Cardiac Flashcards
PVR
Mean PA P- LA P/ pulmonary blood flow(Qp) 1-2= normal 2-4= mile elevation 4-6= moderate >7.9 severe
Cardiac output
Qs= VO2 (oxygen consumption) / A02 - MV02 AO2 = (AoSaO2 x Hb X1.36) + dissolved o2
Qp/Qs
AoO2-MV02/ Pulm V O2 - pulm A o2
Causes Heart failure from CHD by ages
Foetal:
o severe anaemia (haemolysis, parvovirus, foetal-maternal transfusion)
o arrhythmia: SVT, VT, CHB
Birth:
o severe LVOTO – HLHS severe coarctation (interrupted aortic arch) severe AS
o severe birth asphyxia (hypoxia/ acidosis)
o volume overload – severe TR/PR large systemic AV fistula
1st week in premature infant:
o PDA o fluid overload
o cor pulmonale
1st week in term infant:
o TGA
o TAPVD
o any of above if less critical ie systemic AV fistula,
~ 4 weeks:
o critical AS
o large L-R shunts in premature infants (present earlier as quicker fall in PVR) 4-6 weeks:
o some shunt lesions ie. complete AVSD
6 weeks – 4 months:
o large VSD/ ASD
o ALCAPA
CHF treatment
General measures:
o often feel better sleeping semi-upright
o diet - adequate calories important, if find it difficult to feed b/c of SOB, may need NG feeding
o digoxin - eliminated by kidney ; increases CO
crosses placenta (can be given to mother for foetal tachycardia)
↓K, ↓Mg, ↑Ca, myocarditis and prematurity will exacerbate digoxin toxicity
levels - usually pre dose (minimum of 4 hours after last dose)
o diuretics (reduce preload), improve congestive symptoms but no effect on CO:
frusemide - inhibits Na/Cl reabsorption in distal tubules and loop of Henle SE Hypokalemia, Hypochloraemic alkalosis
spironolactone - (aldosterone inhibitor)
o dilators (reduce aferload and improve SV):
ACE I
Tet spells
Physiology Any event that ↓ SVR suddenly (i.e. crying, defecation, tachycardia, hypovolemia or activity) produces a large right to left shunt that may initiate a hypoxic spell as pulmonary blood flow reduces The resulting drop in Pa02 and PaCO2 and reduced pH stimulate respiratory centres causing hyperpnoea This increases venous return to the RV which causes further 02 desaturation, and repeats the cycle You see worsening cyanosis and disappearance of the pulmonary stenosis murmur The baseline arterial sats (75-80%) are the best indicator of whether cyanotic episodes while crying are actually Tet spells May be worse in children with mild cyanosis (aren’t used to hypoxemia) Clinically During the first two years of life Hypoxia/ acidosis results in cyanosis/breathlessness/pallor Reduced intensity of pulmonary stenosis murmur (reduced flow through valve, pulmonary stenosis murmur is a crescendo then decrescendo murmur with severity) Mostly self-limited (lasts <30 mins), but can lead to syncope/seizure/stroke or death More frequent in mornings on first waking, or following vigorous crying Followed by weakness or sleep Treatment ABC + oxygen (acts as a pulmonary vasodilator and a systemic vasoconstrictor, though maybe limited effect as primary problem is reduced pulmonary blood flow) - high flow via mask Posture – knee-chest (on abdomen), or squatting posture Increase the SVR by kinking popliteal/femoral arteries (increasing the afterload) Increase the venous return by increasing abdo pressure (increase preload) If getting better - let settle, IVF (reduced glucose due to increased consumption) Squatting in older children- Increases systemic venous return and systemic arterial resistance Increases LV size and pressure Reduces right to left shunting and increases pulmonary blood flow If not getting better – IV fluids, morphine (to suppress the respiratory centre and abolish hyperpnoea), aramine (increase CO/increase SVR to increase the blood pressure IV beta blocker (propranolol) Relaxation of the RVOT with improved pulmonary blood flow; Reduces the frequency/severity of spells (but usually surgical referral is required
Pulmonary slings
Supracristal VSD associated with
Aortic Regurg
Supracristal = 5% of all patients with VSD; incidence is highest in Asian children.
The VSD, which may be small or moderate in size, is located anterior to and directly below the pulmonary valve in the outlet septum, superior to the crista supraventricularis.
A supracristal VSD is complicated by prolapse of the aortic valve into the defect and aortic insufficiency, which may eventually occur in 50-90% of patients.
