1. ā¢ References:
1. Sarawak Handbook Of
Medical Emergencies 3rd
Edition
2. Guide to The Essential in
Emergency Medicine by
Shirley Ooi.
3. Parrillo & Dellinger: Critical
Care Medicine, 3rd ed.
4. Civetta, Taylor, & Kirby's:
Critical Care, 4th Edition
5. http://www.cc.nih.gov/ccc/ped
web/pedsstaff/ivf.html
(Intravenous Fluid
Management)
Lim Jun Sian Batch
12
2. ā¢ Clinical syndrome that is results from
ā¢ Circulatory failure
ā¢ Reduction in oxygen deliver
ā¢ inadequate peripheral tissue and organ perfusion leading to a
ā¢ eventual cellular hypoxia with all its attendance sequalae.
ā¢ Clinically characterized by
ā¢ hypotension (Hemodynamic instability)
ā¢ SBP < 90mmHg or < 30mmHg from baseline
ā¢ Mean arterial pressure < 65mmHg
ā¢ Oliguria
ā¢ Altered mentation
ā¢ Organ failure
4. Pathophysiology
ā¢ resulting from a decreased circulating blood
volume
Types of Hypovolemia
ā¢ Blood Loss
ā¢ Fluids/Plasma Loss
Most common type of shock
Diagnosis
ā¢ Readily diagnosed based on the etiology
ā¢ Pitfall
ā¢ Difficult to differentiate from cardiogenic
ā¢ A normotensive patient maybe in shock ( hypertensive patient)
6. Class I Class II Class III Class IV
Blood loss
mL <750 750-1500 >1500-200 >2000
% <15 15-30 >30-40 >40
Heart rate
(beat/min)
<100 >100 >120 >140
Systolic
blood
pressure
Normal Normal Decreased Decreased
Pulse
pressure
Normal Decreased Decreased Decreased
Capillary
refill normal
Delayed Delayed Delayed Delayed
Respiratory
rate (min)
14-20 20-30 30-40 >35
Urine output
(mL/h)
>30 20-30 5-15 Minimal
7. ā¢ Cardiogenic shock (CS) is characterized by
systemic hypoperfusion due to
ā¢ cardiac pump failure caused by loss of myocardial
contractility
ā¢ severe depression of the cardiac index [<2.2 (L/min)/m2]
and
ā¢ sustained systolic arterial hypotension (<90 mmHg)
despite an elevated filling pressure [pulmonary capillary
wedge pressure (PCWP) >18 mmHg].
ā¢ Most common cause: MI
ā¢ 15% of cardiogenic shock occurs during MI attack
ā¢ 50% occurs 6 hours after MI attack
9. ā¢ Septic Shock:
ā¢ sepsis-induced hypotension (systolic blood pressure
<90 mm Hg [or a drop of >40 mm Hg]) with
ā¢ signs of tissue hypoperfusion
ā¢ despite adequate fluid resuscitation for at least 1 hour
ā¢ Refractory septic shock
ā¢ Septic shock that lasts for >1 h and does not respond to
fluid or pressor administration
ā¢ Principle of mechanism
1. Peripheral vasodilation and pooling of blood
10. ā¢ Symptoms:
FEVER/hypothermia,
depends on site of
infection.
ā¢ Signs:
ā¢ Warm peripheral
extremities (due to
vasodilation)
ā¢ Febrile
ā¢ hypotension
ā¢ Tachypnea, tachycardia
ā¢ Oliguria
ā¢ Rash
ā¢ History taking:
comorbidities
ā¢ DM,
ā¢ Chronic lung disease
ā¢ alcoholism,
ā¢ liver cirrhosis,
ā¢ Recent invasive
procedure (especially in
CKF)
ā¢ HIV
ā¢ Immunosuppressive agent
(Steroid)
ā¢ Malignancy
11. ā¢ An allergic, IgE mediated, hypersensitivity
response to a foreign substance to which a
patient has been previously sensitized
ā¢ Type I hypersensitivity
ā¢ Causes:
ā¢ Drugs: penicillin, aspirin, streptomycin
ā¢ Vaccines: measles
ā¢ Blood products
ā¢ Insect bites: bees
ā¢ Food: seafood
12. ā¢ Onset:
ā¢ Commonly: 5-60min of exposure
ā¢ Delayed onset: after few hours
ā¢ Biphasic response: recurrence of symptoms 1-8 hrs later
due to late phase reaction
ā¢ Protracted anaphylaxis : persistence of symptoms up to
48hrs despite therapy
ā¢ Skin :
ā¢ Urticaria (200 cases):Area of focal dermal edema
ā¢ angioedema (20cases): Localized non-pitting deeper
edematous process
ā¢ Pruritus
ā¢ Tingling of face (usually at mouth)
13.
