raisis, a. and musk, g. (2012) respiratory and cardiovascular …€¦ · introduction maintenance...

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Raisis, A. and Musk, G. (2012) Respiratory and cardiovascular

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INTRODUCTION

Maintenance of normal oxygenation, ventilation andperfusion (the ABC of resuscitation) is essential in theneurological patient to prevent secondary neurologicalinjury or exacerbation of the underlying condition. Inaddition, correction of hypoxaemia, hypercapnia andpoor perfusion are the most important strategies forreducing intracranial pressure (ICP). The type andextent of supportive care required will depend on thecause of respiratory and/or cardiovascular impairmentand the severity of disruption to normal oxygenation,ventilation and perfusion. Techniques for maintainingnormal respiratory and cardiovascular function and,therefore, adequate oxygen delivery to the tissues areoutlined in this chapter.

PROVIDING AN ARTIFICIAL AIRWAY

The indications for providing an artificial airway arelisted below:• Laryngeal paresis or paralysis, which can be caused

by cranial nerve deficits associated with disorders ofthe brainstem or generalized neuromusculardisease.

• Laryngeal spasm (e.g. tetanus).• An inability to protect the airway adequately

(e.g. severe depression/recumbency associated withintracranial disease).

• Mechanical ventilation.

Treatment methods for acquiring and maintaininga patent airwayOral endotracheal intubation Specific indications • Emergency management of upper airway

obstruction (e.g. laryngeal spasm, laryngealparalysis).

• Protection of airway in an obtunded/unconsciousanimal.

• Animals that need mechanical ventilatory support.

Precautions Oral endotracheal intubation in most animals willrequire sedation or anaesthesia. Details of how tosedate/anaesthetize a neurological patient safely aredescibed in Chapter 29.

Selection of an appropriately sized endotrachealtube (ETT) is essential (19). Resistance to breathingis markedly increased as the diameter of the ETTdecreases. If the diameter of the tube is halved, resistanceincreases 16-fold. To minimize resistance to breathing,the largest diameter tube that can be easily and safelypassed should be used. If the ETT is too long, resistanceto expiration will also increase (doubling the length willdouble the resistance to flow) and the risk of excessive

RESPIRATORY AND CARDIOVASCULAR SUPPORT

Anthea Raisis & Gabrielle Musk

ADMISSION AND NEURODIAGNOSTIC TESTS Chapter 2

35

! 19 Selection of an appropriate endotracheal tube foreach animal is required to ensure that resistance tobreathing is not excessive. When preparing for intubation,select the most appropriate endotracheal tube size inaddition to tubes 0.5–1.0 mm above and below that size asshown here.

9.0 mm

8.5 mm

8.0 mm

equipment dead space or inadvertent endobronchialintubation increases (20).

The increased work of breathing associated withincreased resistance can be overcome by mechanicalventilation. The potential for this increased work toreduce the adequacy of ventilation and cause hypercapniawill be greatest in any animal expected to breathe sponta-neously or when attempting to wean an animal off theventilator. An excessively long ETT will also increase theapparatus dead space, leading to rebreathing of expiredcarbon dioxide (CO2). This also increases the risk ofhypercapnia and increased ICP in the neurologicalpatient.

As oral intubation bypasses the nasal cavity, whichnormally humidifies inspired air, the airways are predis-posed to desiccation. Humidification of gases is essentialto minimize drying of lower airways and should alwaysbe used in patients that are ventilated for anythingother than a short period of time.

Inflation of the ETT cuff is required to prevent aspi-ration of saliva or gastric contents. The cuff should beinflated just enough to create a seal. If excessive or pro-longed inflation pressure is created, the risk of pressurenecrosis of the tracheal mucosa increases. The pressureof the small arterioles in the tracheal mucosa is very low,so the pressure within the cuff should not exceed

25 mmHg. Careful inflation of the cuff is required tominimize damage to the mucosa. During prolongedintubation, occasional repositioning of the endotrachealtube may help reduce mucosal ischaemia; however, repositioning the ETT increases the risk of aspiration ofsecretions that have accumulated above the cuff. If thetube is repositioned, the pharynx and oesophagus shouldbe suctioned prior to cuff deflation to reduce the risk ofsecretions entering the airway.

Tracheostomy Specific indications• Chronic management of airway dysfunction in

conscious patients (e.g. animals with tetanus,laryngeal paresis).

• To reduce the amount of sedation/anaesthesiarequired to immobilize animals requiringmechanical ventilation.

• Severe laryngeal trauma.

PrecautionsThe tracheostomy tube must be secured adequately inplace to prevent accidental removal and loss of theairway. It is essential that the tube can still be removedrapidly should obstruction occur. Tying the tube in placeis preferred over suturing (21).

AD M I S S I O N A N D NE U R O D I A G N O S T I C TE S T S36

" 20 Endotracheal tubes and other apparatus (such asthe capnograph sampling connector; arrow) extendingbeyond the level of the animal’s incisors may increaseapparatus dead space, resistance to expiration and thework of breathing. Always pre-measure the endotrachealtube before placement.

" 21 A tracheostomy tube is used to provide a patentairway in animals with severe compromise of the upperrespiratory tract. The tube should be tied in place (arrow)to allow rapid removal should obstruction of the tubeoccur.

The accumulation of secretions may occlude thetube. When mechanical ventilation is not required andthe risk of aspiration is considered minimal, it is rec-ommended that an uncuffed tube is used (22). It is alsorecommended that the diameter of the tube is one halfthe diameter of the trachea, so the animal can breathearound the tube for short periods should the tubebecome occluded.

Care of the tracheostomy site is labour intensive.Animals need constant monitoring, as occlusion of thetube can result in death within minutes. Regular suction-ing is required to prevent accumulation of secretions.The tube should be replaced 1–2 times a day.

Intratracheal catheter If the upper airway is completely obstructed, an intratra-cheal catheter or needle (large dog: 16 g; small tomedium dog: 18 g) can be placed (23). Oxygen can beinsufflated via these catheters/needles for <5 minutes.

Specific indications• Obstructed airway and impending respiratory

arrest.• Short-term oxygenation while oral intubation or

tracheostomy is performed.

Precautions This method of oxygenation is for short-term use only(<5 minutes) and must be used with conservative oxygenflow rates. When the airway is completely obstructed,oxygen insufflated into the lung via a narrow needle orcatheter cannot be expired, therefore there is a risk ofrupturing the lung, resulting in a pneumothorax. Todetermine suitable flow rates, the volume of the animal’slungs must be considered. For example: a 20 kg dogwould have an approximate tidal volume of 200 ml (basedon 10 ml/kg). Therefore, an oxygen flow of 1 litreminute-1 would fill the tidal volume of the lungs in 12seconds, while an oxygen flow rate of 200 ml/minutewould take 1 minute.

This method does not allow for mechanical venti-lation of the animal, and hypercapnia will occur. Intu-bation should be performed promptly and mechanicalventilation instigated as soon as a patent airway isavailable.

37RE S P I R AT O RY A N D CA R D I O VA S C U L A R SU P P O RT

" 22 A cuffed tracheostomy tube (a) is required whenmechanical ventilation is being performed. However,when the animal is conscious and spontaneouslybreathing, an uncuffed tracheostomy tube (b) is preferred.

" 23 An intratracheal catheter, as shown here, can beused to provide short-term (<5 minutes) oxygen supple-mentation in animals that are completely obstructed.

a

b

BREATHING

Adequate oxygenation (arterial oxygen partial pressure[PaO2] !80 mmHg [10.7 kPa]; saturation of haemo-globin with oxygen [SpO2] !95%) and ventilation (arte-rial carbon dioxide partial pressure [PaCO2] 35–40mmHg [4.7–5.3 kPa]; end-tidal carbon dioxide partialpressure [P’ETCO2] 30–35 mmHg [4–4.7 kPa]) arerequired to maintain cerebral oxygen delivery andprevent increases in ICP.

