Heart failure ภาวะหัวใจล้มเหลว · Chronic heart failure (ภาวะหัวใจล้มเหลว เรื้อรัง) •อาการไม่หนัก
Heart Failure 101
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Transcript of Heart Failure 101
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Armaan Khalid
Heart Failure 101
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HF is a syndrome that manifests as the inability of the heart to fill with or eject blood
HF can result from any structural/functional cardiac disorder that impairs the ability of the heart to function normally
Coronary Artery Disease (CAD) is the most commonest cause of HF
Anything that ↑ myocardial work may aggravate/initiate HF
What is Heart Failure?
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Ischaemic Heart Disease (35-40%)Cardiomyopathy (dilated) (30-34%)Hypertension (15-20%)
Common Causes of HF
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EXTREMELY COMPLEX!Compensatory physiological changes that
eventually get overwhelmed & become pathological
Factors involved are:Venous return (preload)Outflow resistance (afterload)Myocardial contractility (inotropic state)Salt & water retention
Pathophysiology
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Stroke work is increased as ventricular end diastolic volume is raised (e.g. ↓ ejection fraction)↑ Preload will ↑ cardiac contractilityCompensatory mechanism
Frank-Starling’s Law of the Heart
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SV is the volume of blood pumped from one ventricle of the heart with each heart beatUsually assumed to be the Left
SV = EDV – ESVEjection Fraction = SV / EDVDeterminants
PreloadSV is controlled by preload due to Frank-Starling’s Law
Afterload↑ Afterload will ↓ SV
Contractility↑ Ca2+
Stroke Volume
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In HF, ejection fraction ↓Can be compensated by ↑ heart rate (sinus
tachycardia)In severe myocardial dysfunction, cardiac output can
only be maintained by ↑ venous pressure (Preload) &/ ↑ tachycardiaLow functional reservePerfusion only maintained to vital organs (huge
impact)Causes dyspnoea,
hepatomegaly, ascites, oedemaDue to ↑ venous pressure
Venous Return (Preload)
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Afterload is defined as the myocardial wall tension developed during systolic ejection
It is formed by:Pulmonary & systemic resistancePhysical characteristics of the vessel wallsVolume of blood that is ejected
↑ in afterload ↓ cardiac output↑ end-diastolic volume↑ dilatation of the ventricle↑ AFTERLOAD
Vicious cycle
Outflow Resistance (Afterload)
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Sympathetic nervous system is activated in early HF as a compensatory mechanism Inotropic support & maintains cardiac output
Chronic sympathetic activation leads to ↑ neurohormonal activation & myocyte apoptosis
Also causes ↑ cytosolic Ca2+ entryAugments myocardial contractility Impairs myocardial relaxation (lusitropy)
Myocardial Contractility
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↓ CO leads to diminished renal perfusionActivation of RAAS↑ Aldosterone production to retain salt &
waterExacerbates increased venous pressure
Salt & Water Retention
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Primary response to chronic ↑ wall stress is myocyte hypertrophy, apoptosis & regeneration
Myocardial remodelling is pathological (eccentric)Worsens the situation↑ stress on remaining myocytes
Myocardial Remodelling
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Left Heart FailureClinical features
Fatigue, dyspnoeaCardiomegalyOn auscultation,
gallop rhythmCrackles in lung
basesPulmonary oedema
Clinical featuresFatigue, dyspnoea,
anorexia, nauseaJugular venous
distensionHepatomegalyPitting oedemaAscitesPleural transudates
Findings
Right Heart Failure
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FBE/LFT/U&E/TFT/Cardiac troponinsCXR (to be discussed)ECG
Signs of ischaemia, MI, ventricular hypertrophy, LBBB
Echo (TTE/TOE)? Stress
BNPHighly indicative of CHF & poor prognosis factor
? Cardiac Biopsy? Cath Lab
Workup
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Diagnosing Heart Failure
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EducateObesity controlDietary modification
Low salt, minimise EToH +/- fluid restrictionSmokingSexual activityExercise
Light exercise is encouragedVaccination
General Lifestyle Advice
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Heart Failure Treatment Guidelines
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Overall Management Plan
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Presents typically as 1 of 2 radiographic patterns:Pulmonary interstitial oedemaPulmonary alveolar oedema
Which radiographic pattern appears depends on the pulmonary (venous) capillary wedge pressure (PCWP)
Radiological Findings in CHF
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4 key radiographic signs:Thickening of the interlobular septa
Kerley B linesNamed after Irish neurologist & radiologist, Peter
James KerleyPeribronchial cuffingFluid in the fissuresPleural effusions
Pulmonary Interstitial Oedema
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Spot diagnosis!