14.
15. ā¢ CVS:
ā¢ Arrhythimias
ā¢ RS:
ā¢ Laryngeal edema: hoarseness of voice, stridor, ālump in
the throatā
ā¢ Wheeze
ā¢ Dyspnea due to bronchospasm
ā¢ Coughing: ominous sign ļ portend onset of pulmonary
edema
ā¢ GIT
ā¢ Nausea, abdominal cramp
23. Hypovolemic Shock
Cardiogenic Shock
Obstructive Shock
Distributive Shock
Neurogenic Shock
Check the Pulse
Tachycardia
Dysrhythmia
s(by ECG)
Bradycardia
Neurogeni
c
AnaphylacticCardiogenicSepticHypovolemic
Other
Features:
Trauma
diarrhea
vomiting
Other
Features:
Fever
Rash
others
Other
Features:
Post ā MI
Sign of CCF
Other
Features:
Allergy
Urticarial
angioedema
Other
Features:
Spinal
injury
RS
Examination
Tension
Pneumothor
ax
Cardiac
Tamponad
e
BECKāS TRIAD
24.
25. Airway Maintenance If GSC < 8 ļ ETT intubation
Breathing ā by SP02
100% oxygen
oyxgen to maintain PaO2 >
60mmHg or SaO2 > 90%
Circulation
2 large wide bore
ā¢ Size: 16G
ā¢ Route: peripheral ļ
central line ļ Intraosseos
line
ā¢ Wide bore
ā¢ Purpose:
ā¢ Give bolus or infuse
fluids
ā¢ Drugs administration
ā¢ blood Investigation
Bladder
catheterization
26. ā¢ Supine or
Trendelenburg
position
ā¢ Raise the leg up
Non-
cardiogenic
Shock
Cardiogenic
Shock
Fluids therapy
(at least
1000ml)
+/- Fluids
therapy (500-
1000ml max)
Investigation CVP or PAC
Fail to respond to Fluid therapy
Sympathomimeti
cs
ā¢ Mean arterial pressure >60-
65 mm Hg (higher in the
presence of coronary artery
disease)
ā¢ Pulmonary wedge pressure
15-18 mm Hg (may be higher
for cardiogenic shock)
ā¢ Cardiac index >2.1 L/min/m2
for cardiogenic and
obstructive shock
ā¢ Cardiac index >4-4.5
L/min/m2 for septic and
resuscitated
traumatic/hemorrhagic shock
29. ā¢ Crystalloid is preferred over than colloid because
colloid :
1. inhibition of the coagulation system;
2. the risk for anaphylactoid reactions;
3. inhibition of renal salt and water excretion;
4. Over-administration ļ risk of ARF
5. expensive
30. ā¢ Choice of Crystalloid
ā¢ Theoretically: Ringer Lactate or Hartman solution is
preferred over Normal saline
ā¢ Resemble the plasma electrolytes level
ā¢ However, Normal saline is used because
ā¢ it is cheaper.
ā¢ Isotonic Normal saline 0.9% is used in all shock
condition excepts:
ā¢ Burn shock (use Parkland formula)
ā¢ Dextrose 5% Ā½ NS ļ Maintenance therapy
31. 1. The value of Glucose, Na, K must be
memorized.
ā¢ Primarily used to
maintain water
balance in patients
who are not able to
take anything by
mouth
For Fluid Resuscitation
(shock, dehydration)
Fluids
Maintenance
33. Fluids loss
ā¢ Fluids replacement : (NS) to restore the
circulatory volume
ā¢ Adult: at least1000ml over 30minutes bolus
ā¢ Pediatrics ā 20ml/kg
ā¢ Calculating the % loss
ā¢ According to the sign and symptom
ā¢ Dehyration ā mild moderate severe
ā¢ Blood loss ā class I,II, III, IV
ā¢ According to weight loss
ā¢ (Previous healthy weight ā current body weight) x
100%
34. ā¢ Fluids maintenance: daily fluid loss (about 2L) +
additional fluid deficit + ongoing loss
ā¢ (fever āincrease in 1degree celcius =10ml/hr
loss)
ā¢ Paediatrics age group ā Must use Holliday-
Segard Formula
ā¢ Adult ā can use wt + 40 formula
ā¢ Maximum fluid maintenance for normal daily loss
: 120ml/ hr
35. Rule of 4 -2-1 (Holliday-
Segard Formula)
- 4 ml per kg for the first 10
kg of body weight;
- 2 ml per kg for the next 10
kg (11-20kg);
- 1 ml per kg for any weight
>20 kg
Weight + 40
Example: Calculating
maintenance fluid
requirements for 70 kg male.