Oxygen supplementationIndications Oxygen supplementation is indicated if there is a criticaldecrease in oxygen delivery to the brain. Oxygen delivery(DO2 ) is a product of cardiac output (CO) and oxygencarrying capacity (CaO2) measured as the oxygencontent of arterial blood:

DO2 = CO "CaO2

The oxygen content of arterial blood is a combination ofoxygen bound to haemoglobin (haemoglobin " SpO2 "1.34) and that dissolved in the plasma (0.003 " PaO2). Asthe majority of oxygen is carried in the blood bound tohaemoglobin, decreases in oxyhaemoglobin saturationand haemoglobin concentration have the greatest influ-ence on oxygen delivery to tissues, including the brain.Decreases in oxygen saturation of haemoglobin mayoccur due to decreased inspired oxygen percentage,decreased ventilation or decreased transfer of oxygenacross the alveoli, or ventilation/perfusion mismatch orright-to-left shunting of pulmonary blood flow. Adecrease in haemoglobin concentration (anaemia) willoccur due to blood loss or red cell destruction.

Hypoxaemia Definition Although only a small amount of oxygen is carrieddissolved in blood, assessment of oxygenation isfrequently performed by measurement of PaO2. Severehypoxaemia is defined as a PaO2 of <60 mmHg (8 kPa).This is equivalent to an SpO2 of 90% (24). SpO2 is meas-ured using pulse oximetry (see below). For animals withintracranial disease, it is recommended that the PaO2 ismaintained at >80 mmHg (10.7 kPa) to prevent increas-es in ICP.

Common causes of hypoxaemia in animals withneurological disease • Aspiration pneumonia. Animals with CN deficits

associated with brainstem or neuromusculardisease are predisposed to regurgitation andaspiration due to impairment of upper respiratorytract (URT) function. Recumbency andsevere depression also predispose the animal toaspiration.

• Atelectasis (25). Recumbency, immobility and ahigh inspired oxygen concentration all predisposeto alveolar collapse. This creates a mismatch inventilation and perfusion and results in shunting ofblood through the lungs. The shunt preventsoxygenation of the blood as it bypasses ventilatedalveoli.

• Acute lung injury (ALI). Lung injury secondary tosystemic inflammation, prolonged exposure to highinspired oxygen concentrations and trauma due tohigh ventilation pressures all contribute to theincidence and severity of ALI. These processescause the release of inflammatory mediators withinthe lung, which stimulate a vicious cycle of patho-logical changes within the alveoli and surroundinglung tissues. The net result is interference withpulmonary gas exchange. ALI is tentativelydiagnosed when the ratio of arterial oxygen tension


" 24 Oxygen–haemoglobin dissociation curve.

Arterial (90%)

Mixed venous (75%)

2 4 6 8 10 12Oxygen tension (kPa)

Oxygen tension (mmHg)20 40 60 80 100

Oxy

gen

satu

ratio

n(%

)

100

80

60

40

20

05.3 13.3

to fractional inspired oxygen concentration(PaO2:FiO2) is <300. Supportive care of ALI isbased on supplemental oxygenation via mask, nasalcatheters or oxygen cage.

• Acute respiratory distress syndrome (ARDS).ARDS occurs as the pathological changes in ALIprogress and cause greater interference with gasexchange. ARDS is defined as a PaO2:FiO2 ratio of<200. These patients require ventilatory support.

• Pulmonary contusions or pneumothorax (26) inanimals with concurrent chest trauma.

• Neurogenic or non-cardiogenic pulmonary oedemaoccurs in response to increased sympathetic nervoussystem stimulation and blood pressure (BP)secondary to brainstem ischaemia or compression.URT obstruction may also cause pulmonaryoedema if the negative pressures generated during

RE S P I R AT O RY A N D CA R D I O VA S C U L A R SU P P O RT 39

# 25 Recumbency and immobility are very commoncauses of atelectasis and hypoxaemia in the neurologicalpatient.

$ 26 Pneumothorax secondary to chest trauma, as shownin this lateral radiograph, can contribute to hypoxaemia inanimals with concurrent head trauma. (Photo courtesyShannon Holmes)

inspiration damage the alveolar membrane, causingfluid to flood the alveoli.

• Hypoventilation. In an animal breathing room air,hypoventilation causes increased alveolar CO2,which dilutes alveolar oxygen and results in lessoxygen being available to diffuse into the arterialblood. Restoring normal CO2 values by the use ofventilation should also correct the hypoxaemia. Ifthe hypoxaemia is not corrected with ventilationand the return of CO2 to normal, then other causesof hypoxaemia need to be investigated.

ManagementHypoxaemia is managed by treating the underlying causewhen possible and providing supplemental oxygen(see below) until the cause of the hypoxaemia has beencorrected.

Anaemia The clinical significance of anaemia varies according towhether the anaemia is acute or chronic:• Acute anaemia (e.g. haemorrhage): clinical signs

will usually occur if the PCV (packed cell volume) is<0.30 l/l (30%) in dogs and <0.25 l/l (25%) in cats.

• Chronic anaemia (e.g. haemolytic anaemia): clinicalsigns will generally be apparent when the PCV is<0.20 l/l (20%) in dogs and <0.15 l/l (15%) in cats.

Causes of anaemia in neurological disease The most common cause is haemorrhage secondary totrauma or surgical blood loss.

Management The definitive treatment for reduced tissue oxygenationdue to anaemia is whole blood or red blood cell (RBC)transfusion. For further information on blood transfu-sion see Chapter 31.

If there is a delay in administering blood or RBCs,oxygen supplementation can be useful. While oxygensupplementation in these cases may only provideextremely small amounts of dissolved oxygen in theblood, this can be life saving in the short term.

Treatment methods for supplementing oxygenIncreasing the FiO2The aim of techniques that increase the inspired per-centage of oxygen is to use the lowest FiO2 that willmaintain the PaO2 at between 80 and 100 mmHg (10.7–13.3 kPa). As haemoglobin is fully saturated when thePaO2 is approximately 100 mmHg (13.3 kPa), furtherincreases in arterial oxygen tension produce very littleincrease in the amount of oxygen carried by the blood. Inaddition, there is an increased risk of lung damage asexposure to higher than normal levels of alveolar oxygentriggers pathological changes within the pulmonarytissues (oxygen toxicity). The higher the alveolar oxygentension and the longer the duration of treatment, thegreater the risk of irreversible alveolar damage.

Increased inspired oxygen can be delivered by anumber of methods, including oxygen cage, head collar,mask or nasal catheter.

• Oxygen cage. Cages are useful for initial stabiliza-tion of small dogs and cats in respiratory distresswhile minimizing the stress of handling (27). Theadvantage of using an oxygen cage is that an FiO2of >50% can be achieved when the cage remainsclosed. The disadvantages include limited access tothe patient if continuous oxygen support isrequired. In addition, patients are also at risk ofhyperthermia and should be monitored carefully.

• Head collar. Head collars can be used for largeranimals where size prevents the use of oxygencages. The use of head collars covered with plasticfilm can provide a personalized oxygen cage.Oxygen is delivered via tubing attached on theinside of the head collar (28). Head collars have theadvantage of providing a high FiO2 while stillallowing access to the rest of the animal. Thedisadvantages include: • The risk of jugular occlusion and increased ICP

if the collar is too tight. • Hypercapnia can occur if the collar is tight, the

oxygen flow is too low or the supply tubingbecomes disconnected, allowing CO2 to build upwithin the enclosed head collar. Hypoxaemia willalso develop if the oxygen tubing detaches. Flowrates equivalent to those used in non-rebreathing anaesthetic systems (200–300ml/kg/minute) are probably adequate.

• Hyperthermia can also occur with this techniqueas the animal is rebreathing expired warm andhumidified air.


! 27 An oxygen cage can be used to provide oxygensupplementation in small- to medium-sized animals.


" 29 Face masks can be used to provide oxygen duringinitial stabilization or prior to induction of anaesthesia.

" 30 ‘Flow-by’ oxygen therapy can be used to provideshort-term oxygen supplementation to animals that willnot tolerate a face mask.

" 31 Nasal catheters can be used to provide continuousoxygen supplementation and also allow continuous access.They should be avoided in animals with increasedintracranial pressure, coagulopathy and nasal fractures.

" 28 A head collar covered in plastic film can be used toprovide oxygen supplementation to larger animals whenother methods are not feasible. Care should be taken toavoid jugular vein compression and overheating.

• Face mask. Face masks are generally used for initialstabilization only, particularly in animals notamenable to oxygen cages due to their size (29). Theadvantage of using face masks for oxygensupplementation is that they are easily accessible andallow for prompt administration of oxygen in anemergency setting. One of the disadvantages is thatanimals in respiratory distress may not tolerate amask held over their face. In these cases ‘flow-by’

oxygenation can be used (30). A tight-fitting maskcan also exacerbate hyperthermia, as rebreathing ofexpired humidified gases occurs. An open mask orflow-by technique provides limited increase in FiO2.

