Flashcards in CCF (inc pulmonary oedema) Deck (50):
What is heart failure?
Clinical syndrome resulting from almost any cardiac disorder that impairs ability of ventricle to fill with or eject blood.
i.e. CO less than body needs.
What is forward heart failure?
Heart unable to maintain adequate CO to meet demand, or can only do so by elevating filling pressure.
What is backward heart failure?
Heart unable to accommodate venous return resulting in elevated filling pressure and vascular congestion (systemic or pulmonary).
Signs and symptoms of low CO LHF?
-Slow capillary refill
Signs and symptoms of backward (venous congestion) LHF?
-Dyspnoea, orthopnoea, PND
Signs and symptoms of forward RHF?
-LHF symptoms if RHF leads to LV underfilling
Signs and symptoms of backward RHF?
-Pulsatile liver (if TR)
-elevated JVP w/ abdominal jugular reflex and Kussmaul's sign
Outline the pathophysiology of heart failure.
Compensatory vascular and cardiac changes to maintain CO. As HF progressives, mechanisms overhwelmed: peripheral vasoconstriction and Na+ retention due to RAAS activation (decompensation).
What is the systemic response in heart failure?
SNS activation. Systemic response to ineffective circulating volume:
-RAAS activation (retain H20 and Na)
-increased HR and contractility
What is systolic dysfunction?
Impaired myocardial contractile function -> decreased LVEF and SV -> decreased CO.
Signs systolic dysfunction?
-Displaced apex beat
-increased heart size on CXR
Causes LV systolic dysfunction?
-Ischaemic: e.g. CAD, MI
-Non-ischaemic: HTN, DM, alcohol/toxins, myocarditis, dilated cardiomyopathy.
What is heart failure with preserved ejection fraction also known as?
What is the difference b/w systolic dysfunction and HFPEF?
Up to 50% HF pts have normal systolic fxn i.e. preserved ejection fraction; heart failure caused by impaired diastolic filling.
Pathophysiology of HFPEF?
Impaired diastolic filling -> increased LV filling pressures -> upstream venous congestion (pulmonary, systemic).
-Apex beat sustained
-Normal heart size on CXR
-LVH on ECG/Echo
Causes of decreased compliance in HFPEF?
>severe hypertrophy (HTN, AS, HCM)
>restrictive cardiomyopathy (e.g. amyloid)
Describe NYHA heart failure classification.
i: ordinary physical activity does not cause symptoms.
ii: comfortable at rest, ordinary activity causes symptoms
iii: limitation of ordinary activity, less than ordinary physical activity causes symptoms
iv: inability to carry out any physical activity without discomfort; symptoms may be present at rest.
What is high output heart failure?
Demand for increased CO; often exacerbates existing HF of decompensates pt w/ other cardiac pathology
Ddx high output heart failure?
-A-V fistula / L>R shunting
Precipitants of heart failure?
-Endocrine (phaechromocytoma / hyperaldosteronism)
-RHD / other valvular disease
-Failure to take Rx
-Infection / ischaemia / infarction
-Lung (PE / pneumonia / COPD)
-Endocarditis / environment
-Dietary (e.g. FR non compliance)
Blood Ix heart failure?
ECG features to look for in heart failure?
-Ischaemia / infarction
CXR features to look for in heart failure?
-Re-distribution (alveolar oedema)
-B Lines (Kerley B lines)
Echo features in heart failure?
-Wall motion abnormalities
What is the acute treatment of heart failure?
Treat precipitants! +
-L) Lasix: frusemide 40 - 500mg IV
-M) Morphine: 2-4mg IV
-N) Nitroglycerin: topical / IV/ SL
-O) Oxygen: in hypoxemic patients
-P) Position/positive airway pressure (CPAP/BiPAP)
Why is morphine given in acute treatment heart failure?
Decreases anxiety and preload.
Conservative measures for symptomatic management of HF?
Oxygen in hospital, bed rest, elevate head of bed.
Lifestyle measures for conservative management of heart failure?
-Diet / exercise
-FR and Na restriction
Pharmacological management of heart failure?
1) Vasodilators (ACEi / ARB)
4) Aldosterone antagonist
In which pts should ACEi be instituted?
-All symptomatic pts class II-IV
-Asymptomatic pts LVEF
When should ARB be instituted?
-Second line to ACEi if not tolerated; adjunct to ACEi if B-blockers not tolerated
-Consider in acute renal failure until creatinine stabilises
Which pts should receive B-blocker therapy?
-Class I - III with LVEF
Which pts should receive spironolactone?
Class IIIb and IV CHF already on ACEi and loop diuretic.
Indications for inotropes in heart failure?
- Patient in sinus rhythm and symptomatic on ACEi,
- or CHF + AF
When should biventricular pacemaker be considered?
What are the pathophysiological changes in heart failure?
-Increased collagen synthesis
-Increased ANP secretion
-Na+ and water retention
What is after load?
Outflow Resistance (afterload): load the heart pumps against = pulmonary/systemic resistance + physical characteristics of vessel walls + volume of blood ejected.
Effect of neurohormonal activation in HF?
-SNS activated by baroreceptors early in HF, provides inotropic support to maintain CO.
-Chronic SNS ==> increases neurhormonal activation + myocyte apoptosis —> B-receptor downregulation.
What are the major Framingham criteria for HF? (dx = 1 major, 2 minor)
◦S3 heart sound present (‘gallop’ sound)
◦Acute pulmonary oedema (left side of heart is unable to clear fluid from lungs)
◦Weight loss of more than 4.5kg in 5 days when treated (patients lose retained fluids)
◦Paroxysmal nocturnal dyspnoea
◦Abdominojugular reflux (JVP waveform rises when pressure applied over liver area)
◦Neck vein distended (i.e. JVP elevated at rest)
◦Increased cardiac shadow on X-ray (cardiomegaly: heart occupies more than ≈50% of chest diameter)
◦Crackles heard in lungs
What are the minor Framingham criteria for HF?
-Ankle oedema bilaterally
-Vital capacity decreased by 1/3 max value
What are Starling Forces across capillaries?
Fluid leaks in/out according to balance of forces (hydrostatic, oncotic).
Tends out at arterial; in at venous.
In relation to Starling Forces at Capillaries, alteration at which end causes pulmonary oedema?
Fluid tends out at arterial; in at venous.
Increases in VENOUS pressure causes fluid to leak out and oedema.
What are the causes of oedema?
-Increased venous pressure e.g. HF
-Decreased osmotic pressure e.g. plasma protein loss (hep/ren failure)
-Blockage of lymphatics e.g. cancer
-Increased capillary permeability e.g. infection
Alterations in pressure in which vessels cause oedema?
VENOUS not arterial.
What is indicated by elevated JVP?
High RA pressure (therefore high RVED pressure).
Generally also thus high LA (&LVED) pressure.
Causes of pure RHF?
-PAH: Cor pulmonale e.g. COPD / CF; PE
-Right structural disease: pul or tricuspid valves; R ventricular cardiomyopathy
What are the 4 key components of pt diagnosis of HF?
1) Is it HF?
2) What is underlying cause?
3) Precipitating cause of this episode?
4) What other problems? (i.e. CV/ Renal / hepatic)
Principles of HF treatment?
-Reduce venous pressure
-Blocks SNS (B blocker)
-Treat underlying and precipitating causes