Download Heart failure - Modest Mango

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Cardiac contractility modulation wikipedia , lookup

Cardiovascular disease wikipedia , lookup

Electrocardiography wikipedia , lookup

Lutembacher's syndrome wikipedia , lookup

Cardiac surgery wikipedia , lookup

Hypertrophic cardiomyopathy wikipedia , lookup

Heart failure wikipedia , lookup

Jatene procedure wikipedia , lookup

Coronary artery disease wikipedia , lookup

Quantium Medical Cardiac Output wikipedia , lookup

Mitral insufficiency wikipedia , lookup

Dextro-Transposition of the great arteries wikipedia , lookup

Arrhythmogenic right ventricular dysplasia wikipedia , lookup

Transcript
PALi Cardiology Revision:
Heart Failure
Lucille Ramani
[email protected]
Heart Failure
Definition
“a complex of signs and symptoms that occurs when the heart
fails to pump adequate CO”
Epidemiology
• Prevalence: 3-20 per 1000
• 5% emergency admissions
•  by 50% in the next 25 years
• 50% dead by 5 years
• Mainly a disease of the older population (>65 years)
Aetiology
Cause
Cardiovascular disease
Pulmonary disease
Specific Examples
IHD; cardiomyopathies; HTN; myocarditis;
valvular heart disease; congenital heart diseases
Pulmonary HTN; pulmonary valve stenosis; PE; chronic
pulmonary disease; neuromuscular disease
Toxins
Heroin; alcohol; cocaine; amphetamines; lead; arsenic;
cobalt; phosphorus
Infection
Bacterial; fungal; viral (HIV); Borrelia burgdorferi (Lyme
disease); sepsis
Electrolyte imbalance
Endocrine disorders
 calcium, phosphate, potassium, sodium
DM; thyroid disease; hypoparathyroidism;
phaeochromocytoma; acromegaly
Systemic collagen vascular
diseases
Drug-induced
Nutritional deficiencies
Pregnancy
SLE; RA; systemic sclerosis; polyarteritis nodosa; Reiter’s
syndrome
Adriamycin; cyclophosphamide; sulphonamides
Thiamine; selenium; L-carnitine
Peripartum cardiomyopathy
Right Heart Failure (RHF)
• Aetiology:
–
Chronic pulmonary disease cor pulmonale
–
Left-sided heart failure
–
Patent ductus arteriosus
–
Isolated right-sided cardiomyopathy
– Tricuspid
valve disease
•  RV pressure  backward failure  systemic
venous congestion
RHF: Clinical Features
• Symptoms
–
Fatigue
–
Dyspnoea
–
Anorexia, nausea
–
Nocturia
• Signs
–
 JVP
–
Smooth, tender hepatomegaly
–
Ascites
–
Pitting oedema (sacral, ankle)
–
Hypotension
–
Cyanosis, cool peripheries
LHF: Aetiology
• Ischaemic heart disease
• Chronic systemic HTN
• Cardiomyopathy (usually dilated)
• Mitral / Aortic valve disease
–
Mitral regurgitation: volume overload ( preload )
–
Aortic stenosis: pressure overload ( afterload)
• Consequence = pulmonary congestion
LHF: Clinical Features
• Symptoms
–
Fatigue
–
Dyspnoea: exertional; orthopnoea;
paroxysmal nocturnal
–
Cough ± frothy pink sputum; haemoptysis
• Signs
–
Few, but prominent at late stage
–
Weight loss; muscle wasting
–
Cardiomegaly
–
Pulmonary oedema (creps)
–
Hypotension; cool peripheries
–
S3 and tachycardia: triple gallop rhythm
Pathophysiology
• Compensatory mechanisms become overwhelmed
and thus pathological (cardiac decompensation)
• Key concepts:
–
CO is a function of preload and afterload
–
Preload: end-diastolic wall stress (initial stretching of myocytes)
–
Afterload: the resistance against which the heart has to pump
–
Frank-Starling mechanism: change in SV
in response to change in preload
–
 in preload via Rx is beneficial
–
 in workload and symptoms arising from
venous congestion
Compensatory Changes
1.  filling pressures to maintain SV
2. Dilation: increased wall tension  ischaemia
3. Hypertrophy to balance pressure overload
4. Sinus tachycardia
5. Neurohormonal mechanisms
• Activation of RAAS
-  systemic vascular resistance
- Aldosterone release (Na+ and water retention)
- ADH release (water retention)
•  Sympathetic activity ( catecholamines)