The clinical manifestations vary widely from trivial aortic regurgitation and small left-to-right shunts in asymptomatic children to florid aortic incompetence and massive cardiomegaly in symptomatic adolescents.
Mecanism of action of NO
Inhaled nitric oxide is a selective pulmonary vasodilator. It works through guanylyl cyclase activation - leading to the production of cyclic guanosine monophosphate and subsequent smooth muscle relaxation.
Nitric oxide is endothelial derived relaxing factor. It is produced in the endothelium of blood vessels and diffuses out of the cells. It then enters vascular smooth muscle cells and activates guanalate cyclase which forms cyclic guanosine monophosphate (cGMP)(a smooth muscle relaxant).
Nitric oxide is bound to haemoglobin and inactivated instantly in the blood to nitosylhaemoglobins and methaemoglobin. The half life of NO is 3-6 seconds.
Difference between BT shunt and Sano shunt
BT shunt consists of anastamosis between subclavian artery and ipsilateral pulmonary artery
Sano shunt is a conduit from RV to pulmonary artery
Fontan procedure and complications
3rd stage of procedure for HLHS, consists of rerouting systemic blood flow from IVC to pulmonary arteries via intracradiac baffle or extracardiac conduit, performed 2-4years.
Complications:
- Heart failure
- Right sided pleural effusion
- SVT (15-20%)
- Arrythmias, may need atrial pacing due to loss SA node
- Intra-atrial re-entry tachycardia
- Protein losing enteropathy (2-10%)
Drugs used to treat pulmonary hypertension
Pulmonary hypertension - mean pulm pressure >25mmHg
Can cause RV failure (SOBOE, fatigue, cyanosis)
Loud S2, RV heave , systolic murmur TR, hepatomegaly, peripheral oedema
Rx
- Sildenafil (PDE5 inhibitor)
- Bosantan (Endothelin receptor antagonist)
- NO (upregulates cGMP, causes vasodilation)
- Iloprost (PGI2) - prostacyclin derivative, causes vasodilation and inhibits platelet aggregation
Acute pulmonary hypertensive crisis:
- O2, avoid high PCO2, treat acidosis, fluid resusc
- iNO, inotropes, sedation
- ECMO
Kawasaki disease diagnosis and treatment
Kawasaki Disease is a multisystem illness with fever and rash, which occurs mainly in children less than 5 years old. Within 3 days of the abrupt onset of fever, the other characteristic features usually appear:
- Bulbar conjunctivitis (no exudate)
- Mucositis: red cracked lips, red mouth and throat, strawberry tongue
- Polymorphous generalized rash that can be morbilliform, maculopapular, scarlatiniform or may resemble erythema multiforme
- Induration of the hands and feet with red palms and soles
- Cervical lymphadenopathy (usually a solitary, unilateral node > 1.5 cm in size)
- BCG site reactivation (erythema around BCG scar, usually on left upper arm)
Other Findings
- Extreme irritability, severe abdominal pain, diarrhoea and vomiting are common. Other features may include:
- Urethritis with sterile pyuria (70% of cases)
- Hepatic dysfunction (40% of cases)
- Arthritis or arthralgias (35%)
- Aseptic meningitis (25%)
- Pericardial effusion or arrhythmias (20%)
- Gallbladder hydrops (<10%)
- Carditis with congestive heart failure (< 5%). This can occur at any time in the first 3 weeks, and usually resolves by 6 to 8 weeks.
- Other arterial aneurysms (e.g. iliac, femoral, renal, axillary) may occur
Diagnosis is fever >5 days and >4 clinical features
Fever lasts 1-3 weeks, resolves within 36hrs completion IVIG
Rx
IVIG within 10 days of fever ideally (decreases risk CA aneurysms from 24% at 4 weeks to 4%), usually single dose (2g/kg) ; may need 2nd dose if fever persists>48-72hrs
Aspirin high dose initially, then low dose(can stop if no CA aneurysms at 6 weeks)
Rheumatic fever diagnostic criteria
2 major or 1 major and 2 minor and evidence of preceding GAS infection
Major criteria
- Carditis (on Echo) (MR>AR>pancarditis)
- Polyarthritis or aseptic monoarthritis (large joints)
- Chorea (15%)
- Erythema Marginatum (5%)
- Subcutaneous nodules (<5%)
Minor criteria
- Fever
- Raised ESR/CRP
- Polyarthralgia
- Prolonged PR interval
Carey coombs murmur
Carey Coombs murmur is short mid-diastolic murmur caused by active rheumatic carditis with mitral-valve inflammation.
