Heart Failure
Heart Failure
called Congestive Heart Failure if leads to pulmonary oedema, plural effusions, ascites or periorbital/sacral/pedal pitting oedema
CO = SVxHR
determinants of SV are preload, afterload and contractility
Tachyarrhythmias reduce filling time so compromise SV
Anaemia reduced the oxygen capacity of blood, reducing VO2 max that can be achieved for same max CO
CO proportional to filling volume and inversely proportional to resistance
High output failure is signs and symptoms of HF in normal heart failing to meet increased oxygen demands
Heart failure is the failure to meet the demand for CO
Frank Starling curve relates increasing end-diastolic pressure to cardiac output
As pressure increased, CO increased until it reaches max
In heart failure this curve is flattened
Failing heart required increased dilation to produce the same CO
In children dilation in less, HR is the main mechanism, less ability to compensate
?difference between cardiogenic shock and heart failure??
Native response
Adrenaline
> B adrenergic receptors > increase HR and contractility
> A adrenergic receptors > vasoconstriction Skin/Gut/Kidney more than Heart/Brain
Short term good
Chronic > increased systemic metabolic demands/cardiac metabolic demands, high afterload, arrhythmias, GIT/Kidney
Also down regulates B adrenergic receptors impeding future response
Hx
Poor feeding (sweating/dyspnoea/fatigues)
Poor wt gain
Fatigue
Exercise intolerance
Abdominal pain/nausea/Anorexia
Dyspnoea / orthopnoea
Cough
Ex
Systemic venous pressure (JVP/Hepatomegaly)
Crackles / resp distress
Clubbing
Dependant oedema periorb / sacral / peripheral / scrotal / anasarca
Gallop rhythm
Holosystolic murmur (MR/TR from vent dilation)
CXR
cardiomegaly
L>R shunt > increase pulm vascular markings
LHF > venous congestion, pulmonary oedema
ECG low voltage QRS and ST changes can be seen in myocarditis (but also pericarditis)
ECHO:
Etiology
Anaemia
Arrhythmia
Cardiomyopathy (Myocarditis, asphyxia, kawasakis, anomalous coronary artery, radiotherapy, Acute chest syndrome (SSA))
CongHD
Endocarditis
Fluid overload
Hypertension (HUS, GN, )
Cor pulmonale (RHF): bronchopulmonary dysplasia, CF..
AV Malformation (haemangioma...
Thyrotoxicosis
Hemochromatosis-hemosiderosis
Complications
Metabolic acidosis
Respiratory acidosis
Hyponatremia from renal water retention
Rx
Treat cause
Medical management
Sleep head elevated if symptoms require
CPAP for pulmonary oedema
Adrenergic agonists (NB B-blockers useful in chronic management but contraindicated in acute phase as antagonise agonists!)
Concentrate feeds to optimise caloric intake, NG if compromised
Implantable cardioverter-defibrillator (ICD) if high risk of arrhythmia
Experimental resynchronisation pacing to overcome bundle branch blocks (pumping together is more efficient
called Congestive Heart Failure if leads to pulmonary oedema, plural effusions, ascites or periorbital/sacral/pedal pitting oedema
CO = SVxHR
determinants of SV are preload, afterload and contractility
Tachyarrhythmias reduce filling time so compromise SV
Anaemia reduced the oxygen capacity of blood, reducing VO2 max that can be achieved for same max CO
CO proportional to filling volume and inversely proportional to resistance
High output failure is signs and symptoms of HF in normal heart failing to meet increased oxygen demands
Heart failure is the failure to meet the demand for CO
Frank Starling curve relates increasing end-diastolic pressure to cardiac output
As pressure increased, CO increased until it reaches max
In heart failure this curve is flattened
Failing heart required increased dilation to produce the same CO
In children dilation in less, HR is the main mechanism, less ability to compensate
?difference between cardiogenic shock and heart failure??
Native response
Adrenaline
> B adrenergic receptors > increase HR and contractility
> A adrenergic receptors > vasoconstriction Skin/Gut/Kidney more than Heart/Brain
Short term good
Chronic > increased systemic metabolic demands/cardiac metabolic demands, high afterload, arrhythmias, GIT/Kidney
Also down regulates B adrenergic receptors impeding future response
Hx
Poor feeding (sweating/dyspnoea/fatigues)
Poor wt gain
Fatigue
Exercise intolerance
Abdominal pain/nausea/Anorexia
Dyspnoea / orthopnoea
Cough
Ex
Systemic venous pressure (JVP/Hepatomegaly)
Crackles / resp distress
Clubbing
Dependant oedema periorb / sacral / peripheral / scrotal / anasarca
Gallop rhythm
Holosystolic murmur (MR/TR from vent dilation)
CXR
cardiomegaly
L>R shunt > increase pulm vascular markings
LHF > venous congestion, pulmonary oedema
ECG low voltage QRS and ST changes can be seen in myocarditis (but also pericarditis)
ECHO:
- fractional shortening (End-diastolic diameter - End-systolic diameter/End-diastolic diameter) Normal = 28-42%
- Estimation of volumes can be made from above 2D data to give Ejection Fraction (normal =55-65%)
- Doppler studies can also estimate CO
- MRA also useful
Etiology
Anaemia
Arrhythmia
Cardiomyopathy (Myocarditis, asphyxia, kawasakis, anomalous coronary artery, radiotherapy, Acute chest syndrome (SSA))
CongHD
Endocarditis
Fluid overload
Hypertension (HUS, GN, )
Cor pulmonale (RHF): bronchopulmonary dysplasia, CF..
AV Malformation (haemangioma...
Thyrotoxicosis
Hemochromatosis-hemosiderosis
Complications
Metabolic acidosis
Respiratory acidosis
Hyponatremia from renal water retention
Rx
Treat cause
Medical management
- To optimise for surgery
- To delay transplant
Sleep head elevated if symptoms require
CPAP for pulmonary oedema
Adrenergic agonists (NB B-blockers useful in chronic management but contraindicated in acute phase as antagonise agonists!)
- dopamine (B-adrenergic agonist at low doses, A as well at high doses) i.e. inotrope without significant vasoconstriction
- dobutamine (B-adrenergic agonist) inotrope with some vasodilation
- epinephrine (mixed adrenergic) i.e. good for warm (vasodilated) shock
- milrinone (inotrope, vasodilatory)
- nitroprusside
- ACE inhibitors
- ARBs
- Frusemide (beware K loss, supplement K unless concomitant spironolactone
- Chlorothiazide
Concentrate feeds to optimise caloric intake, NG if compromised
Implantable cardioverter-defibrillator (ICD) if high risk of arrhythmia
Experimental resynchronisation pacing to overcome bundle branch blocks (pumping together is more efficient