Cardiology Flashcards
Acute Heart Failure treatment ladder
Universally poor prognosis
Hyponatraemia is a VERY POOR PROGNOSTIC MARKER
Implies severe fluid overload
Treatment:
avoid B blockade = further exacerbate
off load and fluid balance is key
RALES STUDY : Randomised Aldactone Evaluation study showed SPIRONOLACTONE in as small doses as 25mg reduced mortality by 30%
Paroxysmal AF
Definition:
Spontaneous onset and remission of AF
Treatment:
First line is bisoprolol as it will provide rate control and reduce risk of onset - negatively chronotropic.
Also beneficial for cardiac remodelling if evidence of LVF
Digoxin does not reduce the risk of onset of AF / frequency
Anticoagulation:
CHA2DS2VASC2 risk stratification
HASBLED
Risk balance anticoagulation Vs bleed risk
score >1 CHA2DS2VASC2 = low moderate risk
score >2 moderate to high risk
consider warfarin /apixaban / rivaroxaban / dabigatran
note renal dose / increased bleeding profile with dabigatran
also consider risk of UGIB
Decompensation post MI
Many causes
1. Ventricular free wall rupture:
frequency x10 than post infarct septal wall rupture
11% of patients post-MI
Ventricular rupture and cariogenic shock
are the leading causes of death in acute phase post MI
together = 60% of death post 1st MI
Cardiac Cycle - the 8 steps
1. Isovolumetric Contraction begins Systole = S1 MITRAL AND TRICUSPID CLOSE 2.Rise in Atrial Pressure - passive filling JVP C wave due to tricuspid closure 3.Ventricular pressure overcomes diastolic pressure Aortic valve opens first Pulmonary valve opens second
4.Ejection of blood
CAROTID UPSTROKE
JVP X-DESCENT due to atrial relaxation
- ISOVOLUMETRIC RELAXATION - end systole
Aortic valve closes A2
Pulmonary valve closes P2
S2 - Rapid inflow - EARLY DIASTOLE
JVP: V WAVE peak
Passive atrial filling begins to rise past ventricular pressure creating V wave ascent. Once this pressure overcomes the diastolic ventricular pressure the AV valves open - peak
MITRAL AND TRICUSPID VALVES OPEN - Atrial Pressure falls
JVP Y descent
PASSIVE VENTRICULAR FILLING
S3 or gallop - LATE DIASTOLE
ATRIA CONTRACTION
JVP-A WAVE +/- S4
JVP A wave
A wave corresponds to Atrial contraction and ventricular diastole - mid to late.
Large A waves: contraction against increased pressure Tricuspid stenosis RV stiffness Pulmonary Hypertension Pulmonary stenosis Pulmonary regurgitation PE
Cannon waves:
Basically seeing the full pressure of atrial contraction against a closed or restricted system
a. Atrial and Ventricular asynchrony as in complete heart block - Atrial contraction against a closed tricuspid during ventricular systole will result in all the pressure being redirected backwards creating cannon A waves
b. VT - again asynchrony
c. tamponade or restrictive pericarditis
JVP C wave
C wave corresponds to Tricuspid valve closure -i.e. when Ventricular pressure overcomes Atrial pressure in late diastole and late atrial systole
JVP V wave
V wave corresponds to the passive atrial filling pressure increasing to a peak until the pressure is greater than in the ventricles in early diastole leading to the AV valves opening - peak V
Dominant V waves:
Tricuspid regurgitation:
During Ventricular systole some blood will be ejected back into the atria. Thus leading to a higher than normal pressure within the atria and therefore a higher than normal V peak
JVP Y descent
Y wave corresponds to point after tricuspid valve opens - passive atrial filling in mid diastole
Sharp Y descent:
Tricuspid regurgitation:
larger base volume in Atria due to incompetent valve causes a sharp fall in pressure
slow Y descent:
Atrial Myxoma / Atrial Thrombus:
Smaller volume in atria = less pressure = slower delivery of passive filling to ventricle and therefore slower Y descent. May also be physical obstruction to filling caused by tumour
absent Y descent:
Implies that ventricular filling passively is restricted due to an inherent problem with higher than normal ventricular diastolic pressure
cardiac tamponade
restrictive pericarditis
JVP X descent
X descent corresponds to atrial volume depletion
broken by C wave which is the point at which tricuspid valve closes and passive atria filling continues draining JVP
Prominent X descent:
implies rapid falling in atrial pressure post Atrial systole
restrictive pericarditis / tamponade
absent X wave
AF
Aortic Stenosis
CLICK whhOOOSSSHHhh
crescendo decrescendo systolic murmur radiating to carotids associated with ventricular heave and LVH
Aetiology:
Calcificative degeneration commonest
Congential - bicuspid
Rheumatic heart disease - POST STREP A
Differentials:
Aortic Sclerosis - overlaps
PULMONARY STENOSIS- A2 should be louder than P2 - compare sides. Murmurs both louder on inspiration
VSD: loud frequently. Note if very large no murmur. Loudest at sternal edge but heard all over chest Vs restricted to one area. THRILL vs HEAVE
HOCM: Murmur gets quieter when squatting. This increases venous return and preload and also increases afteroad and splints open the outflow tract by increasing diastolic pressure so reduces the obstruction. NO EJECTION CLICK PRECEDING MURMUR. NORMAL S2
SUPRA-VALVULAR OBSTRUCTION: Coarctation / normal s2 - no click
SUBAORTIC MEMBRANE - UBER RARE - Normal S2
Pulse:
slow rising
Left ventricular heave due to LVH against restricted outflow
murmur:
radiates to carotid
Early Ejection systolic click may precede murmur implying the valve still has play - e.g. bicuspid valve or young patient
quiet S2 as valve opening impaired so closes with less impact.
normal S2 - may only be mild disease
Severe AS may have an absent S2
Investigation:
If AS heard with carotid radiation and LV heave disease must be at least mild to moderate and therefore requires workup ECHO - grade and severity ECHO VALVE AREAS and gradients Mild - >1.5cm sq + > 20mmHg Moderate 1-1.5cm sq + 20-40mmHg Severe - <1cm sq + > 40mmHg
Valve area better as the gradient may change with any evidence of LV impairment.
