Abhishek Narayan, 2007

1. General guidelines and of anaesthesiology and intensive care

•

Peri-operative Care

o Assessment

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

o Prep of the Patient

o Intra-operative care

Painless, amnesia, hypnosis, relaxation

o Postoperative care

PACU

• Mointor vitals, support if needed, pain therapy, treat any complications,

“ICU or normal ward”

•

Intensive ( Critical) Care Medicine

Management of pt with life threatening patho-physiological conditions

Vital functions

• Resp, Cardio Vascu, Metabolic, Neuro

Main Characteristics

Life threatening conditions can be

• Broad spectrum of illnesses, of extreme severity, cause complications

Multidisplinary

Special facilities and staff

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 achieved

in all patients.

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 is

appropriate to limit treatment.

Priority 1 patients

• critically ill, unstable patients in need of intensive treatments such as

ventilator 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 little

likelihood 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 has

diminished.

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 for

“comfort care” only.

• Permanent vegetative state

• Physiologically stable patients who are at statistically low risk for

requiring ICU treatment

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2. Severity Scoring Systems

•

Two Outcome Prediction Models

o Disease specific: Focus on predictors that are specific or peculiar to the problem.

Ranson criteria: for acute pancreatitis

Child-Turcotte classification: for cirrosis hepatis

Burns index

Injury Severity Score system (ISSS)

Glasgow Coma Scale (GCS)

o General: Are intended for a broad variety of diseases and circumstances.

The use of general prediction models:

• Clinical research, quality improvement, to assist in decision making about

ICU admission and discharge, auditing performance, comparison in the

same ICU or between ICUs, an index of workload and consumption of

resources

ASA Physical Status ( American Society of Anesthesiologists) . Defining and

quantifying anesthetic risk.

APACHE (Acute Physiology And Chronic Health Evaluation ) Score

SAPS II ( Simplified Acute Physiology Score)

TISS ( Therapeutic Intervention Scoring System)

•

ASA Physical Status:

Category

Description

ASA I

Healthy patient

ASA II

Mild systemic disease, no functional limitation

ASA III

Severe systemic disease, definite functional limitation

compensated by medications

ASA IV

Severe systemic disease, decompensated state that is a

constant threat of life

ASA V

Moribound patient

ASA VI

Organ donor

“E”

Emergency

•

APACHE: A point score derived from the degree of abnormality of readily obtainable

physiological and laboratory variables in the first 24 h of ICU admission, plus extra points for

age and chronic ill health

•

SAPS II:

12 physiology variables + age + GCS in the first 24 h. ( T, MAP, P, RR, SaO2 or PaO2,

pH, Na, K, Creatinin, Htc, WBC, Na, + HCO3)

o Score

Mortality

4 points

10 points

20%

20 points

50%

> 21 points

> 80 %

•

TISS: attaches a score to procedures and techniques performed on an individual patient (1 - 4

points).

o Used for costing services by attaching a dollar vaule to each TISS point

o It is also used as an index of workload activity, or further work load

40-50 points

The most critically ill of the patients requiring intensive

therapy. Lethality: 73%

20-39 points

Patients requiring intensive care. Lethality 21 %

10-19 points

Patients need of intensive monitoring only. Lethality: 15 %

< 10 points

There is no need for intensive care.

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3. Securing Airways

•

Main purposes of airway management

o Avoidance of airway obstruction

o Removal of foreign bodies

o Desuction: aspiration, mucus, edema

o Tongue

•

Oxygen therapy

•

Mechanical ventilation

•

Without Equipment:

o Airway Cleaning

o Head tild chin lift

o Jaw thrust manoeuvre

o Recovery Position

•

Non invasive:

o bag and mask

o Mayo tube (oropharyngeal)

o LMA

o Intratracheal: oro-, nasotracheal Combitube

•

Invasive :

o non surgical

• direct laryngoscopy

• bronchoscopy

• retrograde

o surgical

• cricothyroidotomy

• tracheostomy

•

Complications of Endotracheal Intubation

o During intubation :

• incorrect tube placement, laryngeal trauma

• cardiovasculare response, hypoxaemia

o Tube is in place: blockage

o Following extubation:

• aspiration, airway obstruction, tracheal stenosis

o Prolonged Intubation:

• Damage to vocal cord

Grading 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 visible

2. Anterior glottis is not visible

3. Epiglottis but not glottis is visible

4. Epiglottis is not visible

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

•

Factors influencing Respiration

o Appropriate content of the inspired air

o 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 blood

o Cellular metabolism

•

Alveoli

300 million in an adult

The surface is appr.70-80 sq.meter

Close connection with a capillary

Gas exchange: alveolar epithel - basal membrane - capillary endothel

Surfactant, produced by the pheumocytes inreseaes surface tension

•

Breathing:

o Breathing frequency: 14-18/min.

