Peri- or Myo- carditis alone BUT there must be evidence of ENDOCARDITIS (clinically relates to Valvulitis- regurgitant murmur)
Minor Jones Criteria ??
Raised ESR or CRP
Pyrexia
Arthralgia (NOT if arthritis a Maj. criteria)
Prolonged PR interval
Dx. of RF ??
Evidence of Strept. Infection +
- 2 major criteria
- 1 major & 2 minor criteria
Evidence of Recent Strept. infection
- Raised or Rising Strept. antibodies
- (+)ve throat swab
- (+)ve Rapid Grp. A Strept. antigen test
Rx. of Rheumatic Fever ??
Antibiotics: Oral Penicillin V
Anti-inflammatories: NSAIDs (1st line)
Rx. of any complications that develops eg.- HF
ASCHOFF Bodies describe the Granulomatous nodules found in RF
What is Heart Failure ??
Heart can’t pump enough blood to meet the body’s need; arises from Str. or Func. heart issues & is categorised by
- EF
- Timing
- Anatomical involvement
Classification of HF ??
1) HFrEF (LVEF < 40%)
Systolic Dysfunction + Impaired Myocardial Contraction
Causes: IHD, DCM, Myocarditis, Arrhythmias
2) HFpEF (LVEF > 50%)
Diastolic Dusfunc. + Impaired Ventricular Filling
Causes: HOCM, Restrictive CM, Constrictive Pericarditis, Cardiac Tamponade
3) HFmrEF (Borderline LVEF)
- LVEF 40%- 49%
- Features overlap b/w HFrEF & HFpEF
Classification of HF based on
- Timing ??
ACUTE HF (AHF)
Sudden worsening of Chr. HF
- Features: Pulm. Oedema, Severe dyspnea needing urgent care
CHRONIC HF (CHF)
Slow onset + Progressive C/F
- Leads to Functional decline
Classification of HF based on
- Anatomical involvement ??
LEFT-Sided HF
- Pulm. Edema
- Dyspnea, Orthopnea, PND & Fine Bibasal Crackles
RIGHT Sided HF
- 2ndary to Left-sided or Pulm. HTN
- Peripheral Oedema, Raised JVP, Hepatomegaly, Ascites & Wt. gain
BI-VENTRICULAR HF
- Combination of Left & Right HF
Symptoms & Signs of HF ??
Dyspnea, Fatigue, Exercise intolerence
Left-sided: Orthopnea, PND
Rt.-Sided: Peripheral Swelling
SIGNS-
- HRrEF: Tachycardia, Displaced apex beat & S3 gallop
- Rt.-sided: Raised JVP, Hepatomegaly
- Pulm. Crackles & Oedema
Ix. done in HF ??
Dx.- BNP or NT-proBNP: Elevated
CBC, LFT, RFT
TFT to exclude 2ndary causes
IMAGING
1) Echo: Check LVEF & Str.
2) CXR: Pulm. Congestion or Cardiomegaly
3) Cardiac MRI: Detects Myocardial Fibrosis or Infiltrative CM
ECG
Rx. of HFrEF ??
1st Line
- ACEi or ARBs
- Beta-blockers (Bisprolol, Carvedilol)
- Sacubitril-Valsartan: used when ACEi & Beta-blockers are not relieving C/F + LVEF < 35%
Add on Therapy
- MRAs : Spironolactone
- SGLT2i : Dapagliflozin
Symptomatic Relief: Diuretics
DEVICE Therapy
- ICDs to prevent Arrhythmias
- C Resynchronization Therapy (CRT)
LifeStyle Modifications
- Salt & Fluid restriction
- Regular Physical activity as tolerated
Indications of CRT ??
Importance of ICD ??
LVEF <= 35%
Symptomatic despite Medical Rx
- NYHA Class 2- 4
QRS duration >=130ms + LBBB
Benefits of CRT
- Reduces symptom & Mortality
- Improves quality of life & Decreases Hospitalizations
ICDs prevent SCD
Rx. of HFpEF ??
