LI

1. PENURUNAN KESADARAN
2. SEPSIS
3. GANGGUAN ASAM BASA
4. PATFIS
Ketoasidosis Diabetikum
Rosen’s
• DKA is a syndrome
• Insulin deficiency + glucagon excess  hyperglycemic, dehydrated, acidotic patient, with
profound electrolyte imbalance
• DKA may be caused by cessation of insulin intake or by physical or emotional stress
• ↑hyperglycemic  renal threshold is excessed  glucose excreted in the urine
• Glucose in the renal tubules draws:
• water, sodium, potassium, magnesium, calcium, phosphorus, and other ions from the
circulation into the urine
• Osmotic diuresis + poor intake and vomiting  dehydration and electrolyte
imbalance associated with DKA
• Cells unable to receive fuel substances from the circulation  decrease amino acid
uptake and ↑proteolysis to produce energy source
• Insulin deficiency  activation of a hormone-sensitive lipase  ↑circulating FFA
 partially oxidized and converted in the liver  acetoacetate and β-
hydroxybutyrate
• Body ↑ ketones production but ↓use of ketones as fuel 
ketoacidosis
• Acidosis px
• Incraese lung ventilation to rid the body of excess acid with Kussmaul’s
breathing
• Ketoalkalosis: diabetic px vomiting for several days and in some with
severe dehydration and hyperventilation
• Rare
• Causa:
• DM1 px and is associated with inadequate administration of insulin, infection, or MI
• Can also occur in DM2  associated with any type of stress (such as sepsis or GI bleeding)

• Most patients with DKA complain of a • 50% of px (esp. children) report:

recent history of: abdominal pain
• Polydipsia • Abdominal pain in children is idiopathic
• Polyuria and due to gastric distention or
• Polyphagia stretching of the liver capsule
• Visual blurring • In adults, abdominal pain indicate
• Weakness abdominal disease that may be the
• Weight loss trigger of DKA
• Nausea
• Physical examination:
• Vomiting
• tachypnea with Kussmaul’s breathing
• Abdominal pain
• Tachycardia
• Frank hypotension or orthostatic blood
pressure changes
• Odor of acetone on the breath
• Signs of dehydration
Diagnostic Testing
• Lab studies: serum glucose,
electrolyte, and blood gas levels
• serum ketoacid levels: not
necessary to diagnose DKA and
make be elevated in non-DKA
states (eg, starvation ketosis
from inadequate utilization of
glucose stores) or dehydration
• Determination of pH: venous
blood gas samples can be used
(corelates well with arterial pH)
• Arterial blood gas sample should
be tested if there is concern for
the adequacy of respiratory
compensation or concern for a
mixed disorder
• Winter’s formula (expected Paco2 = [1.5 x serum HCO3] + [8 ± 2]) to determine if
there is appropriate respiratory compensation or the presence of multiple acid-
base disorders
• Glucose level: usually >350 mg/dL
• Blood gas measurement: low pH
• ↑ plasma levels of acetoacetate and β-hydroxybutyrate  acidosis with an
anion gap
• Rare: normal anion gap in a px with DKA  happen if the vomiting was sufficient to cause
a concomitant metabolic alkalosis and bicarbonate level appear to be in the normal range
• ECG: sign of hyperkalemia or hypokalemia
• In DKA serum potassium levels are typically normal of high due to intracellular potassium
shifting out of cells in exchange for elevated serum hydrogen ions
• A basic metabolic panel should be obtained to evaluate: renal function, acid-
base status, and glucose and electrolyte levels
• Determine Mg and K levels due to its deficits are common
• Urinalysis: help confirm a UTI as a precipitant of DKA
• Blood or urine culture determined by the clinical picture
• serum sodium level
• Often low in the presence of significant dehydration because it is strongly
affected by hyperglycemia, hypertriglyceridemia, salt-poor fluid intake,
increased GI and renal losses, and insensible loss
• Dilutional hyponatremia: due to hyperglycemia  water flows from the
cells into the vessels
• Elevated lipid levels  pseudohyponatremia by decreasing the fraction
of serum that is water
• true value of the sodium level: adding 1.6 mEq/L to the sodium value
on the laboratory report for every 100 mg/dL glucose above the norm
• Acidosis and the hyperosmolarity induced by hyperglycemia  shift
potassium, magnesium, and phosphorus from the intracellular to
extracellular space
• Dehydration  hemoconcentration
• contributes to normal or high initial serum potassium, magnesium, and
phosphorus readings in DKA