o Tidal volume: 500 ml

o Minute volume: 14-18 x 500 ml= 7-9 liter

• Respiration volume: volume of 1 breath =500

• Inspiratory reserve: the additional volume which

may 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 be

exhaled after forced inspiration followed by a

forced expiration = 2500 + 500 + 1000= 4000

• 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, O₂ therapy

• Respiratory stimulant (doxapram 1.5-4mg/min IV) may be given if no

improvement with O₂ therapy

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5. Monitoring Ventilation

Signs and Symptoms:

•

Inspection:

Respiration pattern

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

• Apnea

• Cheyne-Stokes breathing: both frequency and amplitude increases until a certain

point, than apnea and starts the next periodical phase (lower brainstem damage)

• Atactic: irregular frequency and amplitude (upper brainstem damage)

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

dyspnea,

clinical signs of hypoxemia

• Incoordinated movements , consciousness disturbance, agitation, tachycardia,

slight hypertension, peripheral vasoconstriction, cyanosis

( Red. Hgb >

50g/L)

• Bradycardia, bradyaritmia, hypotension severe hypoxemia

accidental respiratory muscle use

• COPD-patients: sitting position, fixing the upper part of the body on their

extended 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 muscle

paradoxical breathing, cyanosis

•

Ausculation

Diagnostic:

• Chest X-Ray-helical CT, Pulsoxymetry

• Capnography

o Look at pictures at the bottom of the topic

o 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 paO2

o Below SaO2 of 90%: measures are needed to improve oxigenation

o 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 O₂ in inspired air

o 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 disturbance

o 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

3-8 % - Normal

5-20 % - Usually tolerable

20-30 % - May be life threatening if cardiac function is deceased

> 30 % - Life threatening, severe hypoxemia

•

FiO₂

o PaO₂ is 5 x higher than FiO₂

o FiO2 = 0.21

o The FiO2- PaO2 ratio reflects the alveolo-capillary gas exchange

o Shows pulmonary dysfunction even in case PaO2 is normal

o PaO2 may be normal or elevated during oxygen therapy

Normal: 4.0 -5.0

Moderate Pulmonary dysfunction: 2.0 - 3.9

Sever Pulmonary dysfunction: <2.0

o An example:

PaO2 = 80 Hgmm

• at FiO2 0.21: normoxemia

• at FiO2 0.8: pulmonary dysfunction

Indications for mechanical ventilation

• respiratory failure

• prolonged postoperative recovery,

• altered conscious level,

• inability to protect the airway or exhaustion when the patient is likely to proceed to respiratory

failure.

• Criteria for starting mechanical ventilation are difficult to define and the decision is often a

clinical one. Indicators include:

o Respiratory rate >35 or <5 breaths/ minute

o Exhaustion, with laboured pattern of breathing

o Hypoxia - central cyanosis, SaO2 <90% on oxygen or PaO2 < 8kPa

o Hypercarbia - PaCO2 > 8kPa

o Decreasing conscious level

o Significant chest trauma

o Tidal volume < 5ml/kg or Vital capacity <15ml/kg

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Basic Forms of Respiratory Care:

• Patient effort

o None: controlled mode

o Needs support: assisted mode

o Uncertain or changing: assist-control mode

• According to invasiveness

o Invasive

o Non-invasive

• Administered pressure

o Positive

o Negative (iron lung)

Mechanical Ventilation

• Controlled:

o No patient trigger

o 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 and

facilitates airway suctioning.

• However, it is also possible to deliver positive pressure ventilation to cooperative patients in a

non-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.

•

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' the

inspiratory 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 and

unassisted.

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 be

reduced 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 by

intravenous volume loading.

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

breathing patients.

Ventilation Parameters

Tidal Volume

o No ALI: 10 ml/kg

o ARDS: outcome is better in case of low TV

6 ml/kg

12 ml/kg

Frequency

o ACV : 4/min (only for backup is needed)

o SIMV: 10/min. at the beginning, should be increased when needed

o PSV: no frequency preset is necessary

Sensitivity trigger

o May be:

Flow, pressure, time

o Usually it is negative pressure: 1- 3 H₂Ocm

o Appropriate trigger sensitivity is important: low sensitivity → too frequent triggering →

danger of respiratory alkalosis

FiO2

o High FiO2 potentially toxic

Limit: 0,6

o Goal: the lowest FiO₂, resulting in acceptable oxygenation

o What is acceptable?

60 mmHg O₂, saturation above 90%

PEEP

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 FiO2 at 1.0 and then wean rapidly to a FiO2 adequate to maintain SaO2 of >93%.

