anaesthesiology and intensive care

7/24/2019 Anaesthesiology and Intensive Care

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Abhishek Narayan, 2007

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1. General guidelines and of anaesthesiology and intensive care

Peri-operative Careo Assessment

Anamnesis, lab test, risks of anesthesia, types, how to prepare pt

o Prep of the Patiento Intra-operative care

Painless, amnesia, hypnosis, relaxationo Postoperative care

PACU

Mointor vitals, support if needed, pain therapy, treat any complications,ICU or normal ward

Intensive ( Critical) Care Medicineo Management of pt with life threatening patho-physiological conditions

Vital functions

Resp, Cardio Vascu, Metabolic, Neuro

o Main Characteristics Life threatening conditions can be

Broad spectrum of illnesses, of extreme severity, cause complications Multidisplinary Special facilities and staff

o Goals of ICU Maintaining meaningful life Relief of suffering Avoiding harm to the patient Restoration of health. The ultimate goal of treatment in the ICU is a total recovery enabling the patient

to fully participate in society.

As Intensive Care physicians we need to realize that this goal cannot be achievedin all patients.

o Guidelines for ICU Admission and Discharge Criteria

should receive appropriate advanced life-support.

If treatment is unlikely to be associated with a favorable outcome, it isappropriate to limit treatment.

Priority 1 patients

critically ill, unstable patients in need of intensive treatments such asventilator support, continuous vasoactive drug infusions, etc.

Discharge Criteria:o No more need for intensive treatment

o treatment has failed and short term prognosis is poor with littlelikelihood of recovery or benefit from continued intensive

treatment.

Priority 2 patients

patients require the advanced monitoring services of an intensive care unit.

These patients are at risk for the need of immediate intensive treatment,and therefore benefit form intensive monitoring using methods such as

central venous or pulmonary arterial catheters.

Discharge Criteria:


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o the likelihood of suddenly requiring intensive treatment hasdiminished.

Priority 3 patients

These are critically ill, unstable patients whose previous state of health, -underlying disease, or acute illness, either alone or in combination, -

severely reduces their likelihood of recovery and / or benefit from ICU

treatment.

Discharge Criteria:o the need for intensive treatment is no longer present,o But they may be discharged earlier if there is little likelihood of

recovery or benefit from continued intensive treatment.

Exclusions

Confirmed brain death (if donor management is not necessary)

Patients who refuse aggressive life-supporting therapy and are forcomfort care only.

Permanent vegetative state

Physiologically stable patients who are at statistically low risk forrequiring ICU treatment


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3. Securing Airways

Main purposes of airway managemento Avoidance of airway obstructiono Removal of foreign bodieso Desuction: aspiration, mucus, edemao Tongue

Oxygen therapy Mechanical ventilation

Without Equipment:o Airway Cleaningo Head tild chin lifto Jaw thrust manoeuvreo Recovery Position

Non invasive:o bag and masko Mayo tube (oropharyngeal)o LMAo Intratracheal: oro-, nasotracheal Combitube

Invasive :o non surgical

direct laryngoscopy

bronchoscopy

retrogradeo surgical

cricothyroidotomy

tracheostomy

Complications of Endotracheal Intubationo During intubation :

incorrect tube placement, laryngeal trauma cardiovasculare response, hypoxaemia

o Tube is in place: blockageo Following extubation:

aspiration, airway obstruction, tracheal stenosiso Prolonged Intubation:

Damage to vocal cordGrading a difficult airway

Opening the mouth:1. Visible soft palate, uvula, fauces and pillars

2. Visible soft palate, uvula and fauces

3. Visible soft palate and base of uvula

4. Soft palate is not visible

Laryngoscopy:1. Complete glottis is visible2. Anterior glottis is not visible3. Epiglottis but not glottis is visible4. Epiglottis is not visible


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4. Respiratory Insufficiencies: definition, causes, types, and basic guideline of treatment

Factors influencing Respirationo Appropriate content of the inspired airo Respiratory system

airways

Alvoelo-capillary gas exchange Mechanical factors (respiratory muscles, chest wall rigidity)o Circulation/blood

Function of the circulation itself

Buffer-systems of the bloodo Cellular metabolism

Alveolio 300 million in an adulto The surface is appr.70-80 sq.metero Close connection with a capillaryo Gas exchange: alveolar epithel basal membrane capillary endothelo Surfactant, produced by the pheumocytes inreseaes surface tension

Breathing:o Breathing frequency: 14-18/min.o Tidal volume: 500 mlo Minute volume: 14-18 x 500 ml= 7-9 liter

Respiration volume: volume of 1 breath =500ml

Inspiratory reserve: the additional volume whichmay be inspired after normal inspiration,

followed by forced inspiration =2500 ml

Expiratory reserve: normal expiration followed

by forced expiration =1000 ml Vital capacity: the volume which may beexhaled after forced inspiration followed by a

forced expiration = 2500 + 500 + 1000= 4000

ml

Residual volume: may not be exhaled even after forced, voluntary expiration =1500 ml Functional residual capacity: expiratory reserve + residual volume: 1000+1500= 2500 ml. FEV1: forced inspiration- forced expiration. The amount of volume which may be exhaled

within 1 second= approx. 80%

Respiratory insufficiency

An acute or chronic condition in which pulmonary function is markedly impaired, usually

characterized by elevated carbon dioxide or decreased oxygen (or both) in the arterial blood.Patients in respiratory failure often require ventilators to breathe.

Type 1: Failure of oxygenation: hypoxemia Due to ventilation/perfusion mismatch Cause: Pneumonia, PE, pulmonary edema, asthma, emphysema, ARDS, fibrosing

alveolitis

PaO2< 70(60) Hgmm Causes: hypoventilation, shunt, VA/Q disturbance, low FiO2, diffusion disturbances. Symptoms of hypoxia: dyspnoea, restlessness, agitation, confusion, central cyanosis


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Type 2: Failure of ventilation: hpyercapnia Due to alveolar hypoventilation with/without ventilation/perfusion mismatch Causes increased pCO2 and or decreased pO2 Severe hypoxaemia may be treated by increasing FiO2 Severe hypocapnia may me an earlier sign than hypoxemia Causes: breathing center problem, spinal cord injury, peripheral nerve injury,

neuromuscular junction (M Gravis), respiratory muscles paralysis, chest wall defect,

Restrictive lung diseases Static lung volume decreases Affects:

Lung parenchyma, pleura, chest wall Spirometry: FRC, RV, TLC Symptoms: Dyspnea, coughing, right cardiac failure, cyanosis, fast superficial

breathing

Forms:

Extrinsic: PTX, pleural effusion

Chest wall deformity Respiratory muscle fatigue Nerve and neuromuscular diseases Obesity

Intrinsic Pulmonary edema, pulmonary embolism

Investigations:

Blood test: FBC, U&E, CRP, ABG, CXR, Micro, Spirometry Management

Type 1: Treat underlying cause, O2 (35-60%) by face mask Assisted ventilation of O2 still low even at 60%

Type 2: Underlying cause, O2therapy Respiratory stimulant (doxapram 1.5-4mg/min IV) may be given if no

improvement with O2therapy


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5. Monitoring Ventilation

Signs and Symptoms:

Inspection:o Respiration pattern

Hyperventilation: deep and frequent (e.g. Kussmaul)

Apnea Cheyne-Stokes breathing: both frequency and amplitude increases until a certainpoint, than apnea and starts the next periodical phase (lower brainstem damage)

Atactic: irregular frequency and amplitude (upper brainstem damage)o Frequency

Tachypnea or bradypnea

Tachypnea is always a compensation:

Oxygen demand increased

Oxygen transport is disturbed: e.g.o Circulatory, Anemia

Alveolo-capillary gas exchange is disturbed:o O2 uptake and/or removal of CO2

o dyspnea,o clinical signs of hypoxemia

Incoordinated movements , consciousness disturbance, agitation, tachycardia,slight hypertension, peripheral vasoconstriction, cyanosis ( Red. Hgb >

50g/L)

Bradycardia, bradyaritmia, hypotension severe hypoxemiao accidental respiratory muscle use

COPD-patients: sitting position, fixing the upper part of the body on theirextended arm (use of scalenus muscles, elevating the 1st rib)

Active, forced exspiration: the use of abdominal muscles and inner intercostals(expiration normally is a passive process)

Others: pars alaris of nasal muscleo paradoxical breathing, cyanosis

Ausculation

Diagnostic:

Chest X-Ray-helical CT, Pulsoxymetry

Capnographyo Look at pictures at the bottom of the topico Normal ETCO2 Vaules:

30-43 mmHG, 4.0-5.7 kPa, 4.0-5.6%

Blood gas analysis

Spirometry Ventilated patients:

o Volumes, pressures, fFlows, curve and loop analysis of pressure-volume curve

Goal of Ventilation:o SaO2 above 90%o SaO2 90% corresponds to 60 mmHg paO2o Below SaO2 of 90%: measures are needed to improve oxigenationo Clarify to cause, treat the cause, administer respirator or O2


