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8/11/2019 Dr Muthalib

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POST ANESTHESIA CARE UNIT(PACU)

A. Muthalib Nawawi, dr.SpAnKBag/SMF Anestesiologi & Intensive Care Unit

FK.Unpad/RS Hasan Sadikin Bandung


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Design of PACU

Near the operating room and other IntensiveCare facilities

Open ward (to facilitate observation of all patients simultaneously)

well lighted (day light)


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Equipment Pulse oxymetri ECG BP monitor Warming/cooling blanket Emergency trolley outlets : oxygen, electrical, suction minor set infusion/syringe pump


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Before world war IIPost operative death after anesthesia andsurgery is high

This period is characterized by relatively highincidence of potentially life threatening.Respiratory and circulatory complications.After world war IISuccess of RR factor in evaluation ofmodern ICU/PACU


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Staffing

Nurses - trained in care of emergingPatients ( ACLS)

- I Nurse for 2 Beds ( Patients ) Medical direction of an Anesthesiologist

Coordinated to Surgeon and any consultants


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Emergence from Anesthesia

Because post operative is a time of great physiologic stress.

Ex.. - Airway obstruction

- Shivering- Vomite ...etc.

Delayed Emergence When the patients fail to regain

consciousness 60-90 minute followinggeneral anesthesia ( G.A.)


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The causes

Residual Anesthetic Sedative Prolong effect of opiate Hypothermia

Metabolic Disturbances Perioperative stroke (rare)


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Post op/post anesthesia Management

Monitoring: - vital sign - BP Pulse/HR RR

- Oxygen supplementation (SpO2)- Temp- Sensory and motor level (Regional

Anesthesia)


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Pain control

- parenteral- Regional anesthesia- Nerve Block

Agitation/Restlessness- cause ? (hipoxemia, acidosis etc)

Nausea and vomitingcause ? hypotension by

- regional anesthesia- opioid- vagal tone


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Shiveringcause ?- Unwarmed I.v. fluids- Exposure of large wound- AC

- Hyperthermia- Metabolic acidosis ect


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Complications in PACU 1. Airway obstruction

- Unconscious patients tonguefalling

back against the posterior pharynx- Larynx spasm- Glottic edema etc


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2. Hypoventilation- Defined as PaCO2 > 45 mmHg

pH < 7,25- Causes

- Residual depressant effect ofanesthesia agents (overdose)

- In adequate reversal

- Severe pain- Tight abdominal dressing- CO2 production is high


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3. Hypoxaemia Defined as PaO2 < 70 mmHgCauses

- Hypoventilation- Oxygen consumption - FRC - Lung - edema


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4. Hypotension - Defined as A 20-30% reduction of

BP- Causes

- Hypovolemia- Ventricular dysfunction- Impaired cardiac filling


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5. Hypertension Defined as BP > 20-30% of base line

Causes Sympathetic activation- pain

- hypercapnia


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6. Arrhythmia - Hypercarbia- Electrolyte disturbances- Residual effects of cholinesterase

inhibitor


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Discharge criteria- must be evaluated- after 60 minutes in the PACU

_____________________________________Parameters Value

____________________________________

color - pink 2- pale 1- cyanotic 0

_____________________________________Respiration - Breathe deeply & cough 2- Shallow but adequate 1- apnea 2


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_____________________________________CirculationBP within 20% of normal 2

20-50% 150% from normal 0

_________________________________________________Consciousness- awake/alert 2- arousable 1- no response 0

_________________________________________________

Activity- move all extr 2- move 2 extr 1- no movement 0


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INTENSIVE CARE UNIT (ICU)

- Multi disciplinary- As intensive care with potentially lifethreatening illness

- Supporting therapies- neurologic- cardiovascular/hemodynamic

- Pulmonary/respiratory- Electrolyte/metabolism- Nutritional


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NEUROLOGIC SUPPORT- CBF is constant auto regulation

at range of BP (MAP 50-150mmHg)- Injury losses of ability autoregulation- CBF related to CPP

(CPP = MAP-ICP)


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ACUTE CNS INJURY - Ischemia (focal or generalize)- Structural distortion of brain

- Scoring GCS- CNS support is focused on- optimizing systemic & cerebral B.F- normalizing ICP


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-Immediate concerns- airway/ventilation/oxygenation- hemodynamic issues

-Hypotension (loss of automatic control)- Hypertension (hyper adrenergic state)

- Cardiac dysfunction- Seizures control (metabolic/infections)

- Neurologic exam

- Is there a surgical lession ?- GCS- Laboratory- CT Scan


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SUPPORTIVE CARE - General treatment

- Oxygenation- Correct anemia- Hemodynamic stability

- Establish normovolemia- Control hyperthermia- Control seizures

- control pain- Avoid agitation/shivering- correct metabolic abnormalities


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-Control ICP- CSF (volume reduction)- Hyperventilation- Osmotic agent- Barbiturate- Head position

- To be prevent vasospasm

- Steroid (?)