• FiO2 of greater than 0.6 for long periods should be avoided if possible because of the risk of

oxygen-induced lung damage.

• Strategies to improve oxygenation (other than to increase FiO2) include increasing the mean

airway 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 this

may cause barotrauma to the lungs.

• More complex strategies to improve oxygenation may be required in severely hypoxic patients

eg 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 PEEP

further 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 by

the patient requiring intravenous fluid loading and inotropic or vasopressor therapy.

• Another strategy is to prolong the inspiratory time. Normal inspiratory to expiratory ratio is 1:2

but 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 require

heavy sedation.

o Not infrequently, due to a reduced minute volume the PaCO2 may 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 approach

should 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 in

respiratory 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 holding

and coughing.

Decreased pulmonary compliance - pulmonary pathology, including oedema or

infection 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 <10 cmH2O

o Tidal volume > 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 CPAP

weaning 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 support

overnight 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 status

o Cardiac: chest pain, ischemia on ECG, and wall motion abnormalities on echocardiogram

o Renal: decreased urine output, BUN/creatinine increases,

o GI: abdominal pain, decreased bowel sounds,

o Periphery: cool limbs, poor capillary refill, weak pulses

•

Shock:

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)

Patho-physiology of shock:

Prolonged hypotension (decreased DO2)

Neurohumoral response. Stress hormones: catecholamines, ADH, ACTH,

glucagon (enhanced myocardial contractility, peripheral vasoconstriction)

Metabolic response (hyperglycemia)

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. DIC

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 suctioning

o Patophysiology - Decreased venous return -low RR

o Clinical presentation - hypotension, weak pulses, flat neck veins, cold and clammy skin

o Therapy:

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

(hydroxyethyl starch, dextrans)

Human albumin, blood products

Vasopressors

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•

Cardiogenic Shock:

Causes: AMI and its complications, dysrhytmias, acute myocarditis, contusion,

pharmacologic depressants, proximal aortic dissection)

Pathophysiology: Decreased contractility causes decreased SV, CO, RRsyst

Clinical manifestation: hypotension with cutaneous vasoconstriction, cold extremities,

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

Therapy:

Inotropic drugs

• Dobutamin (ß1,ß2, 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 ß1 effect increases contractility, HR,

RRsyst

• Norepinehrine (alfa1, alfa2, ß1)

o Dosage: 1-20 ug/min

o Increases vascular tone, so can treat hypotension.

o Adverse effects: Intense peripheral vasoconstriction can cause

organ hypoperfusion and ischemia.

• Epinehrin (alfa1, alfa2, ß1, ß2)

o Indications: Refractor hypotension. Bronchospasm, anaphylaxis,

cardiac arrest.

o Effects: 1-2 µg/min ß2 bronchodilatation

o ß1: 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, abnormal

liver function test.

Vasodilatators (nitrates, labetalol, ACE inhibitors)

Intravenous sedatives and analgesics. (bezodiazepins, opioids)

Thrombolysis, PTCA, cardiac surgery

Intraaortic balloon counterpulsation (IABC)

Bradycardia:

HR<40/min

Atropine max:3mg, Epinehprine 5-10ug/min

Pacemakers (transcutaneous, transvenosous)

Tachycardia

HR>150/min

Drugs: cordarone, lignocaine, propafenon

Cardioversion (synchronised, 100, 200, 360J)

Defibrillation (, 200, 200, 360J) No pulse.

•

Neurogenic Shock:

o Traumatic spinal injury

o 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 and

equalization 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 Pressure

Possibilities:

Fluid manometry

Electrical

Veins used:

V. Subclavia, V. jugularis interna, V. Femoralis, V.

cephalica and basilica

Spontaneously breathing patient: 5-10 H₂O cm

Artificially ventilated patients:

3-5 H₂O cm higher

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 normal

Three spikes (a, c, v)

Two descents (x, y)

a: atrial contraction

x: atrial relaxation

c: ventricular contraction

v: atrial filling

y: opening of tricuspidal valve

before ventricular filling

Possible Complication

Carotid puncture, PTX, Air

embolism, arrhythmias,

perforation, cardiac tamponade

Brachial plexus, vagus damage

chylothorax

•

Pulmonary Artery Catheter

o Also called the Swan Ganz catheter

Inserted into the Subclavian vein

or Internal jugular vein

Swimmed up to the pulmonary artery by the blood flow.