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6. Oxygen therapy and artificial ventilation

Reasons of hypoxemia in postoperative period

Low concentration of O2in inspired airo Normal FiO2 = 0.21, insufficient when under that

Alveolar hypoventilation

o Normal: 4.2L/min Diffusion disturbance

o Type 1 respiratory insufficiency

Ventilation/perfusion ratio disturbanceo Normal V*/Q* = 0.8

Pulmonary shunt (Q*s / Q*T)o The % amount of the circulatory minute volume passing the pulmonary capillary network

without getting in contact with alveoli

o 3-8 % - Normalo 5-20 % - Usually tolerableo 20-30 % - May be life threatening if cardiac function is deceased

o >30 % - Life threatening, severe hypoxemia

FiO2o PaO2is 5 x higher than FiO2

o FiO2 =0.21o The FiO2- PaO2 ratio reflects the alveolo-capillary gas exchangeo Shows pulmonary dysfunction even in case PaO2 is normalo PaO2 may be normal or elevated during oxygen therapy

Normal: 4.0 -5.0 Moderate Pulmonary dysfunction: 2.0 3.9 Sever Pulmonary dysfunction: 35 or


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Basic Forms of Respiratory Care:

Patient efforto None: controlled modeo Needs support: assisted modeo Uncertain or changing: assist-control mode

According to invasivenesso Invasiveo Non-invasive

Administered pressureo Positiveo Negative (iron lung)

Mechanical Ventilation

Controlled:o No patient triggero What is controlled:

Inspiratory time

Pattern of inspiration

o Exspiration is passive

Types of mechanical ventilation

Intermittent positive pressure ventilation (IPPV).o The lungs are intermittently inflated by positive pressure generated by a ventilator, and

gas flow is delivered through an endotracheal or tracheostomy tube.

o Tracheal intubation not only allows institution of IPPV, but also reduces dead space andfacilitates airway suctioning.

However, it is also possible to deliver positive pressure ventilation to cooperative patients in anon-invasive manner through a tight- fitting face or nasal mask (NIPPV).

Two main types of ventilators commonly in use in ICU

those that deliver a preset tidal volume

those that deliver a preset inspiratory pressure during each inspiration.

Modern ventilators allow different modes of ventilation

Types of Ventilation

Volume-cycled ventilation occurs when the ventilator delivers a preset tidal volume regardless of

the pressure generated. The lung compliance (stiffness) of the lungs determines the airway

pressure generated, so this pressure may be high if the lungs are stiff, with the resultant risk of

barotrauma (rupture of the alveoli resulting in pneumothoraces and mediastinal emphysema). Pressure-preset ventilation aka PCV (Pressure Controlled Pressure) is where the ventilator

delivers a preset target pressure to the airway during inspiration. The resulting tidal volume

delivered is therefore determined by the lung compliance and the airway resistance.


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Modes of ventilation

Controlled Mechanical Ventilation (CMV).

o Ventilation with CMV is determined entirely by machine settings including the

airway pressure/tidal volume, respiratory rate and I:E ratio. This mode of ventilation

is not often used in ICU as it does not allow any synchronization with the patient's

own breathing.

o As a consequence, CMV is not well tolerated and patients require heavy sedation or

neuromuscular blockade to stop them 'fighting' the ventilator, thereby resulting in

inefficient gas exchange.

o CMV is normally used in theatre when the patient is receiving a full general

anesthetic to optimize surgical conditions.

o Uncomfortable for the patient, triggers only additional mechanical breaths, possible

baro-trauma, choice of inspiratory flow is difficult, difficult to set in active patients,

may increase WOB.

o

Assisted Mechanical Ventilation (AMV).

o designed to work with the patients' own respiratory effort.

o

The patient's inspiratory effort is detected and triggers the ventilator to 'boost' theinspiratory breath.

Possible triggers: time, pressure, flow

o These modes have two important advantages;

better tolerated by the patient and so reduce sedation

allow patients to perform muscular work throughout the breath, thereby

reducing the likelihood of developing respiratory muscular atrophy.

o The ventilator-assisted breaths can be supported either by a preset inspiratory

pressure or by a preset tidal volume. There are several variations of assisted

ventilation.

Intermittent mandatory ventilation (IMV) is a combination of spontaneous and mandatory

ventilation.

o Between the mandatory controlled breaths, the patient can breathe spontaneously andunassisted.

o IMV ensures a minimum minute ventilation, but there will be variations in tidal

volume between the mandatory breaths and the unassisted breaths.

o Problem: no synchronization between patient effort and mechanical breaths (danger

of lung over distension)

Synchronised intermittent mandatory ventilation (SIMV).

o With SIMV, the mandatory breaths are synchronised with the patient's own

inspiratory effort which is more comfortable for the patient.

Pressure-support ventilation (PSV) or Assisted spontaneous breaths (ASB).

o A preset pressure-assisted breath is triggered by the patient's own inspiratory effort.

o This is one of the most comfortable forms of ventilation.

o The preset pressure level determines the level of respiratory support and can bereduced during weaning.

o There are no mandatory breaths delivered, and ventilation relies on the patient

making some respiratory effort.

o There is, however, no back up ventilation should the patient become apnoeic, unless

this mode is combined with SIMV.

o Does not work in paralyzed patients. Minute ventilation is not guaranteed


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o Positive End Expiratory Pressure (PEEP) is used with all forms of IPPV.o A positive pressure is maintained during expiration expanding under ventilated lung, and

preventing collapse of the distal airways.

o This results in improved arterial oxygenation.o PEEP causes a rise in intrathoracic pressure and can reduce venous return and so

precipitate hypotension, particularly in hypovolaemic patients.

o With low levels of PEEP (5-10cmH2O), these effects are usually correctable byintravenous volume loading.

Continuous Positive Airway Pressure (CPAP) is effectively the same as PEEP, but in spontaneously

breathing patients.

Ventilation Parameters

o Tidal Volumeo No ALI: 10 ml/kgo ARDS: outcome is better in case of low TV

6 ml/kg 12 ml/kg

o Frequencyo ACV : 4/min (only for backup is needed)o SIMV: 10/min. at the beginning, should be increased when neededo PSV: no frequency preset is necessary

o Sensitivity triggero May be:

Flow, pressure, timeo Usually it is negative pressure: 1- 3 H2Ocmo Appropriate trigger sensitivity is important: low sensitivity too frequent triggering

danger of respiratory alkalosis

o FiO2

o High FiO2 potentially toxic Limit: 0,6

o Goal: the lowest FiO2, resulting in acceptable oxygenationo What is acceptable?

60 mmHg O2, saturation above 90%o

o PEEPo Inspiratory flow


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7. Practical demonstration of oxygen therapy and mechanical ventilation.

8. Practical conduct of mechanical ventilation

From: http://www.nda.ox.ac.uk/wfsa/html/u16/u1609_01.htm

NOTE: I am not sure what topics 7 and 8 require. Listed is general info about ventilation and their

uses. Refer to topic 6 as and when needed.

Initiating Mechanical Ventilation

When initiating artificial ventilation the aim is to provide the patient with a physiological tidal

volume and ventilatory rate adapted to meet the patient's underlying condition

Initial ventilator settings:

FiO2 1.0 initially but then reduce

PEEP 5 cm

H2O Tidal volume 7-10 ml/kg

Inspiratory pressure 20 cmH2O (15cmH2O above PEEP)

Frequency 10 - 15 breaths per minute

Pressure support (ASB) 20 cmH2O (15cmH2O above PEEP)

I:E Ratio 1:2

Flow trigger 2 l/min

Pressure trigger -1 to -3 cmH2O

'Sighs' Nil - formerly thought to prevent atelectasis, but

no longer considered effective

These settings should be titrated against the patient's clinical state and level of comfort.

OPTIMIZING OXYGENATION

Initially set FiO2at 1.0 and then wean rapidly to a FiO2adequate to maintain SaO2of >93%.

FiO2of greater than 0.6 for long periods should be avoided if possible because of the risk ofoxygen-induced lung damage.

Strategies to improve oxygenation (other than to increase FiO2) include increasing the meanairway pressure by either raising the PEEP to 10cmH2O or, in pressure-preset ventilation modes,

by increasing the peak inspiratory pressure.

However, care should be taken to avoid very high inflation pressures (above 35cmH2O) as thismay cause barotrauma to the lungs.

More complex strategies to improve oxygenation may be required in severely hypoxic patientseg acute respiratory distress syndrome (ARDS) or acute lung injury from a variety of causes.

o In severe hypoxia, it may be possible to improve oxygenation by increasing the PEEPfurther to 15 cmH2O (or above) and using small (6-8mls/kg) tidal volumes more

frequently.


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o However, this may cause a reduction in blood pressure and may be poorly tolerated bythe patient requiring intravenous fluid loading and inotropic or vasopressor therapy.

Another strategy is to prolong the inspiratory time. Normal inspiratory to expiratory ratio is 1:2but oxygenation may be improved if this ratio is changed to 1:1 or even 2:1.

o However, these alterations are often not well tolerated by the patient who may requireheavy sedation.

o Not infrequently, due to a reduced minute volume the PaCO2may rise.o In some patients this technique is used deliberately 'Permissive Hypercapnia'.

