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P

P value,  see Probability

P wave.  Component of the ECG representing atrial depolarisation. Normally positive (i.e. upwards) in lead I, and best seen in leads II and V1 (see Fig. 59b; Electrocardiography). Maximal amplitude is normally 2.5 mm in lead II, and its duration 0.12 s (three small squares). In right atrial enlargement, the P wave is tall and peaked (P pulmonale); in left atrial enlargement, it is wide and notched (P mitrale).

See also, P–R interval

Pacemaker cells.  Cardiac muscle cells that undergo slow spontaneous depolarisation to initiate action potentials. Their activity results from a slow decrease in membrane potassium ion permeability, resulting in gradual increase in intracellular potassium concentration. Rate of discharge depends on the slope of phase 4 depolarisation, resting membrane potential and threshold potential. Pacemaker cells exist in the sinoatrial (SA) node, atrioventricular (AV) node, bundle of His and ventricular cells. Spontaneous rates of discharge for the different sites: SA node 70–80/min, AV node 60/min, His bundles 50/min and ventricular cells 40/min. Impulses from the faster SA node usually reach and excite the slower pacemaker cells before the latter can discharge spontaneously.

See also, Heart, conducting system

Pacemakers.  Devices implanted subcutaneously, usually outside the thorax, that provide permanent cardiac pacing (to distinguish them from temporary pacing devices).

Modern devices consist of a titanium casing, containing the pulse generator and lithium iodide battery (the latter lasting > 10 years). Electrodes are usually unipolar; i.e. one intracardiac electrode, with current returning to the pacemaker via the body. The heart electrode is usually endocardial, passed via a central vein; epicardial electrodes have been used. Leads may be steroid-eluting to reduce inflammation at the site of contact. Modern pacemakers are checked and adjusted via radiofrequency programming without requiring removal, and recorded data downloaded for analysis of cardiac function.

Indicated if an arrhythmia is associated with syncope, dizziness and cardiac failure, e.g. in sick sinus syndrome, heart block or post-MI. Prophylactic use is controversial.

A generic pacemaker code identifies function (Table 34), the first three positions indicating basic pacing function. Thus VVI denotes ventricular pacing and sensing, with inhibition of pacing if any spontaneous ventricular complex occurs (e.g. as would apply in temporary transvenous pacing). DDD denotes pacing and sensing of both chambers, with inhibition or triggering to maintain sequential atrial and ventricular contraction, allowing spontaneous activity if it occurs. Rate modulation implies the ability to alter the heart rate in response to the patient’s level of activity; rate-adaptive devices respond to physiological parameters normally associated with changes in heart rate (e.g. body movement, Q–T interval, respiration, temperature, pH, myocardial contractility, haemoglobin saturation) by increasing the pacing rate. The fifth position is allocated to multisite pacing, which refers to stimulation of different sites either within one chamber (e.g. right ventricle) or within two chambers of the same type (e.g. both ventricles). With the development of implantable cardioverter defibrillators, much of the latter functions are covered within the defibrillator codes (see Defibrillators, implantable cardioverter).

• Anaesthesia for patients with pacemakers:

ent preoperatively:

– preoperative assessment is particularly directed towards the CVS.

– pacemaker type and indication are ascertained. Pacemakers are usually checked regularly (e.g. every 3 months).

– ECG:

– if pacing spikes occur before all or most beats, heart rate is pacemaker-dependent.

– although traditional advice was to convert older demand pacemakers to fixed rate by placing a magnet over the pulse generator, this is no longer recommended outside specialist cardiac pacing units since the effect on the device’s programming is unpredictable.

– CXR: pulse generator and lead position may be identified.

ent perioperatively:

– potential electrical interference or pacemaker damage by diathermy is more likely if the latter is applied near the device. Sensing may be triggered, with resultant chamber inhibition, or arrhythmias induced. Diathermy may also reprogramme the pacemaker to a different mode.

– if avoidance of diathermy is not possible, risks are reduced by using bipolar diathermy, or placing the plate distant from the pacemaker if unipolar diathermy is used. Current should not be applied across the chest, and its strength and duration of use should be minimal.

