1. Cardiology Consultant
Broken Hearts
Acute Heart Failure
Dr Andrew Turley
Cardiology Consultant
South Tees

2. Overview: Acute Heart Failure
New ESC guidelines
Diagnosis
Serum natriuretic peptides
Non-invasive ventilation
Inotropes
Nesiritide
Cardiac Devices

3. Overview: Acute Heart Failure
New ESC guidelines
Diagnosis
serum natriuretic peptides
Non-invasive ventilation
Inotropes
Nesiritide
Cardiac Devices

4. Overview: Acute Heart Failure
Complex syndrome caused by impaired cardiac function
2 types:
left ventricular systolic dysfunction (LVSD)
Heart failure with preserved ejection fraction (HFPEF/HFNEF/Diastolic dys.)
Commonest cause(s):
IHD, Hypertension, alcohol, cytotoxics
30–40% of patients die within a year of diagnosis
Around 900,000 people in the UK
Expected to rise in the future
The cardiac dysfunction may be related to
Ischaemia
Arrhythmias
Valvular dysfunction
Pericardial disease
Increased filling pressures
Elevated systemic resistance.
NOTES FOR PRESENTERS:
Key points to raise:
Heart failure is a complex clinical syndrome of symptoms and signs that suggest the efficiency of the heart as a pump is impaired. It is caused by structural or functional abnormalities of the heart. Some patients have heart failure due to left ventricular systolic dysfunction (LVSD) This is caused by impaired left ventricular contraction, and is usually characterised by a reduced left ventricular ejection fraction. Others have heart failure with a preserved ejection fraction (HFPEF). This is usually associated with impaired left ventricular relaxation, rather than left ventricular contraction, and is characterised by a normal or preserved left ventricular ejection fraction.
The most common cause of heart failure in the UK is coronary artery disease, and many patients have had a myocardial infarction in the past.
Around 900,000 people in the UK have heart failure. Almost as many have damaged hearts but, as yet, no symptoms of heart failure1. Both the incidence and prevalence of heart failure increase steeply with age2, as a result the prevalence of heart failure is expected to rise in future, with the ageing population3.
Heart failure has a poor prognosis: 30–40% of patients diagnosed with heart failure die within a year – but thereafter the mortality is less than 10% per year, and there is evidence of a trend of improved prognosis in the past 10 years4,5,6.
On average, a GP will look after 30 patients with heart failure, and suspect a new diagnosis of heart failure in perhaps 10 patients annually7. Heart failure accounts for a total of 1 million inpatient bed days – 2% of all NHS inpatient bed-days – and 5% of all emergency medical admissions to hospital. Hospital admissions because of heart failure are projected to rise by 50% over the next 25 years – largely as a result of the ageing population7,8,.
It is clear that heart failure has an adverse effect on patients’ quality of life and can place a financial burden upon carers, patients and health service providers. It is important that these patients receive the highest quality of care in order to minimise these negative effects.
For references please see last slide

5. Drugs

6. Diagnosis ECG CXR ABG Laboratory Tests Echo
A small elevation in cardiac troponin may be seen in patients with AHF without ACS.
Echo