• Nasal catheter. An intranasal catheter is insertedinto the ventral nasal meatus, directing the catheterventromedially (31). The tip can be positioned justinside the nostril or in the nasopharynx.

To position the catheter tip in the nasopharynx, thecatheter should be pre-measured to the level of themedial canthus to ensure correct positioning. If thetip is inserted too far, it risks being introduced intothe oesophagus, causing aerophagia and gastricdilation. Most animals will tolerate an oxygen flowof 100 ml/kg/minute/nostril. Higher flows maycause increased irritation, sneezing or removal ofthe catheter by the patient. If flows >100 ml/kg/minute are required to achieve adequate oxygena-tion, a catheter can be placed in each nostril,allowing a total oxygen flow of up to 200 ml/kg/minute to be delivered comfortably. Nasal cathetershave the advantage of allowing long-term supple-mentation of oxygen in animals with respiratorydisease and continuous access to the patient.Furthermore, there is no risk of hyperthermia orhypercapnia. The disadvantages include sneezingassociated with placement of nasal catheters, whichcan be detrimental if there is: (1) increased ICP, assneezing will cause further increases, which mayresult in fatal herniation of the brainstem, or (2)coagulopathy, as sneezing may cause bleeding fromthe nostril or haemorrhage into the eye or brain.This procedure should also be avoided in the head-trauma patient, when fractures within the nasalcavity can lead to misplacement of the catheterwithin neural tissue. Finally, there is a limitedincrease in FiO2 of 0.3–0.4 (30–40% inspiredoxygen concentration) observed with this method.

Endotracheal intubationEndotracheal intubation and connection to a breathingsystem may be necessary when other methods ofincreasing FiO2 fail to achieve adequate arterial oxygentension or if the animal becomes increasingly depressed(32). Intubation must be performed before the animalbecomes unconscious. This will require careful admin-istration of intravenous anaesthetic agents. If intubationis delayed until the animal becomes unconsciousbecause of the pathological process, cardiopulmonaryarrest is highly likely.

Endotracheal intubation has the advantage of allow-ing connection to a breathing system and the delivery of100% oxygen. The clinician can therefore be more con-fident of the delivered FiO2. Disadvantages include:(1) maintenance of oral endotracheal tubes generally

requires some degree of sedation or anaesthesia and(2) the depressant effects of sedative and anaestheticagents will also necessitate some form of positive pres-sure ventilation, particularly in animals with intracranialdisease where maintenance of normal PaCO2 is essential.

Assisted ventilation is indicated when increasing FiO2fails to correct hypoxaemia (33). Details of ventilationtechniques are described in the next section.


" 32 Endotracheal intubation and delivery of highinspired oxygen concentration may be needed in animalsthat do not improve with other methods of oxygensupplementation.

" 33 Mechanical ventilation is commonly used to‘breathe’ for patients that have inadequate spontaneousventilation or are unresponsive to other methods ofoxygen supplementation.

VENTILATION

The aim of mechanical ventilation is to recruit andstabilize alveoli and deliver oxygen to and removecarbon dioxide from them without causing lung injury.Careful monitoring of ventilation to ensure normo-capnia and satisfactory oxygenation is essential to guidemanagement strategies. Furthermore, the haemodyn-amic consequences of mechanical ventilation should becontinuously monitored. During spontaneous ventila-tion, a negative pressure is created within the thoraciccavity to draw air into the lungs. During mechanicalventilation, a positive pressure is generated to push gasinto the lungs. This positive pressure compresses bloodvessels within the chest, especially in the low-pressurevenous circulation and right side of the heart. The neteffect is a decrease in cardiac output. Ideally, cardiacoutput should be monitored in ventilated animals, butarterial BP measurement is a common surrogate measurein a clinical setting.

Mechanical ventilation is indicated in animals withrespiratory failure. Respiratory failure can be dividedinto two types:• Hypercapnic ventilatory failure (inadequate

alveolar ventilation = hypoventilation): generallyconsidered to be present when the PaCO2 is>50 mmHg (6.7 kPa). Ventilatory failure shouldalso be considered in animals with normal PaCO2if there is: (1) clinical evidence of increasedrespiratory work and impending fatigue (highrespiratory rate; change in respiratory pattern;increased inspiratory effort; erratic changes in

tidal volume and/or respiratory frequency), or(2) inadequate respiratory compensation formetabolic acidosis. In animals with intracranialdisease, any increase in CO2 may have detrimentaleffects on ICP. Mechanical ventilation is requiredin any animal with intracranial disease if thePaCO2 is >40 mmHg (5.3 kPa). The causes ofventilatory failure in animals with neurologicaldisease include:• Neuromuscular weakness: tetrodotoxin, snake

envenomation, tick paralysis, botulism,polyradiculoneuritis, myasthenia gravis (MG).

• Cervical spinal cord injury.• Intracranial disease with involvement of

respiratory centres (i.e. caudal fossa pathology).• Drug-induced CNS depression: anaesthesia,

opioid overdose.• Hypoxaemic respiratory failure (inadequate

oxygen exchange): generally defined as arterialoxygen tension <60 mmHg (8 kPa) when the FiO2is >0.5.

Treatment methods for providing ventilationThe most common type of ventilation used routinely inanimals is intermittent positive pressure ventilation(IPPV). The factor determining the termination of inspi-ration and the onset of expiration is most often volume,pressure or time. Positive end-expiratory pressure(PEEP) and continuous positive airway pressure (CPAP)are also used, particularly in animals with pulmonarypathology. Table 6 gives a summary of the modes of ven-tilation that can be used in neurological patients.


Table 6 Modes of mechanical ventilation

MODE MECHANISM USES/ADVANTAGES DISADVANTAGES/CAUTIONS

Volume-cycled IPPV Inspiration terminated when Preferred use in normal lungs Increases risk of lung injury pre-set volume delivered. in animals with altered lung Delivers desired VT regardless complianceof lung compliance

Pressure-cycled IPPV Inspiration is terminated when a Preferred method for animals Poor airway, lung or chest wallpre-set pressure is delivered. VT with altered lung compliance compliance will require high will therefore be determined by or very small patients inflation pressures to achieve anlung and chest wall compliance adequate minute volume

(Continued)

A wide range of other ventilation strategies are usedto promote ventilation and oxygenation, minimize lunginjury and prevent haemodynamic compromise. Tech-niques including high-frequency ventilation, inverseratio ventilation, biphasic airway pressure and extra-corporeal membrane oxygenation have been used toreduce airway pressures in human patients with severepulmonary disease. These techniques are limited tospecialist centres with specialist equipment, a thoroughunderstanding of which is essential before embarking oneither short- or long-term management. A detaileddescription of the equipment and techniques is beyondthe scope of this book. For more information, the readeris referred to the Further reading list, p. 623.

Adverse effects of ventilation Mechanical ventilation may have numerous adverseeffects on a variety of body systems, including thecardiovascular, respiratory, neurological, renal andgastrointestinal systems. A summary of these effects andhow to minimize them is given in Table 7. Before ventila-tion of any animal is undertaken it is essential to under-stand the potential adverse effects and how to avoidthem.

Guidelines for use of mechanical ventilationThe aim of ventilation is to optimize oxygenation andventilation, while minimizing adverse effects on cardio-vascular, pulmonary and neurological functions.

Different ventilatory strategies are used to managedifferent types of respiratory failure. The ventilationstrategy may need to be further altered if the animal hasconcurrent intracranial disease. Guidelines for use ofventilation in these situations are described below (seealso Table 8, page 46).


Table 6 Modes of mechanical ventilation (continued)

MODE MECHANISM USES/ADVANTAGES DISADVANTAGES/CAUTIONS

Time-cycled IPPV Inspiration is terminated when Infrequently used in current PIP is determined by lung and a set inspiration time has passed. clinical practice chest wall compliance. Decreases VT is determined by lung and in compliance will cause chest wall compliance increases in PIP and increase

risk of injury

OTHER DEFINITIONSPEEP Maintains positive pressure Minimizes atelectasis and High PEEP may compromise

at the end of expiration during associated ventilation/perfusion venous return and cardiac controlled ventilation, preventing mismatch in normal lungs. output. Decreased venouscomplete alveolar collapse at Minimizes volutrauma in lung return can lead to increased the part of the respiratory cycle pathology cerebral blood volume and when airway pressure is usually increased ICP0 cmH2O

CPAP Technique used in spontaneously Can help stabilize open alveoli Animals may not tolerate nasalbreathing animals to prevent and prevent alveolar collapse. catheters or prongs. Higher alveolar collapse at the end of May improve oxygenation in than normal pressure at the expiration and increase spontaneously breathing end of expiration may functional residual capacity animals and negate need compromise venous return and

for IPPV cardiac output

VT = tidal volume; PEEP = positive end-expiratory pressure; CPAP = continuous positive airway pressure; ICP = intracranial pressure;

PIP = peak inspiratory pressure; IPPV = intermittent positive pressure ventilation.