– care should be taken with CVP/pulmonary artery catheters since they may dislodge the electrodes.

– temporary pacing facilities (or non-invasive transthoracic pacing) and an external defibrillator should be available.

– isoprenaline may be required if pacemaker failure occurs.

– alteration of pacemaker sensitivity by halothane has been described in older pacemaker models.

– avoidance of suxamethonium has been suggested in case fasciculations are sensed as arrhythmias.

– MRI may be hazardous since the pacemaker may be switched to asynchronous mode, may fail altogether or may move within the chest.

ent postoperative pacemaker checking may be required.

American Society of Anesthesiologists (2011). Anesthesiology; 114: 247–61

Packed cell volume,  see Haematocrit

Paediatric anaesthesia.  Main considerations are related to the anatomical and physiological differences between adults and children, especially neonates (defined as < 1 month old; infants are < 1 year old).

• Thus in children compared with adults:

ent RS:

– the tongue is large and the larynx situated more anteriorly and cephalad (C3–4). The epiglottis is large and U-shaped. A straight laryngoscope blade is thus often preferred for tracheal intubation, and the head should be in the neutral position (as opposed to the ‘sniffing position’ in adults).

– the cricoid cartilage is the narrowest part of the upper airway up to 8–10 years of age (cf. glottis in adults). A small decrease in diameter (e.g. caused by oedema or stricture formation following prolonged tracheal intubation) may lead to airway obstruction.

– the left and right main bronchi arise at equal angles from the trachea. At birth, the tracheobronchial tree is developed as far as the terminal bronchioles. Alveoli number 20 million, increasing to 300 million by 6–8 years.

– respiration is predominantly diaphragmatic, and sinusoidal and continuous instead of periodic. Neonates are obligatory nose breathers. Respiratory rate is increased. Tidal volume is about 7 ml/kg as in adults. The infant lung is more susceptible to atelectasis because the chest wall is more compliant and therefore pulled inwards by the lungs, decreasing FRC. Closing capacity may exceed FRC during normal respiration in neonates and infants. Surfactant may be deficient in premature babies.

– response to CO2 is reduced at birth, and irregular breathing may also occur. Premature babies may suffer from apnoeic episodes; they are at risk of postoperative apnoea up to about 50 weeks postconceptual age. Gasp and Hering–Breuer reflexes are active.

– basal metabolic rate and O2 consumption are high (the latter is 5–6 ml/kg/min, compared with about 3–4 ml/kg/min in adults). Hypoxaemia thus occurs more rapidly than in adults.

– the oxyhaemoglobin dissociation curve of fetal haemoglobin is shifted to the left (P50 of 2.4 kPa [18 mmHg]). Haemoglobin concentration falls from 18 g/dl (1–2 weeks of age) to 11 g/dl (6 months–6 years).

ent CVS:

– cardiac output is 30–50% higher than in adults, largely due to increased heart rate. Arterial BP is lower (Table 35).

Table 35 Normal heart rate and BP at different ages

Age Heart rate (beats/min) BP (mmHg)
0–6 months 120–180 80/45
3 years 95–120 95/65
5 years 90–110 100/65
10 years 80–100 110/70

– left and right ventricles are similar at birth, the former fibrous and non-compliant, making stroke volume relatively fixed.

– blood volume at birth is up to 90 ml/kg (or 50 + haematocrit). It falls to 80 ml/kg for children and 70 ml/kg by 14 years.

– veins are more difficult to cannulate.

– reversion to fetal circulation may occur in severe hypoxaemia.

ent CNS:

– the spinal cord ends at L3 at birth, receding to L1–2 by adolescence.

– the immature blood–brain barrier results in increased sensitivity to centrally depressant drugs, particularly opioid analgesic drugs.

– vagal reflexes are particularly active in children. Bradycardia readily occurs in hypoxaemia.