o Makes use of Ficks principle of diffusion

3 West zones of the lung

I. zone: P_A>P_pa >P_pv

II. zone : P_pa > P_A > P_pv

III:zone: P_pa > P_pv > P_A

o Complications

Thrombosis, Pulmonary artery rupture,

Sepsis, Endocarditis, Lung infarction,

Valve damage

o Can measure: CVP, RVEDP, PAP, PCWP

o 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 Output

o VO₂: Oxygen consumption

Oxygen consumption depends upon the peripheral metabolism and its alterations,

such as:

• Exercise, fever, hypermetabolism

o ScvO₂ - central venous oxygen saturation

Oxygen saturation in the superior vena cava

Normal value is: 70-80 %

• Decreased DO₂ or increased VO₂

o 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 Output

o Uses principle of Thermo-dilution

o This system can measure intra- and extrathoracic volumes and monitors both left and

right side of the heart function.(CO, preload volume, contractility, resistance, volume

responsiveness, extravascular lung volume)

o Applies thermodilution to measure CO

o 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 intracardiac

shunts, 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 Monitoring

o Calculating circulating minute volume based upon the exhaled CO2-concentration (Fick-

principle)

o Measures hemodynamical and respiratory parameters

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11. Life-threatening disturbances of fluid-electrolyte balance.

ECF

ICF

intravasc. interstic.

Normal Values:

Na⁺

142

138

•

Bodywater-content: 42 l (60%)

o IC-water: 28 l (40%)

K⁺

136

o EC-water: 14 l (20%)

Ca⁺⁺

interstitial: 10,5 l (15%)

Mg⁺⁺

intravascular: 2,8 l (4%)

Cl^-

103

111

transcellular: 0,7 l (1%)

HCO₃

•

Sodium

HPO²⁴

110

Hyponatremia ( Se Na < 135 mmol/l)

SO²⁴

se osmolarity < 280 mosm/l

Protein

IC volumen increases

Signs:

• Confusion , restless, edema, weakness, convulsion, coma

Causes:

• TUR syndrom, SIADH, pneumonia, central nervous system illness,

diuretics, vomiting, diarrhea

Therapy:

• Water restriction

• Se Na < 130 mmol/l - sodium (not allowed if Se Na >130 mmol/l!)

• Hyperhydration - Furosemid, dialysis

• Rapid correction may result central pontin myelinolysis

Hypernatremia (Se Na > 145 mmol/l)

Se osmolarity is high (> 320-330 mosm/l)

IC volume decreases

Signs:

• Neurologic disturbances, restless, fever, weakness, confusion,

intracerebral or subarachnoideal bleeding, dry mucous membranes, thirst

Causes:

• Free water loss > intake of water, great diuresis (diabetic ketoacidosis),

hyperalimentation, intake of medicine containing sodium (sodium

bicarbonate), diabetes insipidus, kidney insuffiency with polyuria

Therapy:

• Aim: to compensate fluid deficiency in 48 hours

• Intake of free water - 5% glucose

• Slow correction!

o Decrease of Se Na < 0,5 mmol/l/h (danger of quick correction:

edema, convulsion)

•

Potassium

o Hypokalemia

Mild hypokalemia: 2,5-3,5 mmol/l

Serious hypokalemia: < 2,5 mmol/l

• Muscle weakness, convulsion, paralytic ileus, prolonged effect of non-

depolarisating muscle relaxants

• ECG: ST- depression, flat T wave, U wave

Causes:

• Intracellulary transport:

o Extracellulary alkalosis (hypokalemic alcalosis) or intracellular

acidosis, Altering of potassium - glucose-Insulin therapy

• Gastrointestinal losses

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o Diarrhea, preoperative anterograd rinsing of the bowels, intestinal

polyposis, Intestinal fistulas in Crohn’s disease

• Renal losses:

o Diuretics, hypomagnesemia, hyperaldosteronism, glucocorticoid

effect

Therapy

• Potassium supplement ( p. Os, i.v.) 2-3 mmol/kg/day

o max. speed of infusion: 20 mmol K+ / hour

• Potassium deficiency in mmol =

=( 4,5 mmol/l - Se K+) x ECF(1) x 2 == (4,5 mmol/l - Se K+ ) x 0,4 x BWkg

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

•

Calcium

Calcium norm. value: 2,2-2,6 mmol/l

Ionized calcium norm. value : 1,1- 1,4 mmol/l

Regulation:

Parathormon, calcitonin, vitamin D

Contraction of muscles, release of neurotransmitters, coagulation, bones

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.

