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Approach to Cardiac Failure
Dr J Strange
7th November 2013
Case
• 24 year old male
• Previously well
• Developed shortness of breath, pyrexias over
a 5 day period
• Observations
– HR 130, regular
– BP 87/45
– O2 Sats 88% on room air
• ABG
– pO2 11 pCO2 5.1 BE -12 lactate 6

•
•
•
•
•

Hb 130g/L WCC 14 Platelets 180
Na 132 K 5.2 Urea 15 Creat 210 CRP 180
PT 16, elevated transaminases
Oliguric, peripheral oedema
Intubated and commenced vasopressors
TTE
• Globally reduced LV function
• Estimated EF 15%
• Transferred to Alfred
– Noradrenaline @ .35 microgram/kg/min
– MAP 68
– CVP 21
– PAOP 26
– CI 1.7
INITIAL ASSESSMENT
Immediate assessment and
resuscitation
•
•
•
•
•

Resuscitation
Basic monitoring
History
Examination
Assessment of severity
How does CPAP work?
• Recruitment
• Increased FRC
• Improved pulmonary
compliance
• Reduced
transdiaphragmatic
pressure swings
• Decreased work of
breathing
• Reduction in ventricular
transmural pressure –
reduced afterload
Circulation
• Therapies dependent on patho-physiological
classification
• Maintenance of appropriate blood pressure
and cardiac output essential
Key questions…
• Is the patient dyspnoeic?
• De novo or on a background of cardiac
problems?
• Symptoms of ACS?
• Medications?
Examination
Congestion
• JVP
• Pulsus alternans
• HJR
• Parasternal lift
• Displaced apex
• Gallop
• MR/TR murmur
• Oedema
• Ascites
• Hepar

Low CO
• Cool peripheries
• Decreased LOC
• Confusion
• Hypotension
• Low volume pulse
• Inappropriate tachycardia
Severity
• Who should be transferred to ICU?
• NYHA classification
Framington Heart Study
• Life-time risk 20% for men and women
• Hypertension is the biggest modifiable risk
factor
• Median survival after development of 1.7
years in men and 3.2 years in women
Diagnostic category
•
•
•
•
•

Pressure overload
Volume overload
Impaired ventricular filling
Myocardial diseases
Dysrhythmias
Pathophysiology
• Right and/or left
• Forward/backward
• Systolic and/or diastolic
Cardiogenic shock
•
•
•
•
•
•
•

Oliguria
Clouded sensorium
Cool, mottled peripheries
SBP <90
HR >90
CI <2.2
PAOP >15
Forward failure
• Signs
– reduced tissue perfusion at
rest with weakness
– confusion and drowsiness
– pallor with peripheral
cyanosis
– cold clammy skin
– low blood pressure
– oliguria
– culminating in the full
blown cardiogenic shock

• Causes
–
–
–
–
–

acute myocardial infarction
acute myocarditis
acute valvular dysfunction
pulmonary embolism
cardiac tamponade
Left heart backward failure
Right heart backward failure
• Right heart ischaemia
• Syndrome of chronically elevated systemic
venous pressure
INVESTIGATIONS
ECG
• The negative predictive value of a normal ECG
to exclude LV systolic dysfunction exceeds 90%
• Presence of anterior Q waves and LBBB in
patients with IHD are good predictors of
decreased EF
CXR
Troponin
• I or T
• Increased in shock, renal failure, sepsis,
hypovolaemia
• Values need to be interpreted in context
BNP
• Elevated in accordance with severity of heart
failure
• High negative predictive values
ECHO

• Function
• Mechanics
Other invasive monitors
• PAC
• PiCCO
• Oesophageal Doppler
MANAGEMENT
Reducing demand
• Reducing heart rate
• Reducing afterload
• 30 to 40% of cardiac output may be required
to support the work of breathing in a
dyspnoeic patient
Increasing supply
• Vasodilator
• Blood transfusion
• Judicious inotropes
Non-specific therapy
•
•
•
•
•
•

General care
Adequate oxygenation
Adequate heart rate
Optimise preload
Increasing cardiac output
Correct structural problems
SPECIFIC PROBLEMS
Forward acute heart failure –
Cardiogenic shock
•
•
•
•

Most commonly MI
5 -10% of MI’s
50 – 80% mortality
Reperfusion vital
IABP
VA - ECMO
VAD
Left heart backward failure
• ? ACS – reperfusion
• Oxygen, Diuretics, Vasodilators, Morphine
Right heart backward failure
•
•
•
•