In severe ARDS the patient can be repositioned and ventilated in the prone (face down) position.o This may improve oxygenation by re-expanding collapsed alveoli and improving the

distribution of blood perfusion in the lung relative to ventilation.

o In this position, patient monitoring and care is obviously difficult, and this approachshould be undertaken with careful monitoring and care.

Problems during mechanical ventilation

o 'Fighting the ventilator'o When the patient starts to breathe out of phase with the ventilator or becomes restless or

distressed during IPPV, there is a fall in the delivered tidal volume due to a rise inrespiratory resistance.

o This results in inadequate ventilation and hypoxia.o There are a number of causes including:

Patient factors - Breathing against the ventilators inspiratory phase, breath holdingand coughing.

Decreased pulmonary compliance - pulmonary pathology, including oedema orinfection and pneumothorax.

Increased airway resistance - bronchospasm, aspiration, excess secretions Equipment - ventilator disconnection, leak, failure. ET tube blocked, kinked,

dislodged

Weaning

Patients recovering from prolonged critical illness are at risk of developing 'critical illness

polyneuropathy'. In this condition, there is both respiratory and peripheral muscle weakness, with

reduced tendon reflexes and sensory abnormalities. Treatment is supportive. There is evidence that

long-term administration of some aminosteroid muscle relaxants (such as vecuronium) may cause

persisting paralysis. For this reason, vecuronium should not be used for prolonged neuromuscular

blockade.

Indications for weaning

The decision to start weaning is often subjective and based on clinical experience. However, there

are some guidelines that may be helpful:

Underlying illness is treated and improving

Respiratory function:

o Respiratory rate < 35 breaths/minute

o FiO2< 0.5, SaO2> 90%, PEEP 5ml/kg

o Vital capacity > 10 ml/kg

o Minute volume < 10 l/min

Absence of infection or fever


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Cardiovascular stability, optimal fluid balance and electrolyte replacement

Modes of Weaning

There is debate over the best method for weaning and no one technique has been found to be

superior to others. There are several different approaches.

Unsupported spontaneous breathing trials. The machine support is withdrawn and a T-Piece

(or CPAP) circuit can be attached intermittently for increasing periods of time, thereby

allowing the patient to gradually take over the work of breathing with shortening rest periods

back on the ventilator.

Intermittent mandatory ventilation (IMV) weaning. The ventilator delivers a preset minimum

minute volume which is gradually decreased as the patient takes over more of the respiratory

workload. The decreasing ventilator breaths are synchronised to the patient's own inspiratory

efforts (SIMV).

Pressure support weaning. In this mode, the patient initiates all breaths and these are 'boosted'

by the ventilator. This weaning method involves gradually reducing the level of pressure

support, thus making the patient responsible for an increasing amount of ventilation. Once

the level of pressure support is low (5-10 cmH2O above PEEP), a trial of T-Piece or CPAPweaning should be commenced.

Failure to wean

During the weaning process, the patient should be observed for early indications of fatigue or failure

to wean. These signs include distress, increasing respiratory rate, falling tidal volume and

haemodynamic compromise, particularly tachycardia and hypertension. At this point it may be

necessary to increase the level of respiratory support as, once exhausted, respiratory muscles may

take many hours to recover.

It is sensible to start the weaning process in the morning to allow close monitoring of the patient

throughout the day. In prolonged weaning, it is common practice to increase ventilatory supportovernight to allow adequate rest for the patient.


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9. Intensive treatment of the hemodynamically unstable critically ill

Signs and Symptoms:o Central Nervous System: decreased mental statuso Cardiac: chest pain, ischemia on ECG, and wall motion abnormalities on echocardiogramo Renal: decreased urine output, BUN/creatinine increases,o GI: abdominal pain, decreased bowel sounds,o Periphery: cool limbs, poor capillary refill, weak pulses

Shock:o Shock is a syndrome of hypotension and decreased tissue perfusion. Initially

neurohumoral compensatory mechanisms can maintain perfusion to vital organs. If

appropriate treatment is not promptly instituted, these comp. mech. are overwhelmed,

producing ischemia, cellular damage, multiple organ failure, and death.

Types of shock:

Hypovolaemic (acute loss>20% of blood), Carcinogenic, Obstructive(mech. obstacle to venous return or arterial outflow), distributive

(decreased vascular tone)

o Patho-physiology of shock:

Prolonged hypotension (decreased DO2) Neurohumoral response. Stress hormones: catecholamines, ADH, ACTH,

glucagon (enhanced myocardial contractility, peripheral vasoconstriction)

Metabolic response (hyperglycemia)o Effect of Shock:

CNS - confusion and obtundation Cardiovascular - MI, impaired contractility, dysrhythmias Resp. syst. - Acute resp. failure, bronchospasm, a. pulm. hypertension, V/Q

mismatch, ALI-ARDS

Renal system - GFR decreases, Acute tubular necrosis Gastrointestinal damage to GI mucosa, predispose to translocation of bacteria.

GI hemorrhage, ileus, pancreatitis, hepatic failure.

Haematologic syst. - Platelets and factors may be depleted. DICo Management

Airway, Positive-pressure ventilation Peripheral iv. access. Standard monitoring.(ECG, SpO2, NIBP, urinary output, core temperature) Extra monitoring (IBP, CVP measurement, PAC, PICCO)

Hypovolaemic Shock:o Etiology - hemorrhage, vomiting, gastric suctioningo Patophysiology - Decreased venous return low RRo Clinical presentation - hypotension, weak pulses, flat neck veins, cold and clammy skino Therapy:

Volume replacement: Crystalloids. (Saline, RL), Hypertonic saline 3%, Colloids(hydroxyethyl starch, dextrans)

Human albumin, blood products Vasopressors


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Cardiogenic Shock:o Causes: AMI and its complications, dysrhytmias, acute myocarditis, contusion,

pharmacologic depressants, proximal aortic dissection)

o Pathophysiology: Decreased contractility causes decreased SV, CO, RRsysto Clinical manifestation: hypotension with cutaneous vasoconstriction, cold extremities,

cyanosis, Jugular Venous Distension, new murmur, S3 gallop, pulmonary rales.

o Therapy: Inotropic drugs

Dobutamin (1,2, alfa1)o Pos. Inotropic and chronotropic effects.o Central line is preferable.o low dose:2-5 ug/kg/min dopaminerg effect, increases renal and

splancnic blood flow.

o medium dose: 5-10ug/kg/min 1 effect increases contractility, HR,RRsyst

Norepinehrine (alfa1, alfa2, 1)o Dosage: 1-20 ug/mino Increases vascular tone, so can treat hypotension.

o Adverse effects: Intense peripheral vasoconstriction can causeorgan hypoperfusion and ischemia.

Epinehrin (alfa1, alfa2, 1, 2)o Indications: Refractor hypotension. Bronchospasm, anaphylaxis,

cardiac arrest.

o Effects: 1-2 g/min 2 bronchodilatationo 1: HR, contractility increases.o Alfa1: vascular tone increases.o Inhibition of inflammatory mediator release by mast cells, and

basophils.

Phosphodiesterase inhibitors (amrinone, milrinone)

Positive inotrop and vasodilator effect.

Adverse effects: tachycardia, dysrhytmias, thrombocytaemia, abnormalliver function test.

Vasodilatators (nitrates, labetalol, ACE inhibitors) Intravenous sedatives and analgesics. (bezodiazepins, opioids) Thrombolysis, PTCA, cardiac surgery Intraaortic balloon counterpulsation (IABC)

o Bradycardia: HR150/min Drugs: cordarone, lignocaine, propafenon Cardioversion (synchronised, 100, 200, 360J) Defibrillation (, 200, 200, 360J) No pulse.

Neurogenic Shock:o Traumatic spinal injuryo Clinical presentation: hypotension, peripheral neurologic deficit.o Management: Patent airway, ventilation, fluid resuscitation, alfa agonists, stabilizing

surgery.


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Anaphylactic Shock:o Antibody mediated reaction that occurs on response to a particular antigen in previously

sensitized individuals.(IgE)

o Clinical manifestations: Skin: flushes, urticaria, pruritus. Resp. System: upper airway obstruction, bronchoconstriction, produces dyspnoe.

o Management: Identification and discontinuation of the suspected antigen. Airway management, volume resuscitation. Epinehrin 0,1-0,5 mg. Corticosteroids maximal effect 4-6 hours later. Dose: hydrocortison 4*200 mg

Obstruction Shock:o Causes: tension PTX, pericardiac tamponade, abdominal compartment sy. , pos. Pressure

ventilation, PEEP, auto PEEP, pulmonary embolism.

o Clinical features: Hypotension, tachycardia, resp. Distress, JVD, increase andequalization of central pressures.

o Management: Volume resuscitation. Inotropic support. Tension PTX :emergency needle aspiration Abdominal compartment: decompressive laparotomy Cardiac tamponade: pericardiocentesis. Pulmonary embolism: thrombolysis.