VALVE AREA SHOULD BE NORMALISED TO BODY SURFACE AREA - severe AS <0.6cm sq/metre sq
STRESS ECHO:
good to use to decide if AS is causing LV impairment and therefore may benefit from surgery.
e.g. demonstrated BP drop during exercise
If AS is not connected to LV impairment then there is no point in doing surgery
Cardiac Catheterisation:
Catheterisation of stenosed Aortic valve is associated with MRI evidence of stroke in 22% of cases and neurological defect in 3%
Management: 6-12 month follow-up if asymptomatic Surgery if symptomatic / stenosis severe recommended OR >40mmHg or <1cm sq / 0.6cm sq / m sq (in LV imp) EJF< 45% LVH>15mm BP drop during exercise VT AS with syncope = median survival of 4 months without surgery
Surgery:
AS differentials:
Differentials:
Aortic Sclerosis - overlaps
PULMONARY STENOSIS- A2 should be louder than P2 - compare sides. Murmurs both louder on inspiration
VSD: loud frequently. Note if very large no murmur. Loudest at sternal edge but heard all over chest Vs restricted to one area. THRILL vs HEAVE
HOCM: Murmur gets quieter when squatting. This increases after load and splints open the outflow tract by increasing diastolic pressure so reduces the obstruction. NO EJECTION CLICK PRECEDING MURMUR. NORMAL S2
SUPRA-VALVULAR OBSTRUCTION: Coarctation / normal s2 - no click
SUBAORTIC MEMBRANE - UBER RARE - Normal S2
AS classification
Pulse:
slow rising
Left ventricular heave due to LVH against restricted outflow
murmur:
radiates to carotid
Early Ejection systolic click may precede murmur implying the valve still has play - e.g. bicuspid valve or young patient
quiet S2 as valve opening impaired so closes with less impact.
Mild AS: normal S2 - may only be mild disease
Severe AS: may have an absent S2 / slow rise pulse +/- oedema
ECHO VALVE AREAS and gradients
Mild - >1.5cm sq + > 20mmHg
Moderate 1-1.5cm sq + 20-40mmHg
Severe - <1cm sq + > 40mmHg
Valve area better as the gradient may be reduced with LV impairment giving a false low gradient when stenosis might actually be mod/severe.
VALVE AREA SHOULD BE NORMALISED TO BODY SURFACE AREA - severe AS <0.6cm sq/metre sq
AS complications
- Endocarditis
- Collapse / syncope
- Thromboembolism - spontaneous / arrhythmia induced / iatrogenic during cardiac Cath if Cath passed through lesion
- AV block - invasion of calcium form valve ring into HIS-PURKINJE system
Aortic stenosis or Aortic sclerosis?
In mild disease may be difficult to distinguish Sclerosis: no opening click - fixed no slow rising pulse - fixed normal A2 ELDERLY
ECHO to see valve movement and outflow jet
AS associations
- Rheumatic heart disease think MITRAL REGURG
- Angiodysplasia of colon
- Aortic coarctation
AS surgery indications:
Gradient across valve >40mmHg - severe
Gradient <1cm sq / <0.6cm sq / m sq - severe
OR
plus
A. EJF<45%
B. Syncope - median survival <4 months without surgery
C.Exercise intolerance - BP drop during stress ECHO
D. VT - Calcium at valve ring invades into HIS-PURKINJE system
E. LVH>15mm
Aortic Regurgitation
Causes: Acute: Infective endocarditis aortic dissection prosthetic valve failure ruptured sinus of valsalva acute rheumatic fever - rare in western world
chronic:
1. congenital: biscuspid valves / marfans / aorta annular ectasia
2. rheumatic heart disease
3. infective - rheumatic post strep / endocarditis
4. Seronegative arthritis
5.Syphillis
6.Osteogenesis imperfect due to calcium deposition and PTH axis
A small degree of AR may be normal as with all valvular regurgitation
Presentation: SOBOE Chest pain Overloaded with signs HF Asymptomatic even when severe in some cases
Pulse
Water-hammer collapsing pulse due to rapid fall in diastolic pressure - corrigans pulse
Definition:
pulse systolic pressure is more than double the diastolic pressure
Wide pulse pressure due to raised LVESD and LVEDD
De Musset sign
head bobbing with each pulse
Durozier’s sign
Femoral bruit
Quinke’s sign: pulsation in nail bed - depress end of nail with your nail and observe pulsation in capillary bed
Corrigans sign:
Forceful bilateral carotid pulsation which suddenly falls away - i.e. full expansion and quick collapse
Palpation:
Apex thrill to mid axillary line as flow returns and hits LV
Displaced APEX due to LV dilatation
MURMUR: Early / mid diastolic with radiation to left sternal edge and aortic area esp if AR root dilatation present e.g. Marfans
Shorter murmur = more severe AR
More severe flow of blood back to LV causing faster rise in LV pressure.