1) Symptomatic Rx. & Comorbidity Rx
Diuretics (To relieve Fluid Overload)
- Manage Pulm. Congestion & Edema
2) Rx. of Underlying Condition
- HTN (ACEi, ARBs, CCBs)
- AF (Rate & Rhythm control & use AC based on CHA2DS2 VASc score)
- Ischaemia : Optimize CAD Rx. with Anti-anginal Rx. & Revascularization
3) LifeStyle & Supportive
- Physical activity & Cardiac Rehabilitation
- Na+ restriction & Wt. loss
Prognosis in HF ??
HFrEF generally has a worse outlook than HFpEF
- Severity, Cause & Co-morbidities impact prognosis
What is High Output HF ??
NORMAL Heart is unable to pump enough blood to meet the metbolic needs of body
Signs & C/F of HF + CO >= 8L/min or Cardiac Index >= 4L/min/m2
Causes of High Output HF ??
Anaemia
AV Malformation
Paget’s disease
Pregnancy
Thyrotoxicosis
Wet Beri-beri (Thiamine deficiency)
What id Kawasaki Disease ??
Type of Vasculitis predominantly seen in Children
- CA Aneurysm is a serious complication
FEATURES
- High-grade fever for > 5 days; resistant to Antipyretics
- Conjunctival injection (Red eyes)
- Bright red, Cracked lips
- Strawberry tongue
- Widespread Rash
- Cervical LNpathy
- Red Palms & Soles which later Desquamates
Dx. & Rx. of Kawasaki Disease ??
Clinical Dx. [No specific Dx. test]
TREATMENT
- High-dose Aspirin
- IVIGs
Initial Screening test for CA Aneurysm - ECHOCARDIOGRAM (rather than Angio)
Hallmark of Takayasu’s Arteritis ??
Large Vessel Vasculitis
- Typically causes occlusion of Aorta
- Questions commonly refer to an ABSENT/ WEAK limb pulse
- MC in Young Females (10-40 yrs)
- MC in Asians
Associations: Renal Artery Stenosis
Features of Takayasu’s ??
Systemic features of Vasculitis
- Malaise, Headache
UNEQUAL BP in Upper Limbs
Carotid Bruit & Tenderness
Absent or Weak Peripheral pulses
UL & LL Claudication on Exertion
AR (20% cases)
Ix. & Rx. of Takayasu’s ??
Dx.- MRA or CTA
- Vascular Imaging of Arterial tree
Treatment
- Steroids
Hallmarks of ACE inhibitors ??
MoA: Angiotensin-1 =(-)=> AT-2
- ACEi are activated by Phase-1 Metabolism of liver
S/E
- Cough (15% pts.) due to increased Bradykinin levels
- Angioedema
- HYPER[K+]
- 1st dose Hypotension: MC in pts. taking Diuretics
Interactions of ACEi ??
High-dose Diuretics (> 80mg of Furosemide a day)
- Significantly increases the risk of Hypotension
1st Dose Hypotension
- MC in pts. taking Diuretics
CI of ACEi ??
Pregnancy & Breastfeeding
Renovascular disease- may result in Renal impairment
AS : may cause Hypotension
Hereditary Idiopathic Angioedema
Seek Specialist advice before starting if K+ >= 5mmol/L
Monitoring of ACEi ??
U&E checked before starting Rx. & after increasing dose
- A rise in Cr. & K+ is expected
Acceptable changes
- Rise in S Cr. upto 30% from baseline
- Rise in S. K+ upto 5.5mmol/L
Fall in eGFR of < 20% (SIGN) & < 25% (NICE CKD) is acceptable
What is suspected if there is a significant change in U&E after starting ACEi ??
Undiagnosed B/L Renal Artery Stenosis
Hallmarks of ARBs ??
Indications
- Used when ACEi are not tolerated (Cough)
- Afro-Caribbean pts.
Should be used with caution in pts. with RenoVascular disease
Features of ARBs ??
MoA: Blocks effects of AT-2 at [AT-1r]
Candesartan, Losartan, Irbesartan
- LOSARTAN reduces CVA & IHD mortality in HTN pts.
Centrally Acting Anti-HTN ??
