Heart failure Flashcards
What is CHF?
CH 442: CONGESTIVE HEART FAILURE (CHF)
- Syndrome in which the heart is unable to pump blood
to the body to meet its needs, or to dispose of
pulmonary/venous return adequately
What are the causes of CHF?
Causes
- Usually secondary to volume/pressure overload
- Congenital heart disease
- MC cause of CHF in infancy
- Volume overload lesions (VSD, PDA, OCD): MC cause of
CHF in the 1st 6 MOL
- ASD rarely cause CHF in pedia
- Large L-R shunt lesions (VSD, PDA) do not cause CHF
before 6-8 weeks
o Due to inc PVR at this time - Acquired heart disease
- Dilated cardiomyopathy: MC cause of CHF beyond
infancy. Usually idiopathic
- Myocarditis sec. to Kawasaki disease in 1-4yo
- Viral myocarditis more common <1yo
- Acute rheumatic carditis
- Rheumatic valvular heart ds (MR, AR) usually in older
children - Miscellaneous
a. Metabolic (hypoxia, acidosis, hypogly,
hypoCa)
b. Hyperthyroidism
c. Severe anemia (Hgb <6)
d. Acute systemic HTN (PSGN)
What is the pathophysio?
Pathophysio
- Cardiac output is determined by: HR x SV
- SV is determined by 1.preload, 2.afterload 3.Contractility
- Preload – volume before systole
- Frank Starling Law: inc preload, the healthy heart inc
CO until a maximum is reached. At maximum point, CO cannot be further inc –> LV end diastolic pressure reaches a certain point, pulmonary congestion develops (tachypnea, dyspnea) - Afterload – volume after systole
- Dec SV, dec EF from inc afterload - Wall stress – Laplace law: wall P = P x ½ radius x wall thickness
- 2 most impt points:
o The bigger the LV and higher radius, higher
wall stress
o At any LV size: inc P = higher wall stress
- Thus, dilated ventricles require more O2 demand
Compensatory mechanisms
- Activation of SNS and RAAS
1. Inc epi/NE –> inc sympathetic tone –> inc HR, inc
contractility –> inc CO
- However, chronic bad because: inc afterload, inc
metabolism, inc arrhythmogenesis, inc myocardial
toxicity
- Dec B adrenergic receptors on myocardial cell
(maladaptive)
2. Oliguria –> inc renin –> inc angiotensin II –> constrict arterioles, inc reabsorption of salt and water -> inc myocardial fibrosis –> hypertrophic response in
attempt to restore wall (maladaptive)
- Thus, tx for CHF = beta blocker, ACEI to block maladaptive roles
Hallmark of CHF
Hallmark of CHF:
a. Tachypnea
b. Tachycardia
c. Cardiomegaly
Clinical manifestations of CHF
CM
1. Hallmark of CHF:
a. Tachypnea
b. Tachycardia
c. Cardiomegaly
d. Edema + organomegaly
- Infants – poor feeding, tachypnea during feeding, poor weight gain, cold sweat, puffy eyelid
- Older child – SOB, easy fatigability, bipedal edema
- Compensatory responses – tachycardia, gallop rhythm,
weak thready pulses, cardiomegaly, inc sym. Activity (growth failure, perspiration, cold sweat) - L-sided failure – pulmonary venous congestion: tachypnea (common and early), exertional dyspnea (poor feeding in infants), orthopnea, wheezing & pulmo crackles
- Pulsus alterans – beat-to-beat oscillation in strength of
cardiac muscle contraction at a constant HR (severe
CHF) due to LV dysfunction.