10 ml Ca-Gluconicum 10 % (0,225 mmol/ml)

10 ml Ca Gluconicum 20 % ( 0,45 mmol/ml)

10 ml CaCl2 (0,5 mmol/ml)

Hypercalcemia

Cause:

• Primary hyperparathyreosis, Vitamin D in toxicity, paraneoplastic

syndrome, sarcoidosis

Sings

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

fibrillation

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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

•

Magnesium

o Hypermagnesemia

Causes:b

• Antacids, Iatrogenic

Signs:

• Sedation, weakness of muscles, hyporeflexion, blood pressure decreases

Therapy:

• I.v. Ca++, Diuretics

o 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 Ringer’s lactate:

273 mosmol/l

o NaHCO3 8,4%:

2000 mosmol/l

5% glucose :

253 mosmol/l

NaCl 0,9% :

308 mosmol/l

•

Possible disturbances of water and salt distribution

o Isotonic dehydration

o Hypertonic dehydration

o Hypotonic dehydration

•

Signs of Dehydration

5%: Thirst and dry mouth

5-10%: Decreased peripheral perfusion, decrease skin turgor, postural dizziness,

oligurria, decrease CVP, tachycardia

10-15%: Increase in respiratory rate, hypotension, anuria, delirium, coma

>15%: Life threatening

•

Crystalloids

o Cheap effective, few side effects

o Balanced Salt Solutions (BBS)

Hartmann’s (Ringers), osmolality is similar to ECF, good for restoring extra

cellular 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

•

Colloids

o 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 dehydration

o Laboratory data: Htc, acidosis, urine density (>1020), Na <10 mol/l, osmolality >450

mosmol/kg

o Hemodynamics: CVP, Pulm.art.pressure

o Administer:

Crystalloids- extreme volumes may cause edema

Colloids- i.vasculary (3-6h) + complications!

o Indication: i.v. deficiency (bleeding, shock) in hypoalbuminemia, fluid resuscitation

o Dextran40,70,starch,HES,Voluven,Gelifundol,Salt1o%

• Hyperhydration:

o Heart insufficiency

o Kidney insufficiency

o Iatrogenic

o 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% more

Determination of Energy Needs:

• Estimated needs: 30 kcal/kgBW/day x CF

• Calculated needs: Basic needs x CF

o 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/kgBW

o Protein

20%

o Fat

30%

o Carbohydrates

50%

o Protein

1.2-1.5-2.0 g /kg/day

o carbohydrates

1-5 g/kg/day (max. 5!)

o Fat

1-2 g/kg/day

o Water

1 ml / kcal

o 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 patients

o Nutrition plan (caloric and composition)

o Decision about the proper nutrition

o Continuous control

• Indications for clinical nutrition:

o Inappropriate food intake for more than 5 days

o More than10% loss in body weight within 1 month

o Actual body weight < 80% of ideal body weight

o BMI<18 kgBW/m²

o Antropologial parameters measured< 80% of the ideal

o Serum albumin < 30g/l (normovolemia)

o Ly: <1,2 G/l

o Decreased immune function

MUST MEET AT LEAST 4 OF THE ABOVE

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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 solutions

o 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 work

increases, hepatic steatosis, immune disturbances

•

Enteral Nutrition:

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

Speed: 25-30 ml / hour, followed by an increase of 10-25 ml/1-4 hours

Indication: Dysphagia, mechanical causes, diseases of the stomach , appetite disturbance,

special need for food intake

Contraindication: insufficient bowel function, illues, peritonitis, postaggression syndrome

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 tube

o Surgical method, endoscopic, PEJ (Percutanenous Endoscopic

Jejnostomy)

Dosage:

1 g protein/kg/day + 150-200 kcal ( fat, CH)

Requirements: Motility, resorption

Contraindications: Absorption disturbance, Technical problems

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• Refeeding Syndrome:

o related to oral anteral or parenteral feeding

o In patients with absolute nutritional deficiencies

o 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 Nutrition

o First phase: the amount of structural proteins is maintained.

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

lipolysis

< 7-10 days: use of stores along with normal serum levels

After 7-10 days: tissue and serum decrease of nutrition and functional disturbance (

organ symptoms),

o After 10-15 days: pronounced weight loss

o 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 renal

diseases.

• 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 HCO3

and the anion gap remains normal.

• Organic acidosis: the lost bicarbonate is replaced by the acid anion which is not

normally 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 CO₂is 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 the

metabolic 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

pCO2

HCO3-

Acute ventilatory failure (respiratory

↓

↑

acidosis)

Acute alveolar hyperventilation

↑

↓

(respiratory alkalosis)

Acute metabolic acidosis

↓

Acute metabolic alkalosis

↑

Chronic Acid Base Disturbances

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 Alkalosis

o underlying cause must be corrected.

o Oral or intravenous replacement of extracellular volume

o 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 Acidosis

o correct the underlying disorder

o 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 in

cardiopulmonary arrest at extremes of pH (<7.0-7.1). In most other situations, it has no

role in the treatment of respiratory acidosis.