7. Diagnosis: Cardiac Biomarkers
In patients with symptoms and signs of heart failure:
Measure serum natriuretic peptides
Refer to have echocardiography and specialist assessment within 2 weeks if
Previous MI
BNP > 400 pg/ml or
NTproBNP > 2000 pg/ml
If BNP < 100 pg/ml or NTproBNP < 400 pg/ml, heart failure is unlikely in an untreated patient
Natriuretic peptides
Negative predictive value
There is no consensus regarding BNP or NT-proBNP reference values in AHF.
Important prognostic information.
NOTES FOR PRESENTERS:
Key points to raise:
Measure serum natriuretic peptides (B-type natriuretic peptide [BNP] or N-terminal pro-B-type natriuretic peptide [NTproBNP]) in patients with suspected heart failure without previous MI. [new 2010] [ ]
Refer patients with suspected heart failure and previous myocardial infarction (MI) urgently, to have transthoracic Doppler 2D echocardiography and specialist assessment within 2 weeks. [new 2010] [ ]
Because very high levels of serum natriuretic peptides carry a poor prognosis, refer patients with suspected heart failure and a BNP level above 400 pg/ml (116 pmol/litre) or an NTproBNP level above 2000 pg/ml (236 pmol/litre) urgently, to have transthoracic Doppler 2D echocardiography and specialist assessment within 2 weeks. [new 2010] [ ]
Related recommendations:
Consider a serum natriuretic peptide test (if not already performed) when heart failure is still suspected after transthoracic Doppler 2D echocardiography has shown a preserved left ventricular ejection fraction. [ ]
There are further recommendations specifically about transthoracic Doppler 2D echocardiography [ , , ]. These are the same as in the guideline.
The following recommendations identify the need to be aware when measuring serum natriuretic peptides.
Be aware that:
obesity or treatment with diuretics, angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, angiotensin II receptor antagonists (ARBs) and aldosterone antagonists can reduce levels of serum natriuretic peptides
high levels of serum natriuretic peptides can have a cause other than heart failure (for example, left ventricular hypertrophy, ischaemia, tachycardia, right ventricular overload, hypoxaemia [including pulmonary embolism], renal dysfunction [GFR  60 ml/minute], sepsis, chronic obstructive pulmonary disease [COPD], diabetes, age  70 years and cirrhosis of the liver). [new 2010] [ ]
For more information about all the recommendations for the diagnosis of chronic heart failure see pages 4 and 5 of the quick reference guide and slide 16

8. Cardiac Biomarkers
Troponin/BNP/CRP

9. New Classification of MI-Type 2?
Secondary to spasm,
embolism, anaemia,
arrhythmia, BP changes
Troponinitis

10. Natriuretic Peptides: Origin and Stimulus of Release
Peptide Primary Origin Stimulus of Release
ANP Cardiac atria Atrial distension
BNP Ventricular myocardium Ventricular overload
CNP Endothelium Endothelial stress
This slide lists the origin and stimulus for the release of the natriuretic peptides. Note that BNP is specifically released from the ventricles of the heart in response to ventricular stretch and volume overload.
Relaxation of smooth muscle cells
Vasodilatation of veins and arteries
GFR , Na+ reabsorption inhibited  diuresis
SNS and RAS activity reduced
ANP = Atrial Natriuretic Peptide
BNP = B-type Natriuretic Peptide
CNP = C-type Natriuretic Peptide
Adapted from Burnett JC, J Hypertens 2000;17(Suppl 1):S37-S43
The Triage® BNP Test is indicated for use as an aid in the diagnosis of congestive heart failure.

11. The natriuretic peptides: Biochemistry of NT-proBNP
—COOH H P L G S A Y T R K M V Q C F D I
H2N— 1 10 70 76 80 90
100
108
proBNP
Cleavage
H2N—
—COOH S P K M V Q G C F R D I L H
H2N— H P L G S A Y T R 1 10 70 76
NT-proBNP
BNP
—COOH
t½ min
t½ 20 min

12. Clinical Potential of BNP/NT-proBNP
Extensively studied
A “blood test for heart failure”
Diagnosis-Raised in LVSD/AF/LVH/VHD/ACS
Screening for asymptomatic LVSD
Risk stratification & Prognosis in established HF
Therapy monitoring
Treatment of HF
Normal BNP makes LVSD very unlikely
NEGATIVE PREDICTIVE VALUE

13. Overview: Acute Heart Failure
New ESC guidelines
Diagnosis
serum natriuretic peptides
Non-invasive ventilation
Inotropes
Nesiritide
Cardiac Devices

14. Acute Cardiogenic Pulmonary Oedema
Common
15-20,000 hospital admissions per annum in UK
Deadly
15-20% in-hospital mortality
Costly
6.5 million hospital days per annum in USA

15. Initial Treatment
The evidence in favour of morphine use for AHF is limited.
Multiple agents are used to manage AHF, but there is a paucity of clinical trials data and their use is largely empiric.
Most agents improve haemodynamics but no agent has been shown to reduce mortality.

