Analgesia and sedation

Cite this article as:
Marc Anders. Analgesia and sedation, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3867

Intravenous anaesthetic agents (see table):

  • classified as barbiturates (thiopentone) and non-barbiturates (propofol and ketamine)
  • thiopentone use is largely limited to induction in status epilepticus and for treatment of raised ICP; it has no analgesic properties and is in fact anti-analgesic at sedative doses
  • propofol is suitable for induction (bolus) and maintenance of sedation/anaesthesia (infusion); it is suitable for discrete painful procedures but has only minimal analgesic properties at sedative doses and so must be combined with a suitable analgesic
  • propofol is a direct myocardial depressant and so should be used in caution in patients in (or at risk of) low cardiac-output syndrome (LCOS). It obtunds the normal baroreceptor reflex and so causes a decrease in blood pressure and heart rate
  • ketamine is a dissociative anaesthetic that is also a potent analgesic; it is suitable for discrete painful procedures but increases respiratory secretions and is complicated by psychadelic phenomena (midazolam is suitable to treat or obviate ketamine’s emergence phenomena but will prolong recovery time)
  • combined ketamine and propofol in a ratio ranging from 1:1 to 1:4 (ketofol) is becoming a popular awake-sedative to facilitate medical procedures

Narcotics (see table):

  • morphine, fentanyl and methadone are effective analgesics and sedatives; oxycodone is also a popular analgesic but is less sedating
  • levels of sedation, analgesia and respiratory depression do not correlate (patients may be well sedated and have respiratory depression but not have adequate analgesia)
  • morphine is not a suitable narcotic for discrete painful procedures due to its long and unpredictable effect site equilibration time (fentanyl is more appropriate)
  • fentanyl is often used epidurally and results in significant systemic absorption of drug and resulting side effects
  • sufentanil, alfentanil and remifentanil are phenylpiperidine narcotics used to provide the analgesic component of general anaesthesia. They are very infrequently used in PICU
  • all have predictable effects which include respiratory depression, cough suppression, sedation, meiosis, biliary spasm, constipation, nausea and vomiting, urinary retention and cutaneous flushing (especially about the face)

Benzodiazepines (see table):

  • midazolam and diazepam are effective sedative agents commonly used in PICU
  • they are direct myocardial depressants via blockade of voltage-gated calcium channels (use carefully in patients with LCOS)
  • midazolam is also used to acutely treat seizures in bolus doses and in infusions (up to 1 mg/kg/hour)
  • they are less likely to produce withdrawal syndromes than barbiturates and narcotics (but no analgesic effect)

Alpha2 agonists (see table):

  • clonidine and dexmedetomidine are sedative/anaesthetic agents employed as sedatives in PICU; they also treat symptoms of drug withdrawal
  • their main advantage is lack of respiratory depression which allows quicker weaning of mechanical ventilation
  • they obtund central (brain and spinal cord) sympathetic outflow resulting in negative inotropy and chronotropy and so should not be combined with direct myocardial depressants (benzodiazepines, propofol etc.) in patients at risk of (or in established) LCOS.
  • they cannot be bloused as this can lead to transient alpha1-agonism and severe hypertension

Local anaesthetics:

  • local anaesthetics block voltage gated sodium channels and so prevent conduction along central and peripheral nerve pathways
  • lignocaine is commonly locally infiltrated for short painful procedures (e.g. suturing, insertion of chest drains etc)
  • bupivacaine and ropivacaine are generally used for regional blocks and neuraxial infusions
  • levobupivacaine (S-bupivacaine) and ropivacaine are enantiopure preparations. Cardiotoxicity is less
  • 0.5% solutions contain 5 mg/mL; 1% solutions contain 10 mg/mL; 2% solutions contain 20 mg/mL etc. (1% = 10 mg/ml)
  • onset of effect is related to the pKa of the drug; potency is related to lipid solubility; and duration of action is related to protein binding
  • systemic absorption of local anaesthetics depends on site of infiltration: intercostal > subarachnoid > epidural > brachial plexus > femoral > subcutaneous
  • vasoconstrictors (adrenaline) slow systemic absorption and increase the maximum safe dose
  • EMLA is a mixture of 2.5% lignocaine and 2.5% prilocaine used for topical anaesthesia prior to cannulation/incision; prilocaine can inducemMethaemoglobinaemia and application to mucous membranes will result in rapid systemic absorption of drug
  • CNS toxicity manifests first as excitatory phenomena (circumoral tingling, tinnitus, dizziness and tremors/seizures) followed by CNS depression (unconsciousness, apnoea and coma)
  • CVS toxicity manifests as systemic hypotension, myocardial depression, ventricular arrhythmias and cardiovascular collapse
  • treatment of local anaesthetic toxicity is by supportive therapy (airway management, treatment of seizures with benzodiazepines, fluids +/- inotropes/vascoconstrictors) and administration of 20% lipid emulsion (Intralipid) if in cardiac arrest: 1.5 mL/kg over 1 minute followed by an infusion of 0.25-0.5 ml/kg/min; repeat bolus doses every 5 minutes during CPR

Non-steroidal anti-inflammatory drugs (NSAIDs):

  • classified as specific (COX-2 e.g. parecoxib) or non-specific (COX-1 and COX-2 e.g. ibuprofen)
  • adverse GI effects are due to decreased mucosal blood flow and decreased secretion of mucus and bicarbonate
  • platelet thromboxane A2 is produced from prostaglandins and so NSAIDs impair platelet aggregation
  • prostaglandins are vasodilators involved in physiologic control of vasomotor tone (especially in the kidneys) and their inhibition leads to unopposed vasoconstriction
  • inhibition of prostaglandin synthesis leads to shunting of arachnidonic acid to lypoxygenase which is a bronchoconstrictor
  • specific COX-2 inhibitors are considered to lack effects on platelets and the GIT but will still affect vasomotor tone
  • their use in PICU needs careful consideration due to their wide range of potential side effects
  • paracetamol is generally considered a (central) COX-3 inhibitor; it also acts peripherally by inhibiting bradykinin-chemoreceptor associated pain impulse generation

Other (see table):