o Bronchodilators such as beta-agonists (eg, albuterol, salmeterol), anticholinergic agents

(eg, ipratropium bromide, tiotropium), and methylxanthines (eg, theophylline) are helpful

in treating patients with obstructive lung disease and severe bronchospasm. In addition,

theophylline may improve diaphragm muscle contractility and may stimulate the

respiratory center.

o Oxygen therapy

o Because many patients with hypercapnia also are hypoxemic, oxygen therapy may be

indicated. Oxygen therapy is indicated to prevent the sequelae of long-standing

hypoxemia..

o Medroxyprogesterone increases the central respiratory drive and is effective in treating

obesity-hypoventilation syndrome.

o Acetazolamide is a diuretic that increases bicarbonate excretion and causes a metabolic

acidosis. The metabolic acidosis subsequently stimulates ventilation.

•

Respiratory Alkalosis

o rarely life threatening; therefore, treatment is usually not indicated unless the pH level is

greater than 7.5.

o Because respiratory alkalosis usually occurs in response to some stimulus, treatment is

usually unsuccessful unless the stimulus is controlled.

o If the PaCO2 is corrected rapidly in patients with chronic respiratory alkalosis, metabolic

acidosis may develop due to the previous compensatory drop in serum bicarbonate.

o In respiratory alkalosis complicating mechanical ventilation, changes that can lead to

improvement and resolution involve decreasing the tidal volume and respiratory rate.

o For patients who are receiving mechanical ventilation and are breathing above the set

ventilator rate, adequate sedation and control of pain may also be helpful in controlling

hyperventilation.

o In hyperventilation syndrome, patients benefit from reassurance, rebreathing into a paper

bag during acute episodes, and treatment for underlying psychological stress. Sedatives

should be reserved for patients who have not responded to conservative treatment. Beta-

adrenergic blockers may help control the manifestations of the hyperadrenergic state that

may lead to the hyperventilation syndrome in some patients.

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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 present

o Body temp.: <36 °C, or >38 °C, Pulse rate: >90/min, Breathing frequency 20/min,

PaCO2<30 mmHg, WBC count: <4 G/l or >12 G/l, or more than 10% immature forms

• Severe sepsis: sepsis + organ dysfunction, hypoperfusion, hypotension related to inflammation

• Septic shock: sepsis-induced shock symptoms

o Systolic BP: <90 mmHg, or decreased by 40 mmHg to baseline , Need for vasopressors,

Tissue and organ perfusion disturbances

• Multiple organ dysfunction: acute dysfunction of two or more organs, homeostasis may be

maintained only by organ-preserving measures

• Sepsis Steps:

o Infection Entry into Circulation Acute Phase Systemic inflammatory

Organ Dysfunctions:

• Respiratory

o Tachypnea, orthopnea, cyanosis, Need for artificial ventilation, ARDS

o PaO2 <70 mm Hg, SaO2 <90%, PaO2/FiO2 ≤300

• Renal

o Oliguria, Anuria, ↑ Creatinine

• Hepatic

o Icterus

o Hyperbilirubinemia, AST, ALT increased, LDH elevated, AP elevated, Hypalbuminemia,

PT elevated

• Cardiovascular

o Tachycardia, Hypotension, Arrhythmias, P/MAP ratio, Heart failure, Need for

hemodynamic support

o CVP, PAOP altered, decreased EF, decreased CO

o Septic Sock:

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Cardiovascular decomposition caused by infection or infection-induced mediator

production

• 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 capillary

permeability, frequent myocardial dysfunction, severe cellular

dysfunction, apoptosis, MOF

•

Hematological

o Bleeding, Thrombotic episodes, DIC

o Thrombocytopenia, pathological RBC count, PT and aPTT increased, Protein C

decreased, FDP increased, D-dimer increased

•

Gastrointestinal

o GI bleeding or perforation, Ileus, Bowel ischemia, infarct, Acute pancreatitis

o Amylase and lipase increased, pH decreased

•

Neurological

o Consciousness disturbance, Confusion, Delirium, Septic encephalopathy

o BIS, EEG

•

Endocrine, Immune

•

Diagnostic: Inflammatory Markers:

o Interleukin -1, -6, -8, -10

o TNF α, CRP

o Procalcitonin: most sensitive and earliest

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17. Intrahospital transport of the critically ill

• Types of transfer:

o Hospital to hospital transfer

o 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 activity

o Clinical neurological signs

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

o 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 testing

o 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 Donor

o Kidney, bone marrow, liver, cutis

•

Cadaver Donor

o Kidney, liver, pancreas, hear, lung

•

Conditions not suitable for donations:

o Patient refused donation

o Medical causes

Malignancy, sepsis, infectious disease (HIV, Tbc), metabolic coma, intoxication,

muscle relaxation, hypothermia, mechanical ventilation for more than 7 days (?)