– subependymal vessels are fragile in premature neonates, with risk of rupture if BP and ICP increase.

ent temperature regulation is impaired. Ratio of body surface area to body weight is greater than in adults and there is less body fat. Thus heat loss is rapid, compounded by impaired shivering and increased metabolic rate. Brown fat is metabolised to maintain body temperature. Insensible water loss is increased in premature babies.

ent prolonged fasting may cause hypoglycaemia in small children, and oral clear fluids are usually allowed up to 2 h preoperatively (4 h for milk). IV administration of dextrose may be required.

ent fluid balance is delicate, since a greater proportion of body water is exchanged each day. Total body water is normally increased, with a higher ratio of ECF to intracellular fluid (ECF exceeds intracellular fluid in premature babies). The kidneys are less able to handle a water or solute load, or to conserve water or solutes. Thus dehydration readily occurs in illness.

Appropriate maintenance fluid requirements (using dextrose/saline) have traditionally been calculated thus:

  4 ml/kg/h for each of the first 10 kg, plus

  2 ml/kg/h for each of the next 10 kg, plus

  1 ml/kg/h for each kg thereafter.

  More recently, because of the risk of perioperative hyponatraemia (children being at particular risk from resultant encephalopathy), and because perioperative hypoglycaemia is less of a problem than traditionally thought, there has been a move away from hypotonic solutions such as dextrose/saline, with maintenance fluids given as 0.45–0.9% saline or Hartmann’s solution, and isotonic fluids avoided if plasma sodium concentration is under 140 mmol/l.

Blood is traditionally given above 10% of blood volume loss, but larger blood losses are increasingly allowed if starting haemoglobin concentration is high. In hypovolaemia, 10 ml/kg colloid is a suitable starting regimen.

ent actions of drugs may be affected by the above factors, or by lower plasma albumin levels (up to 1 year of age), resulting in greater amounts of free drug. Renal and hepatic immaturity may contribute to reduced clearance. MAC of inhalational anaesthetic agents is increased in neonates, but may be reduced in premature babies. Neonates are more sensitive to non-depolarising neuromuscular blocking drugs, probably due to altered pharmacokinetics. They may be resistant to suxamethonium, requiring up to twice the adult dose.

• Practical conduct of anaesthesia:

ent children are placed first on the operating list, to allow as short a fasting time as possible.

ent most standard drugs are used, administered according to weight. As a rough guide the following scheme may be useful:

– 14 years: adult dose.

– 7 years: image adult dose.

– 4 years: image adult dose.

– 1 year: image adult dose.

– newborn: image adult dose.

– premature: image adult dose.

ent premedication is often given orally, to avoid injections, but standard im drugs are also given. Rectal administration has also been used. Atropine may be given to reduce excessive secretions and vagal reflexes.

ent induction of anaesthesia:

– cyclopropane was popular but is no longer available in the UK. Halothane has been replaced by sevoflurane. Inhalational induction is rapid because of increased alveolar ventilation, a low FRC and a high cerebral blood flow.

– standard iv anaesthetic agents are suitable. Administration im (e.g. ketamine) is also used. EMLA or topical tetracaine (amethocaine) is routinely used before iv induction.

The presence of parents at induction is usually allowed, depending on the circumstances.

ent appropriately sized laryngoscope handles and blades are employed. Uncuffed tracheal tubes are commonly used (usually until ~10 years), with a small air leak at 15–25 cmH2O airway pressure, to avoid subglottic stenosis. The approximate size may be calculated thus:

– diameter = (age/4) + 4.5 mm.

   For neonates:

– under 750 g/26 weeks’ gestation: 2.0–2.5 mm.

– 750–2000 g/26–34 weeks: 2.5–3.0 mm.

– over 2000 g/34 weeks: 3.0–3.5 mm.

– length = (age/12) + 12 cm.

More recently, cuffed tubes have been used in term neonates and children, on the basis that a smaller tube with a low-pressure, high-volume cuff is better able to provide an adequate conduit for ventilation whilst minimising pressure on the cricoid cartilage (from the tube itself) and the trachea (from the cuff). A formula for cuffed tubes has been suggested: diameter = (age/4) + 3.0 mm.

ent dead space and resistance should be minimal in anaesthetic breathing systems; adult forms are suitable if the child weighs over 20–25 kg but the Bain system is often avoided because of increased resistance to expiration. Ayre’s T-piece is suitable up to 25 kg. Spontaneous ventilation via a facemask or LMA is usually suitable for short procedures in children older than 3 months. Below this, tracheal intubation and IPPV are traditionally performed, although the LMA is preferred by some.

ent for IPPV using a T-piece, the following fresh gas flows have been suggested, producing slight hypocapnia:

– 10–30 kg: 1000 ml + 100 ml/kg per min.