  • chloral hydrate is a prodrug that produces the halogenated alcohol chloroethanol; its mechanism is poorly understood but probably acts in a similar way to the volatile halogenated gases via central GABA-A receptors
  • first-generation antihistamines (e.g. promethazine, cyclizine etc.) are also effective sedatives by virtue of their anticholinergic properties; they are generally only used when specific antihistaminergic and/or anticholinergic properties are desired (e.g. antisialogogue for secretions, antitussive)Table: intravenous anesthetic agents
    Thiopentone Propofol Ketamine
    Type/class Barbiturate Isopropylphenol Phencyclidine
    Mechanism GABAA & glycine agonist GABAA & glycine direct agonist and central nicotinic antagonist(Possible 5HT3 blockade) NMDA non-competitive antagonist & blocks central catecholamine reuptake
    Oral bioavailability 25%
    Oral dose n/a n/a 5mg/kg
    IV Bolus 2-7mg/kg 1.5-2.5mg/kg 0.25-0.5mg/kg (analgesia)1-5mg/kg (GA)
    IV Infusion 1-5mg/kg/hour 1-4mg/kg/hour (sedation)5-15mg/kg/hour (GA) 10-40mcg/kg/hour
    Onset time IV < 30seconds < 30seconds 30-60seconds
    ESET 30 seconds < 30 seconds 60seconds
    pKa 7.6 11 7.5
    UNionised fraction 60% > 99% 45%
    Protein binding 80% 99% 25%
    Vd 2.5L/kg 4L/kg 3L/kg
    Clearance 3mL/min/kg 50mL/min/kg 15mL/min/kg
    t ½-dist 8minutes 4 minutes 12minutes
    t ½-elim 12hours 30-60minutes 2-3hours
    Metabolism Hepatic (may become zero-order with prolonged infusion)Some active metabolites Hepatic (CYP2C9 & 2B6) & extrahepatic (site/s unknown)Inactive metabolites HepaticActive metabolites
    Excretion Urine Urine Urine
    Hepatic failure No effect No effect Decreased clearance
    Renal failure Active metabolites will accumulate No effect No effect
    Pros Rapid onsetAnticonvulsantCan produce isoelectric EEG (maximal decreased cerebral metabolic O2 demand)

    Rapid onset & titratabilityBronchodilatorWill obtund airway reflexesAnticonvulsant

    Antiemetic & antipruritic properties at low doses

    Can produce isoelectric EEG

    Mild analgesic properties

    Stable CSHT (<40mins even after >8 hrs infusion)

    Intense analgesia at low doseFavourable haemodynamic profile due to increased central sympathetic outflowBronchodilatorPrevents & treats opioid tolerance

    No respiratory depression/apnoea

    Cons

    Resp depression/apnoeaAntanalgesicCan produce paradoxical excitementWill accumulate with prolonged infusion (long CSHT)

    Tolerance & withdrawal are a problem

    Resp depression/apnoeaMyocardial depressantCan cause a refractory bradycardia (need β-agonist)Rarely causes propofol-infusion syndrome

    Formulation contains soybean oil & egg lecithin

    Myocardial depressantEmergence delirium (especially in older patients – consider midazolam)Increased secretions (consider glycopyrrolate)BrainZ/BIS inaccurate
    Other points ↓BP (↓SVR)↑HR (reflex)Won’t obtund airway reflexesRacaemic formulation ↓BP(↓SVR & ↓CO)↓HR (obtunded baroreceptor reflex) EEG dissociation between thalamus & cortexWon’t obtund airway reflexesTypical induction agent in asthma & sepsis

    Table: benzodiazepines

    Midazolam Diazepam Flumazenil
    Type/class BDZ BDZ BDZ
    Mechanism GABAA receptor indirect-agonist GABAA receptor indirect-agonist BDZ receptor competitive antagonist
    Oral bioavail 40% 95% 25%
    Oral dose 0.5mg/kg up to 20mg 0.05-0.2mg/kg n/a
    IV Bolus 0.05-0.2mg/kgup to 5mg/dose 0.05-0.4mg/kgup to 10mg/dose 8-15mcg/kgup to 200mcg/dose
    IV Infusion 10-100mcg/kg/hour n/a 2-10mcg/kg/hour
    Onset time IV 1-2mins 1-2mins 1-2mins
    ESET 5mins 5mins 5-10mins
    pKa 6.2 3.3 1.8
    % UNionised 90% >99% >99%
    Protein binding 95% 95% 50%
    Vd 1.5L/kg 1.5L/kg 0.5L/kg
    Clearance 10mL/min/kg 1mL/min/kg 20mL/min/kg
    t ½-dist 5mins 5mins 5mins
    t ½-elim 1-4 hours 24-36 hours 60mins
    Metabolism Hepatic (CYP3A4)Active metabolites Hepatic (CYP3A4/5)Active metabolites HepaticNo active metabolites
    Excretion Urine Urine 90% urine
    10% bile
    Hepatic failure Decreased clearance Decreased clearance Decreased clearance
    Renal failure Active metabolite may accumulate Active metabolites will accumulate No effect
    Pros Sedation, amnesia & anxiolysisAnticonvulsantDecreases cerebral metabolic O2 demand Effective orallySedation, amnesia & anxiolysisAnticonvulsantDecreases cerebral metabolic O2 demand Allows specific reversal of BDZ component of resp depression and / or polypharmacy overdoseRarely causes acute anxiety &/or agitation
    Cons Myocardial depressantResp depressionCan cause paradoxical excitement Myocardial depressantResp depressionCan cause paradoxical excitementPainful on injection Can precipitate seizures in epileptics on maintenance BDZs
    Other points ↓BP(↓SVR & ↓CO)[↑HR (reflex)] ↓BP(↓SVR & ↓CO)[HR (reflex)] Is probably a partial agonist