Increased portal venous pressures
Care with volume replacement therapy
Increase in PVR can be devastating
Aim to reduce RV afterload without affecting
systemic blood pressure
Takotsubo’s cardiomyopathy
Filtration or pharmacology
• Ultrafiltration was inferior to pharmacology at
96h
• Higher creatinine level
• No difference in weight loss
• Higher serious adverse events
Cardiac re-synchronisation therapy
• ICD and CRT used for wide range of patients
with heart rhythm disturbances
• Reduction in sudden death
• Improved ventricular performance
Institution of long-term therapy
• Evidence for long-term benefit of:
– ACEi
– β blockers
– Spironolactone
Case
• 30 yo man post arch and aortic valve
replacement
• Marfan’s
• Post-op
– HR 86
– BP 120/85
– CVP 9
• 6h later
– HR 125
– BP 70/50
– CVP 20
– TR
– Lactate 2  9
– Cool to touch, chest clear
Tests
•
•
•
•
•
•

ABG
LFT – elevated transaminases
Cardiac enzymes – elevated
CXR
ECG – RBBB, ST elevation II, III, aVF
ECHO – no effusion, severely dilated and
hypokinetic RV, hypertrophied LV, TR
Management
• ABCs
• Further fluid may be detrimental
• Drugs to increase RV contractility and
decrease RV afterload
• Return to theatre
• Consider PAC
• Death from any cause or hospitalization for
worsening heart failure
– 50.7% vs 49.5% (p=0.87)

• Stroke
– 3.7% vs 2.7% (p=0.23)

• Thromboembolism
– 13.5% vs 10.0% (p=0.01)
QUESTIONS?
Heart failure

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Heart failure

Hinweis der Redaktion

  1. TTE confirmed global LV impairmentCommenced Adrenaline8 days on VA ECMOCardiac biospyMycoplasmatitre positive
  2. Airwat, breathing….CPAPContinuous electrocardiogramBloodpressureRespiratoryrateTemperatureContinuous oxygen saturation with a pulse oximeter
  3. 40% of cardiac output expended on work of breathing
  4. C circulation
  5. History is essential
  6. NYHA
  7. Hypertension serious risk factor in women
  8. Heart failure should never be the final diagnosisCauses of each to be listed here Pressure overload – hypertension, Aortic stenosis, PEVolume overload – aortic regurg, High output failureImpaired filling – Mitral stenosis, Tamponade, pericardial constriction/restricitionMyocardial disease – IHD, myocarditis, Metabolic/toxicDysrhythmias – ischaemia, brady/tachy
  9. Definition of cardiogenic shock – inadequate tissue perfusion
  10. Conduction abnormalities
  11. Cardiac size and shapeCT ratioPulmonary venous congestion
  12. Remain elevated 7 -10 days
  13. Hr - Anxiolytics, adequate preloadAfterolad – vasodilators, diuretics if overloaded
  14. NB problem of increased intra-thoracic pressure in right ventricular dysfunction leading to elevated rvafterloadTachycardias poorly tolerated – rapid DCC bestElevation of venous pressure often the result of reduced forward flowBeneficial effect of furosemide often as a vasodilatorIncreasing CO – decreased SVR or increased inotropy. Do not compromise coronary artery flowUse of mixed venous oxygen saturation
  15. Documentation of myocardial dysfunction and exclusion or correction of factors such as hypovolaemia, haemorrhage, sepsis, pulmonary embolism, tamponade, aortic dissection, pre-existing valvular disease, hypoxia and acidosis
  16. Contraindications
  17. No significant difference in mortality between the 2 groups when early revascularisation was planned
  18. Interestingly pulmonaryoedema with VA ECMOTreatment before development of end-organ dysfunction
  19. bridge to recovery in certain causes of heart failure e.g. myocarditis.Or destination therapy
  20. ‘FOAM’
  21. Ventricular interdependence and decreased perfusion of the right heartRV diameter should be &lt; 0.7 of LV diameterRV afterload dependentMost common cause is PEHow to do it? NO or protacyclin
  22. Apical ballooning syndrome or broken heart syndrome
  23. Cardiorenal syndrome = worsening renal function in patients with acute decompensated heart failure
  24. Advnaced systolic dysfunction
  25. Clinically shockedPositive HJ Reflex
  26. PAC normal PA values; low mixed venous oxygen saturation; low CI