2. Pain is an unpleasant sensory and emotional
experience, associated with actual or potential
tissue damage, or described in terms of such
damage (The International Association for the
Study of Pain, IASP).
Etymology: “Pain” came from Latin poena,
"punishment, penalty" and as well from Greek
"ποινή" (poine), generally "penalty", "punishment“.
INTRODUCTION
3. Acute pain in perioperative setting is defined as
pain that is present in a surgical patient because
of pre-existing disease, surgical procedure or a
combination of these.
Pain is ubiquitous, is an intolerable sensation
and makes the patient vulnerable.
There is no gain without pain!
INTRODUCTION
4. � Tachycardia
� Increased cardiac output
� Increased blood pressure
� Raised systemic and coronary vascular resistance
� Reduction of lung volumes (tidal volume, vital capacity
and FRC)
� Reduced alveolar ventilation
� As result hypoxemia and hypercapnia
� Reduced ability to cough
� Reduced mucociliar clearance and retention of
secretions
PHYSIOLOGIC RESPONSES
5. � Decreased gastrointestinal motility (gastric stasis
and paralytic ileus)
� Increased smooth muscle sphincter tone
� Increased intestinal secretions
� Increased motility of the urethra and bladder and
consequent difficulty with micturation
� Catabolic state of metabolism (weight loss and
negative nitrogen balance)
PHYSIOLOGIC RESPONSES
6. � Fear
� Anxiety
� Anger, resentment and animosity towards medical
personnel (if left unattended)
� Sleep deprivation
� Depressive state and felling of helplessness
PSYCHOLOGICAL RESPONSES
7. Surgery produces biphasic insult on human
body, which has implications for pain
management:
- Trauma to tissue, which produces noxious
stimuli and great nociceptive input
- Following surgery there is inflammatory
process at the surgical site with noxious input.
They occur at peripheral (stimulates
nocioceptive afferents) and central level
(excitation of spinal neurons).
MECHANISMS OF PAIN
13. It is an opioid agonist. Acts on mu-receptors.
Effects:
- Analgesia
- Euphoria
- Sedation
Protein binding – 35%
Peak effect: 15-30 min IV; 45-90 min IM
Duration of action: 3-4 hrs
MORPHINE
14. Cardiovascular system
- direct myocardial depression
- hypotension (drug-induced histamine release)
- bradycardia (increased parasympathetic effect)
Respiratory system
- dose-dependent depression of ventilation
- reduced breathing pattern to CO2
- an increase in PaCO2
- transient apnea
MORPHINE
15. Central nervous system
- Vasoconstrictor for cerebral vessels, therefore, an
ability to reduce ICP in the absence of hypoventilation
- Miosis (excitatory action on the oculomotor nerve)
- Decreases MAC (minimal alveolar concentration) for
volatile agent
Gastrointestinal system
- Spasm of sphincter Oddi (biliary spasm)
- Decreases peristaltic activity
- Enhance the tone of the pyloric sphincter, contributing
to delayed gastric and intestinal tract emptying
MORPHINE
16. Dosages (for adults)
- As premedicant: 0.05-0.1 mg/kg
- As component of anaesthesia: SC – 0.1-0.2 mg/kg;
IV – 0.05-0.2 mg/kg
- As continuous infusion (e.g. PCA – 0.02-0.05
mg/kg/h)
- Maximal daily dose: 1.5 mg/kg
MORPHINE
17. Cause:
⮚ Direct stimulation of dopamine receptors in the
chemoreceptor trigger zone in the floor of the 4th
cerebral ventricle
⮚ IV<IM
⮚ Management: antagonists 5HT-serotonine
receptors (ondansetron, tropisentron and
granisetron). Efficacy > 95%
MORPHINE, NAUSEA AND
VOMITING
18. � Mu-agonist
� It has structural similarities to atropine and may
have some of their effects and side effects
(tachycardia, midriasis, dry mouth)
� Duration of action: 120-150 min
� It has an active metabolite – norpethidine – with a
strong potential to precipitate seizures in
compromised patients
� It readily crosses blood-brain and placental barrier
PETHIDINE
19. Dosages:
� 1-2 mg/kg IV, IM QID
Contraindications:
� Renal failure
� Hypovolemic patients
� Those on MAOIs (monoamino oxidase inhibitors)
– may produce hypotension or hypertension,
convulsions, hyperpyrexia and even coma
PETHIDINE
20. � Mu-agonist
� Dose-dependent respiratory depressant
� Cardiovascular stability is present
� Duration of action: 30-45 min
� No active potentially dangerous metabolite,
predominately metabolized in the liver and 2/3 of
the dose is excreted in the urine
FENTANYL
21. Effects:
- Analgesia
- Deep sedation (in extremely high doses: 50-150
mcg/kg)
Dosages:
- 0.5-100 mcg/kg IV
Special breathing support systems MUST be
available during fentanyl administration!
FENTANYL
22. Has been in clinical use in Germany since the late
1970s and has proven effective in both
experimental and clinical pain.
Is a synthetic, centrally acting analgesic agent.
It acts as an opioid agonist with selectivity for μ-
receptor and also binds weakly to κ- and σ-
receptors.
Analgesic doses of tramadol are comparable to
those of pethidine.
TRAMADOL
23. Has 2 distinct but complementary mechanisms of
action:
1 – opioid – antagonised (about 30%) by
naloxone
2 – nonopioid – acts on monoamine system to
inhibit the reuptake of noradrenaline and serotonin
(5-hydroxytryptamine)
TRAMADOL
24. Effects on respiration
There is minimal (not clinically relevant) respiratory
depression at the recommended dosages. However,
depression may occur at considerably exceeded
dosages.
Effects on cardiovascular system
Postoperative IM tramadol (0.75-1.5 mg/kg) decreases
both heart rate and diastolic blood pressure but not
clinically relevant. Although there is no effect on systolic
blood pressure*.
* - Schaffer J, Kretz FJ et al. Nalbuphine and tramadol for control of postoperative pain in children.
Anaesthetist 1986;35:408-13.
TRAMADOL
25. Recommended dosages
- oral: 50-100 mg every 4-6 hrs.
The maximum recommended daily oral dose is
400 mg.
- IM, IV: Safe and clinically effective – 1.0-1.5 mg/kg
Maximum IV dosage – 600 mg/day.
TRAMADOL
26. Not recommended for use:
- in patients < 12 years of age
- in patients who are receiving MAOIs or within 2
weeks of their withdrawal
- During pregnancy or in lactating mothers
TRAMADOL