•

Kidney Donation:

Criteria:

age: 4-70 years, maintained circulation

Contraindications:

known kidney disease, kidney trauma, hypotension for more than 1 hour (below

60 mmHg), proteinuria of kidney origin, creatinin>300umol/l

Relative contraindications

severe hypertension , severe long-lasting insulin dependent diabetes

Diagnostic tests:

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

•

Liver

Criteria:

age: 2-60, maintained circulation

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

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:

Criteria:

age: below 45, maintained circulation

Contraindications:

known cardiac disease (valvular lesion, CMP, congenital, coronary artery), severe

hypertension, 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

Criteria

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

below 5 water cm , normal blood gases

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 plateau

pressure (30 water cm or more)

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•

Special Problems:

Hemodynamic disturbances

Hypovolemia

• Systemic vasodilation (sympathicolysis)

• Diabetes insipidus

• Hyperglycemia

• Bleeding (polytrauma)

• Inappropriate volumen therapy

• Treatment goals:

o MAP 65 mmHg or above

o Cardiac index: 2.1 l/min

o PCWP: 12-15 mmHg

o CVP:12 mmHg

o Diuresis: 100 ml/h or above

o 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 diabetes

insipidus

Thermoregulation disturbance

• Causes:

o damage of thermoregulatory center, peripheral vasoparalysis, cold

infusions, low environmental temperature

• Goal: normothermia, passive warming, warmed infusions

Endocrine dysfunction

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 blood

product

• Th: Calcium-chloride

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 observation

Drugs:

•

Rapidly acting (primarily induction) agents

o Barbiturates: methohexital and thiobarbiturates

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

faster 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, and

amnesia

May increase ICP

o 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 depression

o 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 of

their concentration (Henry Laws)

•

Site of Action

o GABA-associated chloride channel: stimulation

o Voltage-dependent Ca-channels (T, L and N type): isoflurane

o NMDA receptor: N₂O, xenon

o Muscarinic effect in CNS (memory and consciousness): desflurane (M1), isoflurane (M1

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

o Nicotinergic: all

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

sevoflurane

•

Solubility

o 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 solubility

o 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 MAC’s

• MAC EI₅₀MACEI₉₅: in 50, or 95% of the patients laryngoscopy and

intubation possible

• MAC BAR₅₀ and MAC BAR₉₅: adrenergic reactions to incision are

blocked in 50, or 95% of the patients

Increases MAC: age (children), hyperthermia, hyperthyreosis, sympathomimetics

Decreases: hypothermia, gravidity, hypoxia, hypotonia, anemia, other drugs

•

Distribution

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 concentration

gradient (Oswald ratio), Duration of anesthesia

o Mostly affect the high solubility group of gases.

•

Anesthesia Systems

o Open

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

Schimmelbush mask

o Semi-open

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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:

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, myocardial

ischemia

• Metabolic: catecholamine-effect, hypo-and hyperkalemia, malignant

hyperthermia

• Surgical: Increase of vagal tone, direct cardiac stimulation,

• Drugs: vagolythic, sympathomimetics, halothane, enflurane,

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, pericardial

tamponade

o Rise in intrathoracal pressure: IPPV/PEEP, PTX

• Myocardial

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

Arrhythmia, Pericardial tamponade

• Drugs:

o Absolute or relative overdose, central regional block

o Allergic reaction (drug, colloid, blood)

o direct histamine release

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 the

3rd space.

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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

Drug side effects

Hypersensitivity, idosynchrasy, drug interations

Embolisation

Gas

Thrombi

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 blood

within the pharynx, irritative inhalational agent, administration of

barbiturates

Bronchospasm

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

release

PTX, Intubation complications

Aspiration of the gastric contents

Improper mechanical ventilation

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)

Physical injuries

Damage to nerves, teeth, corneal drying

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23. Premedication

Goals of Premedicaion:

• Decreasing anxiety

o Information to patient, psychotherapy, anxiolytic

• Decreasing secretion

o Not a concern with current drugs

• Potentiation of hypnotic effect of anesthetics.

• Decreasing Post Operative Nausea and Vomiting (PONV)

o Caused by opioid use

o Prevented by using additional Oxygen and antiemetic

• Amnesia

o Benzodiazepines and propofol

• Decreasing gastric volume / pH

o Gastric emptying: metoclopramide (10mg), decreasing pH: omeprazol (PO 40mg

night before and 2hrs preop), Ranitdine (PO, 150-300mg night before)

• Decreasing vagal reflexes

o Anticholinergic drugs:

Traction of orbital muscles

Repeated use of succinyl choline

Induction with halothane, especially in children

Use of propofol in patients with low heart frequency.