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10. Possibilities of hemodynamic monitoring: CVP, pulmonary artery catheter,

PiCCO, NICO, central venous oxygen saturation etc.

Central Venous Pressureo Possibilities:

Fluid manometry

Electricalo Veins used:

V. Subclavia, V. jugularis interna, V. Femoralis, V.cephalica and basilica

o Spontaneously breathing patient: 5-10 H2O cmo Artificially ventilated patients: 3-5 H2O cm highero CVP = pressure in the right atrium

Determined by right heart function and pressure in the vena cava Thus, it reflects:

Volume status, right heart status

Changes in value are more important then the value it self Normally CVP reflects the left atrial pressure, if and only if no right sided heart

failure and pulmonary vascular resistance is normalo Three spikes (a, c, v)o Two descents (x, y)

a: atrial contraction x: atrial relaxation c: ventricular contraction v: atrial filling y: opening of tricuspidal valve

before ventricular filling

o Possible Complication Carotid puncture, PTX, Air

embolism, arrhythmias,

perforation, cardiac tamponade

Brachial plexus, vagus damage chylothorax

Pulmonary Artery Cathetero Also called the Swan Ganz catheter

Inserted into the Subclavian veinor Internal jugular vein

Swimmed up to the pulmonary artery by the blood flow.o Makes use of Ficks principle of diffusiono 3 West zones of the lung

I. zone: PA>Ppa>Ppv II. zone : Ppa> PA> Ppv III:zone: Ppa> Ppv> PA

o Complications Thrombosis, Pulmonary artery rupture,

Sepsis, Endocarditis, Lung infarction,

Valve damage

o Can measure: CVP, RVEDP, PAP, PCWPo Can calculate: CO, CI, SV, SVR, PVR


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Central Venous Oxygen Saturation (ScvO2)o DO2: the amount of oxygen transported by the circulation to the tissues

Determinants:

Oxygen content: Hemoglobin (Hb), Oxygen saturation (SO2)

Cardiac Outputo VO2: Oxygen consumption

Oxygen consumption depends upon the peripheral metabolism and its alterations,such as:

Exercise, fever, hypermetabolismo ScvO2 central venous oxygen saturation

Oxygen saturation in the superior vena cava Normal value is: 70-80 %

Decreased DO2or increased VO2o SvO2 mixed venous oxygen saturation

the saturation of the Hgb in the pulmonary artery, i.e. just after the right heart

PiCCO - Pulse Contour Cardiac Outputo Uses principle of Thermo-dilution

o This system can measure intra- and extrathoracic volumes and monitors both left andright side of the heart function.(CO, preload volume, contractility, resistance, volume

responsiveness, extravascular lung volume)

o Applies thermodilution to measure COo Necessary cannula:

Central venous arterial

o Advantages: Easy use, less invasive, beat-to beat registration of the actual parameters

o Indications: Patients in whom cardiovascular and circulatory volume status monitoring are

necessary.

o Contraindications: Patients in whom there are arterial access restrictions, for example due to femoral

artery grafting or severe burns in areas where the arterial catheter would normally

have been placed.

Note: The Axillary or Brachial artery can be used as an alternative site.Additionally a long radial artery catheter can be placed for short term use.

May give incorrect thermodilution measurements in patients with intracardiacshunts, aortic aneurysm, aortic stenosis, mitral or tricuspid insufficiency,

pneumonectomy, macro lung embolism and extracorporeal circulation (if blood is

either extracted from or infused back into the cardiopulmonary circulation).

NICO Non Invasive Cardiac Output Monitoringo Calculating circulating minute volume based upon the exhaled CO2-concentration (Fick-

principle)

o Measures hemodynamical and respiratory parameters


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o Diarrhea, preoperative anterograd rinsing of the bowels, intestinalpolyposis, Intestinal fistulas in Crohns disease

Renal losses:o Diuretics, hypomagnesemia, hyperaldosteronism, glucocorticoid

effect

Therapy

Potassium supplement ( p. Os, i.v.) 2-3 mmol/kg/dayo max. speed of infusion: 20 mmol K+ / hour

Potassium deficiency in mmol =o =( 4,5 mmol/l - Se K+) x ECF(1) x 2 == (4,5 mmol/l - Se K+ ) x 0,4 x BWkgo Hyperkalemia

>5.5 mmol/l ECG: high, peaked T waves, wide QRS, AV block, loss of p wave Causes:

Metabolic acidosis, lack of mineralocortikoids, hypoxia, Olyguria, anuria,hemolysis, over correction of hypokalemia, drug side effects

Therapy:

Treat it over > 6mmol/l with

20-30 ml calcium gluconicum 10% 100 ml 20% glucose + 20 IE Insulin ( 1 IE Insulin / 2 g glucose), in 30

minutes control

40-100 ml 4,2 % Na HCO3 ( 0,5 mmol/ ml)

Low dose epinephrine, furosemid

Calciumo Calcium norm. value: 2,2-2,6 mmol/lo Ionized calcium norm. value : 1,1- 1,4 mmol/lo Regulation:

Parathormon, calcitonin, vitamin D Contraction of muscles, release of neurotransmitters, coagulation, bones

o Hypocalcemia Se Ca < 2,2 mmol/l, ionized Ca < 1,1 mmol/l Cause:

Massive transfusion, use of heart-lung machine, Hypoparathyreosis,Kidney disease. Enteral absorption disturbances, lack of vitamin D, lack

of magnesium

Signs:

Cardiac signs < 0,75 mmol/l , ECG-elonged QT

Paresthesia, laryngospasm, convulsion Therapy

Ca++substitution is indicated in decreased ionized Ca value.

Ca++substitution with the help of Ca-gluconicum, CaCl2.

o 10 ml Ca-Gluconicum 10 % (0,225 mmol/ml)o 10 ml Ca Gluconicum 20 % ( 0,45 mmol/ml)o 10 ml CaCl2 (0,5 mmol/ml)

o Hypercalcemia Cause:

Primary hyperparathyreosis, Vitamin D in toxicity, paraneoplasticsyndrome, sarcoidosis

Sings

ECG: Shorter AP, RF, QT distance. If Se Ca > 9 mmol/l ventricularfibrillation


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Therapy:

Glucose 5 %

Diuretics (Furosemid)

Isotonic Na-Sulphuricum ( 1 liter every 3-6 hours, with 20-40 mmol K+).

EDTA in arrhythmic disorders

Hemodialysis

Magnesiumo Hypermagnesemia

Causes:b

Antacids, Iatrogenic Signs:

Sedation, weakness of muscles, hyporeflexion, blood pressure decreases Therapy:

I.v. Ca++, Diureticso Hypomagnesaemia

In critically ill patients Signs:

Weakness, paresthesia, contraction of muscles, atrial fibrillation,

increasing muscle irritability Therapy:

MgSo4


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12. Guidelines of volume therapy

Isomosis:

Norm. osmolality: 290 mosmol/kg water= = 2 X Na + BUN + Glucose Hypoosmolarity -> hyponatremia Hyperosmolarity -> Na^, Glu^, BUN^

o

Ringers lactate: 273 mosmol/lo NaHCO3 8,4%: 2000 mosmol/lo 5% glucose : 253 mosmol/lo NaCl 0,9% : 308 mosmol/l

Possible disturbances of water and salt distributiono Isotonic dehydrationo Hypertonic dehydrationo Hypotonic dehydration

Signs of Dehydrationo 5%: Thirst and dry moutho 5-10%: Decreased peripheral perfusion, decrease skin turgor, postural dizziness,

oligurria, decrease CVP, tachycardia

o 10-15%: Increase in respiratory rate, hypotension, anuria, delirium, comao >15%: Life threatening

Crystalloidso Cheap effective, few side effectso Balanced Salt Solutions (BBS)

Hartmanns (Ringers), osmolality is similar to ECF, good for restoring extracellular volume

First line in preoperative period Reduce iatrogenic hyperchlormemic metabolic acidosis

o Normal Saline 0.9% Common for electrolyte replacement Contain high sodium and Cl, can cause hyperchlormemic metabolic acidosis Preferred in hypovolemic resuscitation, good for replacing fluid lose via

electrolyte rich GI loses

o Glucose Solution Aka Dextrose, 5% or 4%-saline 0.18% Glucose 5% - way of giving free water, used to restore dehydration associated

with water loss. Hyponatraemia may occur.