    Table: narcotics

    Morphine Fentanyl Methadone Naloxone
    Type/class Phenanthrene opiate Phenylpiperidine opioid Diphenyl-propylamine opioid Phenanthrene opioid
    Mechanism Non-specific OR agonist MOR agonist with some mild activity at KORs MOR agonist (L-isomer) & NMDA antagonist (D-isomer) Non-specific OR competitive antagonist
    Oral Bioavail. 30% n/a 75% <1%
    Oral dose 0.2-0.5mg/kg q4-6h n/a 0.1-0.2mg/kg q6-24h n/a
    IV bolus dose 0.05-0.2mg/kg 1-10mcg/kg 0.1mg/kg 10mcg/kg
    IV infusion 5-100 mcg/kg/hr 1-10 mcg/kg/hr n/a 10 mcg/kg/hr
    Onset time IV 15-30mins 1-2mins 10-20mins 1-2mins
    ESET 30-90mins 3-6mins 10-20mins 5-10mins
    pKa 8.0 8.4 9.2 7.9
    % UNionised 25% 10% 1% 30%
    Protein binding 35% 85% 90% 50%
    Vd 3L/kg 4L/kg 3.5L/kg 0.2L/kg
    Clearance 25
    mL/min/kg
    10-20 mL/min/kg 1-3 mL/min/kg 30 mL/min/kg
    t ½-dist 2-3mins 1-2mins 1-2 mins
    t ½-elim 2-4hours 2-4hours 18-36 hours 45-60mins
    Metabolism Hepatic & renal10% to active M6G Hepatic (CYP3A4)No active metabolites Hepatic (CYP3A4)No active metabolites HepaticNo active metabolite
    Excretion 90% urine
    10% bile
    90% bile
    10% urine
    50% urine
    50% bile
    Urine
    Hepatic failure May precipitate encephalopathy No effect reduced clearance reduced clearance
    Renal failure Morphine & M6G will accumulate No effect No effect No effect
    Pros No myocardial depressionSedation & euphoriaAntitussive No myocardial depressionSedation & euphoriaAntitussiveNo histamine release Effective enterallyHelpful in withdrawal syndromesSuitable for chronic pain (NMDA actions) Acts rapidly & is titratableAntiinflammatory properties
    Cons

    Respiratory depressionHistamine releaseNausea & vomitingPruritis

    Urinary retention

    Constipation

    Respiratory depressionNausea & vomitingPruritisUrinary retention

    Constipation

    Prolonged CSHT

    Respiratory depressionNausea & vomitingConstipationHistamine release possible but rare

    Prolongs QT interval

    Can precipitate acute withdrawalRarely may cause pulmonary oedema & arrhythmiaUsually needs repeat dosing
    Other points Meiosis↓ HR & BP (↓SVR) Meiosis↓ HR & BP (↓SVR) Meiosis↓ HR & BP (↓SVR) 1mcg/kg effective for narcotic pruritisBP may rise or fall

    Table: alpha2 agonists

    Clonidine Dexmedetomidine
    Type/class Synthetic imidazoline Synthetic imidazoline
    Mechanism α2 adrenoceptor partial agonist α2 adrenoceptor agonist
    Oral bioavail >99% 15%
    Oral dose 1-5mcg/kg up to 300mcg n/a
    IV bolus dose 1-5mcg/kg 1-2mcg/kg
    IV infusion dose 0.5-2mcg/kg/hour 0.2-0.7mcg/kg/hour (sedation)5-10mcg/kg/hour (GA)
    Onset time IV 10-30minutes 10minutes
    ESET 20-30minutes 10-20minutes
    pKa 8.0 7.1
    UNionised % 20% 50%
    Protein binding 20% 95%
    Vd 2L/kg 1.5L/kg
    Clearance 5mL/min/kg 10mL/min/kg
    t ½-dist 30minutes 10 minutes
    t ½-elim 12-18hours 2-3hours
    Metabolism 50% hepatic50% excreted unchanged HepaticNo active metabolites
    Excretion Urine (50% unchanged) Urine
    Hepatic failure No effect Decreased clearance
    Renal failure Active drug will accumulate No effect
    Pros

    Effective sedativeNo respiratory depressionSpinal-mediated analgesia (very effective neuraxially)Known to be useful in opioid & alcohol withdrawal syndromes

    Raises the shivering threshold

    Prolongs regional block by local anaesthetics

    Effective sedativeNo respiratory depressionSpinal-mediated analgesiaUseful for symptoms of opioid withdrawal

    Raises shivering threshold

    Prolongs regional block by local anaesthetics

    Short(er) half time

    Cons

    Rapid IV administration will agonise α1 receptors (↑BP)Negative inotropy & chronotropyDry mouthRebound hypertension can occur (worse if patient is on a TCA or β-blocker)

    Long half time

    Rapid IV administration will agonise α1 receptors (↑BP)Negative inotropy & chronotropyDry mouthCannot be used neuraxially due to glycine in preparation
    Other points ↓HR & ↓BP↓CODry mouth may be used therapeutically if secretions are an issue ↓HR & ↓BP↓CODry mouth may be used therapeutically if secretions are an issue

    Table: others

    Chloral hydrate Promethazine
    Type/class Halogenated alcohol Phenothiazine
    Mechanism Prodrug – below data is for trichloroethanol (active drug)Probably a GABAA agonist H1 receptor antagonist & anticholinergic (antimuscurinic)
    Oral bioavail >99% 25%
    Oral dose 10-100mg/kg 0.25-1.5mg/kg
    IV bolus dose n/a 0.25-1.5mg/kg
    IV infusion dose n/a n/a
    Onset time IV 15minutes (oral) 30-60minutes
    ESET 30-60minutes (oral) 1-3hours
    pKa 12.7 9.1
    UNionised % >99% <1%
    Protein binding 50% 80%
    Vd 1L/kg 7L/kg
    Clearance not known 15mL/min/kg
    t ½-dist n/a 1-2hours
    t ½-elim 4-8hours 12hours
    Metabolism HepaticMetabolites of trichloro-ethanol are inactive Hepatic (CYP2D6)Inactive metabolites
    Excretion Urine Urine
    Hepatic failure Decreased clearance Decreased clearance
    Renal failure No effect No effect
    Pros

    Effective sedative & anxiolyticRapid onset following enteral administrationMild anticonvulsantRelatively wide therapeutic index

    Minimal interference with REM-sleep

    Effective antihistamine & antiemetic at low dosesEffective sedative/hypnotic at high dosesAntitussiveEffective in motion sickness

    Useful in allergic pruritis but not opioid induced pruritis

    Respiratory depression is rare

    Cons

    Respiratory depression in high dosesIrritant to GI mucosaArrhythmias in high dosesTrigger for porphyria

    Patients can develop tolerance & withdrawal

    Anticholinergic effects (dry mouth, blurred vision, urinary retention etc)Central anticholinergic syndrome in overdoseProlonged QT-interval & AV-blockParadoxical excitement may occur
    Other points ↓BP (↓SVR)↑HR (reflex)Actual half time of chloral hydrate is minutes (metabolised by esterases) [↑HR & ↑BP]Antidopaminergic propertiesLocal anaesthetic properties

    All Marc’s PICU cardiology FOAM can be found on PICU Doctor and can be downloaded as a handy app for free on iPhone or AndroidA list of contributors can be seen here.