Dec EF –> dec SV –> inc
LVEDV - R-sided HF – systemic venous congestion: hepatomegaly, puffy eyelids (infant), distended neck
veins, dependent edema (sacral (infant), back) - Anginal sx – due to dec EF, dec CO to coronary sinus
Modified Ross classification of HF in children
Modified Ross classification of HF in children
I – asymptomatic
II – mild tachypnea with feeding diaphoresis
III – marked tachypnea, diaphoresis during feeding
IV – tachypnea, grunting, retractions, diaphoresis at rest
Diagnostics for CHF
Dx
1. ECG – ID cause of CHF, least helpful in CHF
2. CXR – cardiomegaly, pulmonary edema, congestion
3. 2D echo – most helpful non-invasive study that
confirms CHF and estimates severity of HF; useful in
determination of efficacy of Tx
- Ejection fraction NV = 55-70%
4. Cardiac catheterization – endomyocardial biopsy
5. CBC,BUN, Crea, ABG, e’s, BCS
Management of CHF
Mgt
Goals:
1. Elimination of underlying cause – most desirable approach
- Treatment of contributing causes
- Control of HF state
The required calorie intake of infants = 150-160 kcal/kg/d - Preload unloaders
a. Diuretics – principal tx to control pulmonary
and systemic venous congestion and salt and water retention
- Decrease preload (no effect on CO/myocardial contractility)
- SE: hypoK (except spironolactone), hypochloremic alkalosis (due to loss of Cl ions –> inc HCO3 levels),
hypotension
- Hydrochlorthiazide 2-4mkd BID/TID (non popular)
- Furosemide 1mkdose IV or 2-3mkdose po BID or TID:
DOC, most potent
- Spironolactone 1-3mkd po BID or TID: anti-aldosterone
and K sparing effect. Good to combine with
furosemide. - Inotropes
a. Rapidly acting inotropic agents – inotropic, vasodilating for acute situations
- For critically-ill infants with renal dysfunction, post op pxs with HF
- SE: HTN, arrhythmia, vasodilation, tachycardia
- Epinephrine 0.1-1 ug/kg/min IV (rare)(a>B1>B2)
- Dobutamine 2-8 ug/kg/min IV (B1>B2)
- Dopamine 5-10 ug/kg/min
o Dose related CV effects:
§ 2-5: renal vasodilation
(dopaminergic R)
§ 5-8: inotropic (B & dopa R)
§ >10: mild vasoconstriction (a
adrenergic R)
§ 15-20: vasoconstriction
o Onset of action: 1 min
b. Digitalis glycosides (digoxin) – inc CO; diuretic and PSY (slows HR, inhibits AV conduction) properties
- SE: shortening of QTc (earliest sign), slowing of HR
- CM: anorexia, nausea, vomiting, diarrhea, restlessness, drowsiness, fatigue, visual disturbance
- Half-life: 36-48h (N renal fxn); 3-5d (impaired renal fxn)
- Toxicity: PR interval prolongation à 2nd degree HB, profound sinus bradycardia, SVT and ventricular
arrhythmia, PVC
- Dosage: infants and children require larger dose
Age Total digitalizing
dose (ug/kg) Maintenance dose
(ug/kg/d)
PT 20 5
FT 30 8
<2yo 40-50 10-12
>2yo 30-40 8-10
How to digitalize?
How to digitalize?