Table 7 Adverse effects of mechanical ventilation

SYSTEM EFFECT METHODS OF MINIMIZING ADVERSE EFFECTS

Cardiovascular

Pulmonary

Renal function

Gastrointestinal system

Central nervous system

VT = tidal volume; RR = respiratory rate; PIP = peak inspiratory pressure; PEEP = positive end-expiratory pressure;CPAP = continuous positive airway pressure; ICP = intracranial pressure; CVP = central venous pressure; CO = cardiac output;GFR = glomerular filtration rate; SIRS = systemic inflammatory response syndrome; MOF = multiple organ failure;ADH = antidiuretic hormone; ANP = atrial natriuretic peptide; IPPV = intermittent positive pressure ventilation.

Positive airway pressure during IPPV interfereswith venous return and CO during inspiration.CPAP and PEEP interfere with venous return and CO during expiration. PEEP in combinationwith IPPV interferes with venous returnthroughout the respiratory cycle. Decreased CO leads to decreased oxygen delivery to thetissues and may offset improvement in oxygencontent

Barotrauma: excessive airway pressure causesphysical disruption of lung tissue and extra-alveolar air (e.g. pneumothorax). Volutrauma:overdistension of alveoli causes increased perme-ability, oedema and inflammation. Repetitivestretching and recoil of alveoli induces inflamma-tory and structural changes, leading to increasedpermeability of alveoli and oedema formation.Inflammation associated with ventilator-inducedlung injury may be an important inciting factor fordevelopment of SIRS and MOF

Decreased urine output due to release of ADH anddecreasing ANP production causing fluid retention.Decreased GFR and intrarenal blood flow redistrib-ution may interfere with the renal elimination ofdrugs

Increased incidence of gastric ulceration and liverdysfunction. Decreased portal blood flow may alsoreduce the elimination of drugs that undergohepatic metabolism

Interference with venous return can lead toincreased cerebral venous blood volume and ICP

• To minimize the detrimental effects on cardio-vascular performance it is important to ensureadequate blood volume and minimize PIP, theamount of time spent in inspiration (inspiratorytime) and PEEP.

• Monitor blood pressure and CVP duringventilation.

• Monitor ICP in animals with intracranialdisease.

• Use the minimum VT and PIP necessary toachieve adequate oxygenation and ventilation.

• Lung disease: lower VT, higher RR and PEEP.Slight hypoventilation and permissive hyper-capnia (PaCO2 45–60 mmHg).Note: Permissive hypercapnia must be avoidedin patients with intracranial disease.




• Neuromuscular relaxation in anaesthetizedanimals can help reduce the PIP required toventilate to normocapnia.

• Use PEEP very carefully in animals with intra-cranial disease.

• Monitor CVP and ICP in animals with intra-cranial disease.


Table 8 Guidelines for mechanical ventilation

NORMAL LUNGS ABNORMAL LUNGS INTRACRANIAL DISEASE

Preferred Pressure or volume cycled Pressure cycled Pressure cycledventilator type

Settings

VT 10–20 ml/kg <6 ml/kg

RR Comparable to resting respiratory Adequate to maintain appropriate rate F’EtCO2

I:E ratio 1:3 1:3

PIP 10–20 cmH2O will adequately Higher PIP required due to reduced ventilate most animals with compliance (see Further reading)normal lungs; cats will sometimesrequire <10 cmH2O due to higherchest compliance

PEEP 0–5 cmH2O Start at 3 cmH2O and increase up to 10 cmH2O as required to achieve adequate oxygenationwithout decreasing oxygen delivery

VT = tidal volume; RR = respiratory rate; I:E ratio = inspiratory:expiratory time ratio; PIP = peak inspiratory pressure;PEEP = positive end-expiratory pressure; ICP = intracranial pressure; F’ECO2. = Fractional concentration of carbon dioxide in mixed expired air

Mechanical ventilation in cases of ventilatory failureIn animals with ventilatory failure, peak inspiratorypressure (PIP) is adjusted until the minimum pressurethat maintains adequate ventilation and oxygenation isobtained. For normal chests, a PIP of 8–10 cmH2O indogs and slightly less in cats will adequately ventilatemost animals in normal body condition. Higher pres-sures may be required in obese animals and animalswith barrel chests.

The majority of these animals will have normal lungsat least initially, so only conservative PEEP may berequired (up to 3 cmH2O). This will help prevent thedevelopment and progression of atelectasis, especially ifa high FiO2 is used. PEEP must be used with extremecare in animals with increased ICP.

Mechanical ventilation of animals with lung pathology in the absence of intracranial diseaseSmaller tidal volumes (5–6 ml/kg) and higher respiratoryrates are recommended in animals with diseased lungs toprevent overdistension of normal lung tissue. Over-distension of normal lungs occurs as gas delivered during

the inspiratory phase follows the pathway of leastresistance and distributes to areas of lung that are morecompliant (i.e. normal lung tissue is preferentiallyventilated compared with less compliant diseased tissue).Overdistension of normal lung contributes to ventilator-induced lung injury (VILI) and triggers a cascade ofworsening pulmonary function and the developmentof multiple organ failure. Unfortunately, this type ofventilation strategy is unable to maintain normal CO2.However, in animals with normal intracranial compli-ance the increases in PaO2 are generally tolerated.

PEEP is particularly useful in animals with reducedlung compliance, as there is a tendency for lungs tocollapse during expiration. In these conditions, PEEPprevents alveolar collapse and atelectasis. By preventingalveolar collapse, PEEP prevents the cyclic collapse andre-opening of alveoli that contribute to VILI. By mini-mizing atelectasis, PEEP also reduces physiological deadspace and improves pulmonary gas exchange.

Adverse effects of PEEP includes interference withnormal venous return during the expiratory phase of ven-tilation. To minimize this effect, the amount of PEEP

Settings are a compromise betweenpre-existing lung condition andneed to maintain normocapnia andprevent increased ICP

Use the minimal PIP required toachieve normoxia and normocapnia,but limit adverse effects on venousdrainage and ICP

Avoid/use carefully in animals withintracranial hypertension

applied is adjusted to optimize arterial oxygenation whilemaintaining normal cardiac output (and oxygen deliv-ery). Clinically, where measurement of cardiac output isnot available, the effect of IPPV on arterial BP andcentral venous pressure (CVP) can be used to assess theimpact on cardiovascular function.

Mechanical ventilation of animals with lung pathology in the presence of intracranial disease Ventilation of animals with both lung and intracranialdisease presents a unique challenge, as many of theventilator strategies designed to minimize VILI have adetrimental effect on ICP.

The low tidal volume ventilation strategies recom-mended in animals with lung pathology cause permissivehypercapnia and are harmful in animals with intracranialdisease, as a marked increase in ICP accompaniesincreasing PaCO2. Increasing mean airway pressure alsohas the potential to increase ICP due to detrimentaleffects on venous return increasing cerebral bloodvolume. The level of PIP required to ventilate theseanimals adequately may be reduced by use of non-depo-larizing neuromuscular blockers, which increase compli-ance of the chest wall. Venous return is optimized byincreasing expiratory time and, thus, the time for blood

to return to the heart. PEEP should be avoided or usedextremely carefully in animals with intracranial disease.(For details of neuromuscular blockers see Chapter 29.)

Increases in ICP negate any improvement inoxygenation by reducing cerebral perfusion pressure(CPP). Furthermore, increased ICP increases the riskof herniation and death. The use of ICP monitoringmay be worthwhile in animals with concurrent intra-cranial disease and lung disease warranting mechanicalventilation to ensure ventilation strategies do not exacer-bate intracranial hypertension. (For more details on ventilation in ARDS see Further reading.)