Glucose 10%, 20% and 50% for resorting normal glucose levels

Colloidso Homogenous, non-crystalline substances that have large molecules or ultramicroscopic

particles, which stay in the vascular compartment to expand the functional plasma

volume

o

HAS- Human Albumin Solution MW = 69 000, used as a 4.5% solution for hypovolemia and as a salt poor 25%

for the treatment of hypoalbuminaemia

o Gelatins Succinylated gelatins (MW 30 000), 4% in NaCl solutions Made from bovine collagen from BSE-free herds

o Hydroxyethyl starches (HES) MW 70 000 to 450 000 Made from hydrolysed amylase resistant maize. Vary in MW, molar substitution,

and degree of substitution


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o Dextrans Branched polysaccharides from bacterial actions on sucrose 10% dextran 40 (MS 40 000), 6% dextran 70, and supplied in 0.9% saline

solutions

Used as plasma expanders

Therapy of dehydrationo Laboratory data: Htc, acidosis, urine density (>1020), Na 450

mosmol/kg

o Hemodynamics: CVP, Pulm.art.pressureo Administer:

Crystalloids extreme volumes may cause edema Colloids i.vasculary (3-6h) + complications!

o Indication: i.v. deficiency (bleeding, shock) in hypoalbuminemia, fluid resuscitationo Dextran40,70,starch,HES,Voluven,Gelifundol,Salt1o%

Hyperhydration:o Heart insufficiencyo Kidney insufficiencyo

Iatrogenico Iso-, hyper-, hypotonic


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13. Indications and practice guidelines of clinical nutrition

Daily energy expenditure

Basic energy requirement: 35-40 kcal/m2/h

Resting metabolic need : 10% moreDetermination of Energy Needs:

Estimated needs: 30 kcal/kgBW/day x CF Calculated needs: Basic needs x CFo Harris-Benedikt equation: basic needs

Male: 66,5(13,8 x weight) + (5,0 x height) (6,8x age) Female: 65,5 (9,6 x weight) + (1,9 x height) (4,7 x age)

o Stein-Levine formula: Male: 1,05 x 24 x height Female: 0,97 x 24 x height

Indirect calorimetry: gold standard

Where CF= correction factor, which changes in fever, surgery, visceral damage, fractures, sepsis,burns

Nutritional Needs:o Energy: 25-40 kcal/kgBWo Protein 20%o Fat 30%o Carbohydrates 50%o Protein 1.2-1.5-2.0 g /kg/dayo carbohydrates 1-5 g/kg/day (max. 5!)o Fat 1-2 g/kg/dayo Water 1 ml / kcalo Minerals, Vitamins

Goals of Clinical Nutrition:

Primary:

o Providing non-protein energy, restoration of wasted structural proteins

Secondary:o support of immune response, prevention of complications

Proper nutrition can help in:o Improvement in wound healing , catabolic reaction decreases, improvement in

gastrointestinal permeability, less complications, shorter hospital stay

Steps of Clinical Nutrition:o Delineation of malnourished patientso Nutrition plan (caloric and composition)o Decision about the proper nutritiono Continuous control

Indications for clinical nutrition:o Inappropriate food intake for more than 5 dayso More than10% loss in body weight within 1 montho Actual body weight < 80% of ideal body weighto BMI


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Forms:o Total

Enteral: Oral or tube feeding

Side effects: gastric residuum, aspiration pneumonia Parenteral

Side effects: gut mucosa atrophy, overfeeding, hyperglycemia, infections

2 forms:

o Total parenteral nutrition (TPN)o Partial/ protein-preservating parenteral nutrition ( PT)

o Partial

Parenteral Nutrition:o Indication:

when enteral nutrition is not possible! (e.g. short bowel syndrome, chylothorax) If gastric emptying is disturbed, jejunal feeding should be administered.

o Peripheral TPN: The limit of administration in peripheral veins 800-1200 mosm/l

o Central venous: Above 1200 mOsm/l of osmolarity

o Solutions: Mono-solutions, multiple component solutionso Complications: Volume overload, Infection, metabolic shifts

Metabolic:

Essential amino acids are not provided during TPN (glutamin, cystein)

Too high CH: energy consumption increases, VCO2 and respiratory workincreases, hepatic steatosis, immune disturbances

Enteral Nutrition:o Advantages:

More physiological G. I. functions may be used: peristaltic, digetive, selective absorption Preserves bowel mucosa! (against bacterial translocation)

Glutamine supplementation is possible Early enteral nutrition: prevents intestinal damage

o Speed: 25-30 ml / hour, followed by an increase of 10-25 ml/1-4 hourso Indication: Dysphagia, mechanical causes, diseases of the stomach , appetite disturbance,

special need for food intake

o Contraindication: insufficient bowel function, illues, peritonitis, postaggression syndromeo Can be Oral, Gastric or jejunal

Gastric:

Nasogastric tube: for les than 4 weeks,

Gastrostomy

Percutaneous endoscopic gastrostomy Duodenal and jejunal feeding:

Nasointestinal tube: balloon, mandrine, Peristaltics pushes forward,endoscopic,

Transcutaneous intraabdominal tubeo Surgical method, endoscopic, PEJ (Percutanenous Endoscopic

Jejnostomy)

o Dosage: 1 g protein/kg/day + 150-200 kcal ( fat, CH) Requirements: Motility, resorption

o Contraindications: Absorption disturbance, Technical problems


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Refeeding Syndrome:o related to oral anteral or parenteral feedingo In patients with absolute nutritional deficiencieso Due to inappriopriate planning of nutritional therapy (not a stepwise increase in calory

during nutrition, immediate giving of large calories for malnourished patients)

o Characteristics: Severe electrolyte disturbances Fluid shifts Metabolic disturbances

Phases of Decreased Nutritiono First phase: the amount of structural proteins is maintained.

The energy need is met through: glycogenolysis, gluconeogenesis, ketogenesis,lipolysis

o < 7-10 days: use of stores along with normal serum levelso After 7-10 days: tissue and serum decrease of nutrition and functional disturbance (

organ symptoms),

o

After 10-15 days: pronounced weight losso After 60-70 days: death

NOTE: Read about Postagression Metabolism / Acute phase reaction from lecture notes


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14 & 15. The diagnostic steps and treatment of acid-base disturbances

Acidosis:

Increased intake of acids: infusions, conserved blood, intoxication with acids Increased acid production: diabetic or alcoholic ketoacidosis, increased protein metabolism

(endocrine crisis)

Removal of the H+ is disturbed (kidney disease) Loss of base, although acid content is normal: diarrhea, loss of intestinal fluids, certain renaldiseases.

The removal of the CO2 is disturbed: severe lung disorder, respiratory innervation failure

Alkalosis

Increased intake of alkaline materials: overcompensated acidosis by external bicarbonate, increased intake of bicarbonate in case of peptic ulcer.

Kidney is not able to excrete bicarbonate, it increases in the blood. As potassium and H+-excretion are connected, hypokaliemia may also produce alkalosis.

Loosing acids: vomiting

Forced ventilation: the removal of CO2 and the oxygen-intake increases: hysteria, chest wall irritation, irritation of the breathing center, fever, intracranial inflammatory disease, inappropriate mechanical ventilation.

Anion Gap: Anion gap = [Na+ + K] - [Cl- + HCO3-]; normal range: 8 to 16 mmol/l. Concentration of all the unmeasured anions in the plasma. Confirms the presence of a metabolic acidosis Differentiate between causes of a metabolic acidosis: high anion gap versus normal anion

gap metabolic acidosis.

Inorganic metabolic acidosis (eg due HCl infusion), the infused Cl- replaces HCO3and the anion gap remains normal.

Organic acidosis: the lost bicarbonate is replaced by the acid anion which is notnormally measured.AG is increased.

Blood Gas Parameters and Values

pH:: 7,35-7,45. Decreased: acidosis, increased: alkalosis.

pCO2:the pressure of the CO2 in the blood.o Normal value in arterial sample: 34-46 mmHg.o Increases: the lung is not able to remove the CO2,o decreases: too much CO2 is removed.

pO2:The partial pressure of the oxygen in the blood.

o Normal value: > 60 mmHg.o decreased: inappropriate gas exchange in the lung,o increased: hyperventilation.

Standard bicarbonate: reflects the concentration of the bicarbonate. information about themetabolic side of the compensation.

o Normal value: 22-26 mmol/l.o Decrease: lack of base, increase: excess of base.


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Actual bicarbonate:Reflects the metabolic side.o Normal value: 25 mmol/l.o Decrease: lack of base, increase: excess of base.

Buffer base (BB):The overall base content of the organism. Reflects the metabolic side.o Normal value: 45-52 mmol/l.

BE (base excess):Reflects the metabolic side.o Positive: base excess or lack of acids,o negative: lack of base or acid excess.o Normal value: -2,5 - +2,5 mmol/l.o Calculation of bicarbonate needed for compensation of a metabolic acidosis: bicarbonate

(ml)= BEx0,3x body weight

Acute Acid Base disturbances

pH pCO2 HCO3-

Acute ventilatory failure (respiratory

acidosis) -

Acute alveolar hyperventilation

(respiratory alkalosis) -

Acute metabolic acidosis -

Acute metabolic alkalosis -

Chronic Acid Base Disturbances

pH pCO2 HCO3-

Chronic ventilatory failure

(compensated respiratory acidosis)-

Chronic alveolar hyperventilation

(compensated respiratory alkalosis)- -

Chronic metabolic acidosis -

Chronic metabolic alkalosis -

Treatment

Metabolic Acidosis:o Correction of the underlying cause.o If needed give bicarbonate (when the pH is less than 7.1-7.2)

Dose (mEq) = 0.3 x Wt (kg) x SBE (mEq/L)o ER Care:raise the systemic pH above 7.1-7.2, a level at which dysrhythmias become less

likely and cardiac contractility and responsiveness to catecholamines will be restored.