16. Non-invasive Ventilation In Acute Cardiogenic Pulmonary Oedema
“When the household vacuum cleaner is employed, the machine should be run for some minutes first of all to get rid of dust”
Poulton EP, Oxon DM: Left-sided heart failure with pulmonary oedema: Its treatment with the "pulmonary plus pressure machine." Lancet (1936);231:

17. Physiological Improvement with CPAP in Patients with ACPO
Reduced acidosis, respiratory rate and heart rate
Kelly et al. Eur Heart J 2002;23:

18. Mortality Benefit of CPAP/NIPPV in Patients with ACPO
Mortality reduced
from 22% to 11%
RR 0.53
(95% CI )
(Individual Group
Sizes small)
However, in 3CPO,
a large RCT
Masip et al. JAMA 2005;294:

19. 3CPO Trial summary Background Intervention Aims
Clinical effectiveness of non-invasive ventilation
Comparative effectiveness of CPAP and NIPPV
Safety of non-invasive ventilation
Hypothesis:
Non-invasive ventilation reduces mortality
Randomised (1:1:1)
Standard oxygen therapy (by facial mask)
CPAP (5 cmH2O up titrated to a maximum of 15 cmH2O)
NIPPV (8/4 cmH2O up titrated to a maximum of 20/10 cmH2O)
Inhaled oxygen of 60%
Attending physicians were encouraged to use vasodilator (nitrate) and diuretic therapy
Opiate therapy was administered at the discretion of the treating physician

20. Outcome: Any NIV v Standard Mortality
3CPO
Outcome: Any NIV v Standard Mortality
Standard Therapy
Non-Invasive Ventilation
Odds Ratio
95% Confidence Intervals
P Value
7-Day
9.8%
9.5%
0.97
0.63 to 1.48
0.869
30-Day
16.7%
15.4%
0.93
0.65 to 1.32
0.685
Active Trial 1069 patients ~ 350 per arm
Baseline Characteristics matched
Baseline Medications matched
Baseline Interventions matched (nitrate, diuretic, opiate, oxygen)

21. Outcome: Hospital stay
3CPO
Outcome: Hospital stay
Standard
CPAP
NIPPV
P-value
Admitted to intensive Care
8.8%
9.1%
6.6%
0.411
Admitted to high-dependency Care
7.7%
10.3%
10.9%
0.301
Admitted to coronary Care
38.1%
43.7%
40.9%
0.337
Median length of hospital stay in days ( IQR)
8 (5-13)
9 (5-16)
0.313
No significant differences (P>0.05)

22. 3CPO
CONCLUSIONS
In patients with acute cardiogenic pulmonary oedema non-invasive ventilation (1069 patients)
UK study, RCT:
Produces more rapid resolution of metabolic abnormalities
and respiratory distress
Has no major effect on 7-day or 30-day mortality
Is beneficial irrespective of the mode (CPAP or NIPPV) of delivery

23. Overview: Acute Heart Failure
New ESC guidelines
Diagnosis
serum natriuretic peptides
Non-invasive ventilation
Inotropes
Nesiritide
Cardiac Devices

24. Inotropes
Inotropic agents should only be administered in patients with low SBP or a low measured cardiac index in the presence of signs of hypoperfusion or congestion.
Dobutamine
Positive inotropic agent acting through stimulation β1-receptors to produce dose-dependent positive inotropic and chronotropic effects.
The infusion rate may be progressively modified according to symptoms, diuretic response.
The elimination of the drug is rapid after cessation of infusion.
Care should be exercised in weaning patients from dobutamine infusion.