– > 30 kg: 2000 ml + 50 ml/kg per min.

Set minute volume should equal twice fresh gas flow.

ent routine monitoring, including temperature measurement.

ent anaesthetic rooms and operating theatres should be warmed. Warming blankets and reflective coverings should also be used, with humidification of inspired gases.

ent tracheal extubation may be performed with the child awake or anaesthetised, depending on the clinical context.

ent regional techniques are effective for peri- and postoperative analgesia, e.g. caudal analgesia, inguinal field block, penile block. Local wound infiltration is also effective. Spinal and epidural anaesthesia have also been used.

ent paracetamol and codeine are often used for postoperative analgesia, with morphine for severe pain. Antiemetic drugs are given as required; ondansetron and cyclizine are commonly used.

• Other problems are related to the procedure performed, e.g.:

ent repair of congenital defects, e.g. tracheo-oesophageal fistula, pyloric stenosis, gastroschisis, diaphragmatic hernia, congenital heart disease.

ent related to trauma.

ent ENT, dental and ophthalmic surgery.

The National Confidential Enquiry into Patient Outcome and Death (as NCEPOD) focused for its first year on paediatric anaesthesia. It concluded that general care was good, although outcome was related to clinicians’ experience.

Paediatric intensive care.  Classified into levels 1, 2 and 3, primarily on the basis of interventions undertaken. Level 1 is high dependency care; level 3 is almost always provided in tertiary paediatric centres. In general, differs from adult intensive care by virtue of anatomical and physiological differences between adults and children (see Paediatric anaesthesia) and the range of conditions seen.

• Main clinical problems encountered include:

ent acute respiratory failure:

– upper airway obstruction:

– neonates: choanal atresia, congenital facial deformities, laryngeal/tracheal abnormalities.

– infants/children: inhaled foreign body, tonsillar/adenoidal hypertrophy, croup, epiglottitis and angioedema.

– lung disorders:

– neonates: meconium aspiration, respiratory distress syndrome, diaphragmatic hernia, pneumothorax, chest infection.

– infants/children: pneumonia, asthma, bronchiolitis, cystic fibrosis, congenital heart disease, trauma, near-drowning, burns.

– in neonates, respiratory impairment may result in the development of a persistent fetal circulation.

ent neurological disease:

– neonates: birth asphyxia, central apnoea, convulsions.

– infants/children: meningitis, encephalitis, status epilepticus, GuillainBarré syndrome.

ent trauma: the leading cause of death in children under a year old and the third leading cause in older children (after sudden infant death syndrome and congenital abnormalities). Non-accidental injury must always be considered.

– head injury occurs in 50% of cases of blunt trauma. A modified Glasgow coma scale is used for assessment; otherwise, management is along similar lines to that of adults.

– spinal cord injury and thoracic/abdominal trauma is usually caused by road traffic accidents.

ent poisoning and overdoses.

• Specific attention must be paid to:

ent smaller equipment, drug doses and fluid volumes; specialised equipment.

ent nutrition and electrolyte/fluid balance.

ent temperature regulation.

ent sedation and analgesia.

ent educational and psychological needs.

ent the risk of retinopathy of prematurity in neonates.

In 1997, the Department of Health recommended that level 3 paediatric intensive care should be primarily delivered in lead centres supported by district general hospitals (capable of initiating intensive care), major acute general hospitals (large adult ICUs already managing critically ill children at level 2 or 3) and specialist hospitals (e.g. those caring for children with burns or requiring cardiac or neurosurgery). Each centre must comply with specific standards relating to training, equipment, the experience of medical and nursing staff, access to specialist services and advice, treatment protocols, facilities for families and audit. Regional paediatric retrieval teams have also been established.