o LD given over 12-18h followed by MD
§ Results to pharmacokinetic
steady state in 3-5d
o Baseline ECG and serum e’
§ ECG: rhythm and PR
§ E’s: hypoK, hyperCa predispose
to digitalis toxicity
o Calculate total digitalizing dose
o Give ½ TDD à ¼ à ¼ q6-8h intervals
o ECG again – start MD 12h from final part of
TDD
- Monitoring toxicity
Monitoring toxicity
o Best determined by ECG monitoring during
the 1st 3-5d after digitalization
§ Prolonged PR interval
§ Profound sinus bradycardia/ SA
block
§ SV arrhythmia – atrial/nodal
ectopic beat
§ Ventricular arrhythmia -isolated
PVC
o Serum digoxin levels: therapeutic range = 0.8-2 ng/ml
§ Blood should be collected >6h
from last dose
§ Drugs that inc levels: quinidines,
verapamil, amiodarone, B
blockers
§ Drugs that dec levels: rifampicin,
neomycin, cholestyramine
Digitalis toxicity
o Stop drug immediately then resume MD after 3-5d
o Correct hypoK/hyperCa
o Treat arrhythmia with anti-arrhythmic drug
Management
- Afterload reducing agents – facilitate ventricular emptying by dec wall tension and inc CO
- augments SV w/o damage in contractile state (no inc in O2 consumption)
- SE: dizziness, syncope, hypotension
a. Arteriolar vasodilator: Hydralazine 0.1-0.2 mkdose q4-6h IV (max 2 mg/kg q6h), 0.75-3
mkd BID-QID (max 200mg/d)
b. Mixed vasodilator: Captopril – vasodilator of choice due to AgII suppressing effect
§ NB: 0.1-0.4 mkdose OD-QID po
§ Infant: 0.5-6mkd OD-QID
§ Child: 12.5 mg/dose OD-BID
c. Mixed vasodilator: Nitroprusside 0.5-8
ug/kg/min IV
d. Mixed: Prazosin5 ug/kg (1st dose) –> 25 ug/k/d QID po
e. Venodilator: Nitroglycerin 0.5-1 ug/kg/min IV
- Other drugs
a. B blockers – prevent LV remodeling and myocardial fibrosis
- SE: dizziness, headache, hypotension
- Metoprolol 0.1-0.2 ug/kg/dose BID then slow inc to 1.1 mkd over weeks - Surgical mgt – consider if no improvement in sx after medical tx
- Cardiac transplant – progressively deteriorating cardiomyopathy despite maximal medical tx - Supportive mgt – semiFowler position, oxygen, hypoNa and hyperK supplementation, enhance physical and
metabolic requirements (inc pH, glu, Ca, Hgb), control HR, e’ and metabolic balance, peritoneal dialysis and mech vent
What is myocarditis?
CH 439: MYOCARDITIS
- Inflammation of the myocardium
- Cell-mediated immunologic reaction of myocardium:
soft, flappy, pale with areas of scarring
Etiology of myocarditis
Etiology
1. Infections – enterovirus (MC), Coxsackie A&B, adenovirus, parvovirus, EBV, CMV, HIV, HepC, Dengue, HSV, Infuenza, VZV, MMR, rabies, HepB
- Bacteria (rare): C.diphtheria toxin, MTb, Streptococcus, Mycoplasma, C.perfringens, Salmonella
- Fungal, protozoal, parasites
- Immunologic: ARF, Kawasaki, RA, SLE
- Drugs: sulfonamides, penicillin, phenytoin,
Carbamazepine - Toxins/chem: radiation, drugs, Ca, Hc, Hg, lead
Pathophysio of myocarditis
Pathophysio
- Pathogens/causative agent: infectious/ non-infectious
- Immune response –>
o Innate: activate cytolytic T cells, apoptosis,
dec T cell regulatory function, inc inflamm
mediators (cytokines, interferon)
o Acquired: further T cell and subsequent Bcell activation, Ab against endogenous
epitopes (cross-reaction)
- Myocardial inflammation: direct damage by causative agent, additional injury may be caused by immunologic mechanisms, inflammatory cell infiltrates, myocyte
necrosis and degeneration –>
- Resolution or persistence:
o Resolution: eradication of pathogen,
dampened immune response
o Persistence: viral persistence and/or
continuous immune activation; myocardial
fibrosis, cardiac remodeling
What are the clinical manifestations of myocarditis?
CM
1. Infant/young child: hx of preceding URTI/GIT infection,
fever, poor feeding, irritability, lethargy, vomiting,
pallor, diaphoresis (fulminant, severe s/sx)
2. Older child: recent Hx of flu-like illness, headache,
muscle pain, diarrhea, sore throat, rashes, chest
discomfort, exertional dyspnea, syncope/nearsyncope
3. CHF signs (RD, tachypnea, tachycardia, hepatomegaly)
soft systolic murmur (MR due to dilated MV annulus),
gallop rhythm (poor ventricular compliance),
arrhythmia (universal sx), cardiomegaly, poor
peripheral perfusion, hypotension