Methyldopa (Rx. of HTN in Pregnancy)
Moxonidine
- Rx. of Essential HTN when conventional Anti-HTNs have failed
Clonidine
- (+) Alpha-2 r in Vasomotor centre
- Anti-HTNs effects
Hydralazine ??
Used in Pregnancy & in Severe HTN
MoA: Increase cGMP => SM relaxes
CI: SLE, IHD, CerebroVascular D
S/E: Tachycardia, Palpitations, Flushing, Fluid retention, Headache, Drug induced Lupus
Adenosine ??
MC used to terminate SVTs
Adenosine effects are enhanced by
- Dipyridamole (Antiplatelets)
Adenosine effects are blocked by
- Theophylline
CI: Asthma (bronchospasm)
S/E: Chest pain, Bronchospasm, Transient flushing, Can enhance Conduction down accessory pathway => Increased Ventricle Rate (WPW)
MoA of Adenosine ??
Causes TRANSIENT HB in AVN
- A1 r agonist in AVN =(-)=> Adenylyl Cyclase ==> Reduces cAMP ==> Hyperpolarisation by Increasing K+ Efflux
- 1/2 life: 8- 10 sec
- Infused ideally via Large-calibre Cannula due to its Short 1/2 life
What are ADP receptor Inhibitors ??
ADP is a main Plt. Activation factor, mediated by G-coupled r P2Y1 & P2Y12
Main target of [ADPr i] is [P2Y12 r], as this leads to -
- Sustained Plt. aggregation & stabilisation of Plt. plaque
Eg.- Clopidogrel, Prasugrel, Ticagrelor, Ticlopidine
Dual Anti-Platelet Therapy ??
[Aspirin + ADP i] work by blocking different Plt. aggregation pathway, which have Synergistic effect
Moderate-High Risk ACS pts.
- [Prasugrel + Aspirin] causes marked reduction in ischaemic events than [Clopidogrel + A]
NICE guideline for 2ndary prevention of ACS
- Aspirin 75mg + Ticagrelor 90mg BD
DAPT for ACS undergoing PCI ??
Aspirin (75- 100mg) OD + Prasugrel 10mg (OR) Ticagrelor 90mg BD
If newer Anti-Plt. are CI
- Use Clopidogrel 75mg
Given for 12m with Aspirin
S/E of Ticagrelor ??
Dyspnoea (due to impaired Adenosine clearance => increased conc. in blood => (+) Adenosine r in lungs => Adenosine (+) sensory nerve fibres => Dysponea)
Drug interactions of ADP i (Clopidogrel & Prasugrel) ??
Clopi + PPIs (Ome- & Esmo- prezole) => Reduced Antiplatelet effect
CI of Prasugrel
- Prior Stroke or TIA + High risk of Bleeding
- Prasugrel Hypersensitivity
Drug interactions of ADP i
- Ticagrelor ??
CI of Ticagrelor
- High risk of bleeding,
- H/o Intracranial Bleeding
- Severe hepatic dysfunction
Use Ticagrelor with caution in
- Acute Asthma
- COPD
- Due to higher rates of Dyspnoea
Hallmarks of Loop Diuretics ??
Works by (-) Na+/K+/2Cl- in Thick Ascending Limb of L of H
- Reduces NaCl
There are 2 variants of NKCC; Loop D acts on NKCC2, which is more prevalent in Kidneys
- They must be Filtered INTO Tubules by Glomerulus before they can have an effect
Indications & S/E of Loop D ??
Heart Failure: Acute (IV) & Chronic (Oral)
Resistant HTN, particularly in pts. with Renal Impairment
S/E
- HYPO: Na+, K+, Mg2+
- HYPOCALCAEMIA
- Hypotension
- Hyperglycaemia (less common than Thiazides)
- Gout
- Hypochloraemic Alkalosis
- Ototoxicity
- Renal Impairment (Dehydration + Direct Toxic efect)
Why should we increase the dose of Loop D in Renal Impairment ??