Metabolic Alkalosiso underlying cause must be corrected.o Oral or intravenous replacement of extracellular volumeo alkalosis cannot be corrected until potassium is repleted.o In severe cases, unresponsive to other measures, ammonium chloride may be given (1 to

2 g orally every 4 to 6 hours to a maximum of 4 g every 2 hours; or by intravenous

infusion of 100 to 200 mEq dissolved in 500 to 1000 ml of isotonic saline) in addition to

potassium replacement.


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Respiratory Acidosiso correct the underlying disordero Rapid correction of the hypercapnia can alkalinize the cerebrospinal fluid, causing

seizures and also inducing a metabolic alkalemia.

o Infusion of sodium bicarbonate rarely is indicated. It may be considered incardiopulmonary arrest at extremes of pH (


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16. Sepsis and Multiple Organ Failure

Terms to know:

Sepsis: inflammatory reaction related to infection, provided that 2 of the following are presento Body temp.: 38 C, Pulse rate: >90/min, Breathing frequency 20/min,

PaCO2


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Cardiovascular decomposition caused by infection or infection-induced mediatorproduction

Characteristics:o Hypotension lasting for > 1 hour despite adequate volume therapy

(SAP < 90 mmHg, or decrease exceeds > 40 mmHg)

o Distributive shock, low SVR, high CO, Increased capillarypermeability, frequent myocardial dysfunction, severe cellular

dysfunction, apoptosis, MOF

Hematologicalo Bleeding, Thrombotic episodes, DICo Thrombocytopenia, pathological RBC count, PT and aPTT increased, Protein C

decreased, FDP increased, D-dimer increased

Gastrointestinalo GI bleeding or perforation, Ileus, Bowel ischemia, infarct, Acute pancreatitiso Amylase and lipase increased, pH decreased

Neurologicalo Consciousness disturbance, Confusion, Delirium, Septic encephalopathy

o BIS, EEG Endocrine, Immune

Diagnostic: Inflammatory Markers:o Interleukin -1, -6, -8, -10o TNF , CRPo Procalcitonin: most sensitive and earliest


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17. Intrahospital transport of the critically ill

Types of transfer:o Hospital to hospital transfero Transport within the hospital.

Pre-transport coordination and communication.

Personnel who accompany the patient. Equipment for monitoring and therapy.

Provide immediate medical and nursing care for resuscitation of patient.

Documentation

Risk to the patient and sometimes to the personnel.

Decision on transport: potential benefits of transport weighted against the potential risk.

A period of transport = period of potential instability.

Does the planned diagnostic procedure alter the treatment of the patient?o Could it not be performed at the ICU?


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18. Brain Death

Steps of Diagnosis:

Complete absence of brain activityo Clinical neurological signs

Dolls Eyes, Pupil light reactions, corneal reflex, auditory reactiono

Apnea test Arterial cannul Breathing with FiO2 1,0 -10 min Disconnecting from the respirator, providing oxygen: 6 l /min. Undress the patient, check breathing movements Serial arterial blood gas measurements Brain death: pCO2: 60 Hgmm or above, no spontaneous breathing activity Return to mechanical ventilation, donor management

o Vestibulo-ocular testingo Other investigations:

EEG, EP, TCD, angiography

Irreversibility

o Regular observation of all clinical signs primary brain damage year 3- childhood-adulthood: 12 hours secondary brain damage: 72 hours 5 weeks- 3 years: 24 hours (both primary and secondary) newborns: 72 hours

o OR: proven clinical signs + other tests


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19. Donor Conditioning

Live Donoro Kidney, bone marrow, liver, cutis

Cadaver Donoro Kidney, liver, pancreas, hear, lung

Conditions not suitable for donations:

o Patient refused donationo Medical causes

Malignancy, sepsis, infectious disease (HIV, Tbc), metabolic coma, intoxication,muscle relaxation, hypothermia, mechanical ventilation for more than 7 days (?)

Kidney Donation:o Criteria:

age: 4-70 years, maintained circulationo Contraindications:

known kidney disease, kidney trauma, hypotension for more than 1 hour (below60 mmHg), proteinuria of kidney origin, creatinin>300umol/l

o Relative contraindications severe hypertension , severe long-lasting insulin dependent diabetes

o Diagnostic tests: KN, creatinin, urine, Others: abdominal US, chest X-ray., serological assessments

Livero Criteria:

age: 2-60, maintained circulationo Contraindications:

Known liver disease, alcohol, drug-abuse, hepatotoxic drugs, liver damage,abdominal infection, long lasting hypernatremia (Na: higher than 170 mmol/l),

Long lasting respirator therapy, severe obesity

o Diagnostic tests: liver functions: Se Bilirubin, GOT, GPT, gamma GT, AP, prothtrombin, urine

bilirubin, ubg, serum albumin, serology: HIV 1-2, HBsAg, Hepatitis C, CMV,

Other: abdominal US

Heart:o Criteria:

age: below 45, maintained circulationo Contraindications:

known cardiac disease (valvular lesion, CMP, congenital, coronary artery), severehypertension, heart trauma or damage, chatecholamine in high dose (10 ug/kg/min

or more), long-lasting mechanical ventilation( 7 days), Long lasting hypotension

Diagnostic tests:

serology: HIV 1-2, Hepatitis C, CMV, auscultation, 12 lead EKG, BP,pulse rate, CVP, chest X-ray, Others: CK, CK-MB, LDH,

echocardiography, chest X-ray Lungs

o Criteria Age below 65, maintained circulation, ventilation: FiO2 below 40 %, PEEP:

below 5 water cm , normal blood gases

o Exclusion criteria: known pulmonary disease (tbc. asthma), smoking history, severe thoracic trauma,

infection, atelectasis, high arterio-alvelolar oxygen gradient (FiO2= 1, PEEP= 5

water cm, arterial oxygen below 35 mmHg), ventilation with high plateaupressure (30 water cm or more)


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Special Problems:o Hemodynamic disturbances

Hypovolemia

Systemic vasodilation (sympathicolysis)

Diabetes insipidus

Hyperglycemia Bleeding (polytrauma)

Inappropriate volumen therapy

Treatment goals:o MAP 65 mmHg or aboveo Cardiac index: 2.1 l/mino PCWP: 12-15 mmHgo CVP:12 mmHgo Diuresis: 100 ml/h or aboveo Arterial O2 (PaO2): 100 Hgmm or above

Myocardial ischaemia

Hypertension (catecholemine-storm): beta-blockers

Bradyarrhythmia: atropin ineffective, catecholamin (dobutamin) Supraventricular and ventricularis tachycardia: beta-blocker or

antiarrythmics

Hypotension: catecholamine, volume therapy, treatment of diabetesinsipidus

Thermoregulation disturbance

Causes:o damage of thermoregulatory center, peripheral vasoparalysis, cold

infusions, low environmental temperature

Goal: normothermia, passive warming, warmed infusions

Endocrine dysfunction

o Metabolic disturbances Hypernatremia

cause: diabetes insipidus, diureticum

Th: isotonic saline, 5% glucose, spironolacton, substitution Hypokalaemia, hypomagnesaemia, hypophosphataemia

cause: volume loss Hypocalcaemia

Cause: acut tubular necrosis, insufficient intake, CPD-conserved bloodproduct

Th: Calcium-chloride

o Mechanical ventilation Goals:

pH=7.4, SpO2 >95%, Tidal volume: 8-10 ml/ kg, FiO2 < 40%

PEEP< 7 wcm, normocapnia,


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20. Intravenous Anesthesia

Phases of Anesthesia:

Premedication (Topic 23)

Anesthesia induction

Anesthesia maintenance

Recovery phase Postoperative observationDrugs:

Rapidly acting (primarily induction) agentso Barbiturates: methohexital and thiobarbiturates

Thiopental and methohexital: high lipid solubility, promotes entry into brain, andfaster surgical anesthesia

Used for short procedures Note: respiratory and circulatory depressants, also decrease cranial blood flow

o Imidazole compounds: etomidate Rapid induction with minimal change in cardiac function or respiratory rate, but is

not analgesic

o Sterically hindered alkyl phenols: propofol Raster and better recovery then barbiturates Antiemetic actions, may cause hypotension via decrease in peripheral resistance

Slower acting (basal narcotic) agents:o Ketamine

Dissociative anesthesia: pt awake but has marked catatonia, analgesia, andamnesia

May increase ICPo Benzodiazepines: diazepam, flunitrazepam, midazolam

Used with inhaled, and with IV opioids Slower but longer acting then the barbiturates

Can use Flumazenil to speed recovery

o Large-dose opioids: fentanyl, alfentanil sufentanil, remifentanil Very helpful in high risk patients who may not survive a full general May cause chest wall rigidity

o Neuroleptanesthesia combination: opioid + neuroleptic State of analgesia and amnesia produced when fentanyl is used with droperidol

and nitrous oxide.