Ventilation of animals with pulmonary disease andconcurrent CNS disease requires intensive monitoringof pulmonary, cardiovascular and neurological functions.This is limited to referral hospitals.

CARE OF THE VENTILATED ANIMAL

Appropriate monitoring and supportive care of theventilated patient are required to minimize adverse effectsof chronic intubation, ventilation and recumbency. Thissection discusses some important aspects of this care.Table 9 gives a summary of the general nursing require-ments of these animals.


Table 9 General nursing of the ventilated patient

PROCEDURE RATIONALE

Lubricate eyes Paralysed animals are unable to close eyelids and are predisposed to cornealulcers if eyes are allowed to dry out

Moisten and reposition tongue every 1–2 hours Prevents desiccation, circulatory stasis and swelling. Wrapping the tongue in a swab soaked with water can be useful for preventing desiccation

Reposition endotracheal tube every 2 hours Prevents local tracheal necrosis at site of inflated cuff. Do not inflate the cuff ofthe ETT excessively. The cuff should be inflated until there is no audible leakduring inspiration. High-volume low-pressure cuffs are preferred. Ties used tosecure the ETT in place should also be repositioned every 2–4 hours to preventcirculatory stasis of muzzle

Swab pharynx and suction stomach/ Helps minimize regurgitation and aspiration. Even when the cuff of the ETT is oesophagus every 2 hours inflated, fluid can accumulate proximal to the cuff and enter the airway when

the cuff is deflated. It is important that animals with intracranial disease areadequately sedated or anaesthetized during this procedure, as coughing willcause a marked increased in ICP

(Continued)


Table 9 General nursing of the ventilated patient (continued)

PROCEDURE RATIONALE

Positioning Maintain in sternal recumbency if possible, as this optimizes pulmonary andcardiovascular functions. If positioned in lateral recumbency, turning every 2hours may help prevent atelectasis and compression of dependent muscle groups

Head elevation In animals with intracranial disease the head should be supported so that it islevel with or slightly above the heart in order to encourage venous drainage.Excessive elevation of the head will impair perfusion. Care must be taken to avoidjugular venous occlusion

Environmental temperature control Monitor body temperature and warm as needed using circulating warm air,blankets, heating pads or hot water bottles. Care must be taken to avoiddiscomfort or burns from the heat source

Clean and dry Incontinence pads can be used, but must be changed regularly; alternatively,place an indwelling urinary catheter

Sedation/analgesiaMost animals with respiratory disease will require anaes-thesia to allow endotracheal intubation and ventilation.Some degree of sedation or anaesthesia will also berequired in animals with neuromuscular disease, particu-larly during recovery when animals will attempt to move,but are still too weak to maintain their own spontaneousventilation or protect their upper airway. If anaesthesia isnot required to maintain immobility (e.g. animal paral-ysed by snake envenomation), it is important to remem-ber that these animals are conscious and aware ofenvironmental stimuli, including noise and touch. Someform of analgesia/sedation is recommended to minimizethe stress associated with handling. Agents used tosedate/anaesthetize animals requiring ventilation arediscussed in Chapter 29.

MonitoringAs mechanical ventilation may have detrimental effectson a variety of organ systems, close monitoring of venti-lated animals is essential.

Cardiovascular functionTo ensure adequate circulating blood volume and BP andto minimize the detrimental effects of ventilation on car-diovascular function, measurement of arterial BP andCVP should be performed in ventilated animals. Thesetechniques are described in detail in Monitoring thecardiovascular system, p. 56.

Pulmonary functionAdequacy of ventilationAssessment of the adequacy of ventilation can be made bymeasurement of airway pressure, capnography (see p. 50)and measurement of arterial CO2.

Measurement of airway pressure is essential whenevermechanical ventilation is performed, as sudden changesin pressure can have dramatic consequences. Failure toachieve a predetermined airway pressure indicates inad-equate delivery of volume to the patient and may be dueto insufficient gas supply, leaks in the breathing system ordisconnection. Abrupt increases in airway pressuresuggest sudden changes in compliance or resistance andcan be caused by obstruction or kinking of tubing, acutebronchoconstriction or development of pneumothorax.Gradual increases in airway pressure suggest deteriora-tion in pulmonary function, with associated decreases incompliance and increases in resistance.

Adequacy of oxygenationThe amount of oxygen within the blood can be assessedby measuring oxyhaemoglobin saturation (SpO2) with apulse oximeter (34) and measuring the partial pressure ofoxygen in arterial blood (PaO2). Calculation of oxygendelivery to the tissues requires measurement of botharterial oxygen content and cardiac output. Measure-ment of mixed venous oxygen can provide an indirectmeasure of adequacy of oxygen supply to the tissues.Details of these techniques are described below.

Neurological function Neurological function is influenced by the adequacy ofoxygenation, ventilation and perfusion, and a reductionin these variables can lead to neurological deterioration.Deterioration of neurological status will be observedclinically by progressive mental depression in consciousanimals, dilation of pupils with absence of a PLR anddevelopment of cardiorespiratory abnormalities (e.g.cardiac arrhythmias, Cushing reflex [reflex bradycardia],abnormal breathing patterns). ICP monitoring may also be useful in animals with concurrent intracranial and pulmonary disease, particularly in those requiringventilation.

Renal function Measurement of urine output (see p. 60) and urine specific gravity (SG) should be performed regularly inchronically ventilated animals to monitor the effects ofventilation on renal function and to assess fluid balance.Ideally, this should be performed via a sterile indwellingurinary catheter and closed collection system (35). Measurement of blood urea, creatinine and electrolytesshould also be performed daily to monitor for changes inrenal function.

Fluid therapy (for more details see Chapter 31)Once volume deficits have been corrected, crystalloidfluids are required to maintain adequate hydration.As large amounts of water can be lost through evapora-tion from the airways of ventilated animals, particularlywhen non-rebreathing systems are used, it is generallyrecommended that fluid administration is supplied at1.5–2 " maintenance to prevent dehydration andmaintain adequate hydration of the airway mucosa.Humidification of ventilator gases will offset this effect.

In ventilated animals with intracranial disease, fluidtherapy should ideally be monitored using CVP toprevent excessive fluid administration and increases inhydrostatic pressure.


" 35 A closed urinary collection system allows continuousmonitoring of urine output in critical patients.

" 34 Multivariable monitoring recording haemoglobinsaturation and plethysmograph using pulse oximetry. The level of CO2 expired over time is measured usingcapnography (blue wave form). Arrow = end-tidal CO2.

Humidification of the airwayVentilation with dry gases causes drying of airwaysecretions, decreased mucociliary clearance and asso-ciated increased risk of secondary infection. Water lostfrom the airway will increase fluid requirements.Adequate intravenous fluid therapy is essential formaintaining airway hydration, but heat and moistureexchange (HME) devices (see Chapter 29) placedbetween the animal and the breathing circuit can reducewater loss by up to 80%. These devices need to bereplaced every 6 hours to ensure optimal efficiency.

Ideally, humidified gases should be used if ventilationis expected to be prolonged. Even a couple of hours ofventilation with dry gases can cause significant damage tothe upper airways and lungs. Humidifiers can be fitted tomost ventilators and are placed in the inspiratory limb ofthe ventilator breathing system. Sterile saline can beinstilled into the airway at the level of the tracheal bifur-cation and then removed via suctioning every 1–2 hours.As this increases the risk of nosocomial infection, suc-tioning is only recommended when secretions are exces-sive. Suctioning generally requires the patient to bedisconnected from the ventilator (open suctioning). Thispredisposes to alveolar collapse. The performance of analveolar recruitment manoeuvre may be necessary to re-recruit collapsed alveoli. Alveolar recruitment isachieved by manually inflating the lung with a larger thannormal tidal volume or PIP than that being used forventilation, holding for a prolonged inspiratory time.

Cardiovascular support in the ventilated patientVasoactive agents may be indicated in animals withhypotension unresponsive to normalization of bloodvolume and techniques used to reduce mean airwaypressure during ventilation. Conservative approachesto the correction of hypotension should be performedfirst (fluid therapy and minimizing the delivery of vaso-dilating agents such as anaesthetics) and preparationsmade for the administration of vasoactive drugs if indi-cated. Close monitoring must be performed before,during and after pharmacological management of BPabnormalities. Pharmacological manipulation of BP isdescribed in the sections on hypotension (p. 52) andhypertension (p. 55).