Gradient difference between aorta and LV reduces over time and as regurgitation occurs earlier and earlier in diastole
Differential:
Pulmonary regurgitation BUT murmur will not be loudest over left sternal edge - no other peripheral signs present
Associations: Marfans endocarditis Rheumatic heard disease syphillis aortic coarctation ank spond - examine for pulmonary fibrosis at apices
Investigation:
ECHO: - grading - Severe
Width of AR jet LVOF - LV outflow
>65% = severe implying large portion of valve incompetent
Regurg fraction - RF
>50%
Left ventricle end diastolic diameter - LVEDD
>70mm - implying lots of residual volume from previous systole + normal atrial passive and active filling
left ventricle end systolic diameter - LVESD
>50mm
Doppler pressure slope half time
<200Ms - fast drop off of pressure indicating severe AR - in early diastole (short murmur)
MRI
coronary angiography for pre-surgery work up but valves not examined
Management:
ACUTE AR - anything more than mild disease = surgery
CHRONIC AR
ramipril
treat HF - bisoprolol and furosemide +/- ivabridine
ECHO FU
Symptomatic AR:
whatever severity the event rate is low and is less than that of surgery therefore conservative Mx is mainstay = ACEi and Diuresis
Severe AR:
Valve replacement with LVEDD >70mm or LVESD >50mm/ EF<50% / RF>50% / severe AR dilatation
AR Causes
Causes: 200 years ago - Syphillis Acute: Infective endocarditis aortic dissection prosthetic valve failure ruptured sinus of valsalva acute rheumatic fever - rare in western world
chronic:
- congenital: biscuspid valves / marfans / aorta annular ectasia
- rheumatic heart disease
- infective - rheumatic post strep / endocarditis
- Seronegative arthritis
- Syphillis
- Osteogenesis imperfect due to calcium deposition and PTH axis
A small degree of AR may be normal as with all valvular regurgitation
AR Management
Management:
ACUTE AR - anything more than mild disease = surgery
CHRONIC AR
symptoms beyond class I breathlessness = surgery
Symptomatic AR:
whatever severity the event rate is low and is less than that of surgery therefore conservative Mx is mainstay = ACEi and Diuresis
Severe AR:
Valve replacement with LV dilatation / EF<50% / RF>50%
AR dilatation - >55mm or >45 in Marfans >50 in bicuspid valves
AR Severity
Murmur:
Short early diastolic with LV thrill and Apex moved secondary to dilatation and signs of LHF - pulmonary congestion
ECHO: - grading - Severe
Width of AR jet LVOF - LV outflow
>65% = severe implying large portion of valve incompetent
Regurg fraction - RF
>50%
Left ventricle end diastolic diameter - LVEDD
>70mm - implying lots of residual volume from previous systole + normal atrial passive and active filling
left ventricle end systolic diameter - LVESD
>50mm
Doppler pressure slope half time
<200Ms - fast drop off of pressure indicating severe AR - in early diastole (short murmur)
Mitral stenosis
Typical Presentation:
Female
Heart failure - Exertional dyspnoea / orthopnoea / PND
AF - palpitations / stroke / SOBOE
Hoarse voice - Ortner’s sign - compression of left recurrent laryngeal by LA hypertrophy / pulmonary artery
haemoptysis - bronchial capillary veinous haemorrhage in Pulm HTN / pulm oedema
Mallar flush - combination of pulmonary HTN and low Cardiac output with high venous pressures
Pyrexial - Endocarditis - are other valves involved?
Signs:
Mallar Flush - erythema across max sinus and nasal bridge
- pulmonary HTN / high venous pressure / low card output
Ortners sign - hoarse voice
- left rec Laryngeal compression - LA or pulmonary artery
ENDOCARDITIS:
fever
splinter haemorrhages - fingers and toes / lost digits
more than 1 murmur
ROTH SPOTS - immune complex deposition in eyes - red haemorrhage spots with central white
OSLER NODES - immune complex deposition i.e. vasculitis of hands and feet - PAINFUL
JANEWAY LESION - hands and feet - SEPTIC EMBOLI with BACTERIAL INFECTION SECONDARY - painless micro abscess
ENDOCARDITIS SIGNS
Infective
immune complexes
embolism
Major and Minor criteria
INFECTIVE: Fever Changing murmur - RIGHT OR LEFT? appearance of new murmur hepatosplenomegally cardiac decompensation
Immune complex:
vasculitis:
ROTH SPOTS - immune complex deposition in eyes - red haemorrhage spots with central white area
OSLER NODES - immune complex deposition i.e. vasculitis of hands and feet - PAINFUL - typically funger buds and toe pads - ?are they tender?
Renal involvement - GN
Embolism Septic emboli - Evidence of pneumonia? splinter haemorrhages conjunctival haemorrhages retinal haemorrhages Janeway lesions
Conjunctival haemorrhage - look up - thankyou - now look down.
Splinter haemorrhages - fingers and toes / lost digits
more than 1 murmur - embolism
Septic embolism:
JANEWAY LESION - hands and feet - SEPTIC EMBOLI with BACTERIAL INFECTION SECONDARY - painless micro abscess
Infective Endocarditis - DUKES CRITERIA - MAJOR
Need 2 major or 5 minor or 1 major 3 minor
NEED 2 MAJOR OR 1 MAJOR 3 MINOR OR 5 MINOR
MAJOR: A) Positive blood culture 2 separate cultures with a typical micro OR Micro-organism consistent with IE isolated from persistently positive cultures - 2/3 samples 12 hours apart or all 3 samples or majority of 4 samples with first and last culture at least 1 hour apart. OR 1 culture positive for Coxiella Burnetti Or Interphase 1 IgG titre >1:800
- strep viridans
- staph aureus
- strep bovis
- Coxiella Burnetti - Q fever
HACEK GROUP
- Haemophilus parainfluenzae / aphrophilus / paraphrophilus
- Actinobacillus actinomycetemcomitans
- Cardiobacterium Hominis
- Eikinella Corrodens
- Kingella spp
B) ECHO / CT showing endocardial involvment
- vegetations on Mitral or aortic valves with regurgitant jet
- intracardiac abscess
- new dehiscence of a prosthetic valve
- new regurgitant valve
Infective Endocarditis - DUKES CRITERIA - MINOR
Need 2 major or 5 minor or 1 major 3 minor
MINOR CRITERIA:
A) Serological evidence of organism consistent with IE not meeting major criteria e.g. 1 culture +ve / time span insufficient
B)Vascular or Septic Emboli
- Janeway lesions - Septic emboli to buds / pads - dermal microabscesses - PAINLESS
- Splinter haemorrhages - toe and finger nails
- Conjunctival haemorrhages - look up and look down
C)Vasculitis
- Roth spots - Vasculitic haemorrhages on retina
- Osler nodes - Vasculitic micro haemorrhages hands and feet - PAINFUL
- Glomerulonephritis
- RF +VE
D) Pyrexia
E) IVDU or predisposing cardiac condition - prosthetic valve / bicuspid valve
F)ECHO findings supporting diagnosis but not meeting major criteria
Infective Endocarditis: TYPICAL ORGANISMS
- strep viridans
- staph aureus
- strep bovis
- Coxiella Burnetti
Infective Endocarditis: HACEK GROUP
HACEK GROUP
- Haemophilus parainfluenzae / aphrophilus / paraphrophilus
- Actinobacillus actinomycetemcomitans
- Cardiobacterium Hominis
- Eikinella Corrodens
- Kingella spp
Infective Endocarditis Classification?