Overall mortality ranges from 5 to 10% depending on admission criteria. Scoring systems such as the paediatric trauma score, injury severity score and paediatric risk of mortality score attempt to predict outcome and allow audit of care within and between units.

Frey B, Argent A (2004). Intensive Care Med; 30: 1041–6, 1292–7

See also, Brainstem death; Cardiopulmonary resuscitation, neonatal; Cardiopulmonary resuscitation, paediatric; Necrotising enterocolitis

Paediatric logistic organ dysfunction score (PELOD).  Scoring system for the severity of multiple organ dysfunction in paediatric intensive care. Based on 12 variables relating to six organ systems (neurological, cardiovascular, renal, respiratory, haematological and hepatic). Has been used as daily indicator of organ dysfunction.

Leteurtre S, Martinot A, Duhamel A, et al (2003). Lancet; 362: 192–7

Paediatric risk of mortality score (PRISM).  Scoring system used in paediatric intensive care to help predict mortality. Originally used weighted scores for 14 variables related to acute physiological status; the latest version (PRISM III) has 17 and includes additional risk factors, including acute and chronic diagnosis. Has been validated for most categories of paediatric ICU.

Pollack MM, Patel KM, Ruttimann UE (1996). Crit Care Med; 24: 743–52

Paediatric trauma score.  Trauma scale designed to allow triage of paediatric patients. Six variables (weight, patency of airway, systolic BP, conscious level, presence of skeletal injury and skin injuries) attract scores of 2 (normal), 1 or –1 (severely compromised); scores under 8 indicate increased morbidity and mortality and require referral to a paediatric trauma centre.

Tepas JJ, Ramenofsky ML, Mollitt DL, et al (1988). J Trauma; 28: 425–9

Pain.  Classically defined as an unpleasant sensory and emotional experience resulting from a stimulus causing, or likely to cause, tissue damage (nociception), or expressed in terms of that damage. Thus affected by subjective emotional factors, making pain evaluation difficult. Chronic pain may arise from nervous system dysfunction rather than tissue damage and may be associated with damage to pain pathways (neurogenic pain, e.g. trigeminal neuralgia, postherpetic neuralgia, complex regional pain syndrome type 2, phantom limb pain, central pain). Substances released from damaged tissues, and/or reorganisation of somatic and sympathetic spinal reflex pathways, are thought to be involved in the aetiology of chronic pain. Chronic pain is usually more difficult to diagnose and treat than acute pain, and psychological and emotional factors are more important.

See also, Allodynia; Dysaesthesia; Hyperaesthesia; Hyperalgesia; Hyperpathia; Hypoalgesia; Myofascial pain syndromes; Pain clinic; Pain management; Postoperative analgesia

Pain clinic.  Outpatient clinic run by consultants (usually anaesthetists) with a special interest in the management of chronic pain. Its role includes diagnosis of the underlying condition and management directed at reducing subjective pain experiences, reducing drug consumption, increasing levels of normal activity and restoring a normal quality of life. Requires appropriate facilities for consultation, and performance of nerve blocks and surgical procedures. Anaesthetists, physicians, psychologists and neurologists may be involved. Primary referrals to the clinic are usually from general practitioners or hospital consultants.

See also, Pain management

Pain, intractable,  see Pain; Pain clinic; Pain management; individual conditions

Pain management.  Acute pain, e.g. postoperative, is usually treated with systemic analgesics and regional techniques (see Postoperative analgesia).

• Chronic pain management may involve the following, after pain evaluation:

ent simple measures, e.g. rest, exercise, heat and cold treatment, vibration.

ent systemic drug therapy:

– analgesic drugs: different drugs, dosage regimens and routes of administration may be chosen, depending on the severity and temporal pattern of the pain, and efficacy and side effects of the drugs. Drugs used range from mild NSAIDs to opioid analgesic drugs. The latter are usually reserved for severe pain of short duration, or pain associated with malignancy; they may require concurrent antiemetic and aperient therapy. Implantable devices may be used for intermittent iv, epidural or subarachnoid injection or continuous infusion of opioids.

– other drugs used include:

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