Congestive heart failure Flashcards
What CHD lesions present with CHF at birth?
HLHS
Volume overload lesions
Severe tricuspid or pulmonary insufficiency
Large systemic arteriovenous fistula
What CHD lesions present in the first week?
TGA PDA in prem infants TAPV systemic AV fistulas Critical AS or PS
What CHD lesions present with CHF at 1-4 weeks?
COA with associated anomalies
Critical AS
large L -> R shunt lesions in prem
Causes of acquired heart disease leading to CHF, and when the present?
- Dilated CMP: Mostly idiopathic, any age
- Doxyrubicin CMP: months to years post chemo
- CMP with muscular dystrophy, Friedrich’s ataxia: Older children
- Kawasaki’s myocarditis: 1-4 yrs
- Cardiac surgery pts: May remain in or develop CHF
- Viral myocarditis: Small kids >1, in newborns it is fulminant
- Acute rheumatic carditis: School age children
- Rheumatic valvular heart diseases: Volume overload, older kids
What is cardiac output determined by?
- Heart rate
- Preload
- Afterload
- Contractility
How does afterload affect cardiac output?
Afterload is the force that resists myofibril shortening during systole, contributing to myocardial wall stress (tension).
Afterload determined by aortic pressure, systemic vascular resistance, arterial impedance, myocardial peak wall stress.
How is cardiac remodelling defined?
A genomic expression
resulting in molecular, cellular and interstitial changes
manifested clinically as changes in size, shape, and function
after cardiac injury
How is the hypertrophy seen in athletes different from failing hearts?
Both are aimed at reducing the wall stress (and O2 demand) according to Laplaces law.
An athletes hypertrophy is physiological
A failing heart is secondary to remodelling in response to neurohormonal compensatory mechanisms
What two major compensatory mechanisms are involved in heart failure?
- Increased sympathetic tone secondary to adrenergic release of adrenaline and neural release of noradrenaline
- Chronic stimulation leads to increased afterload, hypermetabolism, arrhythmogenesis, and myocardial toxicity - Renin-angiotensin-Aldosterone system.
- Reduced renal blood flow stimulates renin release, leading to angiotensin II formation, which causes reabsorption of salt and water, and can produce a trophic response in vascular smooth muscle.
What are the clinical signs of CHF
- Compensatory:
- Tachycardia, gallop rhythm,
- cardiomegaly,
- increased sympathetic discharge (growth failure, perspiration, cold wet skin.) - Pulmonary venous congestion (Left sided failure):
- tachypnoea
- dyspnoea on exertion (poor feeding)
- orthopnoea
- wheeze and crackles - Systemic venous congestion (RHF)
- Hepatomegaly common, but has wide differential
- Periorbital oedema
- Distended neck veins and ankle oedema (not seen in infants)
- Splenomegaly doesn’t occur, usually represents infection.
What general measures can be used in treating CHF?
- Cardiac chair or infant seat
- Humidified oxygen if respiratory distress and desaturating
- Ensure adequate calories
- Increasing caloric intake
- frequent feeds
- NG feeds overnight and calorie dense oral feeds (encourage normal development of oral-motor function)
- Salt restriction in infants replaced by using DIURETICs
- educate parents
- Salt restriction in older kids
- daily weights for hospitalized children.
What are the common classes of diuretics used in CHF?
- Thiazides (prox and distal tubules) not popular now
- Loop diuretics (Frusemide, ethacrynic acid) Popular
- Aldosterone antagonists (spironolactone): Distal tubule
- advantages over other diuretics; CHF is high aldosterone state, prevent hypokalemia (caution with ACEi)
Common side effects of diuretics?
electrolyte and pH dysfunction
- Hypokalaemia; all except spironolactone
- Hypochloraemic alkalosis: lose more Cl than Na
- Both increase risk of digitalis toxicity!
What are the similarities and differences of dopamine and dobutamine?
They are both inotropes and vasodilators
Both rapidly acting catecholamines with a short duration of action
Dobutamine has fewer chronotropic effects
Dopamine in high doses causes alpha-receptor stimulation with vasoconstriction and reduced renal blood flow
What are the properties of digoxin?
- Inotrope
- Parasympathomimetic
- slows heart, reduces sinoatrial firing, slows AV conduction - Reduces circulating norepinephrine, renin and aldosterone
- Diuretic effect
Increases inotropy without increasing myocardial oxygen consumption