Formally SBE / IE - NOW 6 DOMAINS
Based on path / treatment / prog
Domains: 1 - Disease activity 2 - Diagnostic certainty 3 - Valve involved or IVDU 4 - Right or Left heart 5 - Culture report 6 - Demographic
Disease activity
a) Active = currently positive IE cultures
b) Healed = past IE now biologically sterile
c) Persistent = IE not eradicated after appropriate Abx
d) Recurrent = Recurrence post definitive cure - difficult to differentiate from persistent - POOR PROGNOSIS
Diagnostic Certainty
a) Established = Dukes Criteria Confirmation
b) Suspected = IE infection suspected without evidence of endocardial involvement
c) Possible but other causes also exist
Valve involvement
a) native
b) prosthetic
c) Endocarditis
Right or Left ?IVDU ?Dental work ?VSD / ASD Bubble echo
Culture: Organisms in keeping with BE 1.strep viridans 2.coxiella burnetty 3.staph aureus
HACEK - haemophilus parainfluenza / actinobacillus / cardiobacterum hominis / eikinella corrodens/ kingella
What is the RAAS system
The Renin Angiotensin and Aldosterone system is a feedback mechanism which drives sodium retention and therefore water retention to maintain blood pressure by increasing circulating volume, increase preload and increase CO
It is therefore activated chronically in heart failure and drives its pathogenesis
low BP / hypovolaemia / low CO
renin release from kidneys JM apparatus
-angiontensinogen (liver) –renin–>angiotensin 1
-increase vascular tone
angiotensin 1
-Converted by ACE pleura–> angiotensin 2
angiotensin 2
- Increase Na asborption PCT - Na in / H+ out
- aldosterone release from adrenal cortex
- DCT Na reabsorption / CL and K+ excretion
- increased vascular tone
- Stimulates ADH release from post pituitary
What is the function of natriuretic peptides
There are 3 natriuretic peptides
ANP - atria - endocrine
BNP - ventricular - endocrine
CNP - arterial sheer stress - pararcrine role - inhibitor of vascular and glomerular proliferation and interstitial matrix production
Released in response to plasma volume expansion (STRETCH)
Released in response to rising Ang II as an autofeedback mechanism
They stimulate natriuresis
- dilate afferent arteriole and constrict efferent arteriole
- increased GFR
- increased delivery of sodium to DCT / LoH / PCT for excretion
Arterial dilatation
-ANP and BNP
Vasodilation and VEGF inhibition
- CNP
Inhibit ADH release
-DCT Aquaporin II channels then close
THEREFORE IDEAL WOULD BE TO INCREASE ANP/BNP/CNP half life.
Trials were promising re: Neprilysin inhibitor
BUT combined ACEi + Neprilysin - angioedema
More evidence for combined single agent therapies
Uncontrolled cardiac failure on ACEi
Switch to ARB + NEP = valsartan + SACUBITRIL
PARADIGM-HF trial REDUCED MORTALITY BY 20%
What is Sacubitril
Neprilysin inhibitor
prolong ANP / BNP / CNP halflife
What is Kartageners syndrome
Also known as primary ciliary dyskinesia
- Bronchiectasis
- Dextrocardia - faint heart sounds -
ECG = reverse R wave progression from v1-v6
Inferior MI is associated with
Right ventricular MI in 30% cases
- reduced RV compliance and stroke volume
- reduced LV filling and therefore reduced CO
- activation of RAAS
Tricuspid regurg —>pansystolic murmur
Raised JVP - giant C wave and shallow V trough
What is indapamide
Thiazide like diuretic - missing benzothiadiazine group
Act to block DCT Na+ reabsoprtion via NA+/CL- channel
Thought to have greater efficacy to reduce diastolic and systolic BP
No increased incidence of DM2 / hyponatraemia / hypokalaemia
What is Adenosine
Adenosine is a very short acting agent which causes a transient AV block and is useful in slowing or chemically cardioverting a supra-ventricular tacchyarhythmia
What is Ivabridine
Ivabridine is a sodium funny channel blocker used in ANGINA / HEART FAILURE =If
Particularly present in SAN and AVN. Slows cardiac conduction without negagively impacting on force of contraction i.e. improves diastolic filling and therfore increase stroke volume and CO
Adjunctive medication in heart failure but must be in sinus rhythm.