0-10 kg: 10 * 4 ml = 40 mL
11-20 kg: 10 * 2 mL = 20 mL
21-70 kg: 50 * 1 mL = 50 mL
Total = 110 mL/hr
Example: Calculating
maintenance fluid
requirements for 70 kg male.
70+40 = 110mL/hr
36. ā¢ Indications
ā¢ Severe hemorrhage > 30%
ā¢ Hb < 8%,
ā¢ Whole Blood is used.
ā¢ GXM
ā¢ 1 unit of blood = 450ml of blood
ā¢ During initial resuscitation of acute blood loss and shock,
crystalloid or colloid infused to restore circulatory volume
ā¢ Emergency blood group āOā blood should not be used
indiscrimately
ā¢ Look for side effect of transfusion
37. ā¢ Group O āpositiveā is used as emergency blood for man.
ā¢ Group O ānegativeā is used for female in reproductive
age group.
ā¢ Category of blood according to urgency
Unmatch
Emergency
blood
Rapid
Match
blood
Full
matched
blood
Availability Instant 5-10minutes 30-
45minutes
CXM not done done Done
Antibody
screen
not done not done done
Guide to The Essential in Emergency
Medicine by Shirley Ooi.
38. ā¢ Prevention of stress ulcer
ā¢ Ranitidine or PPI
ā¢ Prevention of deep vein thrombosis
ā¢ UF heparin or LMW heparin if no C/I
ā¢ Prevention of ARF
ā¢ Induce diuresis by furosemide (make sure adequate fluid
therapy) ļ look for hyperkalemia
ā¢ IV 2-5micro g/kg/minute of dopamine (low dose)
ā¢ Glucose control
ā¢ Insulin to prevent DKA in DM patient
ā¢ Metabolic Acidosis
ā¢ treat in severe cases only.
39.
40. ā¢ Blood investigations
ā¢ FBC, RBS
ā¢ HCT is extremely unreliable test
ā¢ GXM
ā¢ BUSE and creatinine, lactate
ā¢ Cardiac enzyme and TnT
ā¢ Exclude acute MI
ā¢ ABG
ā¢ Metabolic acidosis, elevated lactate(>5mmol/L) and significant
base deficit are marker of poor prognosis
ā¢ Correction of these abnormalities will improve outcome (by ABC)
ā¢ However, sodium bicarnoate is not used routinely because it does little
to positively affect morbidity and survival.
ā¢ Coagulation profile , albumin
ā¢ ECG and CXR
ā¢ FAST scan (Focused assessment with sonography for trauma)
41. ā¢ Fluids
Resuscitation -
mainstay
ā¢ All fluids need to be
warmed to prevent
iatro-genically
induced
hypothermia.
ABC + Bladder
catheterization
Active
bleeding
Fluid
Resuscitatio
n
Dopamine
+/-
Dobutamine
Compressi
on
E / NE
HypotensionCVL / PAC
Hypotension
OT if
required
If MAP < 60mmHg
ļ CVL / PAC
sympathomime
tic drugs
external
Internal
42.
43. ā¢ Blood Investigation
ā¢ Cardiac enzyme
ā¢ ABG
ā¢ BUSE and creatinine
ā¢ FBC , RBS
ā¢ ECG
ā¢ CXR
ā¢ Echocardiography if cause is uncertain
44. ā¢ Assessment of Venous Pressure:
reflect Right ventricular filling pressure
ā¢ Pulmonary capillary wedge pressure
(PCWP) with Swan-Ganz catheter
ā¢ useful in suspected ARDS, exclusion of
VSD, associated hypotension requiring
inotrope to guide therapy
45.