Myocarditis

Cite this article as:
Marc Anders. Myocarditis, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3794

See cardiomyopathy , but cardiac MRI or endomyocardial biopsy to confirm diagnosis


Symptoms: 

Very nonspecific in children: malaise, fever, poor appetite, tachypnea, tachycardia, chest pain, abdominal pain, myalgia, fatigue, cough, oedema, hepatomegaly, murmur.


Investigations:

  • See also cardiomyopathy
  • Nonspecific T changes on ECG
  • Cardiac enzymes are not elevated in most patients with myocarditis
  • Echo is mandatory to assess function (systolic and diastolic dysfunction)

Treatment:

1. Symptomatic: see cardiomyopathy

2. IVIG: early, high dose IVIG: 2 g/kg over 24 hrs

3. In chronic DCM: consider interferon with persistent viral genomes


Common differential diagnosis of CM in regards to age:

< 1 year: myocarditis, endocardial fibroelastosis, Barth syndrome, carnitine deficiency, selenium deficiency, anomalous left coronary artery, Kawasaki disease, critical aortic stenosis, supraventricular tachycardia, arterio-venous malformation, calcium deficiency, hypoglycemia, left ventricular non-compaction, mitochondrial cardiomyopathy, nemaline myopathy, minicore-multicore myopathy, myotubular myopathy

> 1 year and < 10 years: familial DCM, Barth syndrome, myocarditis, arrhythmogenic RV dysplasia, endocardial fibroelastosis, carnitine deficiency, selenium deficiency, anomalous left coronary artery, Kawasaki disease, supraventricular tachycardia, toxic (adriamycin), ketothiolase deficiency, ipecac toxicity, systemic lupus erythematosis, polyarteritis nodosa, haemolytic-uraemic syndrome, mitochondrial cardiomyopathy, nemaline myopathy, minicore-multicore myopathy, myotubular myopathy

> 10 years: familial DCM, X-linked DCM, myocarditis, supraventricular tachycardia, congenital heart disease, mitochondrial CM, Chagas disease, arrhythmogenic RV dysplasia, eosinophilic cardiomyopathy, toxic (adriamycin), phaeochromocytoma, Duchenne/Becker muscular dystrophy, Emery-Dreifuss muscular dystrophy, haemochromatosis, limb-girdle muscular dystrophy, myotonic dystrophy, peripartum cardiomyopathy, alcoholic cardiomyopathy


References:

[1] Academic Emergency Medicine, 2008, 15, 355 – 362: Tallmann et all: Noninvasive ventilation outcomes in 2430 acute decompensated heart failure patients: an ADHERE registry analysis

[2] European Journal of Pediatrics, 2010, 169, 269 – 279: Kantor et all: Clinical Practice: Heart Failure in Children. Part I. clinical evaluation, diagnostic testing and initial management

[3] American Journal of Medicine, 2006, 119, S37 – S44: Hill et all: Beyond diuretics: management of volume overload in acute heart failure syndromes

[4] New England Journal of Medicine, 1999, 341, 709 – 717: Pitt et all: The Effect of Spironolactone on Morbidity and Mortality in Patients with Severe Heart Failure

[5] Circulation. 2003;107: 996 – 1002: Hoffmann et all: Efficacy and Safety of Milrinone in Preventing Low Cardiac Output Syndrome in Infants and Children After Corrective Surgery for Congenital Heart Disease

[6] Journal of Intensive Care Medicine, 2006, 21, 183 – 187: Egan et all: Levosimendan for Low Cardiac Output: A Pediatric Experience

[7] Current Cardiology Reviews, 2009, 5, 40 – 44: S. Batra et all: Cardiac Resynchronization Therapy in Children

[8] The Journal of Pediatrics, 2001, 138(4), 457-458: Bruns et all: Carvedilol as therapy in pediatric heart failure: An initial multicenter experience

[9] New England Journal of Medicine, 2006, 355, 1873 – 1884: Birks et all: Left ventricular assist device and drug therapy for the therapy of heart failure

[10] Circulation, 2004, 109, 1250 – 1258: Mahrholdt: Cardiovascular MRI assessment of human myocarditis: a comparison to histology and molecular pathology

[11] Circulation, 1994, 89, 252-257: Drucker et all: Gamma-globulin treatment of acute myocarditis in the pediatric population

[12] Circulation, 2003, 107, 2793 – 2798: Kuhl et all: Interferon-beta treatment eliminates cardiotropic viruses and improves left ventricular function in patient with myocardial persistence of viral genomes and left ventricular dysfunction.


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Heart failure and ventricular assist device (VAD)

Cite this article as:
Marc Anders. Heart failure and ventricular assist device (VAD), Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3790

Modified Ross heart failure classification:

Class Symptoms
I Asymptomatic
II Mild tachypneoa or diaphoresis with feeding. Dyspnea on exertion in older children
III Marked tachypnea or diaphoresis with feeding; marked dyspnea on exertion; prolonged feeding time with failure to thrive
IV Tachypnea, retractions, grunting or diaphoresis at rest

 


Causes:

  • Congenital, skeletal myopathy with cardiac involvment (e.g. Duchenne, Becker, Barth Syndrome, myotonic dystrophy)
  • Metabolic disorders with cardiac involvement (carnitine deficiency, glycogen storage disease, mitochondrial disease)
  • Cardiomyopathy (primary, secondary)
  • Acquired (rheumatic heart disease, myocarditis, tachyarrythmia, toxic, antineoplastic drugs, nutritional deficiency)

Treatment:

Treatment of the underlying cause and cardiomyopathy.