Advantages using IVA for maintenance:o Minimal cardiovascular depressiono Rapid recovery profile (with propofol only)o Higher oxygen concentration in some circumstances, such as:

One-lung anesthesia

Severe trauma Some procedures (laryngoscopy, bronchoscopy, electroshock)

o Situations where avoidance of N2O is necessary


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21. Inhalational Anesthesia

Used mainly for maintaining anesthetic state.

Gas at room temperature: nitrous oxide, xenon

Fluid at room temperature: halothane, enflurane, isoflurane, methoxyflurane, sevoflurane,desflurane vaporizer is needed

o Gases partial pressure in the inhaled air or in the blood or other tissue is a measure oftheir concentration (Henry Laws)

Site of Actiono GABA-associated chloride channel: stimulationo Voltage-dependent Ca-channels (T, L and N type): isofluraneo NMDA receptor: N2O, xenono Muscarinic effect in CNS (memory and consciousness): desflurane (M1), isoflurane (M1

and M3),sevoflurane (M1), halothane (M1 and M3)

o Nicotinergic: allo Voltage-dependent Na-channel inhibition: halothane, enflurane, isoflurane, desflurane,

sevoflurane

o

Solubilityo More rapid the equilibration in the blood, the more quickly the drug passes into the brain

produce anesthetic effects

o Drugs with LOW blood:gas partition coefficient (N2O), equilibrate faster Oswald Ratio

> 1 - better solubility in blood

< 1 less blood solubilityo Greater amount is necessary from the lung to reach the needed

concentration, but if it is in the blood soluble form, the diffusion to

the tissues is easier

o Minimum Alveolar Concentration (MAC): the concentration that eliminates the response

in 50% of patients exposed to a standard painful stimulus Modified MACs

MAC EI50 MACEI95: in 50, or 95% of the patients laryngoscopy andintubation possible

MAC BAR50and MAC BAR95: adrenergic reactions to incision areblocked in 50, or 95% of the patients

Increases MAC: age (children), hyperthermia, hyperthyreosis, sympathomimetics Decreases: hypothermia, gravidity, hypoxia, hypotonia, anemia, other drugs

Distributiono 75% vessel rich group (brain and heart), 8-10% fat, 15% muscle group, rest: vessel poor

group

o Fat: takes relative large amount of anesthetics will be important in the recovery

period. Factors affecting Anesthetics

o Inspired gas partial pressure, ventilation rate, pulmonary blood flow, AV concentrationgradient (Oswald ratio), Duration of anesthesia

o Mostly affect the high solubility group of gases.

Anesthesia Systemso Open

Inhalational anesthetics enters the patient as a transported gas by the room air, ieSchimmelbush mask

o Semi-open


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Narcotics is carried to the patient by fresh gaso Semi-closed

A certain amount of exhaled gases will be re-breathed, another amount will beremoved

o Closed systems Exhaled gas mixture is given back in its total amount to the system, after CO2-

absorption


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22. Anesthesiology Risks

In 9% of all patients, at least one type of complication happens.

Factors increasing the risk:o Duration of surgery,Age, Urgent surgery

Most Frequent complications:

o Cardiac arrhythmias Bradycardia:

Cause:o Drug side effect, Surgical manipulation, Hypotermia, Metabolic

disturbances

Treatment: atropin, catecholamins Tachycardia

Cause:o improper anesthesia or analgesia, hypoxia, hypercapnia,

hypovolaemia

Treatment: treat the cause! Most Frequent Causes:

Cardio-respiratory: hypoxia, hypotension, hypo-hypercapnia, myocardialischemia

Metabolic: catecholamine-effect, hypo-and hyperkalemia, malignanthyperthermia

Surgical: Increase of vagal tone, direct cardiac stimulation,

Drugs: vagolythic, sympathomimetics, halothane, enflurane,o Hypotension

MAP= below 60 mmHg If decrease of systolic BP reaches 25% (especially in previous HT) In coronary artery diseases diastolic BP is important (coronary perfusion) Causes:

Cardiorespiratory:o Hypovolemia: improper preoperative fluid load, gastrointestinal

fluid loss, bleeding

o Obstruction: embolia, aorto-caval compression, pericardialtamponade

o Rise in intrathoracal pressure: IPPV/PEEP, PTX

Myocardialo Decreased contractility: drug effect, acidosis, ischemia, AMI,

Arrhythmia, Pericardial tamponade

Drugs:o Absolute or relative overdose, central regional blocko Allergic reaction (drug, colloid, blood)o direct histamine release

o Hypovolemia: Preoperative:

bleeding: trauma, gynecological, gastrointestinal, rupture of large vessels

Gastrointestinal: vomiting, fistulas, diarrhea

Other: diuretic, fever, burn Intraoperative:

bleeding, Insensible perspiration, Drainage of bowel, ascites, Loose to the3rd space.


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o Hypertension Previous hypertension

Not known, Pregnancy-induced, Stopping antihypertensive treatment Increased sympathetic tone

Improper analgesia, Improper depth of anesthesia, Airway manipulation,Hypercapnia

Drug-overdose:

Epinephrin, ephedrin, Ketamin Other: hypervolemia, aortic clamp, pheochromocytoma, malignant hyperthermia

o Drug side effects Hypersensitivity, idosynchrasy, drug interations

o Embolisation Gas Thrombi

o Respiratory Complication Hypoxemia,

Low Fi02 of the inspired gas

Hypoventilation

Ventilation-Perfusion Insufficiency Hypercapnia ( Elimination failure or Increased production), Hypocapnia Airway obstruction (Equipment failure or Patient Related), Laryngospasm

Can be caused by: insufficient depth of anesthesia, secretum or bloodwithin the pharynx, irritative inhalational agent, administration of

barbiturates

Bronchospasm

Can be caused by: Admin of Beta Blockers, Drugs inducing histaminerelease

PTX, Intubation complications Aspiration of the gastric contents

o Improper mechanical ventilationo Temperature Alterations

Hypothermia

Decreased heat production:o Anesthetics decreases metabolic rate, and shivering

Decreased heat loss:o Vasodilatation, air conditioning,o Exporative heat loss: mechanical ventilation, sweating, open

cavities (especially abdominal and thoracal)

Can lead to:o CO decreases, decrease in tissue oxygenation, in severe cases:

metabolic acidosis, oliguria, Hyperthermia

Causes: Sepsis, Drug effects, Excessive catecholamine-release

Can lead to: CO increases Oxigen demand increases, minute ventilation increases, acidosis Treatment: cooling (surface and intravenous fluid)

o Physical injuries Damage to nerves, teeth, corneal drying


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24. Regional Anesthesia

Definition

Regional anesthesia is the blockade of nerves that causes anesthesia of regional distributionwhile consciousness is preserved.

Full aseptic and antiseptic precautions must be taken.

Advantages:o The patient remains conscious, the recovery is uncomplicated, extension of the blockade

provides effective analgesia, reduces metabolic and endocrine changes, blood loss is

reduced, less expensive, faster discharge

Disadvantageso The patient remains conscious, some blocks need up to 30 min to be fully effective,

analgesia is not always fully effective, generalized toxicity may occur, widespread

sympathetic blockade causes hypotension, not suitable for all operations

Immediate complications:o Sensitivity, hypotension, respiratory paralysis pain on injection, motor paralysis, urinary

renention

Late complications:o Nerve trauma, anterior spinal artery syndrome, adhesive arachnoiditis (spinal, epidural),

pneumothorax (intercostal, interpleural, supraclav. brach. plexus), headache (spinal)

Types:o Central (spinal, epidural, caudal)o Peripheral (any peripheral nerve)

Spinal Anesthesiao Anesthetic agent is injected into the cerebrospinal fluid that causes widespread blockade

of the spinal nerves. Can be single or continuous (catheter)

o Patient position: sitting or lateral with spine fully flexedo Puncture site : L2-3, L3-4, L4-5 interspace

Penetrate: Supraspinous and interspinous lig, lig flavum, dura mater, arachnoid

matter Spinal cord ends at L2, dural sac at S2o Drugs used: bupivacaine, articain, fentanylo Contraindications:

Absolute

Patient refusal, infection at puncture site, uncorrected hypovolemia Relative:

Bacteremia, pre-existing neurologic disorders, heparin therapyo Effects:

Motor and sensory blockade, SNS blockade, bradycardia, venodilatation, decreasein bp,

Epidural Anesthesia

o Blockade of nerves of the epidural space, that lie within the spinal canal but outside thedura mater. Touhy needle is used

o Contraindications are the same as aboveo Single or continuous EDA

First test dose, then main dose is injectedo Anesthesia( concentrated solution in large dose) or pain control (dilute solution in small

dose)

o Drugs: local anesthetics, morphine derivates, alpha-agonists


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o Effects: Motor and sensory block depends on dose and concentration. Hemodynamic effects: SNS blockade is milder and more gradual in onset than

with spinal.

