Heart failure and Pulmonary oedema

1. Heart failure and
Pulmonary oedema
Presentor: Haizewarya and Lee Wai Yern
Supervisors: Dr Wong & Dr Syahirah

2. Case
A 72 years old indian lady, with following underlying:
1. Type 2 DM
On insulin: S/C Actrapid 6 units TDS, S/C Insulatard 22units ON
2. Hypertension
on 2 anti HPT: T Perindopril 2mg OD, T Bisoprolol 1.25mg OD
3. IHD – 2 vessels disease
- H/o acute inferior STEMI - thrombolysed on 4.1.2016
ECHO 15.1.2016
depressed EF, 38%
akinetic at mid lateral , mid to apical septal and mid posterior wall
- angiogram 20.1.2016: 2VD (RCA: diffuse disease 80%, calcified ostial, LCX 80% - for 2 DES to RCA)
- plan for PTCA for RCA
- defaulted TCA, opted for medical therapy
4. CKD IV secondary to DM
eGFR - 31 ( stage III ) >> 236
ROF 500cc/day (but usually took more than 500cc/day)
- Advised for RRT but patient not keen

3. —
Presentation
1/ SOB x 1/52
-Initially occurs when she exerted herself, which resolved by rest
-Symptoms progressively worsens and currently triggered by less than ordinary activities (ex:walking short distance)
-Associated cough, no sputum
- Worsening orthopnea (used to sleep with 2 pillows => 3 pillows) and PND
- Minimal lower limb swelling for 3/7
- Claimed wasn't compliant to ROF for the past 3 days
—
Otherwise
No fever
No vomit
No diarrhea
No runny nose/ No sore throat
No chest pain
No palpitation
No presyncopal attack
No sick contact

4. IN ED:
GCS full
+ mild tachypneic (RR 28)
+ tachycardiec
Warm peripheries
Good PV
CRT immediate
T: 36.8 / BP: 134/98 / PR: 102 / SPO2: 98% under RA
Lungs: A/E equal, crepts over bibasal but more on right LZ
CVS: DRNM
PA : soft non tender, no ascites
pedal edema till upper shin
CXR: cardiomegaly, fluid overload picture, blunted left costophrenic angle, no consolidation
ECG sinus rhythm, no ischemic changes, poor R wave progression
ABG under RA: pH 7.488 / PCO2 23.3 / Po2 114 / So2 98.3 / Lact 2.3 / Base -5.4 / HCO3 21.4

6. Wcc 6.85 / Hb 13.1 / Plt 239
Urea 7.9 / Na 134 / K4.0 / Cr 157
Ca 2.14 / Mg 0.84 / PO4 1.13
CK 50 / LDH 269 / AST 24
Given:
-Put on NP3L
-IV lasix 40mg stat
-IV augmentin 1.2 stat
Imp:
1. Decompensated CCF secondary to non compliance to ROF
2. Cover for CAP

7. In ward (3days)
Saturating well under NP 3L
claimed no worsening of SOB, improving
Ambulating in ward
Started on T spirinolactone 12.5mg OD
Strict IO chart
Strict ROF 500cc/day
And subsequently wean off the NP3L on day 2 of
admissions
Meds:
IV Frusemide 40mg BD
S/C Actrapid 6 units TDS
S/C Insulatard 22units ON
Top up scale B
T Cardiprin 100mg OD
T Atorvastatin 40mg ON
T Pantoprazole 40mg OD
T Bisoprolol 2.5mg OD
T spironolactone 12.5mg OD
Upon discharge
Saturating well under RA, 97-99%
No SOB/ no chest pain/ no dizziness
Ambulating in ward
Feeling much better
Tolerating orally well
Lungs: fairly clear
CVS: DRNM
Discharge meds:
T Frusemide 40mg OD
T spironolactone 12.5mg OD
S/C Actrapid 6 units TDS
S/C Insulatard 20units ON
T Cardiprin 100mg OD
T Atorvastatin 40mg ON
T Pantoprazole 40mg OD
T Bisoprolol 2.5mg OD

8. Definition
• Heart failure (HF) is a clinical syndrome due to any structural or physiological abnormality of the heart resulting in its inability to
meet the metabolic demands of the body or its ability to do so only at higher than normal filling pressures.
• This may be accompanied by signs and symptoms of systemic hypoperfusion and/or volume overload.
Patients may have typical symptoms (breathlessness, ankle swelling, fatigue), signs ( elevated jugular venous pressure, ankle
oedema, pulmonary crackles, and displaced apex beat)
Pulmonary oedema
Cardiogenic pulmonary edema - defined as due to increased capillary hydrostatic pressure secondary to elevated pulmonary pressure
Non cardiogenic pulmonary oedema - caused by changes in capillary permeability as a result of a direct or an indirect pathologic insult
.