Reduces hospital admission and mortality when ready on maximal therapy
What is Anticoagulation:
CHA2DS2VASC2 risk stratification
CHA2DS2VASC2 risk stratification for stroke risk in AF
HASBLED score must be done alongside to also apply risk of bleeding Vs risk of stroke
CHA2DS2VASC2 Congestive heart failure (or Left ventricular systolic dysfunction) 1 Hypertension: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication) 1 Age ≥75 years 2 Diabetes Mellitus 1 Prior Stroke or TIA or thromboembolism 2 Vascular disease (e.g. peripheral artery disease, myocardial infarction, aortic plaque) 1 Age 65–74 years 1 Sex Category (i.e. female sex) 2 score =0 - no anticoagulation score >1 CHA2DS2VASC2 = low moderate risk as for >2 score >2 moderate to high risk consider warfarin /apixaban / rivaroxaban / dabigatran
note renal dose / increased bleeding profile with dabigatran
also consider risk of UGIB
What is HAASBLEDD
Hypertension: (uncontrolled, >160 mmHg systolic)
1
Abnormal renal function: Dialysis, transplant, Cr >2.26 mg/dL or >200 µmol/L
1
Abnormal liver function: Cirrhosis or Bilirubin >2x Normal or AST/ALT/AP >3x Normal
1
Stroke: Prior history of stroke
1
Bleeding: Prior Major Bleeding or Predisposition
1
Labile INR: (Unstable/high INR), Time in Therapeutic Range 65 years
1
Prior Alcohol or Drug Usage History (≥ 8 drinks/week)
1
Medication Usage Predisposing to Bleeding: (Antiplatelet agents, NSAIDs)
1
score of ≥3 indicates “high risk” and some caution and regular review of the patient is needed
>5 = >10per 100
What is Frank-Starling Law
Describes relationship between stroke volume and end diastolic volume
This relies on the constant that ventricular output = atrial input
- stroke volume of the heart increases with ventricular filling
- increased volume = increased stretch = increased contraction force
- The limit of ventricular filling is reached and this results in a plateau of contraction force and ventricular dilatation.
Mitral stenosis
P mitrale
end diastolic murmur
B-Blocker in AF
1st line for atrial tacchyarythmias
- slow sinus rhythm
- increase diastolic filling time
- greater filling = greater stretch = greater recruitment and contractile force = greater CO
Resistance = Amiodarone
Digoxin not good for PAF - does not reduce frequency and does may prolong paroxysm
What is Beckers Muscular Dystrophy?
X linked recessive
mutation in Dystrophin
Similar to DMD but later onset and milder
Present 5-15 years of age or later
- dilated cardiomyopathy - early onset
- Calf hypertrophy
- proximal weakness
What is Ebsteins Anomally?
Critical congenital heart defect of tricuspid valve
<1% of heart defects
1/200,000 live births
- Annulus of tricuspid in normal position
- valve leaflests face into the right ventricle and may be attached to the walls o the septum
- RV becomes atrialised
- RA therefore very enlarged and the RV small in size
Associated tricuspid regurg - pansystolic murmur - right sternal edge
Associated with WPW
-Transient Supraventricular tacchyarhythmia
WPW
pre-excitation syndrome Supraventricular tachycardia due to accessory pathway delta waves short pr rbbb
Also associated with Ebsteins anomally rbbb TR Tricuspid valve leaflets inverted intro RV Atrialisation of RA Small RV Large C waves Deep V wave -large RA reduced CO
DC cardioversion for short term control
RF ablation definitive
avoid digoxin and verapamil
may precipitate greater conduction via accessory pathway
Lown Ganong Levine syndrome
pre-excitation complex accessory pathway short PR no delta wave no rbbb
Describe RBBB ECG changes
positive qrs v1 - rSr pattern = M
negative deflection V6 = W pattern
Diagnostic:
Broad QRS > 120 ms
RSR’ pattern in V1-3 (‘M-shaped’ QRS complex)
Wide, slurred S wave in the lateral leads (I, aVL, V5-6)
Associated Features
- ST depression and T wave inversion in the right precordial leads (V1-3)
- Sometimes rather than an rSr’ pattern in V1, there may be a broad monophasic R wave or a qR complex.
1 - RBBB, activation of the right ventricle is delayed as depolarisation has to spread across the septum from the left ventricle.
2 - The left ventricle is activated normally, meaning that the early part of the QRS complex is unchanged.
3 - The delayed right ventricular activation produces a secondary R wave (R’) in the right precordial leads (V1-3) and a wide, slurred S wave in the lateral leads.
4 - Delayed activation of the right ventricle also gives rise to secondary repolarization abnormalities,
- ST depression
- T wave inversion in the right precordial leads.
- Cardiac axis is unchanged, as left ventricular activation proceeds normally via the left bundle branch.
Causes of RBBB
Inferior MI
Core pulmonale / pulm HTN / CF / COPD / bronchiectasis
PE
Rheumatic heart disease
Degenerative disease of conduction system
What is fondaparinux
Factor Xa inhibitor
What is long QT syndrome (LQTS)
Congenital disorder
genetic mutations in ion channels
2 forms:
ROMANO WARD SYNDROME
JERVELL AND LANG-NIELSON
=QT prolongation on ECG 0 >450ms . Associated with ventricular tachyarrhythmia -syncope -arrest -sudden death
Treatment:
B-blockade
Reduces rate and increases ventricular diastole
Reduces risk of life threatening VT
What is Romano Ward syndrome
One of two recognised sydromes of congenital long QT syndrome
Associated with : VT syncope arrest sudden death
treatment:
B blockade - reduce risk of VT / VF
Implantable defibrillator
What is Lang-Nielson Syndrome
One of two recognised sydromes of congenital long QT syndrome
Associated with : VT syncope arrest sudden death
treatment:
B blockade - reduce risk of VT / VF
Implantable defibrillator
What is the initial management in suspected aortic dissection
- IV beta blockade to reduce BP
- CT aorta angio
- Discussion with cardiothoracics
Mortality untreated is 25-30% at 24 hours and up to 75% at 2 weeks
AD confined to descending aorta (80%) has a better prognosis
What are the signs of aortic dissection
- Inferior ST elevation
- aortic dissection may compress and occlude the RCA ostium - Aortic regurgitation
Corrigans sign in the neck
Quinke’s signs in the nails
Collpasing radial pulse
Early diastolic murmur radiating to axilla
Ventricular heave due to higher end diastic vol
Displaced apex asassociated with dilatation - Pericardial rub
- Retrosternal CP + interscapular tearing pain
RF Marfinoid - dilated Aortic root Ehlers Danos Rheumatic heart disease Trauma
71M presents with exertional dyspnoea. CXR = bibasal congestion only. Started on Furosemide 40mg OD with resolution. Auscultation = EJS radiating to carotids with slow rising pulse. No history of rheumatic heart disease / colonic angiodysplasia or biscuspid valves.