Monitoring oxygenation and ventilationPulse oximetryThe factors that interfere with a reliable pulse oximeterreading include local vasoconstriction, interference fromextraneous lighting, movement, haemoglobin abnormal-ities and pigment. Pulse oximetry can be used to providea guide to oxygenation. It provides a non-invasive beat-by-beat assessment of the amount of oxygen carried byhaemoglobin within the arterial blood. However, toensure accuracy, the pulse quality must be good andreflected in the generation of a continuous plethysmo-gram.

Pulse oximetry measures the percentage of haemo-globin (Hb) molecules that are saturated with oxygen andthe pulse rate. Due to the shape of the oxyhaemoglobindissociation curve (see 24), a saturation of >95% isrequired to ensure a PaO2 of >80 mmHg (10.7 kPa).There are many physiological and technical factors thatcan interfere with the pulse oximeter, so the readingsshould be interpreted with a thorough understanding ofthe limitations of the equipment. (Note: Pulse oximetrydoes not assess the adequacy of ventiliation and severehypercapnia can develop despite adequate oxygen satura-tion, especially if the patient is inspiring gases with a highFiO2. Pulse oximetry can only be relied on to measureoxyhaemoglobin saturation and pulse rate.)

Capnography Capnography provides a breath-by-breath assessment ofthe adequacy of ventilation, assuming normal cardiovas-cular function. This technique measures CO2 in theexpired patient gases (P’ETCO2) (see 34), which approx-imates the CO2 tension in the alveoli (PACO2). As alve-olar gases should be in equilibrium with arterial blood,P’ETCO2 can be used to approximate PaCO2.

Intermittent analysis of arterial blood gas samplesshould also be performed to ensure capnography isproviding a reliable indication of ventilation, as dis-crepancies between arterial and end-tidal CO2 can occur.Differences between PaCO2 and P’ETCO2 are causedby reduced pulmonary blood flow (and increased physiological dead space) due to pulmonary thrombo-embolism, air embolism and reduced cardiac output(heart failure, hypovolaemia). In small animal patients


with cardiovascular compromise, PaCO2 may differ fromP’ETCO2 by 10–20 mmHg or more due to developmentof physiological dead space. Discrepancies will also occurdue to increased dead-space ventilation, as less of theinspired tidal volume actually reaches the alveoli. Anexample of this is panting in a spontaneously breathinganimal.

As capnography provides breath-by-breath informa-tion and is a non-invasive monitor, it is an important toolfor assessing pulmonary and circulatory emergencies inthe ventilated patient (36).


Arterial blood gasesMeasurement of PaO2 is the gold standard for determin-ing the amount of oxygen within arterial blood andshould be performed whenever the accuracy of pulseoximetry is in doubt. Measurement of mixed venousoxygen tension (blood collected from the right atrium viaa central venous catheter) can provide an indication ofthe relationship between oxygen supply and demand.An increase in the difference between arterial and mixedvenous oxygen tension suggests either decreased tissueperfusion or increased tissue consumption.

Calculation of oxygen deliveryOxygen delivery to tissues is a product of cardiac outputand arterial oxygen content (DO2 = CO "CaO2). A cal-culation of DO2 is the ultimate measure of adequacyof tissue oxygenation, but is not always practical. CaO2is easily calculated, as it is the sum of oxygen boundto haemoglobin and oxygen dissolved in the plasma(CaO2 = [SpO2 "Hb " 1.34] + [0.003 " PaO2]). Becauseof the requirement for specialist equipment, assessmentof cardiac output is usually limited to referral institutions.As a result, cardiac output is usually extrapolated fromthe measurement of BP (mean arterial pressure [MAP] =cardiac output " systemic vascular resistance [SVR]). Aninability to obtain direct measurement of cardiac outputprevents the calculation of DO2 in a clinical setting.

CIRCULATION: CARDIOVASCULAR SUPPORT OFTHE NEUROLOGICAL PATIENT

Abnormalities of cardiovascular function can cause sec-ondary neurological damage in animals with intracranialdisease. Hypotension leads to reduced CPP, particularlyin the presence of increased ICP (CPP = MAP # ICP).Hypertension has the potential to increase ICP in thepresence of intracranial disease. This occurs whenincreases in MAP are in excess of normal autoregulationor when autoregulation is impaired. When autoregula-tion is impaired, any increase in MAP can cause linearincreases in cerebral blood volume and ICP. Therefore,cardiovascular function needs to be monitored closely inneurological patients and hypotension and hypertensionmanaged as required.

" 36 A humidifying and moisture exchange (HME)device, placed between the patient and the anaestheticcircuit, prevents excessive heat and fluid loss duringanaesthesia. A capnograph attached to the HME providesbreath-by-breath assessment of adequacy of ventilation.

Circulatory shock/hypotensionDefinitionCirculatory shock causes a significant reduction in organperfusion. During the compensatory phase, BP is main-tained by the responses to reduced tissue perfusion,including increases in heart rate (37, 38), peripheral vaso-constriction, shifts in fluid from the interstitial space tothe intravascular space and reduced urine production.Once the fluid deficit exceeds the ability of the body tocompensate (decompensatory shock), decreases in BPoccur (39).

In humans with head trauma, hypotension is definedas systolic arterial blood pressure (SAP) $90 mmHg.Similar limits of MAP in the trauma patient have notbeen established in small animals, although maintenanceof CPP (MAP # ICP) at between 60 and 70 mmHg andMAP >70 mmHg is associated with a better outcome inhead-trauma cases. In the absence of ICP monitoring it isrecommended that the MAP should be 70–80 mmHgand the SAP should be 100 mmHg to maintain CPP inthe presence of increased ICP. Further increases in CPPabove 70 mmHg are not recommended, as the use ofaggressive fluid therapy and vasopressors to maintainCPP above 70 mmHg is associated with systemic com-plications such as ARDS.

Clinical signs of circulatory shockInstigation of appropriate therapy is dependent on earlyrecognition of shock. This requires a good understand-ing of the clinical signs of circulatory shock. The clinicalsigns of shock will vary depending on the severity, thedegree of compensation and the cause.

Reduction in cardiac output causes sympatheticnervous stimulation, leading to tachycardia and peri-pheral vasoconstriction (pale mucosal membranes, coldextremities, reduced rectal temperature). If these changescan compensate for the reduction in cardiac output, BPwill be normal. Once these compensatory responses areoverwhelmed, BP will decrease. It is essential that therapyis started before decompensation and decreases in BPoccur in order to minimize organ damage.


! 39 Electrocardiogram showing tachyarrhythmia, here associated with poor cardiac output and hypotension.In this case urgent management is required, includingrapid correction of the cause of the arrhythmia.

" 38 When loss of blood volume is severe or prolonged,compensatory mechanisms fail and hypotension occurs, ascan be seen in this recording.

" 37 Recording from a patient taken before blood loss.Heart rate (seen here to be 106 beats per minute) andblood pressure (wave marked with arrow), measured usingan arterial catheter, are within normal ranges.

Management of circulatory shock Appropriate treatment depends on the cause. Arterial BPis influenced by cardiac output and total peripheralresistance. A decrease in either cardiac oputput or totalperipheral resistance will decrease BP. Cardiac output isthe product of heart rate and stroke volume. Strokevolume is determined by preload (blood volume),myocardial contractility and afterload.

Hypovolaemic shock A reduction in circulating blood volume results in adecreased amount of blood returning to the heart(preload), with a resultant decrease in stroke volume andcardiac output and, therefore, BP. The most commoncause of hypovolaemic shock in the neurological patientis haemorrhage associated with trauma or surgical losses.Trauma may also cause hypovolaemia due to loss ofprotein-rich fluid into damaged tissues such as musclebruises and large wounds. In immobile animals unable toaccess water, dehydration may lead to hypovolaemiaonce the fluid deficit exceeds 10% of body weight.

Fluid therapy forms the cornerstone of the manage-ment of hypovolaemia. (For details on fluid therapy seeChapter 31.)