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Thickening of the interlobular septaNot visible on normal CXROnly visible when it accumulates excessive
fluid, PCWP about 15 mm HgVisible on frontal CXR, @ lung bases, @/ near
costophrenic anglesVery short (1-2cm), very thin (1mm) &
horizontal in orientationChronic Kerley B Lines
After repeated episodes of pulmonary interstitial oedema, fibrosis occurs
Kerley B Lines
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A, B, C!
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Yes, there are A & C lines unfortunatelyKerley A Lines
Appears when connective tissue around the bronchoarterial sheaths in the lungs distends with fluid
Extends from the hila (up to 6 cm) & don’t extend to the lung peripheries
Kerley C LinesIf you know what they are, you are wasting
time in this lecture? Overlap b/w A & B Lines? Myth
Kerley A Lines
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Doughnuts!
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Bronchi may only be visible when seen on-end in the region of the pulmonary hilaAnywhere else, it is pathological
Fluid collects in the interstitial tissue surrounding the wall of the bronchiBronchial wall becomes ‘thicker’ & appears as
doughnuts when seen on-endSame mechanics as air bronchograms
Peribronchial Cuffing
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Normal & Pathological
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The fissures may normally be visible however, are almost never thicker than a line drawn with a sharp pencil
Fluid may collect b/w the 2 layers of the visceral pleura or subpleural spaceAccumulated fluid distends the fissure(s)
Thicker, irregular & more visible
Fluids in the Fissures
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Spot the Difference
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Pleural effusions caused by CHF are usually bilateralWhen it is unilateral, almost always right-sided
Therefore when you see a left-sided pleural effusion, considerMets, TB, thromboembolic disease, etc
Laminar Pleural EffusionThin, band-like density along lat chest wall,
esp. near costophrenic angles (still sharp)Almost always due to left atrial pressure ↑↑↑
CHFLymphangitic spread of malignancy
Pleural Effusions
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Which one is it?
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Fluid spills out of the interstitium & into the airspaces when PCWP is sufficiently ↑↑↑ (25 mm Hg)
Almost known as Pulmonary OedemaRadiographic finding
Fluffy, indistinct patchy airspace densitiesOuter 1/3 usually sparedLower zones > Upper zonesButterfly/Bat-wing appearancePleural effusions usually present when the
oedema is cardiogenic in nature
Pulmonary Alveolar Oedema
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Cardiogenic VS Non-cardiogenic Pulmonary Oedema
Imaging Findings Cardiogenic Non-cardiogenic
Pleural Effusions Common Infrequent
Kerley B Lines Common Infrequent
Heart Size Usually enlarged May be normal
PCWP Elevated Normal
Different forms of Pulmonary Oedema
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Mr XY, 80 y/o pensionerHOPC sudden & extreme SOBWheezing & diaphoreticCoughing with pink frothy sputumCold peripheriesGallop rhythm
DifferentialsInvestigationsManagement
Emergency!!!
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a) Asthmab) COPDc) Pneumoniad) Pulmonary oedemae) All of the above
Differentials???
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CXRECGU&E, Cardiac Troponins, ABGBNPEcho
Investigation!!!
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Could this be Pneumonia?
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Sit upright & OxygenIV access & ECG monitoringMorphine (5-10mg) +/- metoclopramide (10mg)
Beware of morphine systolic BP < 90 mm HgIV diuretics (furosemide 40-80 mg slowly)GTN (spray 2 puffs/ 2 x 0.3 mg SL)
Don’t give if systolic BP < 90 mm HgConsider nitrate infusion if systolic BP > 100 mm Hg
Isosorbide dinitrate 2-10mg/h IVEvaluate situation
If worsening, consider more diuretics & venesectionGet HELP!!!
Management