Remember 1 syncopal episode 1 month ago
ECHO = valve gradient 0.5cm sq.
Gradient 120mmHg
a) Diagnosis
b) management
c) how to grade the condition
d) any risk stratification criteria
AS with syncope = median survival of 4 months without surgery
- Aortic stenosis Vs sclerosis due to slow rising pulse
- ECHO shows severe AS an since symptomatic all more reason for urgent valve replacement
- inpatient angio + admission
Criteria for AS: grading MILD >1.5cm sq pressure <20mmHg MOD 0.5-1.5cm sq pressure gradient 20-40mmHg SEVERE <0.5cm sq. pressure >40mmHg
Valve area better as the gradient may change with any evidence of LV impairment / past MI etc
VALVE AREA SHOULD BE NORMALISED TO BODY SURFACE AREA - severe AS <0.6cm sq/metre sq
STRESS ECHO:
good to use to decide if AS is causing LV impairment and therefore may benefit from surgery.
-?BP drop
-?pre-syncope
If AS is not connected to LV impairment then there is no point in doing surgery
Cardiac Catheterisation:
Catheterisation of stenosed Aortic valve is associated with MRI evidence of stroke in 22% of cases and neurological defect in 3%
HOWEVER CORONARY ANGIO USEFUL TO PLAN IF CABG SHOULD BE DONE ALONGSIDE TAVI
Management: 6-12 month follow-up if asymptomatic Surgery if symptomatic / stenosis severe recommended OR >40mmHg or <1cm sq / 0.6cm sq / m sq (in LV imp) EJF< 45% LVH>15mm BP drop during exercise VT on tape
Are ACEi prescribed in AS
NO CONTRAINDICATED
BP modulation is a balance in AS - dropping BP may cause a drop in coronary perfusion pressure and further worsen symptoms of heart failure
35F from Africa presents with SOBOE / fatigue. NO CYANOSIS / NO CLUBBING Right pericordial heave wide split S2 CXR = prominent pulmonary vessels ECG = RBBB
- could be cardiac or pulmonary
- signs of pulm HTN
Diff:
PE = expect nipping of pulmonary arteries are normal or pruned
ASD
- RV heave due to left to right shunt
- development of Eisenmenger syndrome = RVH overcomes LV = right to left shunt
- pulmonary artery engorgment due to higher CO state
- RBBB
Mx:
TOE - ASD visualisation / quantify jet and PA pressure / valve gradient / direction of shunting
Right heart catheter - suitability for closure
Book CTPA if concerned re: PE
What is the target level for digoxin
Heart failure - 0.5-2
AF - 1.5-2.5
What are the consequences of digoxin toxicity and what levels would you expect to see them
Therapeutic levels 0.5-2.5 depending on whether HF or AF / flutter
Toxicity effects seen >10 and definitiely >13
>10mg in adults
>4mg in children
- complete heart block
- bradycardia
- unstable bradycardia - HS instability
- VT - avoid adrenalin
Management:
Digoxin level
If <6 hours - 75g activated charcoal via NG to bind and block further absoprtion
ECG + continuous cardiac monitoring
Atropine 500mcg for symptomatic bradycardia
Repeat atropine 500mcg for recurrence
Further recurrence
A) FAB specific digoxin
FAB fragment works as an opsoniser and is specific to digoxin epitope - binds and excludes
B) Isoprenaline infusion
FAB indications: VT HD instability failed response to atropine hyperkalaemia digoxin level >13 or ingestion >10mg adult or 4mg child Recurrent bradycardia
How does digoxin work
- negatively chronotropic - MYOCARDIAL + AVN
- increases refractory period at phase 4 and 0 due to increased intracellular calcium due to inhibition of the Na/K /Ca pump
- AVN parasympathetic effects - increases contractile force without increasing cardiac workload
- Digoxin exerts a PNS effect on AVN
- Digoxin inihibits Na/K/Ca exchanger in MYOCARDIUM
- Results in higher INTRACELLULAR CALCIUM
- Higher intracellular calcium prolongs phase 4 and phase 0 of cardiac AP
- This results in slower repolarisation
- This results in a decrease in heart rate
- Increased Ca is stored within the sarcoplasmic reticulum and therefore more is available to act as a myosin cofactor and so contractile force is increased without increasing work
DIGOXIN DOES NOT ALTER THE UNDERLIEING RHYTHM
DIGOXIN SLOWS VENTRICULAR RATE AND IMPROVED DIASTOLIC FILLING REDUCING OXYGEN DEMAND
THEREFORE DOES NOT REDUCE FREQUENCY OF ATTACKS OF PAF
What are absolute contraindications to thrombolysis in STEMI?