9. Pathophysiology
The main pathophysiology of HF is due to a decrease in cardiac output which will
result in the following compensatory mechanisms:
1. A higher ventricular end diastolic pressure - This is a compensatory mechanism to
increase stroke volume by the Frank Starling mechanism.
1. Neurohormonal activation of the:
→ Sympathetic nervous system
→ Renin-angiotensin-aldosterone system
→ Vasopressin

10. This neurohormonal activation is aimed at increasing stroke volume and cardiac
output by:
● An increase in heart rate and ventricular contraction
● Vasoconstriction of arterial resistance vessels to maintain blood pressure
● Venous constriction to increase venous preload
● Salt and water retention to increase preload
In general, these neurohormonal responses are compensatory mechanisms. However
they can also aggravate HF by increasing ventricular afterload and increasing preload
to the point where pulmonary and/or systemic congestion and oedema occur

12. Classification
For practical purposes, HF can also be classified according to the clinical
presentation into:
Acute heart failure - defined as the rapid onset of symptoms and signs of HF
due to an acute deterioration of cardiac function in the presence or absence
of previous cardiac disease.
Chronic heart failure - this is a chronic state when patients have stable
symptoms. In these patients, an acute precipitating or aggravating factor(s)
may cause acute cardiac decompensation
Left sided/ Right sided
High output / low output
Systolic / diastolic
acute / chronic

13. Patients with Chronic HF may occasionally develop acute decompensation.
Factors that can contribute to this Acute HF.

14. Classification
2. According to left ventricular ejection fraction (LVEF).

15. Etiology
The common underlying causes of HF in adults are
● Coronary artery disease (CAD)
● Hypertension
● Dilated cardiomyopathy-idiopathic, familial
● Valvular heart disease
● Diabetic cardiomyopathy
Other causes of HF include:
● Congenital heart disease
● Cor pulmonale
● Pericardial disease: constrictive pericarditis, cardiac tamponade
● Hypertrophic cardiomyopathy
● Viral myocarditis
● Acute rheumatic fever

16. Toxic: Alcohol, cardiotoxic chemotherapy e.g. doxorubicin, trastuzumab
(Herceptin), cyclophosphamide.
Endocrine and metabolic disorders: thyroid disease, acromegaly,
phaechromocytoma.
Collagen vascular disease: systemic lupus erythematosis, polymyositis,
polyarteritis nodosa.
Tachycardia induced cardiomyopathy eg uncontrolled atrial fibrillation.
Infiltrative cardiac disease e.g. amyloid, hyper-eosinophilic syndrome.
Miscellaneous.
High output HF e.g. severe anaemia, large A-V shunts/malformations.
Peripartum cardiomyopathy.
Stress (Takotsubo) cardiomyopathy

17. Clinical signs and symptoms

18. Exercise capacity in a patient with heart disease is assessed by the New York Heart
Association (NYHA) functional classification.

23. Management according to Classification
⚫ According to aetiology and precipitating cause
⮚ Myocardial infarction/ischemia
⮚ Arrhythmias:commonly rapid AF
⮚ Acute valvular dysfunction:acute mitral regurgitation
⮚ Severe and uncontrolled hypertension
⮚ Infection: pneumonia
⮚ Non compliance to treatment especially oral diuretics
⮚ Fluid overload
▪ According to clinical presentation
⮚ Warm and wet:adequate perfusion but congested **(lungs and/or periphery)
⮚ Cold and dry: hypoperfusion* and dehydrated/not congested**
⮚ Cold and wet: hypoperfusion* and congested**(lungs and/or periphery)
⮚ Warm and dry:adequate perfusion and dehydrated/not congested **.These patients have either mild HF or are in the
compensated stage of HF
*Hypoperfusion:Cold peripheries,CRT >2sec,diaphoresis,oliguria,dizziness,confusion,narrow pulse presurre,hypotension
**Congestion:Peripheral edema,orthopnea,PND,lung crepitation,JV dilatation,hepatijugular reflex,congested
hepatomegaly,ascites,gut congestion