Mechanical treatment options (ECLS):

Short term support: IABP (diastolic augmentation), Impella axial flow (minimum weight 25 kg), centrifugal pumps (Levitronix), ECMO

Mid-term support /bridge to transplantation/bridge to recovery: Thoratec, Berlin heart


References:

[1] European Journal of Pediatrics, 2010, 169, 403 – 410: Kantor et all: Clinical Practice: Heart Failure in Children. Part II. Current maintenance therapy and new therapeutic approaches

[2] Circulation 110:975-981: Stevenson LW: Left ventricular assist device as destination for patients undergoing intravenous inotropic therapy: a subset analysis from REMATCH (Randomized Evaluation of Mechanical Assistance in Treatment of Chronic Heart Failure).

[3] Ann Thorac Surg 1999; 67: 1415-20. Akomea-Agyin: Intraaortic balloon pumpi in children.

[4] J. Thorac. Cardiovasc. Surg., July 1, 2011; 142(1): 60 – 65. Lamarche et al: Comparative outcomes in cardiogenic shock patients managed with Impella microaxial pump or extracorporeal life support

[5] John et al. J Thorac Cardiovasc Surg.2011; 141: 932-939. Outcomes of a multicenter trial of the Levitronix CentriMag ventricular assist system.

[6] Reinhartz O, Keith FM, El-Banayosy A, et al. Multicenter experience with the thoratec ventricular assist device in children and adolescents. J Heart Lung Transplant 2001; 20: 439-48.

[7] Current Cardiology Reviews, 2010, 6, 46-53. Gazit et al: Mechanical Circulatory Support of the Critically Ill Child Awaiting Heart Transplantation.

[8] J Heart Lung Transplant. 2011 Feb;30(2):115-23: Stevenson et al: Third INTERMACS Annual Report: the evolution of destination therapy in the United States.

[9] Interact Cardiovasc Thorac Surg. 2012 Sep;15(3):426-31. The profile of the systemic inflammatory response in children undergoing ventricular assist device support.


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ECMO antibiotics

Cite this article as:
Marc Anders. ECMO antibiotics, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3783
Indication Prophylaxis Timing Duration
ECMO (cannulation, chest revision, reoperation on ECMO, decannulation) – if not on anitbiotics with both gramnegative and grampositive cover already Cephazolin 50mg/kg up to 1g IV or (if cephazolin unavailable)Cephalothin 50mg/kg up to 2g IV Optimal timing for Beta-Lactams: administer 30 – 60min before incision 2nd dose 25mg/kg if operation > 3hrs, continue 25mg/kg 8hrly, remember to cease after 24hrs
Known MRSA infection or colonization, currently or in the past Cephazolin 50mg/kg up to 1g IV plusVancomycin 25mg/kg up to 1.5g (child < 12yrs: 30mg/kg up to 1.5g) Optimal timing for Beta-Lactams: administer 30 – 60min before incision; for Vancomycin: slow infusion, starting 60min before, and finishing immediately before incision, CVL not required 2nd dose 25mg/kg if operation > 3hrs, continue 25mg/kg 8hrly, remember to cease after 24hrs; no further doses of Vancomycin required
Penicillin / Cephalosporin allergy Vancomycin 25mg/kg up to 1.5g (child < 12yrs: 30mg/kg up to 1.5g) IV plusGentamicin 2mg/kg IV Optimal timing for Beta-Lactams: administer 30 – 60min before incision; for Vancomycin: slow infusion, starting 60min before, and finishing immediately before incision, CVL not required No further doses required
ECMO (cannulation, chest revision, reoperation on ECMO, decannulation) – if on anitbiotics with both gramnegative and grampositive cover already No further prophylaxis required n/a n/a

References:

[1] Therapeutic Guidelines: Antibiotic, 2006: Therapeutic Guidelines Ltd, Melbourne.

[2] Ann Thorac Surg 2006, 81:397-404: The Society of Thoracic Surgeons Practice Guideline Series: Antibiotic Prophylaxis in Cardiac Surgery, Part 1: Duration.

[3] The Society of Thoracic Surgeons Practice Guideline Series: Antibiotic Prophylaxis in Cardiac Surgery, Part 2: Antibiotic Choice. Ann Thorac Surg 2007;83:1596-76.


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ECMO

Cite this article as:
Marc Anders. ECMO, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3778

Inclusion criteria:

>34/40 weeks gestation age, reversible cardiac, pulmonary, or cardiopulmonary failure, mechanical ventilation <14 days.


Exclusion criteria:

Major intracranial haemorrhage, lethal malformation, severe neurological injury, untreatable cardiac or pulmonary malformation.


Clinical indications:

  • Failure to wean off cardiopulmonary bypass, oxygenation index >40 on two or more ABG despite maximum therapy [OI = (MAP * FiO2 * 100) / PaO2]
  • Intractable metabolic acidosis
  • Progressive intractable pulmonary or cardiac failure

Flow rates on full VA ECMO support:

  • In patients <10 kg aim for 100-150 ml/kg/min
  • In patients >10 kg aim for CI 2.4 L/min/m2
  • Consider higher flow rates in septic patients, univentricular hearts with open systemic-pulmonary shunts and extracardiac shunts

Flow rates on full VV ECMO support:

  • In patients <10 kg aim for 70-140 ml/kg/min
  • In patients >10 kg aim for CI 1.8 L/min/m2
  • Consider higher flow rates in septic patients, univentricular hearts (cave: inappropriate high SmvO2 might indicate recirculation)

Cannulation:

  • ABG, FBE, coags, UEC, Ca++, Mg++, LFT, SBR, ABG, obtain blood culture/urine for M, C and S/ETT aspirate for M, S and S, optimise coagulation if possible, consider blood sample storage for genetic analysis
  • Cephazolin (50 mg/kg IV) 30-60 min prior to procedure
  • CXR, ECHO, cranial ultrasound
  • Arterial line placed and secured, central line placed (not RIJ or R subclavian) and secured
  • Chest drain placed, if required and secured
  • Neck cannulation: position patient head outwards in bed space and neck overextended with roll under shoulders
  • Transthoracic cannulation: supine position with roll under back
  • 2 x venous line extensions
  • Fentanyl 5 mcg/kg IV bolus, vecuronium 0.1 mg/kg IV, consider fluid resuscitation/enhance inotropic support if needed
  • Surgical preparation
  • Give heparin on surgical request (50-100 U/kg if appropriate for patient situation), surgical cannulation & connection of tubing (<15 kg → ¼”, >15 kg → 3/8″ circuit)
  • Set FiO2 100% and sweep gas flow, turn RPM to 1000-1200, unclamp venous line, unclamp arterial line, increase slowly RPM to desired flow
  • Reduce inotropic/vasoconstrictor accordingly, observe ABP/inlet pressure/outlet pressure/CVP
  • Recheck ACT every 30 mins, commence heparin infusion 20 U/kg/hr once ACT <250
  • Once on full flow, change to ventilation rest settings (PEEP 10, PS + 10, Vt 6 ml/kg, RR 10, FiO2 30-40% in VA ECMO FiO2 60% in VV ECMO)
  • Secure cannula position, commence analgesia & sedation & paralysis, CXR, ECHO, fluid restriction to 60%