Absolute contraindications for fibrinolytic use in STEMI include the following: [16]
- Prior intracranial hemorrhage (ICH)
- Known structural cerebral vascular lesion
- Known malignant intracranial neoplasm
- Ischemic stroke within 3 months
- Suspected aortic dissection
- Active bleeding or bleeding diathesis (excluding menses)
- Significant closed head trauma or facial trauma within 3 months
- Intracranial or intraspinal surgery within 2 months
- Severe uncontrolled hypertension (unresponsive to emergency therapy)
- For streptokinase, prior treatment within the previous 6 month
How would you control BP in phaeochromocytoma
phenoxybenzamine
gives alpha blockade preventing arterial vasoconstrction and hypertensive crisis - doxazocin
DO NOT B BLOCKADE IN FIRST INSTANCE -
Results in unopposed alpha stimulation and hypertensive crisis
What is the procedure post PPM insertion
1. CXR rule out PTX check lead placement RA + RV LV vai Coronary sinus and LV vein
- Pressure dressing for 24 hours
- Wound review and discharge
RV infarction - what are the signs and where is the likely lesion
40% of inferior MIs
TWI in II / III / AVF - reciprocal depression ST in V5/V6
ECG: New complete heart block
TWI in III / AVF
- Raised JVP
- peripheral oedema
- Hypotension -reduce pulmonary flow - reduced preload
- Very preload sensitive therefore nitrates can drop BP further
LAD supply
LAD supplies
AV septum - EXPECT BBB
anterior and lateral LV
papillary muscle of mitral valve
MOST COMMONLY OCCLUDED
LAD stenosis / blockage - ANTERIOR MI
ECG: ANT changes / INF reciprocal
ST elevation V1 / V2 / and V4/V5 / AVL
ST Depression in 2/3/avf
MORE PROXIMAL OCCLUSION = GREATER DAMAGE - MORE WIDESPREAT ST ELEVATION
CIRCUMFLEX SUPPLY
Circumflex branches off LAD or RCA
majority of people = Right dominant
gives rise to circumflex
ECG =
RCA dominant = post MI changes
st depression v1/2 (anterior leads) ( just circ PDA spared )
IF left dominnant circumflex also supplies posterior descending after circumflex instead of RCA
therefore inferior changes seen too (circ + PDA)
St depression V1/v2
st elevation 2/3/avf
Supplies: SAN in 50% Left atrium Lateral LV wall anterior papillary of mitral valve posterior lateral wall LV (with right coronary)
Right Coronary supply
Comes of aorta and runs in AV groove
gives rise to posterior descending artery
supplies: SAN (50-73%) AVN (50-73%) - via right AV artery Right ventricle IV septum proximal encircling both BB
issue:
infarction = BBB / bifascicular
predispose to conduction abnormality
RV infarction - hypotension / raised JVP / preload sensitive
Right marginal artery
Comes off RCA
supplies Right ventricle
What is Bifascicular block
RBBB + either left anterior fascicular or left posterior fascicular blockage
Sign of extensive conductive disease
Likely RCA infarct - supplies SAN / AVN and prox bundles
Likely LAD - supplies AV septum housing bundles
Hyperkalaemia
Causes: Ischaemic heart disease (40-60% cases) Hypertension (20-25%) Aortic stenosis Anterior MI (occurs in 5-7% of acute AMI) Primary degenerative disease of the conducting system (Lenegre’s / Lev’s disease) Congenital heart disease Hyperkalaemia (resolves with treatment)
ECG:
RBBB + left axis or right axis deviation
-MORROW
-RSR V1-V3
-Wide QRS
Conduction of RV delayed so propogation of RV contraction via myocyte junctions
Majority conduction still via LV in isolated RBBB
-Leads facing RV will see initially depol away as LV goes first then see large second R wave as RV delayed depol
-Lateral leads see a slurred S wave due to Left V dominance but mistimed R V disrupting smooth isovolumetric contraction
What medications can cause long QTc (andtherefore atypical VT / torsades de pointes)
- Erythromycin
- lithium
- amiodarone
- sotolol
- tacrolimus
- quinine
- fluoxetine / citalopram /
What is Multi focal atrial tachycardia?
Atrial tachy SVT with at least 3 different P wave morphologies with variable PR and PP intervals
Trigger:
Hypoxia / hypercapnia
Salbutamol nebs will worsen the SVT but are needed in the first instance to treat the airway
In setting of COPD or asthma B-BLOCKADE is NOT APPROPRIATE - NO METOPROLOL / NO BISOPROLOL
- bronchospasm
- worsen obstruction
Therefore second line = VERAPAMIL
5mg IV bolus load
oral 40-120mg TDS
Repat 72 hr ecg if reverts to SR to see if long term rate control is needed (unlikely)
MOA Verapamil:
block voltage-dependent calcium channels.
calcium channel blockers are considered class-IV antiarrhythmic agents.
Concentrated in the sinoatrial and atrioventricular nodes, Decrease impulse conduction through the AV node, thus protecting the ventricles from atrial tachyarrhythmias.
Calcium channels are also present in the smooth muscle lining blood vessels.
By relaxing the tone of this smooth muscle, calcium channel blockers dilate the blood vessels.
- treating high blood pressure and angina pectoris.
- increases the supply of blood and oxygen to the heart.
-This controls chest pain, but only when used regularly.
What is Ivabridine? What is it used for?
Highly selective If blocker - funny channel blocker in SAN
non inferior to atenolol and amlodipine in management of angina pectoris
improves ET and reduces frequency of angina attacks
Would therefore be good for b blocker contraindicated pathology
What medications in heart failure have been shown to reduce mortality
Spironolactone - reduced mortalitu by 30% at 25mg dose when added to conventional therapy
Bisoprolol - reduced mortality and sudden cardiac death compared to pacebo
Ramipril - reduced mortality by 15-30% in all stages of CHF
inotlerance or ACEi or ARB
USE HYDRALAZONE AND ISMN COMBO
Data predates B blocker data
How is ABPI interpreted
> 1.4 = vascular hardeneing / claudication - VASC
0.9-1.4 = normal
0.8-0.9 - treat risk factors for claudication / BP / lipids / DM
0.5-0.8 = moderate stenosis = VASC - Int Claud
<0.5 = critical claudication = VASC - rest pain
What us Heyde’s syndrome?
Microcytic anaemia + Calcific AS
Cause: Destruct of VwF as platelets (bound to VwF) cross calcific valve. This may cause PR blood loss. OR MICROANGIOPATHIC HAEMOLYSIS
management
VALVE REPLACEMENT
Mesenteric angiography to establish bleeding looking for ANGIODYSPLASIA
What is the treatment for NSTEMI?