46. Supine or Trendelenburg position
ABC + bladder catheterization
Oyxgen 35-100% via facemask
to maintain PaO2 > 60mmHg or
SaO2 > 90%
Continuous cardiac, BP,
HR, Pulse oxymetry
monitoring
ā¢ Increase inspired
oxygen to keep
SaO2 > 90%
ā¢ Mechanical
ventilation is
indicated if
ā¢ hypercapnia
ā¢ hypoxia
ā¢ Patient who are alert
and cooperative may
cope with (NIPPV)
ā¢ Correct severe
metabolic acidosis
(pH < 7.2)
ā¢ Reason: negative
inotrophic and
pro-
47. Treat underlying arrhythmias
ā¢ Insert large cannula and
give:
ā¢ Morphine IV 2.5-5mg
+ metoclopramide
10Mg IV or IM
Reduce
anxiety and
vasodilation
(use carefully)
Notice: SL GTN
and frusemide
are not used in
Cardiogenic
Shock if SBP <
NO CLINICAL OR
HEMODYNAMIC PULMONARY
CONGESTION
ā¢ Look for sign of CCF
48. NO CLINICAL OR
HEMODYNAMIC
PULMONARY
CONGESTION
(Judicious fluid challenge)
Method of giving:
Without invasive
hemodynamic monitoring
ā¢ 100ml NS or
Hartmanās Solution
over 5-10min interval
ā¢ Reassessment of BP,
HR, peripheral
perfusion, breath
sound between
successive
administration
ā¢ Max : 500-1000mL
With invasive
hemodynamic monitoring
Investigation
as above
49. Still Hypotension
Dopamine
Peripheral
hypoperfusion and
significant hypotension
ļ use dopamine ļ
increase MAP + restore
renal and coronary
perfusion
Up to 15-20 Āµg/kg/min
Common desired effect
dosage: 7.5-15Āµg/kg/min
Contraindicated
Dobutamine
Contraindicated in significant
pulmonary congestion and only
mild hypotension
Still Hypotension
50. Still Hypotension
NE/E Phosphodiesteras
e āIII inhibitors
OR
NE/E
NE: beta1 and alpha
adrenergicļ increase
contractility +
vasoconstriction
Use if dopamine fails
Caution: both are
proarrhythmias (if AMI ļ
extensive myocardial
injury)
Phosphodiesterase āIII
inhibitors
Eg. Amrinone and
milrinone
Indication: severe
Treat Pulmonary
Edema
With Frusemide /
GTN
SBP > 100mmHg
AMI if present
- Follow MI protocol
51. ā¢ Aminophylline (rarely use)
ā¢ Increase cardiac contractility
ā¢ Bronchodilatation
ā¢ Vasodilatation
ā¢ Mechanical circulatory support
ā¢ Intra-aortic balloon counterpulsation in tertiary
centers
ā¢ increases myocardial oxygen perfusion while
at the same time increasing cardiac output.
52.
53. ā¢ To establish the definitive diagnosis
ā¢Blood Culture and sensitivity (2 sets)
ā¢ For IV line sepsis:1 set from suspected
IV line, another from peripheral vein
ā¢Urine C&S
ā¢Stool culture
ā¢Sputum culture
ā¢UFEME
56. ABC
Watch I/O
carefully and be
aware of other
losses
Continuous ECG, BP,
HR, Pulse oxymetry
monitoring
Bladder catheterization
Pulmonary arterial catheterization
57. Fluid Challenge
ā¢ Mainstay of
hemodynamic
supports
ā¢ Fast and rapid wide
bore fluid resuscitation
ā¢ urine output rate
should be kept at >0.5
mL/kg per hour by
continuing fluid
administration
ā¢ central venous
pressure should be
maintained at 8ā12
cmH2O
Rate of administration
should be reduced if
cardiac filling
pressure increase
without concurrent
hemodynamic
improvement
58. Give low dose of
vasopressin
ļ increase systemic
arterial pressure to
ļ sustains the ability of
the vasculature to
autoregulate flow on a
tissue and organ level
ļ ļ prevent organ
failure
Low Dose
vasopressor
ā¢ NE /
Dopamine(not in
low dose) 1st
choice
ā¢ Alternate:
Epinephrine (if BP
is poorly
responds)
ā¢ Enhance sensitivity to
vascular smooth muscle to
catacholamine ļ to
minimize the side effect of
using high dose vasopressor
ā¢ beneficial in catecholamine-
resistant septic shock
following adequate volume
59. ā¢ C&S before empirical antibiotic
ā¢ Intravenous broad-spectrum antimicrobials
should be initiated immediately (preferably <30
minutes) following the clinical diagnosis
ā¢ At dosing at the high end of the therapeutic
range
ā¢ Duration of therapy: 7-10 days
ā¢ Empiric antimicrobial therapy should be adjusted
to a narrower regimen within 48 to 72 hours if a
plausible pathogen is identified or patient
stabilizes clinically Where possible, early source
60. ā¢ Indications:
ā¢ Early phase of fibro-proliferative phase of ARDS
and sepsis
ā¢ History of endocrine disease and history of taking
corticosteroid therapy
ā¢ Persistent hypotension after adequate fluids
resuscitation and vasopressin
ā¢ Meta-analysis showed no convincing
evidence that early administration of high
dose corticosteroid is beneficial and they
could be harmful.