25. Treatment related to BP
Respiratory support, Furosemide (infusion)
IV Dobutamine plus low dose IV GTN
± IABP

26. Other treatment options
Vasopressin antagonists
Unproven
Levosimendan is a calcium sensitiser that improves cardiac contractility
Exerts significant vasodilatation mediated through ATP-sensitive potassium channels
Levosimendan infusion increases cardiac output and stroke volume and reduces pulmonary wedge pressure, systemic vascular resistance, and pulmonary vascular resistance.
Vasopressors (norepinephrine) are not recommended as first-line agents

27. Overview: Acute Heart Failure
New ESC guidelines
Diagnosis
serum natriuretic peptides
Non-invasive ventilation
Inotropes
Nesiritide
Cardiac Devices

28. Vasodilators
Vasodilators relieve pulmonary congestion usually without compromising stroke volume or increasing myocardial oxygen demand in acute HF.
Often combined with diuretic ± inotrope
Nitrates: Predominantly venodilator effect.

29. Nesiritide Non-invasive BP measurements are usually adequate.
Intravenous
Recombinant form of human B-type natriuretic peptide,
Venous and arterial vasodilator with a combined modest diuretic and natriuretic effect.
Approved by FDA in 2001
Reduce PCWP 3 hrs!)
Non-invasive BP measurements are usually adequate.
Combination with other i.v. vasodilators is not recommended.
2005
2 meta-analysis ? Renal safety
Nesiritide is not available in most European countries.

30. Minimal symptomatic improvement
Ascend HF*: AHA 14th Nov 2010
7141 patients
1:1
Placebo vs Nesiritide
Safe
No mortality benefit
Minimal symptomatic improvement
*Acute Study of Clinical Effectiveness of Nesiritide in Decompensated Heart Failure Trial

31. Overview: Acute Heart Failure
New ESC guidelines
Diagnosis
serum natriuretic peptides
Non-invasive ventilation
Inotropes
Nesiritide
Cardiac Devices

32. What is the rhythm?

33. Causes of death in heart failure
NYHA II
26%
15%
59%
NYHA III
56%
11%
33%
NYHA IV
64%
12%
24%
Pump failure
I No Limitation
II SOB on severe exertion
III SOB on mild exertion
IV House bound (SOB at rest)
Other
Sudden death

35. Pre-implant counselling How do you want to die?
Heart failure death
Sudden death

36. Device X Rays
ICD Lead
BiV LV Lead position

37. ICD Myths Myths “Diathermy kills patients & devices”
ICDs prevent syncope
Contacts can be electrocuted by ICD discharge
Not safe to use mobile phone, mircowave, playstation etc.
Will stop you dying from VF
“Diathermy kills patients & devices”
PPM – may inhibit (pulse oximetry)
ICD – will detect as VF (reprogram)

38. Consequences of tachycardia therapy
VT Storm
Inappropriate shocks

39. End of life issues: NECVN
Ventricular arrhythmias and/or poor LV function → is an ICD indicated ?
Temporarily disabled with a ring magnet

40. The Future?

41. Intrathoracic Impedance: Concept
The Reality
Intrathoracic Impedance: Concept
Drier lungs means the intrathoracic impedance is higher
Wetter lungs means the intrathoracic impedance is lower
Less Fluid
More Fluid

42. Summary Normal BNP makes LVSD very unlikely Non invasive ventilation
NEGATIVE PREDICTIVE VALUE
Non invasive ventilation
Produces more rapid resolution of metabolic abnormalities and respiratory distress
Has no major effect on 7-day or 30-day mortality
Is beneficial irrespective of the mode (CPAP/NIPPV)
Respiratory support, Furosemide (infusion), IV Dobutamine plus low dose IV GTN, (± IABP)
Nesiritide
Safe, No mortality benefit, Minimal symptomatic improvement
ICD: Temporarily disabled with a ring magnet
End of life issues: NECVN