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CARDIOVASCULAR/HEMODYNAMIC

SUPPORT - Major determinants of cardiac output (C.O)

- Heart rate & Contractility

- Blood Vessels- Volume Intra vascular- Pre Load- After Load- Oxygen Delivery

- C O = HR x 3 V


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* SV Is Determined By

- Preload- After load- Contractility

* Clinical Measurements- Preload - Echo Cardiography

- PCWPAfter load = SVR

= MAF - CV x 80C. O

Contractility = ECHO = EF


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Oxygen Delivery (D O2)D O2 = Ca O2 x C O x 10

= (HB x 1.34 x Sa O2)+ (PaO2 x 0,031) x

C. O x 10


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SHOCK * Characterized BV

- Organ Blood Flow that Is Inadequate

to meet Tissue Demands* Four Categories Of Shock1. Cardiogenic Shock

- Co - PCWP - SVR


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2. Hypovolemic Shock- C O - P C W P - S V R

3. Distributive Shock- C O N / - PCWP N / - S V R

4. Obstructive Shock- C O - PCWP

- S V R


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MANAGEMENT OF SHOCK- Increasing C.O

- Therapy Arrhythmias- To Manage - Pre Load

- After Load- Fluid- Improve Contractility

- Optimize Oxygen Delivery- Hemoglobin- P a O2 (FiO2 & Lung Function)


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- Vaso Pressor & Inotropic Agent- Dopamine. etc- Antibiotic- Decrease Oxygen Demand


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Respiratory SupportOne of Most Common Disorder Leading to1cm Admission is ARF (Acute RespiratoryFailure)ARF. - When the Pulmonary system is no

longer able to meet the metabolicdemands of the body

Two types of respiratory failure (RF)Type I Hypoxemic RF (PaO2 50TORR)

Type II Hypercapmic RF (PaCO2 50TORR)

- with hypoxemic- without hypoxemic


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Causes of RF

Type I (Usually the result of mismatch ofalveolar ventilation and pulmonary perfusion)Example - Acute lung injury

- acute pulmonary edema Type II (Characterized by alveolar

hypoventilation)

Example airflow obstruction- CNS- Neuromuscular disturbances


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CLINICAL MANIFESTATIONS OF ARF IS ARDS

- Onset 12-72 hours after triggers- Respiratory distress (gasping, cyanotic etc)- Lung edema (non cardiogenic)- PaO2 < 50mmHg- CPWP > 18mmHg- PaO2/FiO2 < 200mmHg Management- Oxygen supplement

- nasal canula- face mask

- IPPV non invasive

- Pharmacologic


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ELECTROLYTE DISTURBANCES Es the most common disturbances are in K+

Na+ Ca+A. Potassium (N.3,5-5,5 mEq/L)

1. Hypokalemia (K+ < 3,5 mEq/L)

Causes - Renal & extra renal losses- Transcellular shift- Decreased intake

Clinical

Arrhythmias- ECG. Abnormalities- Muscle Weakness- Ileus Etc.


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TREATMENT- Correcting The Underlying Cause- Stop Offending Drubs

- Correct The Potassium level- K + > 3 Meg /L . KCL 20-40

Meg/4-6 MRS . Orally/NGT

- K +


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2. HYPERKALEMIK ( K+>5,5 mEq/L

- Most often from renal dysfunction- Other Causes

- Acidemia

- Hypoaldosteronism- Cell Death (Hemolysis, Burns etc)- Excessive Intake

Clinical - Arrhythmias- Muscle Weakness- Paralysis. etc.


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TREATMENT- Underlying cause- Stop Offending Drugs- Limitation of Potassium- Correcting

- ECG Abnormalities are present- CaCl2 10 % 5-10 ml (i.v.5-10 mnt)- Sodium Bicarbonate

1 Meg /Kg BW /I.V 5-10 mnt.- 10 IU RI. In 10 Ml Dext.50 %/IV/10 - Dialysis


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3. SODIUM (N 135 - 145 mEq/L)1. Hyponatremia (Na + < 135 mEq/L)Causes- Excess Secretion of ADH- Non Sodium Solute Infusion Clinical.- CNS Disturbances- Muscular Disturbances


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TREATMENT- Treating the Underlying Disease- Stop Offending Drugs- Correcting

- Restricting free water intake- Increasing free water clearing

- Loop diuretic

- Replace with saline 5 %- Limit 15 mEq/L in first 24 hours


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2. HYPERNATREMI (Na + > 145 mEq/L)Cause Intracellular volume Depletion with

A Loss of free water- Excessive sodium intake

Clinical- CNS- Muscle


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TREATMENT Underlying CausesFree water Repletion

L = 0,6 x wt [( Na1 /Na2)-1]

L = Water deficit Na 1 = Normal Sodium Level Na 2 = MeasuredWt = KS

- Correcting . 12-20 Meg /C/24HRS- Dialysis


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METABOLIC DISTURBANCES

Hyperglycemic Syndromes- Life Threatening Hyperglycemic syndrome1. Diabetic Ketoacidosis (DKA)2. Hyperglycemic Hyperosmolar Nonketotic

syndrome (H1 + NK)Clinical

- Osmotic Diuresis Dehydration- Weakness- CNS Manifestation- Odor to the Breath


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TREATMENT

- The Goals are- Restore the Fluid & Electrolyte Balance- Provide Insulin- Identify Precipitating Factor

- NS. 20 ml/ kg for First HourThen. 250-500 ml/Hr AS NeededAfter that

- NS 0,5 % Maintenance-Insulin (R1) 5-10 IU

Followed By 5-10 IU /HR. (0,1 IU /kg/HR)


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IF Glucose Level 250 Mg %- Glucose Containing Fluid (1/V)

(Maintain Glucose level >150By Insulin S.C.

IF Glucose Level < 150 mg %

- Glucose 10 %IF PH < 7.0

- Consider Bicarbonate- Correcting the Serum level (if Present)

- Potasium- Phosphorus- Magnesium

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