Caudal Anesthesiao Injection of local anesthetic through the sacral hiatus into the sacral (epidural) canalo Large dose is needed because of the large canal and free leakage through the foraminao Anesthesia or analgesiao Single or catheter technique

Biers Blocko Limb is isolated from the circulationo Local anesthesia is injected.o The drug reaches the capillaries by retrograde flow, gets

into the extravasc. space and reaches nerve endings

causing paralysis below the cuff

Local Anesthesia drugso Potency is related to lipid solubilityo Duration of action is related to protein binding and blood

supplyo Esters

Long Acting tetracaine, amethocaine Short Acting procaine Surface action benzocaine, cocaine

o Amides Long action bupivacaine, ropivacaine Medium action lidocaine (max 3mg/kg), prilocaine

o Can be combined with Bicarbonate increase pH (increases unionized LA) Adrenaline decrease vascular reabsorption, increasing duration Opiopds synergism with epidural LA, morphine 2-5mg

Clonidine prolongs duration of sensory and motor block

Refer to OXFORD HANDBOOK OF ANAESTHESIA for more info on regional blocks


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25. Guidelines of acute and chronic Pain relief

Pain:

unpleasant sensory and emotional experience associated with actual or potential tissue damage,always subjective

Factors influencing perception

o Physical, Depression, Anger, Anxiety Pain assessment:

o Believe the patients complaint, assess the severity of the pain.o Assess the psychological state of the patient.o Take a detailed history of the pain.o Perform a careful physical examination.o Order, and personally review, any necessary diagnostic investigations.o Consider alternative methods of pain control during the initial evaluation.

Describing Paino Verbal Description Scaleo Numerical Rating Scaleo Visual Analogue Scaleo Ocuher scale for kids

Acute Pain:o Usually self limitingo Usually a progressive improvement over a short periodo Unrelieved pain is associated with:

Outpouring catecholamines, risk of tachycardia, dysrhythmias and decreasedmyocardial oxygenation.

Reduced functional residual capacity Reduced sputum clearance and risk of atelectasis Peripheral vasoconstriction Metabolic acidosis

o Pharmacological Paracetamol:

Inhibit prostaglandin syn, both analgesic and antipyretic

4g/d NSAIDS:

Analgesic, anti-inflam, anti-pyretic, anti-platelet

Diclofenac(50mg), Ibuprofen (400mg),Ketorolac (10mg) Inhalation analgesia:

Entonox (50% nitrous oxide, 50% oxygen)

Isoflurane (0.2-0.75% in Entonox) Opioids:

Morphine, papaveretum, Pethidine, Methadone

Fentanly: highly lipid soluble, short duration, good for trans dermal admin Codeine: prodrug for morphine

Tramadol: synthetic centrally acting opioid like drug,o Inhibit the serotonin and noradrenaline update at never terminals

Infusions for 2-3 days

only, tolerance occurs quickly

Side effects: respiratory depression, sedation, euphoria, nausea andvomiting,

Opioid Antagonist: Naloxone Simple Analgesics


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Ketorolac aka Toradol, IM/IV (0.5mg/kg up to 30mg qds) for post op painfor 5 days

NSAID

Not for use preioperativeo Interruption of Pain Afferents

Direct injection of local analgesic drugs close to peripheral nerves, major nervetrunks or nerve roots: blocking conduction of afferent impulses.

Using Local Anagesic:

Spinal subarachnoid blocko Use long lasting drug like bupivacain for long lasting effects, or

opioid drug before blocks wears

Epidural analgesia, caudal epidural analgesia

Intercostal block, nerve blocks Other Methods:

Inhalational methodso Entonox, note nitrous oxide can cause pancytopenia

Transcutan Electrical Nerve Stimulation (TENS)o TENS acts by increasing c.s.f. levels of B endorphins, together

with activation of the pain gate by counter irritation. Cryotherapy

Physical methods of pain relief

Chronic Pain:o Intractable pain is

severe, incapacitating, resistant to all forms of treatment by non-opioid drugs orphysical therapies.

o Pain is described as chronic when it persists for more than 6 monthso Pain threshold is lowered by continuous paino There are five groups of patients with chronic pain associated with cancer:

Due to cancer, due to treatment, dying, Are / have been drug dependent, pain notdue to cancer but have cancer

o Goal of Therapy: To relieve pain, to manage associated depression or anxiety, to prevent / relieve

side effects of drugs (especially nausea, constipation), to assist sleep.

o Drugs: The simple analgesics

Paracetamol (max 4g.day) and aspirin(max 4g.day) The weak analgesics

Codeine phosphate, Oxycodone The potent opioid drugs

Morphine, Methadone, Dextromoramide, Pethidine, Diamorphine

Note: Morphine is contraindicated in:

o tension headache and migraines, arthritis, muscle spasmo burning pain caused by nerve damage, neuralgic pain

Adjuvant analgesic drugs

anticonvulsant drugs for relief of neuralgic pain

antispasmodic drugs for relief of muscle spasm

in low dose the tricyclic antidepressants will help sleep and they mayhelpful in reducing the burning pain associated with nerve damage.

Corticosteroidso Relief of headce of raised intracranial pressure

Inhalational methods of analgesia


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26. Cardiopulmonary Resuscitation (ALS)

http://www.resus.org.uk/pages/als.pdf

o Arrhythmias associated with cardiac arrest are divided into two groups: shockable rhythms(VF/VT) and non-shockable rhythms (asystole and PEA).

o The principle difference in management is the need for attempted defibrillation in patients with

VF/VT.o Subsequent actions, including chest compression, airway management and ventilation, venous

access, administration of adrenaline, and the identification and correction of reversible factors,are common to both groups.

o The ALS treatment algorithm provides a standardised approach to themanagement of adult patients in cardiac arrest.

Shockable rhythms (VF/VT)o Sequence of actions

o Attempt defibrillation (one shock - 150-200 J biphasic or 360 J monophasic).o Immediately resume chest compressions (30:2) without reassessing the rhythm or

feeling for a pulse.o Continue CPR for 2 min, then pause briefly to check the monitor:

If VF/VT persists

Give a further (2nd) shock (150-360 J biphasic or 360 J monophasic). Resume CPR immediately and continue for 2 min.

Pause briefly to check the monitor.

if VF/VT persists give adrenaline 1 mg IV followed immediately by a (3rd)shock (150-360 J biphasic or 360 J monophasic).

Resume CPR immediately and continue for 2 min.

Pause briefly to check the monitor.

If VF/VT persists give amiodarone 300 mg IV followed immediately by a(4th) shock (150-360 J biphasic or 360 J monophasic).

o Lidocaine 1 mg kg-1 may be used as an alternative if amiodarone

is not available, but do not give lidocaine if amiodarone has beengiven already.

Resume CPR immediately and continue for 2 min.

Give adrenaline 1 mg IV immediately before alternate shocks (i.e.approximately every 3-5 min).

Give a further shock after each 2 min period of CPR and after confirmingthat VF/VT persists.

If organised electrical activity is seen during this brief pause in compressions,check for a pulse.

If a pulse is present, start post-resuscitation care.

If no pulse is present, continue CPR and switch to the nonshockablealgorithm.

If asystole is seen, continue CPR and switch to the nonshockable algorithm.

Non-shockable rhythms (PEA and asystole)o Pulseless electrical activity (PEA) is defined as cardiac electrical activity in the absence of any

palpable pulse.o These patients often have some mechanical myocardial contractions but they are too weak to

produce a detectable pulse or blood pressure.o PEA may be caused by reversible conditions that can be treated if they are identified and

corrected (see below).


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o Survival following cardiac arrest with asystole or PEA is unlikely unless a reversible cause canbe found and treated effectively.

o Sequence of actions for PEAo Start CPR 30:2.o Give adrenaline 1 mg IV as soon as intravascular access is achieved.o Continue CPR 30:2 until the airway is secured, then continue chest compressions

without pausing during ventilation.o Recheck the rhythm after 2 min.o If there is no change in the ECG appearance:

Continue CPR. Recheck the rhythm after 2 min and proceed accordingly. Give further adrenaline 1 mg IV every 3-5 min (alternate loops).

o If the ECG changes and organised electrical activity is seen, check for a pulse. If a pulse is present, start post-resuscitation care. If no pulse is present:

Continue CPR.

Recheck the rhythm after 2 min and proceed accordingly.

Give further adrenaline 1 mg IV every 3-5 min (alternate loops).

o Sequence of actions for asystole and slow PEA (rate < 60 min-1)o Start CPR 30:2.o Without stopping CPR, check that the leads are attached correctly.o Give adrenaline 1 mg IV as soon as intravascular access is achieved.o Give atropine 3 mg IV (once only).o Continue CPR 30:2 until the airway is secured, then continue chest compression without

pausing during ventilation.o Recheck the rhythm after 2 min and proceed accordingly.o If VF/VT recurs, change to the shockable rhythm algorithm.o Give adrenaline 1 mg IV every 3-5 min (alternate loops).

anaesthesiology and intensive care

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