Vasodilatory/distributive shockVasodilatory shock is caused by marked peripheralvasodilation, which results in relative hypovolaemia asthe vascular volume increases relative to the volumeof blood within the circulation. A primary cause ofperipheral vasodilation and hypotension in animals withneurological disease is spinal disease that interferes withthe sympathetic innervation of the splanchnic vascula-ture. A secondary cause is the use of anaesthetic agentsthat cause peripheral vasodilation (e.g. propofol, iso-flurane, sevoflurane). Vasodilation associated withadministration of these agents is dependent on the doseand rate of administration. The higher the dose or thefaster the rate of administration, the greater the amountof vasodilation and the lower the BP. Vasodilation and

hypotension will also occur in any animal that developsconcurrent systemic inflammatory response syndrome(SIRS). SIRS may develop in the presence of any factorthat can stimulate a widespread inflammatory response(e.g. multiple organ trauma, hypoxaemia and ventilator-induced lung injury).

In most cases, management requires treatment of theunderlying cause. Symptomatic treatment includes fluidtherapy and administration of vasoconstrictive agents.Drugs used to increase BP in human patients with headtrauma include noradrenalin (norepinephrine) infusion,dopamine and phenylephrine. Vasopressin has also beenused to increase BP in critically ill animals with SIRS.The dose rates of those agents that have been used insmall animals are: noradrenalin (norepinephrine) (0.05–2µg/kg/minute); dopamine (5–10 µg/kg/minute); vaso-pressin (0.5–2 IU/kg/minute) and phenylephrine (1–3µg/kg/minute) (see Further reading).

When sedative and anaesthetic agents are responsiblefor the hypotension, the dose of the administered agentshould be reduced and fluid therapy given to animals thatdo not respond to the reduction in anaesthesia.

Cardiogenic shockCardiogenic shock may occur due to marked changes inheart rate and rhythm, and reduced myocardial contrac-tility. Abnormalities in cardiac rhythm include thoseassociated with fast heart rates (tachyarrhythmias) andslow heart rates (bradyarrhythmias). Hypotension occurssecondary to fast heart rates, as there is decreased timefor the heart to fill during diastole, resulting in reducedstroke volume and cardiac output. In addition, the highheart rate increases myocardial oxygen demand whenoxygen delivery may be compromised. This predisposesto myocardial ischaemia, which may further exacerbatethe arrhythmia. Slow heart rates cause hypotension, ascardiac output is dependent on heart rate (CO = SV "HR). Poor myocardial contractility decreases theamount of blood able to be pumped by the heart and,therefore, cardiac output.


Abnormalities in cardiac rhythmTachyarrhythmiasCauses of tachyarrhythmias associated with neurologicaldisease include brainstem disease/compression. Myo-cardial degeneration and necrosis are also reported tooccur following cranial and spinal trauma in dogs. Causesassociated with other systemic abnormalities includemyocardial contusions secondary to thoracic trauma andmyocardial ischaemia secondary to hypovolaemia(e.g. haemorrhage from trauma or surgery). Fluid,electrolyte and acid–base abnormalities may also occursecondary to inappetence, an inability to eat and drink orlosses from the gastrointestinal tract or kidneys. (Formore details on fluid and electrolyte abnormalities thatoccur commonly in neurological disease see Chapters 3and 31.) Persistent tachycardia can also lead to myo-cardial ischaemia and arrhythmias, as the increase inheart rate causes both an increase in myocardial oxygenconsumption and a reduction in oxygen delivery due todecreased time for the heart muscle to be perfused.

Management of arrhythmias involves the correctionof all possible underlying causes. Brainstem compressionand/or herniation requires specific treatment forincreased ICP (see Chapter 20). Brainstem ischaemia canoccur due to either increased ICP or decreased BP. Anyconcurrent electrolyte and acid–base abnormalities alsoneed to be corrected. Any cause of persistent tachycardia,including pain, hypovolaemia or hypotension, needs tobe corrected to minimize the risk of exacerbating or con-tributing to the development of tachyarrhythmias.

Specific anti-arrhythmic medication is indicated if thearrhythmia persists despite treatment of all possiblecauses and/or if tissue perfusion is compromised. Specif-ic anti-arrhythmics for ventricular tachyarrhythmiasinclude lidocaine (sodium channel blocker) and betablockers (e.g. esmolol). Supraventricular tachyarrhyth-mias can be treated using beta blockers. (For dose ratescommonly used in clinical cases see Further reading.)

Bradyarrhythmias The main cause of bradycardia and bradyarrhythmias inanimals with neurological disease is brainstem compres-sion (Cushing reflex). Brainstem compression causessympathetic stimulation, which results in a markedincrease in peripheral arterial BP. Initially, the heart rate

also increases; however, the marked hypertension ulti-mately causes a reflex decrease in heart rate due tobaroreceptor stimulation. Bradycardia may also occursecondary to drug overdose (e.g. opioid administration).Severe hypothermia and electrolyte abnormalities(hyperkalaemia and hypokalaemia) may also contributeto bradycardia in any critically ill patient.

Brainstem compression requires specific treatment toreduce ICP (diuretics, hyperventilation). (For details onspecific management of increased ICP see Chapter 20.)Bradycardia secondary to opioid overdose requires areduced dose of opioids +/- administration of reversalagents such as naloxone. Specific treatment of bradycar-dia requires administration of anticholinergics such asatropine. As these agents can mask the signs of brainstemherniation (e.g. pupil and heart rate changes), use of theseagents in animals with intracranial disease needs to beperformed carefully and increased ICP as a cause of thebradycardia needs to be ruled out before these agents areadministered.

Poor myocardial contractilityDecreased cardiac muscle contraction most commonlyoccurs in neurological patients secondary to the use ofanaesthetic and sedative drugs. Development of SIRSsecondary to prolonged hypotension, hypoxaemia, ven-tilator-induced injury or multiple organ trauma may beanother cause of reduced myocardial contractility in theneurological patient.

Improving myocardial contractility requires theidentification and treatment of underlying causes. Fordrug-induced decreases in contractility, delivery of theagent needs to be decreased or stopped if possible. Use ofmultimodal anaesthesia with opioid-based protocols willreduce the requirement for the more cardiovascular andrespiratory depressant anaesthetic drugs. The undesir-able effects of anaesthesia can also be minimized by usingshort-acting agents that can be titrated to effect. (Formore details of methods of reducing anaesthetic-relatedcardiovascular depression see Chapter 29.)

Inotropes are indicated when management of theunderlying cause does not improve myocardial contrac-tility or when urgent improvement in perfusion isrequired. Inotropes that can be used include dopamine(2–5 µg/kg/min) or dobutamine (2–5 µg/kg/min).


Obstructive shockObstructive shock occurs due to physical interferencewith venous return to the heart resulting in decreasedpreload and, therefore, stroke volume and cardiacoutput. In animals with trauma, obstruction to venousreturn may occur in association with pneumothorax. Inthese cases, prompt removal of the air by thoracocentesisor a chest drain will result in resolution of the shock.

HypertensionDefinition In non-neurological patients, hypertension is defined asan MAP of >100 mmHg and a SAP of >150 mmHg. Inneurological patients, increases in mean BP and, there-fore, CPP outside the normal autoregulatory range ofthe brain cause linear increases in blood volume and ICP(40). In addition, abnormal brain tissue loses the ability toautoregulate. In these regions, any increase in mean BP isassociated with an increase in cerebral blood volume and,potentially, an increase in ICP. Maintenance of a stablenormal BP is therefore important in these animals toprevent increases in ICP.

Causes of hypertensionAs described above, MAP = CO "SVR. Cardiac output isdependent on heart rate and stroke volume, which inturn are dependent on preload, contractility and after-load. Therefore, an increase in any of these factors mayincrease BP. The extent of the increase will depend onthe degree of compensation.

Causes of hypertension in neurological patientsinclude peripheral vasoconstriction, tachycardia andhypervolaemia (increased preload). Peripheral vasocon-striction can occur due to increased ICP and brainstemcompression (Cushing reflex) in animals with intracranialdisease. Peripheral vasoconstriction, tachycardia andassociated hypertension may also occur secondary tosympathetic stimulation caused by pain and anxiety.

Management Specific management of increased ICP is detailed inChapter 20. To minimize other causes of hypertension,adequate pain management and careful administration offluids are important. Where hypertension persistsdespite correction of underlying causes, specific pharma-cological treatment may be required to prevent detri-mental effects on ICP and neurological function.