Pt. with poor Renal Func. require escalating doses to ensure sufficient conc. is achieved WITHIN the Tubules
- Loop D to work has to get filtered into Tubules via glomerulus before they have their effect
Hallmarks of Thiazide D ??
Work by (-) Na+ reabsorption at Early DCT by blocking Na+/Cl- Symporter
- K+ is lost as more Na+ reaches the Collecting D
- Mainly used in HTN Rx
NICE now recommends use of other Thiazide like D: Indapamide & Chlorthalidone
S/E of Thiazide D ??
Dehydration, Postural Hypotension
HYPO: Na+, K+
Impotence
HYPER[Ca2+] leads to Hypocalciuria
- Useful in reducing incidence if Renal Stones
Hyperuricaemia (Gout)
Hyperglycaemia (IGT)
Rare S/E
- Thrombocytopaenia
- Agranulocytosis
- Photosensitive Rash
- Pancreatitis
Hallmarks of Amiodarone ??
Class 3 Anti-arrhythmic agent used in Rx of Atrial, Nodal & Ventricular tachycardias
- (-) K+ channels =(-)=> repolarization & hence prolongs AP
- Also has Na+ (-) effect (Class1 effect)
Monitoring
- Before Rx: TFT, LFT, U&E, CXR
- TFT & LFT every 6 monthly
Factors limiting Amiodarone use ??
Very Long 1/2 life (20- 100 days)
- Loading doses are used oftenly
Ideally be given via Central veins
Pro-arrhythmic effect (Prolong QT)
Interacts as P450 inhibitor drugs (decrease metabolism of Warfarin)
Numerous S/E
S/E of Amiodarone ??
Thyroid Dysfunction (Hyper & Hypo)
Corneal deposits
Pulm. Fibrosis or Pneumonitis
Liver fibrosis/ Hepatitis
Peripheral Neuropathy, Myopathy
Photosensitivity
‘SLATE-GREY’ appearance
Thrombophlebitis
Bradycardia
Lengthens QT interval
Hallmarks of Dipyridamole ??
Anti-Platelet mainly used in with Aspirin after Ischaemic Stroke or TIA
- (-) PDE => Elevates Plt. cAMP levels => in turn Reduces Intracellular Ca2+
- Also reduces Cellular uptake of Adenosine
- (-) Thromboxane Synthase
Fondaparinux ??
Direct Thrombin Inhibitors ??
- Activates AT-3 => Potentiates (-) of Factor 10a & is given SC
Often grouped with DOACs
1) Bivalirudin (given as IV) : Is a Reversible direct thrombin inhibitor used as an AC in Rx. of ACS
2) Dabigatran taken Orally
- Used as an alternative to Warfarin
- Do NOT require regular monitoring
Importance of Dabigatran ??
2 main indications
VTE Prophylaxis after Hip/Knee replacement Sx.
Non-Valvular AF (Stroke prevention) who have >=1 of the following RFs
- H/o:- Stroke/TIA/Systemic Embolism
- LVEF < 40%
- NYHA Class >=2 (Symptomatic HF)
- >= 75 yrs old
- >= 65 yrs + one of: DM, CAD or HTN
S/E of Dabigatran ??
- Haemorrhage (Maj. S/E)
- Dose should be reduced in CKD
Higher risk of bleeding & VTE events seen with recent Mechanical HV replacement compared with Warfarin
CI if Cr. Clearance < 30 ml/min
Dabigatran antidote ??
Idarucizumab (rapid reversal of AC)
Hallmarks of Clopidogrel ??
Anti-Platelet Agent & is a 1st line in pts. after Ischaemic Stroke & PAD
Belongs to class of drug called
THIENOPYRIDINES which have similar MoA.
- Eg.- Prasugrel, Ticegrelor, Ticlopidine
MoA & Interactions of Thienopyridines ??
Antagonist of P2Y12 ADP r => (-) Plt. activation
Interactions
- Don’t use with Ome- or Esmo- Prazoles
- Pantoprazole can be used
Secondary prevention of Stable CV disease with an indication for an AC
All must be started on Anti-Platelets
If indication for AC exists (eg. AF)
- Give Only AC Monotherapy without Anti-Platelet agents
How to give a combination of Anti-Platelet & AC in-
- Post ACS or PCI ??
