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