• Decreasing sympatho-adrenal reflexes

o Beta-blocker or Clonidine

Drugs:

• Benzodiazepines:

o Receptors present in many brain regions, including the thalamus, limbic, and cerebral

cortex.

o Form part of GABA_Areceptors-chloride ion channel (inhibitory, via increased chloride

channel opening Note: increase frequency of opening, not duration (barbiturates)

o Lormetazepam (0.5-1.5mg), Temazepam, Lorazepam (2hr preop, 1.0 - 2.5 mg),

midazolam (20-40mins preop, IM, 2-10mg)

• Butyrophenone

o Droperidol

Neuroleptic and antiemeic, dopamine and alfa-blocker

Used as antiemetic, 0.5-2.5 mg, or if used as neuroleptic 0.2mg/kg with fentanyl

4µg/kg

• Phenotiazines

o Chlorpromazine (good for chronic hiccup, upto 25mg), thioridazine, fluphenazine

o Central antiemetic, sedative, Anxiolytic

o H2-receptor antagonist, alfa-adrenerg antagonist, anticholinergic

o potentiating opioid effect

o Side effect: extrapyramidal movements,tachycardia, hypertonia (postop.)

• Other Drugs:

o Thrombosis prophylaxis, Antibiotics (single-shot)

o Treatment of underlying illnesses (DM, hypertension, epilepsy, etc.)

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24. Regional Anesthesia

Definition

•

Regional anesthesia is the blockade of nerves that causes anesthesia of regional distribution

while 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

•

Disadvantages

o 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 Anesthesia

o 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 flexed

o 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 S2

o Drugs used: bupivacaine, articain, fentanyl

o Contraindications:

Absolute

• Patient refusal, infection at puncture site, uncorrected hypovolemia

Relative:

• Bacteremia, pre-existing neurologic disorders, heparin therapy

o Effects:

Motor and sensory blockade, SNS blockade, bradycardia, venodilatation, decrease

in bp,

•

Epidural Anesthesia

o Blockade of nerves of the epidural space, that lie within the spinal canal but outside the

dura mater. Touhy needle is used

o Contraindications are the same as above

o Single or continuous EDA

First test dose, then main dose is injected

o 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 Anesthesia

o Injection of local anesthetic through the sacral hiatus into the sacral (epidural) canal

o Large dose is needed because of the large canal and free leakage through the foramina

o Anesthesia or analgesia

o Single or catheter technique

•

Bier’s Block

o Limb is isolated from the circulation

o 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 drugs

o Potency is related to lipid solubility

o Duration of action is related to protein binding and blood

supply

o 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 patient’s 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 Pain

o Verbal Description Scale

o Numerical Rating Scale

o Visual Analogue Scale

“Ocuher scale for kids

•

Acute Pain:

Usually self limiting

Usually a progressive improvement over a short period

Unrelieved pain is associated with:

Outpouring catecholamines, risk of tachycardia, dysrhythmias and decreased

myocardial oxygenation.

Reduced functional residual capacity

Reduced sputum clearance and risk of atelectasis

Peripheral vasoconstriction

Metabolic acidosis

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 and

vomiting,

• Opioid Antagonist: Naloxone

Simple Analgesics

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• Ketorolac aka Toradol, IM/IV (0.5mg/kg up to 30mg qds) for post op pain

for 5 days

• NSAID

• Not for use preioperative

o Interruption of Pain Afferents

Direct injection of local analgesic drugs close to peripheral nerves, major nerve

trunks or nerve roots: blocking conduction of afferent impulses.

Using Local Anagesic:

• Spinal subarachnoid block

o 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 methods

o 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:

Intractable pain is

severe, incapacitating, resistant to all forms of treatment by non-opioid drugs or

physical therapies.

Pain is described as chronic when it persists for more than 6 months

Pain threshold is lowered by continuous pain

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 not

due to cancer but have cancer

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.

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 spasm

o 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 may

helpful in reducing the burning pain associated with nerve damage.

• Corticosteroids

o 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 the

management of adult patients in cardiac arrest.

Shockable rhythms (VF/VT)

Sequence of actions

Attempt defibrillation (one shock - 150-200 J biphasic or 360 J monophasic).

Immediately resume chest compressions (30:2) without reassessing the rhythm or

feeling for a pulse.

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 been

given 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 confirming

that 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 nonshockable

algorithm.

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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Survival following cardiac arrest with asystole or PEA is unlikely unless a reversible cause can

be found and treated effectively.

Sequence of actions for PEA

o 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).

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).

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