Triple Therapy (2 Anti-P + 1 AC)
- For 4 wks to 6 months after the event
(THEN)
Dual Therapy (1 Anti-P + 1 AC) to complete 12 months
Pt. on Anti-P agent develops VTE, how to treat this pt. ??
ORBIT score calculated
- Low risk bleeders : Continue Anti-P
- Intermediate or High risk bleeder : Stop Anti-P & start AC
Anti-P of choice in
- ACS (medical Rx.) ??
- PCI ??
1st line: Aspirin (life long) + Ticagrelor (12 months)
2nd line: If Aspirin CI, Clopidogrel (LL)
1st line: Aspirin (LL) + Prasugrel or Ticagrelor (12 months)
2nd line: If Aspirin CI, Clopidogrel (LL)
Anti-P of Choice in-
- TIA ??
- Ischaemic Stroke ??
- PAD ??
TIA & Ischaemic Stroke
- 1st line: Clopidogrel (life long)
- 2nd line: Aspirin & Dipyridamole (LL)
1st line: Clopidogrel (LL)
2nd line: Aspirin (LL)
What are GP 2b/3a r Antagonists ??
Abciximab
Eptifibatide
Tirofiban
Hallmarks of Warfarin ??
Oral AC; used previously in the Rx. of VTE & reducing Stroke risk in AF pts.
- Now been superseded by DOACs
MoA: (-) Epoxide Reductase => prevents Vit.K reduction to its active Hydroquinone form
- This in turn acts as in Carboxylation of Factors 2, 7, 9 & 10 & Protein C
Indications of Warfarin ??
Mechanical Heart Valve
- Target INR depends on Valve type & its location
- MV requires higher INR targets than AV
Second line after DOACs
- VTE: Target INR= 2.5 & if Recurrent 3.5
- AF: Target INR- 2.5
Monitoring of Warfarin ??
What are the Factors that potentiate Warfarin ??
Using INR= PTT of Pt. : Normal PTT
- has long 1/2 life & achieving stable INR may take several days
Factors that Potentiate Warfarin are
- Liver Disease
- P450 inhibitors
- CRANBERRY Juice
- Drugs that displace Warfarin from Albumin- eg.- NSAIDs
- Inhibit Plt. func.- NSAIDs
S/E of Warfarin ?
- Haemorrhage
- Teratogenic, but can be used in Breastfeeding mothers
- Purple Toes
Skin Necrosis - When Warfarin is 1st started, Protein C synthesis is reduced => Temporary Procoagulant state
- Thrombosis may occur in venules leading to necrosis
Why is Heparin administered when Warfarin is started ??
When warfarin STARTED => Synthesis of Protein C is reduced => Temp. Procoagulant state => Thrombosis
- To AVOID this, Concurrently Heparin is administered
Rx. of Warfarin induced High INR ??
1) MAJOR Bleed
- Stop W + IV VitK 5mg + PTCC
- FFP given IF PT Conc. Complex not available. FFP can take time to defrost
- Intracranial Bleed: PTCC
2) INR > 8.0 + Minor Bleed
- Stop W + (IV) Vit.K 1- 3mg
- Repeat Vit.K if INR still too high after 24hrs
- Restart W when INR < 5.0
3) INR > 8.0 + No bleeding
Rx. of Warfarin induced High INR ??
3) INR > 8.0 + No Bleeding
- Stop W + Vit.K 1- 5mg by mouth, using the IV preparation Orally
- Repeat dose of Vit.K if INR still too high after 24hrs
- Restart W when INR < 5.0
4) INR 5.0- 8.0 + Minor Bleed
- Stop W + (IV) Vit.K 1- 3mg
- Restart W when INR < 5.0
5) INR 5.0- 8.0 + No Bleeding
- Withhold 1 or 2 doses of W
- Reduce Maintenance dose
Dentistry in Warfarinised pts. ??
Check INR 72hrs before procedure, proceed if INR < 4.0
If H/o an unstable INR, then it should be checked within 24hrs of Dental procedure
What is Thrombolysis ??