• The effect of acidosis on the serum potassium level determination can
be corrected by
• Subtracting 0.6 mEq/L from the laboratory potassium level for every 0.1-
decrease in pH noted in the arterial blood gas analysis
• As insulin is administered and the hydrogen ion concentration decreases, the
patient needs considerable potassium replacement
• DDx: alcoholic ketoacidosis
• Ketoacidosis can also develop with fasting commonly in the third trimester of
pregnancy and in nursing mothers who do not eat
• sepsis, poisoning, or lactic acidosis because physiologic stress from one of
these other causes can precipitate DKA
Management
• comatose patient, esp. if vomiting  intubation
• Hyperventilation to prevent worsening acidosis
• Hypovolemic shock  aggressive fluid resuscitation with isotonic
crystalloids
• Bedside USG: to excluding other causes of hypotension and evaluating
the volume status of an individual patient
• When hyperglycemia, ketosis, and acidosis have been established 
initiate fluid, electrolyte, and insulin therapy
Complications
• iatrogenic causes, infection, and myocardial infarction
• hypokalemia from inadequate potassium replacement
• hypoglycemia from inadequate glucose monitoring
• alkalosis from overaggressive bicarbonate replacement
• pulmonary edema from overaggressive hydration
• Death: infection especially pneumonia, arterial thromboses, and shock
• Cerebral edema: when px becomes altered or lapses into coma after
the reversal of acidosis
• Occurs 6-10 hrs after the initiation of therapy
• Less common in adults or children >5 years
• Treatment: supportive
• Outcomes: poor
 HYPERGLYCEMIC
HYPEROSMOLAR STATE
Rosen’s
• Causes:
• HHS is a syndrome of severe
dehydration that results from a
sustained hyperglycemic
diuresis in which the px is
unable to drink sufficient fluid
to offset the urinary losses
• common in geriatric patients
with type 2 diabetes
• HHS may occur in patients who
are not diabetic, especially after
burns, peritoneal dialysis, or
hemodialysis
• Clinical features:
• extreme dehydration, hyperosmolarity, volume
depletion,
• Px may complain of:
• Fever
• Thirst
• Polyuria or oliguria
• Common associated diseases are chronic renal
insufficiency, gram(-) pneumonia, GI bleeding,
and gram(-) sepsis
• patient often exhibits orthostatic hypotension
or frank hypotension, tachycardia, and fever,
with signs of marked dehydration
• Neurologic findings: decreased level of
consciousness, seizures, stroke syndromes, and
movement disorders
• Diagnostic Testing:
• Blood glucose level >600 mg/dL
• Serum osmolarity >350 mOsm/L
• BUN concentraion: elevated
• Px may have a metabolic acidosis secondary to some combination of lactic
acidosis, starvation ketosis, and retention of inorganic acids
• profound electrolyte imbalance than the patient with DKA
• DDx:
• identical to that of DKA
• diabetic patients receiving chlorpropamide are subject to water intoxication with
dilutional hyponatremia  manifested as coma without acidosis that is clinically
indistinguishable from HHS
• Px with HHS who has a sharply depressed sensorium may not be initially
distinguishable from the px with profound hypoglycemia
 MANAGEMENT
• The fluid, electrolyte, and insulin regimens for the initial resuscitation in HHS
• Intravenous Fluids
• hypovolemic shock -> rapidly as possible
• Glucose should be added to resuscita- tion uids when the blood glucose level drops below
300 mg/dL
• noninvasive or invasive forms of hemodynamic monitoring may be required to guide fluid
administration when there is clinical sus- picion of pulmonary edema or volume overload.
• Electrolytes
• potassium levels more accurately reflect total body stores than they do in DKA
• Insulin
• continuous IV insulin infusion is not required in these patients,
• help lower the glucose concentration in a more controlled fashion
• very high glucose levels (>700 mg/dL)
• hypoperfused
• IV insulin infusion is used, it should be done at an infusion rate similar to that for DKA (0.1
unit/kg/hr).

• Other Considerations
• Phenytoin (Dilantin) is contrain- dicated for the seizures of HHS because it is often
ineffective and may impair endogenous insulin release
• should be given low-dose subcutaneous heparin to lessen the risk of thrombosis
• increased by the volume depletion, hyper- viscosity, hypotension, and inactivity associated with HHS.