-  HR, force of contraction and peripheral vasoconstriction
Diagnosis
Diagnosis of HF (European Society of Cardiology Guidelines)
Essential Features
1. Symptoms and signs of heart failure (e.g. SOB, fatigue, ankle oedema)
2. Objective evidence of cardiac dysfunction (at rest)
Non-essential Features: in cases where there is diagnostic doubt
3. Response to treatment directed towards heart failure
•
•
•
•
Bloods; cardiac enzymes/markers
BNP (>100pg/mL = 95% specificity and 98% sensitivity
ECG
Transthoracic doppler ECHO: EF<0.45
Chest X-ray Findings
• Alveolar oedema (“Bat’s wings”)
• Kerley B lines (interstitial oedema)
• Cardiomegaly
• Dilated prominent upper lobe vessels
• Pleural Effusions
• LV dysfunction  dilation of pulmonary vessels  leakage of
fluid into interstitium  pleural effusion  alveolar oedema
(pulmonary oedema)
Management
• Aims:
–
Treat cause, e.g. valve disease
–
Treat exacerbating factors, e.g. anaemia, HTN
–
Relieve S+S
–
Augment survival
• General Measures:
–
Smoking cessation
–
Salt reduction and fluid restriction if severe
–
Maintenance of optimal weight and nutrition
–
Vaccinations: pneumoccocal (once only) and annual influenza
–
Assess for depression
–
Monitor: functional capacity, fluid status, cardiac rhythm
Pharmacological Rx
• Diuretics
–
Routinely loop diuretics, e.g. Furosemide 40mg/24h po (increase prn)
–
Can add spironolactone or metolazone
• ACEi
–
Long-acting, e.g. lisinopril 10mg/24h po
–
Start with small dose and increase every 2 weeks until at target (30-40mg)
–
Warn patients of side effects: hypotension (esp after first dose- advise to lie
down); dry cough; hyperkalaemia; taste disturbance
– Check
U+E and creatinine before starting and with each titration
Pharmacological Rx
• Beta-blockers
–
–
Initiate after ACEi and diuretic
Start low, go slow e.g. carvedilol 3.125mg/bd  25-50mg/bd (at least 2 week
increments)
• Angiotensin-II receptor antagonists
–
Alternative if intolerant of ACEi
• Digoxin
–
Use if diuretics, ACEi or BB do not control symptoms or if in AF
– 0.125mg-0.24mg/24h
–
po
Monitor U+E and maintain potassium at 4-5mmol/L
Acute HF
• Most commonly occurs in context of acute MI 
extensive loss of ventricular muscle
–
Also: PE, cardiac tamponade, rupture of IV septum (producing VSD), AF
• Clinical presentation:
–
Acute worsening (decompensation) of chronic HF
–
Acute pulmonary oedema: respiratory distress, crackles, pink frothy sputum
–
Cardiogenic shock: hypotension, tachycardia, oliguria
• Investigations:
–
CXR
–
ECG; consider ECHO and BNP
–
U+E; cardiac markers; ABGs
Acute HF Management
• Different to chronic; Rx before Ix
• Sit pt up + high-flow O2 (100% if no lung disease)
• IV access and ECG (Rx any arrhythmia, e.g. AF)
• Diamorphine 2.5-5mg IV slowly
• Furosemide 40-80mg IV slowly
• GTN spray 2 puffs sublingual then infusion of
isosorbide dinitrate 2-10mg/h
• If pt worsening- first get help, then:
–
Further dose of furosemide
–
Consider ventilation or increasing nitrate infusion
MEQ Past Paper
MEQ 1.2
Marks
A 78 year old man had a large anterior myocardial infarction 3 years ago.
Initially he made a good recovery although he has required to take a
diuretic for ankle swelling since. In the last 2 months he has become short
of breath on exertion. You suspect he has developed left ventricular failure
(a)
Give 2 additional symptoms which would support this diagnosis
2
(b)
You arrange for a chest x-ray. Give 4 features which would support the diagnosis of
left ventricular failure
4
(c)
Give 2 neurohumoral mechanisms which may be activated in heart failure
1
(d)
If starting this patient on an ACE Inhibitor give 3 precautions you would take
3
Further Questions
• What are the possible causes for deterioration in
HF? (3)
• Immediate treatment of acute HF and how you would
administer this? (3)
Thank-you!
Any Questions?