Thrombolytic drugs activate plasminogen to form plasmin => this in turn degrades Fibrin & breaks up Thrombi
- Used in ST elevation MI
Other indication: Acute Ischaemic Stroke & PE
Eg.- Alteplase, Tenecteplace, Streptokinase
Physiological effect of Atropine ??
- Tachycardia
- Mydriasis
- Can trigger Acute Angle Closure G in susceptible pts.
CI & S/E of Thrombolysis ??
Active internal bleeding
Recent Bleed, Trauma or Sx (including Dental extraction)
Coagulation & Bleeding disorder
Intracranial Neoplasia
Stroke < 3m ago
Aortic Dissection, Severe Head injury
Severe HTN
S/E: Bleeding, Hypotension (MC with Streptokinase), Allergic Reaction (can occur with Streptokinase)
Hallmark of Atropine ??
Muscuranic ACh r antagonist
Uses:
- Symptomatic Bradycardia (IV Atropine)
- Rx. of OP poisoning
- In ALS, it is no longer recommended for routine use in Asystole or Pulseless Electrical Activity (PEA)
Hallmark of BNP ??
Source: LV Myocardium in response to Strain
Increased Synthesis
- Raised in HF (mainly) but also in
- M Ischaemia, Valvular HD
Reduced Excretion
- CKD
Drugs that reduce BNP are
- ACEi, ARBs, Diuretics
Effects of BNP ??
- Vasodilator
- Diuretic & Natriuretic
- Suppress both Sympathetic tone & RAAS
Clinical uses of BNP ??
1) Dx. Pts. with Acute Dyspnoea
- Low BNP (< 100pg/ml) has a high (-)ve predictive value; makes the Dx. of HF unlikely
- Helps to RULE OUT a dx. of HF
2) PROGNOSIS in pts. with Chr. HF
- Very useful marker of prognosis
3) Guiding Rx.- Effective Rx. lowers BNP levels
Beta-Blockers ??
Beta-1 : Heart (1 heart)
Beta-2 : Lungs (2 lungs)
Cardioselective Beta Blockers
“MANBABE”
- Metoprolol, - Atenelol
- Nebivolol, - Bisprolol
- Acebutolol, - Betaxolol, - Esmolol
Indications of Beta-Blockers ??
- Angina, - Post-MI
- HF (improve both symptom & Mortality)
- Arrhythmias (has replaced Digoxin as the rate control DoC in AF)
- HTN (use here has been diminished)
- Thyrotoxicosis
- Migraine Prophylaxix
- Anxiety
Which Beta-blocker crosses BBB ???
Propranolol (1st Beta-B to be developed)
- Lipid soluble, hence can cross BBB
S/E & CI of Beta blockers ??
- Bronchospasm
- Cold Peripheries, - Fatigue
- Sleep disturbances including Nightmares
- Erectile dysfunction
CI - Uncontrolled HF
- Asthma
- Sick Sinus Syndrome
- Concurrent VERAPAMIL use: can ppt. severe bradycardia
ECG Features of Digoxin toxicity ??
Down-sloping ST depression
- Reverse Tick, Scooped Out
Flat/Inverted T wave
Short QT interval
Arrhythmias (eg.- AV block, Bradycardia)
Hallmarks of Ivabradine ??
Anti-Anginal drug which works by reducing HR
- Acts on “If”(funny) ion current which are highly expressed in SAN
- Reduces Cardiac Pacemaking activity
S/E
- Visual Effects, LUMINOUS Phenomenon is common
- Headache, - Bradycardia, - H Block
Nicorandil ??
Vasodilatory drug used to treat Angina
- K+ channel activator
- Vasodilation occurs via Guanylyl Cyclase activation => Increases cGMP
S/E & CI of Nicorandil ??
Headache, Flishing
Skin, Mucosal & Eye Ulceration
GI ulcers & Anal Ulceration
CI : LV Failure
Hallmark of Nicotinic Acid ??