61. ā¢ Human recombinant activated protein C
(drotrecogin alfa)
ā¢ Indicated in high risk for death (APACHE II > 24 or
multi-organ failure
ā¢ Effect:
ā¢ Antithrombotic
ā¢ Anti-inflammatory
ā¢ Pro-frinolytic
ā¢ Prerequisite: Platelet count > 30,000
ā¢ Main contraindication
ā¢ Active bleeding
ā¢ CRF
62.
63. ABC
Bladder
catheterization
ECG,RR,BP,SaO2
recumbent position
ā¢ High flow Oxygen
with facemask ļ fail
ļ ETT ļ difficult
intubation due to
severe laryngeal
edema ļ
tracheastomy /
cricothyroidotomy
Remove the inciting agent
ā¢ Prompt application of
torniquet proximally
ā¢ Insect: flick out insect
stinger with a tongue
blade
ā¢ Ingestion of allergen :
gastric lavage and
activated charcoal
64. IM aqueous
epinephrine 0.3-
0.5 ml of 1:1000
Repeat every
20minutes
ā¢ Epinephrine is the
mainstay of initial
management
ā¢ controlling symptoms
and maintaining blood
pressure.
IV Epinephrine
3 ā 5ml 1:10
000
Severe
airway
compromise /
hypotension
Repeat every 5-
10min
Epinephrine
Infusion
If require
multiple doses
65. Administer
histamine
antagonists
ā¢ block vasodilation,
capillary leak, and
shock
ā¢ H1 blockade, 25ā50 mg
of diphenhydramine IV
6hrly
ā¢ ; H2 blockade, 50 mg of
ranitidine IV 6hrly
aggressive fluid
resuscitation
500-1000ml of
crystalloid or colloid
in patients
who remain
hypotensive
despite
epinephrine.
Still
Hypotension
67. ā¢ Nebulizer Bronchodilator
ā¢Short acting beta2 agonist every 15-
30minutes
ā¢Due to refractory to epinephrine
ā¢ Consider Corticosteroid
ā¢250mg IV hydrocortisone, repeated 6
hourly
ā¢Reduce protracted anaphylaxis
ā¢not effective therapy for the acute
manifestations
68. ā¢ Consider glucagon administration
ā¢Indicated for those who receive B blocker
therapy in anaphylactic shock
ļ antagonizes the beneficial Ī²-mediated
effects of epinephrine therapy
ā¢1ā5 mg IV over 1 minute, then 1ā5
mg/hour in a continuous infusion
69. ā¢ Continuous ECG monitoring
ā¢ Close monitoring of ABG, CVP, BP
ā¢ Antihistamine 48-72hours to prevent
relapse
ā¢ Short course of steroid for 7-10 days
ā¢ Counseling
70. ā¢ Clinical features:
ā¢ Bradycardia, hypotension, warm peripheral
extremities
ā¢ Mx:
ā¢ ABC + Supine position with leg elevated
ā¢ Fluid resuscitation
ā¢ NE
ā¢ Anal wink or bulbocarvenosus reflex
Editor's Notes
(1) hypovolaemic, due to inadequate venous return (haemorrhage, dehydration), (2) cardiogenic, due to inadequate ventricular pump function (myocardial infarction), (3) obstructive, due to vascular obliteration (pulmonary embolism or tamponade), and (4) distributive, due to loss of vasoregulatory control (sepsis).
Atelectasis - Recumbency and involuntary restriction of ventilation secondary to pain reduce functional residual capacity and may lead to atelectasis
Shock and, in particular, resuscitation-induced oxidant radical generation, is recognized as a major cause of acute lung injury and subsequent acute respiratory distress syndrome (ARDS;
severe sepsis or septic shock may demonstrate persistent vasomotor dysfunction characterized by regional perfusion deficits with or without systemic hypotension despite normal or increased CO. Clinical manifestations may include lactic acidosis and ongoing progression of organ failure.
Acute Physiology and Chronic Health Evaluation
Ī²-blockade antagonizes the beneficial Ī²-mediated effects of epinephrine therapy, thereby resulting in unopposed Ī±-adrenergic and reflex vagotonic effects: vasoconstriction, bronchoconstriction, and bradycardia