Anti-coagulation:

Keep ATIII level >80%: No. IU = (desired – actual level) X Wt, Heparin [Patients <10 kg: 5 KU/50 ml 0.9% NaCl; patients >10 kg: 25 KU/50 ml 0.9% NaCl]

Commence heparin on 20 U/kg/hr, adjust in regards to ACT.

ACT Bolus (U/Kg) % rate change
<160 50 +15%
160-180 30 +10%
180-200 20 +10%
200-220 0 0
220-240 0 -10%
240-260 0 -10%
260-280 0 -10%

Weaning in VA ECMO:

  • Ensure volume status is adequate
  • Ventilate patient with acceptable settings (as blood flow through lungs increased)
  • Decrease pump flows by 10 ml/min every 60 min down to a minimum of 40 ml/kg or 250 ml/min total flow through oxygenator
  • ABG 15 mins post each wean of flow
  • ECHO at lower flows, [do NOT turn sweep gas off – all flow going through circuit bypasses lungs. Minimum sweep gas setting is 200 ml/min], bridge or decannulate

Weaning in VV ECMO:

  • Commence full ventilation
    Sweep gas FiO2 at 0.21 for approx 10 minutes to flush O2 from oxygenator
  • Turn sweep gas to minimum setting of 200 ml/min, run ACT’s 200-220 whilst pt still on ECMO circuit
  • Observe patient saturations, ABG after 30 mins (oxygenator continues to oxygenate for approx 20 mins after sweep gas flow is ceased)
  • Organise for decannulation

References:

[1] Cardiol Young, 2007; Sep;17 Suppl 2:104-15: Cooper et al: Cardiac extracorporeal life support: state of the art in 2007

[2]

[3] Lancet, 1996 Jul 13; 348(9020):75-82: UK collaborative randomised trial of neonatal extracorporeal membrane oxygenation. UK Collaborative ECMO Trail Group

[4] Cochrane Database Syst Rev. 2008 Jul 16;(3):CD001340: Mugford et al: Extracorporeal membrane oxygenation for severe respiratory failure in newborn infants.

[5] Lancet. 2009 Oct 17;374(9698):1351-63: Peek et al: Efficacy and economic assessment of conventional ventilatory support versus extracorporeal membrane oxygenation for severe adult respiratory failure (CESAR): a multicentre randomised controlled trial.

[6] Intensive Care Med (2012) 38:210-220: MacLaren et al: Contemporary extracorporeal membrane oxygenation for adult respiratory failure: life support in the new era

[7] Artif Organs. 2013 Jan;37(1):21-8. Kotani et al: Evolution of technology, establishment of program, and clinical outcomes in pediatric extracorporeal membrane oxygenation: the “sickkids” experience.


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Cardiomyopathy

Cite this article as:
Marc Anders. Cardiomyopathy, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3772

Basic investigation:

ECG, CXR, ECHO, FBE, clotting, UEC  (incl. Ca++, Mg++, Fe++, PO4), CRP, ESR, albumin, LFT, TFT, BNP, troponin I, troponin T, lactate, ABG, VBG.


Extended investigation:

  • Cardiac MRI.
  • 24 hr Holter monitor.
  • Blood: amino acids, carnitine, acyl-carnitine, ammonia, Cu, caeruloplasmin, transferrin ioforms, pyruvate, selenium, vitamins.
  • Urine: amino acids, organic acids, pligosaccharide screen, MPS screen.
  • Autoimmune: ANA, ENA.
  • Genetic: FISH.
  • Endomyocardial biopsy.

Investigation for myocarditis:

  • Blood & Urine for viral cultures (echo, adeno, parvo, coxsackie, CMV, parainfluenza, influenza, HIV, hepatitis screen) and for bacterial (incl. atypical)/fungal/rickettsial/protozoal and helminithic culture.
  • NPA.
  • ETA.

Identifying the high risk patient:

LVEF < 20% or LVEDD >70 mm or increased C/T ratio >0.7 or MR >3 or complex ventricular arrhythmia (NSVT).

All high risk patients require PICU admission !


Acute management guideline for DCM

Is there low perfusion ? Is there congestion ?
NO YES
NO Ward ManagementACEiβ – Blockeroral diuretics PICU admissioniv Frusemide infusionconsider NIV CPAPobserve for minimum of 48 hrwatch BNP & renal function
YES PICU admissionNIV CPAPiv Adrenaline
(max. 0.05 ≈≥g/kg/min)
observe closelyfor need for ECLS
PICU admissioniv Frusemide infusionconsider NIV CPAPintroduce carefully Milrinoneconsider β agonistsobserve for 4 days

 

1. CPAP or BIPAP. Only intubate when ECLS is on stand-by

2. Fluid and water restriction to 25% maintenance

3. Commence IV frusemide infusion. Aim for euvolaemic state in DCM. Mild hypervolaemia may be needed in HCM. Watch renal function. Avoid hypovolaemia.

4. Commence spironolactone (1 mg/kg BD)

5. Commence milrinone if tolerated

6. Commence β-agonists as indicated. Dopamine, dobutamine or adrenaline up to 0.05 mcg/kg/min

7. Consider levosimendan

8. Consider biventricular pacing

9. Consider antiarrhythmic therapy. Consult cardiology. Do not use β-blocker when on β -agonists. β – Blocker might be useful in HCM

10. Consider anticoagulation therapy

11. Ensure appropriate nutrition. Supplemental therapy with carnitine, co-enzyme Q10, vitamins as indicated.

11. Early use of ECLS if patient is deteriorating or not improving (see ECMO)

12. Specific guided therapy in Pompe disease: myozyme


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Berlin heart VAD Excor

Cite this article as:
Marc Anders. Berlin heart VAD Excor, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3797

Definition:

Paracorporal, pneumatically driven, pulsatile flow mechanical support device driven by a central driving unit (Ikus®) and different sizes of blood pumps (10, 25, 30, 50, 60, 80ml), can be used as RVAD, LVAD or BIVAD.