Niacin is used in the Rx. of Hyperlipidaemia & also to lower Cholesterol & TGs
- Raises HDL levels
S/E
- Flushing: mediated by PGs
- Impaired Glucose Tolerance
- Myositis
What is Syndrome X ??
Angina like Chest pain on Exertion
ST depression on Exercise Stress Test
But NORMAL Coronary Arteries on Angiogram
Rx-
- Nitrates
Hallmarks of Nitrates ??
Have Vasodilatory effect
Main Indication:
- Angina & Acute Rx. of HF
Sublingual GTN MC drug used in IHD pts. to relieve Angina attack
S/E
- Hypotension, - Headache
- Tachycardia, - Flushing
What is Nitrate Tolerance ??
Pts. on Nitrates develop Tolerance & Experience reduced Efficacy
Pts. who develop tolerance should take the 2nd dose of Isosorbide Mononitrate after 8 hrs rather than after 12 hrs
- This allows Blood-nitrate levels to fall for 4 hrs & maintain effectiveness
This effect is NOT seen in pts. who take modified release Isosorbide Mononitrate
Broad Complex T + which is most commonly by SVT with aberrant conduction rather than VT ??
Absent QRS concordance in chest leads
- (+)ve QRS concordance in chest leads is a/w VT
- AV dissociation suggests VT
What is Brugada Algorithm ??
Used to differentiate b/w SVT with aberrant conduction & VT
The following suggests VT
- Absent RS complex (ie. either monophasic R or S waves) in all precordial leads (OR)
- An R to S interval is > 100ms in 1 precordial lead
- AV dissociation is also suggestive
Following is suggestive of SVT with Aberrant conduction
- RS wave in precordial lead + AV association
- RSRdash pattern
Pre-eclampsia affects what %age of Pregnancy ??
2- 8% of pregnancies worldwide
MoA of Nitrates ??
Cause Nitric Oxide release in SM
- Activating Guanylate Cyclase which then converts GTP => cGMP => leads to a FALL in Intracellular Ca2+
- They dilate Coronary Arteries & also reduce Venous Return ==> Reduces LV work => Reduce Myocardial O2 Demend
Cardiac X syndrome ??
Microvascular Angina
Normal Coronary angiogram + ECG changes on Exercise Stress testing (ST depression)
ECG normal at rest
Prosthetic valve Thrombotic therapy ??
Bioprosthetic: Aspirin
Mechanical : Warfarin + Aspirin
Statin induced Myopathy ??
Inhibition of Mevalonate pathway => depletion of several metabolites necessary for Muscle function
Admitted to hospital for ACS + DM; how to handle DM ??
Keep BG < 11mmol/L (avoid Hyoglycaemia)
- Stop OHAs & Start Dose adjusted IV Insulin infusion + regular BG monitoring
Variable intensity S1 ??
Loud S1 ??
Soft S1 ??
Loud S2 ??
Soft S2 ??
Variable S1 ??
- MS & TS
- MR, Severe HF, LBBB, 1st degree HB
- Systemic HTN
- Severe AS
- Complete HB
Rx. of Prinzmetal Angina ??
Dihydropyridine CCBs (Felodipine)
Non-Synchronised DC-CV & Synchronised DC-CV ??
N-S DC-CV is Defibrillation & should only be used in Cardiac ARREST cases for Shockable Rhythms (VF & VT)
DC-CV is Synchronised to R wave to minimise the risk of inducing VF
Witnessed Cardiac arrest while on monitor Rx ??
3 successive (Stacked) shocks before CPR
- Start CPR immediately after 3rd shock & continue CPR for 2 min.
- 3 quick successive shocks are regarded as FIRST Shock
Non-Shockable Rhythm (PEA & Asystole) Rx. ??
Give Adrenaline 1mg 1:10000 asap
- Defibrillator will not be able to bring back the pulse
The most important factor predicting outcomes Post-STEMI ??
New onset Systolic HF (suggests a large amount of Myocardial damage)
- 10x more likely to die
Why is Beta blocker not used as an anti Hypertensive ??
Less likely to prevent stroke + Causes Impaired Glucose Tolerance
Regurgitation caused by DCM ??
MR (not AR)