Persistent hypertension, despite adequate analgesia,can be treated by the administration of beta receptorantagonists or calcium channel blockers. Agents thathave been used in human patients with head traumainclude esmolol (% blocker), labetalol (mixed & and %blocker) and nicardipine (calcium channel blocker). Useof these agents in small animal neurological patients hasnot been reported. Esmolol is commonly used to treattachyarrhythmias in small animals and labetolol has beendescribed for use in a hypertensive crisis. Nicardipine isnot used clinically in small animals at present; however,amlodipine, a calcium channel blocker used in smallanimals with cardiovascular disease, may be a suitablealternative. The dose rates of these agents can be foundin critical care texts (see Further reading).

Sodium nitroprusside is also used in small animalpatients with cardiac disease to control hypertension;however, this agent is best avoided in patients withneurological injury due to its risk of causing increasesin ICP.


$ 40 Relationship between cerebral blood flow andintracranial pressure in response to changes in cerebralperfusion pressure, arterial carbon dioxide and oxygentension. Normal pressure autoregulation of blood flow(dotted red line) maintains appropriate cerebral bloodflow despite fluctuation in the mean arterial pressure.Increased PaCO2 (green line) causes a global increase incerebral blood flow that exceeds demand. Cerebral bloodflow is unchanged until PaO2 levels fall below approxi-mately 60 mmHg, when it rises sharply.

0 50 100 150 200MAP (mmHg)

PaCO2

ICP

CPPPaO2

CBF

(ml/1

00 g

m/m

in)

100

80

60

40

20

0


The use of any agent that decreases BP should beassociated with close monitoring of BP to ensure exces-sive reduction and hypotension do not occur.

Monitoring the cardiovascular systemArterial blood pressureArterial BP can be measured non-invasively using oscil-lometric or Doppler techniques (41). Oscillometric tech-niques (e.g. device for indirect non-invasive, automated,mean arterial pressure [DINAMAP]) provide automaticintermittent measurement of mean, systolic and diastolicpressure and pulse rate. The minimum amount of timebetween repeated measurements is 2 minutes. Many ofthe commercial systems available are unreliable in verysmall animals, such as cats, and in hypotensive orbradycardic patients. However, the accuracy in these sit-uations is improving with newer equipment that isbecoming more readily available. The Doppler tech-nique is performed manually and is limited to measure-ment of SAP. However, this technique is more reliable insmall animals and in shocked patients.

In unstable animals or chronically ventilated animals,invasive BP monitoring via an arterial catheter (42) ispreferred over non-invasive methods. Invasive tech-niques allow continuous monitoring of BP. Catheters aremost commonly inserted in the dorsal pedal artery insmall animals. In addition, arterial blood gases can beobtained via the arterial catheter, allowing accurateassessment of pulmonary function and oxygen delivery.

! 42 Arterial blood pressure is commonly measureddirectly via a catheter placed in the dorsal pedal artery. (a) Prior to placement, the hair over the medial surface ofthe dorsal tarsus is clipped and the site disinfected. (b) A small amount of lidocaine (2%) can be injected sub-cutaneously over the artery at the intended site of catheterinsertion. This is particularly useful in conscious animalsto prevent discomfort and movement during insertion. It can also be useful in anaesthetized animals as the vaso-dilation associated with the lidocaine administration canaid catheter placement. (c) Prior to catheter placement, asmall stab incision can be made in the skin. This allowsthe catheter to be inserted with greater control as there isno longer any skin resistance. The artery is then gentlypalpated at the site of insertion and the catheter insertedgently but firmly in the direction of palpation. If the arterycontinues to be palpable as the catheter is inserted, then itis likely that the catheter is too far lateral or medial to theartery. If the artery cannot be palpated, the catheter maybe between the artery and skin. A flash of blood will enterthe hub of the stylet once the arterial wall has beenpenetrated by the bevel of the stylet. It is essential that thecatheter is not separated from the stylet until at least5 mm have been inserted to ensure that both stylet andcatheter have penetrated the wall of the artery. If this hasnot occurred, the catheter will not be able to be inserted.(d) Taping and/or superglue can be used to secure thecatheter in place. (e) The catheter can then be connectedto the fluid line to allow blood-pressure monitoring.

$ 41 The Doppler technique can be very useful formeasuring blood pressure, particularly in small animals.


e

a b

c d

a


c

b

d

f

h

e

g


Central venous pressureCVP is measured using a fluid-filled catheter insertedinto the cranial vena cava via the jugular vein (43).Placement of the catheter in the jugular vein mayincrease the risk of disturbance to venous return andincreased ICP. An alternative is to place a percutaneouscentral catheter, which is passed into the caudal vena cavavia a catheter in the medial saphenous vein (44). Wherethis is not possible, a jugular venous catheter can beplaced, taking care not to occlude the jugular duringplacement (surgical exposure may be required) and utilizing a catheter with as small a diameter as possible to minimize interference with venous return. The use ofneck bandages over these catheters is discouraged inanimals with intracranial disease.

CVP in spontaneously breathing animals is normallybetween 0 and 10 cm H2O. CVP is determined by theamount of blood returning to the heart and the ability ofthe heart to pump this blood. Therefore, measurementof CVP will help differentiate cardiac and hypovolaemiccauses of hypotension and determine appropriate treat-ment. A low BP accompanied by a high CVP suggeststhat the heart is unable effectively to pump bloodreturning to the heart, while low BP and CVP supports areduction in the volume of blood returning to the heart(i.e. hypovolaemia). In contrast, a high CVP and highMAP would suggest hypervolaemia.

Measurement of CVP is helpful to determine theextent of adverse effects of ventilation. A high CVP canbe caused by high mean intrathoracic pressure used forventilation. In such a case, the PIP and/or PEEP requiresadjustment.

# 43 Insertion of a catheter into the jugular vein. Prior to placement, the dead space of the catheter isfilled with saline or heparinized saline and an areaover the selected jugular vein is clipped. The site is thendisinfected. A roll of bandage or gauze placed under theneck can be useful for increasing visibility of the vein,but care should be taken not to occlude the dependentjugular vein in animals with intracranial disease. (a) A small stab incision can be made (carefully) in theskin over the jugular vein, as shown by tenting the skinbetween two fingers; this assists placement of thecatheter. (b) With an assistant compressing the veinproximally, the introducer (a needle or catheter) isinserted through the stab incision into the jugular vein.(c) Once the guide wire has been placed, the needleintroducer is removed, leaving the wire in place. (d) The dilator is then passed over the wire andthreaded into the vein. (e) A gentle but firm twistingaction will help insert the dilator through the skin andvessel wall. The dilator is them removed, again leavingthe wire in place. At this stage some haemorrhage willoccur at the entry site as the hole in the vessel wall islarger than the wire. Gentle pressure at the entry siteusing a sterile swab will reduce the amount ofhaemorrhage until the catheter is placed. (f) Thecatheter is then passed over the guide wire. Duringinsertion of the catheter it is essential to maintain a holdon the guide wire at all times. The wire is inserted intothe proximal end of the catheter and gradually passed upthe catheter. (g) When the hub of the catheter isreached, the injection port is removed and the wirepassed through the end of the catheter. Once the wirepasses through the hub, the operator can hold the wireand pass the catheter over the wire into the vein.The wire is then removed and the injection portreplaced. The catheter is flushed with saline. (h) Thecatheter is sutured in place. A sterile dressing is placedover the entry wound. Neck bandages should not beused in animals with intracranial disease, but can beused in other patients to help secure the catheter inplace.

! 44 Central venous pressure can be measured via acatheter placed in the caudal vena cava via the medialsaphenous vein.

Urine outputUrine output provides an indirect indication of renalperfusion and therefore circulating blood volume andhydration status. It is an extremely valuable tool forassessing the adequacy of cardiovascular function inneurological patients.

Urine output is normally 1–2 ml/kg/hour innormovolaemic patients on normal maintenance fluidrates. Higher rates should be expected in normallyhydrated animals receiving more than maintenance ratesof fluid. Higher than normal output is also expected inanimals that have received diuretics or glucocorticoids.

(For more details on interpretation of changes in urineoutput see Chapter 31.)

Monitoring of urine output is easy, cheap and inform-ative. An indwelling urinary catheter is inserted and aclosed collection system set up. It is an extremely usefulway of assessing fluid balance in unstable neurologicalpatients, particularly those receiving diuretics, wherefluid losses in the urine are higher than normal. Inaddition, animals with traumatic brain injury may havealterations in the reabsorption of renal sodium and water(e.g. central diabetes insipidus [DI] resulting in abnormalurine production and urine SG).


raisis, a. and musk, g. (2012) respiratory and cardiovascular …€¦ · introduction maintenance...

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