Aim:

Bridge to transplant or bridge to recovery


Standard settings:

Driving pressures for Systole and Diastole
(Chamber Size / LVAD / RVAD)
10 ml 225 / 175 – 50 / – 50
25 ml 175 / 150 – 50 / – 50
30 ml 175 / 150 – 50 / – 50
50 ml 175 / 150 – 25 / – 25
60 ml 200 / 150 – 25 / – 25
80 ml 225 / 175 – 25 / – 25

Anticoagulation guide:

Medications / Dosing / Target

start UFH+ >24 hr post OP+ no bleeding

+ platelets >20.000

+ normal TEG

start witha) <12 month:
15 U/kg/hr (no bolus) and increase after 6hrs to 28 U/kg/hrb) >12 month:

10 U/kg/hr (no bolus) and increase after 6 hrs to 20 U/kg/hr

aPTT 1.5-2.5 of normal (check every 6 hrs)or Anti-Xa 0.35-0.50 U/ml (draw level 4 hrs after 2nd dose)

start LMWH+ creatinine normal+ no bleeding

or if

+ unable to tolerate PO

+ unstable INRs

+ convert after UFH and no bleeding

start with Enoxaparina) <3 month: 1.5 mg/kg BDb) >3 month: 1 mg/kg BD

or if low INR 2.0-2.7: 1 mg/kg/ OD

or if low INR <2.0:

1 mg/kg BD

Anti-Xa 0.6-1.0 U/ml (draw level 4th after 2nddose until stable)
start Vitamin K Antagonist
(bridge with LMWH)
+ if age >12 month+ enteral feeds tolerated
Warfarin 0.2 mg/kg/day(maximum 5 mg/day) INR 2.7-3.5(use LMWH if unstable INRs)

start Platelet inhibitorsDipyramidole+ if Platelets >40.000

+ postop Day 2 and

ADP >50%

+ Aspirin

+ if platelets >40.0000

+ postop Day 4 and drains removed and ARA >50%

Dipyramidole 1 mg/kg/dose QID (maximum 15 mg/kg/day)Aspirin 1 mg/kg/day ADP activity <50%ARA activity <30%

 


Trouble shooting: always inform PICU consultant for any changes !

Insufficient filling of VAD (VAD Diastole)
Hypovolaemia check Hb and drain losses → replace volume
changes in intrathoracic pressure check CXR (pneumothorax?), ventilation settings → aim for early extubation to increase CO (negative impact of positive intrathroacic pressure)
Tamponade ECHO warranted, inform surgeon ASAP
increased PVR lower PVR (pulmonary hypertension), check right heart function on ECHO
Kink in inflow cannula check for mechanical obstruction: extracorporal / intracorporal (ECHO)
right heart failure(LVAD only) check right heart function with ECHO → inotropic support of right heart (dobutamine, milrinone), →→ NO , RVAD
too low negative vacuum pressure increase negative vacuum pressure (be careful not to suck air in) → driving pressures
VAD rate too high lower VAD rate, decrease % systole

 

Insufficient emptying of VAD (VAD Systole)
increased PVR (in RVAD) lower PVR (pulmonary hypertension)
increased SVR (in LVAD) lower SVR (vasodilators)
Kink in outflow cannula check for mechanical obstruction
systolic drive pressure too low increase systolic driving pressure (→ driving pressures)

References:

[1] J of Cardiovasc Trans Res (2010) 3:612-617: Bryant 3rd: Current Use of the EXCOR Pediatric Ventricular Assist Device

[2] Artif Organs. 2010 Dec;34(12):1082-6: Humpl et al: The Berlin Heart EXCOR Pediatrics-The SickKids Experience 2004-2008

[3] Ann Thorac Surg. 2005 Jan;79(1):53-60; discussion 61: Groetzner et al: Cardiac transplantation in pediatric patients: fifteen-year experience of a single center

[4] J Heart Lung Transplant. 2009 Apr;28(4):399-401. Irving et al: Successful bridge to transplant with the Berlin Heart after cavopulmonary shunt

[5] Am Heart J. 2011 Sep;162(3):425-35.Almond et al: Berlin Heart EXCOR Pediatric ventricular assist device Investigational Device Exemption study: study design and rationale

[6] J Thorac Cardiovasc Surg. 2011 Mar;141(3):616-23, 623: Hetzer et al: Single center experience with treatment of cardiogenic shock in children by pediatric ventricular assist devices

[7] Artif Organs 2012 Jul;36(7):635-9: Sharma et al: Ventricular assist device support in children and adolescents with heart failure: the Children’s Medical Center of Dallas experience


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ABO incompatible blood transfusion

Cite this article as:
Marc Anders. ABO incompatible blood transfusion, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3786

UNOS Policy: ABO incompatible HTX for children up to 2 years (with acceptable isohaemoglutinin titres – less than 1:4)

Recipient Donor compatible Donor incompatible Antibodies to avoid Plasma / Platelets RBC
0 0 0
0 AB Anti AAnti B AB 0
0 A Anti A AB or A 0
0 B Anti B AB or B 0
A A
A 0
A AB Anti AAnti B AB A or 0
A B Anti AAnti B AB A or 0
B B
B 0
B AB Anti AAnti B AB B or 0
B A Anti AAnti B AB B or 0
AB AB AB
AB A AB
AB B AB
AB 0 AB

 


Preoperative preparation:

Isohaemagglutinin titres. Avoid transfusion. Consider transfusion in regards to guide.


Perioperative management:

If elevated iso-titre: plasma exchange once on CPB, iso-haemagglutinin quick test before AoCx release, repeat plasma exchange as required.


Postoperative management:

Isohaemaggluttinin titres daily of ABOi HTX. Repeat plasma exchange if required.


Outcome:

Similar long term outcome. Reduced rate of infection and rejection compared to ABO compatible blood transfusions.