Aspirin Ticagrelor GTN Oxygen Fondaparinux
Ticagrelor has been shown to be superior to Clopidogrel in the treatment of NSTEMI in reducing all cause mortality including stroke without an increase rate of bleeding (PLATO)
What are the contraindications to fondaparinux
eGFR<20 –> switch to LMWH
active or concurrent bleeding or deranged INR
What are the indications for ICD
1 LVF<35% and NYAC 3 or less 2 inducible arrhythmia 3 non sustained VT 4 familial long QT 5 HOCM 6 Brugada - V1-V3 ST elevation with RBBB 7 RV dysplasia 8 post tetralogy repair
ICD is superior to medication control of VT alone in LVF e.g. amiodarone alone
reduces mortality by 20% vs 14% post MI almost totally due to a reduction in sudden cardiac death.
What are the treatments for PAF
- coag control
- warf
- APIX / RIVAROX
2, rhythm control
- bisoprolol
- amiodarone
How is a myocardial perfusion scan done and when should it be carried out?
Thallium contrast MRI of the heart = CAD evaulate
Shows perfusion to tissue and gives more information than ECHO + angio and is less invasive than angiography
Indications:
>40
atypical CP + HTN
Stress echo in the >40 htn group will have V1-V4 ST depression even without myocardial ischaemia
Dobutamine or thallium labelled can be used for MI perfusion scan
Thallium has greater sensitivity
Dobutamine has greater specificity (stresses heart)
Dobutamine good if patient cannot exercise e.g. stroke / injury / pain / bmi / pvd / arthritis
AVOID IN WPW OR ROLAND LONG
How is Torsades De Pointes managed?
DO NOT GIVE AMIODARONE - this may cause QT prolongation
- Instead this needs IV MAGNESIUM which will reduce the availability of calcium and reduce the amplitude of the arrhythmia resulting in potential termination
- DC CARDIOVERSION
Drugs that cause QT prolongation or low MAG can cause TdP
- erythromycin
- ketoconazole
- tricyclics esp in OD
- sotalol
What is sotalol and when is it used
Competitive B blocker that causes QT prolongation and is useufl in management of VT / AF or flutter resistant to other medications
AVOID in heart failure - increased risk of death likely due to QT prolongation
How does digoxin work
Slows AV conduction
How does amiodarone work
Class III
refractory AF / Broad complex Tachys without HD compromise
Resus: when is amiodarone indicated?
Shockable rhythm - VF or VT
After 3 failed shocks
Resus: when is adrenalin indicated
Shockable: VF or VT
Every other cycle = Amiodarone alternate after 3rd cycle
Unshockable : PEA / asystole
every other cycle of CPR - no amiodarone
When is Dobutamine used?
Stress ECHO
Stress perfusion scans when patient cannot exercise
Positive inotrope for low cardiac output states
- MI
- cardiomyopathy
- sepsis
What is cardiac index and when is it useful
Assessment of LV output
product of HR x SR
normal range 2.5-4
<2.1 = cardiogenic shock
How is MAP calculated?
(Systolic + 2xdiastolic) / 3
What is first line management for stable angina?
B - blocker - cardio selective
Bisoprolol
aim to improve efficiency / contractility
negatively chronotropic to reduce work
Tolerated well even in COPD
What is second line management for stable angina?
Nitrates
Diltiazem or ISMN
do not alter MACE
What is the treatment ladder for Heart Failure - chronic?
Bisoprolol - improve mortality and remodelling
ramipril - improve mortality
candesartan / valsartan if not tolerating ramipril
furosemide
spironolactone - improve mortality
Ivabridine - (BB subs - if HF + HR >75 / LVEF)
- funny channel blocker - improve outcomes
(LVEF severe / b blocker not tolerated / esacalted therapy
Valsartan sacubitril - LVEF<35%
- ARB + natrilutic peptidase inhibtor - reduce hyponatreamia - improves outcomes
What is Long QT and how is it managed
Congenital or Acquired
Acquired:
Drug induced
OD
tricyclics / benzodiazepines
avoid amiodarone / digoxin /
any drug which prolonges AV depol
Congenital
LQT1 - higher risk for VT and SCD
B blockade
- blunt andrenergic tone as thought VT may be induced by high tone and depolarisations
- propranolol bisoprolol nidolol
Lifestyle mod
avoid swimming and contact sports
ICD
pacemaker
How is Brugada diagnosed on ECG
3 Types
Type 1: >2mm ST elevation in V1-V3 + TWI in V1-V3
Type 2: Saddle back ST elevation
Type 3: mix of above but <2mm elevation
Plus collapse / syncopy VT/VF FMH SCD nocturnal agonal inspiration
How does Coxsackie B present?
liver / heart / mouth
Mouth ulcers flu like prodrome myocarditis pericarditis hepatitis
What gene defects are associated with HOCM
MYH7A - 40% HOCM
MYBPC3 - 40% HOCM
What agent can be used in P.HTN to manage symptoms?
BOSENTAN - teratogenic
Endothelin A receptor antagonists
PROSTACYCLIN
- pregnancy
aim decerase pulmonary vascular resistance
What causes sudden death in HOCM
Onset VF
This is due to asymmetrical septal hypertrophy increasing risk of aberrant ventricular rhythm.
What causes Brugada? How can it present?
More than 20 documented gene defects
most commonly affecting a sodium channel
Presentation with VF / VT and collapse
incidental ECG finding
ECG type 1
ST elevation and TWI V1-V3 >2mm
type
ST elevation saddleback - widespread
Type 3 - <2mm type1 or type2 findings
What is Commotio cordis?
Often lethal arrhythmia triggered by contusion to the chest during ventricular repolarisation which induces VT or VF
What is target LDL in a diabetic with previous CAD / MI
Target LDL <1.8 or a reduction by 50% if between 1.8-3.5
Peripheral AD is equivalent to CAD ad cerebrovascular disease risk