References:

[1] Paediatric Heart Transplant Society: www.uab.edu/phts/

[2] Heart Lung Transplant. 2012 Feb;31(2):173-9: Henderson et al: ABO-incompatible heart transplantation: analysis of the Pediatric Heart Transplant Study (PHTS) database.


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Central venous catheters

Cite this article as:
Marc Anders. Central venous catheters, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3767

Use of central venous catheters in the acute care setting is an integral approach to deliver fluids, blood products, nutrients, medications, obtaining blood specimens, maintaining emergency vascular access, and for haemodynamic monitoring.


Risk factors:

Mechanical complications (malposition, occlusion, dislodgement, tamponade), infection, pneumothorax, thrombosis


Insertion:

Ask nurse to complete the checklist and to stop you if you are about to breach the rules!

  • Maximal sterile barriers for insertion
  • Use chlorhexidine lollipops – the use of liquid in pot is absolutely forbidden!
  • Dedicated equipment cart easily accessed
  • Use of a procedural pause “stop the line” if barrier precautions are breached
  • Use of chlorhexidine impregnated patch at insertion site
  • Appropriate dressings used over insertion site
  • Radiographical confirmation of catheter tip position
  • Always transduce pressure waveform (with heparin)
  • Details of insertion documented in patient record

Maintenance:

  • Commence heparin 10 U/kg/hr in patients <5 kg
  • Daily review of lines with prompt removal of unnecessary lines
  • Use of closed needless mechanical valve on each lumen

References:

[1] https://www.cdc.gov/mmwr/preview/mmwrhtml/rr5110a1.htm

[2] The Pediatric Infectious Diseases Journal, 2010; Sept 29(9): 812 -815: Prasad et al: Risk Factors for Catheter-associated Bloodstream Infections in a Pediatric Cardiac Intensive Care Unit.


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Infection

Cite this article as:
Marc Anders. Infection, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3764

Surgical site infection (superficial/deep/organ):

  • Prevalence 5-10%
  • Within 10-14 days post surgery
  • Most common: Staphylococcus aureus
  • Risk factors: neonate, HLHS, hospitalization prior surgery, TPN, emergency procedures, long CPB

Blood stream infection:

  • Prevalence 5-10%
  • Within 10-14 days post surgery
  • Most common: gram negative organism (Pseudomonas, Enterobacter)
  • Risk factors: surgical complexity, open sternum, low body weight, longer duration of central line, prolonged ICU stay

Pulmonary infection:

  • Prevalence 10%
  • Risk factors: prolonged mechanical ventilation, surgical complexity, low cardiac output syndrome, failed extubation

Current recommendation for antimicrobial prophylaxis in cardiac surgery: cefazolin up to 72 hrs (prolonged use may increase antimicrobial resistance). In the setting of either a presumed or known Staphylococcal colonisation, the hospital presence of a high incidence of MRSA, patients susceptible to colonisation, or an operation for a patient having prosthetic valve or vascular graft insertion, it would be reasonable to combine the beta-lactam with a glycopeptide (vancomycin) for prophylaxis.

Special considerations in immunodeficient syndromes (DiGeorge Syndrome, postoperative – see chylothorax).

See also sepsis and fever.


References:

[1] Am J Infect Control 2010 Nov;38(9):706-710: Sohn et al: Risk factors and risk adjustement for surgical site infections in pediatric cardiothoracic surgery patients

[2] Pediatr Cardiol 2010 May;31(4): 483-9: Abou Elella et al: Impact of bloodstream infection on the outcome of children undergoing congenital heart surgery

[3] Am J Health Syst Pharm 2008 Nov 1;65(21): 2008, 2010: Survey of congenital heart surgeons’ preferences for antimicrobial prophylaxis for pediatric cardiac surgery patients

[4] Ann Thorac Surg 2007 Apr; 83(4): 1569-76: Engelman et al: The Society of thoracic surgeons practice guideline series: Antibiotic prophylaxis in cardiac surgery, Part II: Antibiotic Choice


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Formulae

Cite this article as:
Marc Anders. Formulae, Don't Forget the Bubbles, 2013. Available at:
https://doi.org/10.31440/DFTB.3746

Body surface index (BSA) = ( [Height(cm) x Weight(kg) ] / 3600 )½

Mean arterial blood pressure (MAP) = (SBP + 2 x DBP) / 3

Transpulmonary gradient (TPG) = mPAP – PCWP or in Glenn/Fontan: SVC (CVP) – LAP

Cardiac output (CO) = SV x HR. normal: 2.1-3.5 l/min/m2

Cardiac index (CI) = CO / BSA. normal 3.0-5.5 l/min/m2

Systemic vascular resistance index (SVRI) –> 80 x (MAP – CVP) / CI. normal 800-1600 dyne*sec/cm5/m2. SVRI / 80 = normal 15 – 30 Wood unit / m2

Pulmonary vascular resistance index (PVRI) —>80 x (MPAP – LAP) / CI. normal 80-240 dyne*sec/cm5/m2. PVRI / 80 = normal 1 – 3 Wood unit / m2

Stroke volume (SV) = CO / HR. normal 1-1.5 ml/kg

Ejection fraction (EF) = (EDV – ESV) / EDV. normal 55-75 %

Fractional shortening (FS) = (LVEDD – LVESD) / LVEDD. normal 28-45 %

Modified Bernoulli equation: p1-p2=4 x v2 relates the pressure drop (or gradient) across an obstruction

Flow resistance. Poiseuille’s Law: R = 8 x η x L / π x r4 ( η = viscosity, L = length, r = radius). laminar flow only

Right ventricular pressure (RVP) = 4 x TR Vmax2 + RAP

Pulmonary to systemic blood (Qp : Qs) –> (SaO2 – SmvO2) / (SpvO2 – SpaO2). Normal 1.0. In parallel circulation Qp : Qs ~ 25 : (95 – SaO2)

Oxygen Delivery (DO2) = CI x Hb (g/l) x SaO2

Oxygen consumption (VO2) –> CI x Hb (g/l) x 1.36 x ((SaO2 – SmvO2) / 100). Normal: infant 160-180, child 100-130, adult 120-150 ml/min/m2

QT interval. Bazett’s formula: QTc = QT (sec) / SqrRt of previous RR interval (sec). normal approximately <0.44 sec


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