Acute Complications
• many patients with HHS are older adults who have underlying cardiac
and renal disease  high morbidity and mortality rates
• Pediatric HHS: cerebral edema
• Other causes of morbidity and mortality are similar to those
described for DKA
• Mortality rate of treated HHS: 8% - 25%
HYPOGLYCEMIA
Rosen’s
• Common problem in patients with type 1 diabetes, especially if tight
glycemic control is practiced
• Severe hypoglycemia: blood glucose levels <40 – 50 mg/dL and
impaired cognitive function
• Diabetic patients using insulin are vulnerable to hypoglycemia because
of insulin excess and failure of the counterregulatory system
• Counterregulatory system: cessation of insulin release and mobilization of
counterregulatory hormones
• Hypoglycemia has many causes:
• missing a meal (decreased intake)
• increased energy output (exercise)
• increased insulin dosage
• It can also occur in the absence of any precipitant
• Oral hypoglycemic agents
• Hypoglycemia without warning symptoms, or hypoglycemia unawareness 
dangerous complication of type 1 diabetes and is probably caused by previous
exposure to low blood glucose concentrations
• factors associated with recurrent hypoglycemic attacks:
• overaggressive or intensified insulin therapy
• longer history of diabetes
• autonomic neuropathy
• decreased epinephrine secretion or sensitivity
• The Somogyi phenomenon: common problem associated with iatrogenic
hypoglycemia in the type 1 diabetic patient
• Initiated by excessive insulin dosing, resulting in an unrecognized hypoglycemic episode
that usually occurs in the early morning while the patient is sleeping
• Counterregulatory hormone response  rebound hyperglycemia
• Evident when the px awakens
• Often the physician interpret as an indication to increase the insulin dosage 
exacerbates the problem
 Clinical Features
• Symptomatic hypoglycemia: glucose level 40 – 50 mg/dL
• The rate at which the glucose level decreases, however, and the patient’s age,
gender, size, overall health, and previous hypoglycemic reactions contribute to
symptom development
• Signs and symptoms of hypoglycemia are caused by excessive secretion of
epinephrine and CNS dysfunction:
• Sweating
• Nervousness
• Tremor
• Tachycardia
• Hunger
• Neurologic symptoms: bizarre behavior and confusion to seizures and coma
• Px with hypoglycemia unawareness: marked hypoglycemia may be minimal or absent
and px may rapidly become unarousable. May have seizure or show focal neurologic
signs (resolves w/ glucose administration)
Differential Diagnoses
• Hypoglycemia in the nondiabetic patient classified as postprandial or
fasting
• The most common cause of postprandial hypoglycemia: alimentary
hyperinsulinism
• Fasting hypoglycemia is caused when there is an imbalance between
glucose production and use
• Diagnostic Testing:
• blood glucose concentration: perform before
therapy is begun
• Laboratory testing should address any
suggested cause of the hypoglycemia: such as
ethanol or other drug ingestion
• testing for insulin antibodies or low levels of C
peptide: patient who is surreptitiously
administering exogenous insulin will have
normal to low levels of C peptide and markedly
elevated insulin levels
• Management:
• alert patients with mild symptoms: oral
consumption of sugar-containing foods or
beverages
• In other patients: 1-3 ampules of D50W via
IV while the patient’s airway, breathing, and
circulation are assessed and maintained
• If alcohol abuse is suggested 
thiamine 100 mg
• Children < 8 years: D25W or D10W
• 0.5 – 1 g/kg or 2-4 mL/kg when using
D25W
• If IV access cannot be rapidly obtained
 1-2 mg glucagon IM or
subcutaneously and may be repeated
as needed
• Glucagon is ineffective in causes of
hypoglycemia in which glycogen is
absent, notably alcohol-induced
hypoglycemia
• All patients with severe hypoglycemic
reactions:
• Aspiration
• Seizure precautions
• Treatment of hypoglycemia secondary to oral hypoglycemic
agents depends on the agent:
• Metformin and the thiazolidinediones: rarely cause significant or
prolonged hypoglycemia
• Sulfonylureas: do cause hypoglycemia
• Overdose  should be observed for a period of 24 hours if hypoglycemia
recurs in the ED after management of the initial episode
• Patients at risk for hypoglycemia: impaired renal function, pediatric
patients, and patients who are naïve to hypoglycemic agents
• requires treatment with an agent to inhibit further insulin release: such as
octreotide
• Adult: 50-100 µg IV or subcutaneously every 12 hrs
• Pediatric: 0.1 mcg/kg IV or subcutaneously
DENGUE
Rosen’s
• Dengue virus
• Flaviviridae family
• can be found all over the world
• Most infections occuring in: Southeast Asia, the Western Pacific, and
Central and South America
• transmitted via the mosquito vector:
• Aedes aegypti and Aedes albopictus
Clinical Features
• Many individuals are asymptomatic
• fever, headache, retroorbital pain, severe myalgias, and arthralgias
• Symptoms can last up to 1 week
• Dengue hemorrhagic fever (DHF):
• Increased vascular permeability (pleural effusion, ascites, hemoconcentration)
• Thrombocytopenia
• Fever lasting 2 to 7 days
• Hemorrhagic tendency or spontaneous bleeding
• Dengue shock syndrome (DSS): when DHF occurs with circulatory
shock
• Differential Diagnosis:
• malaria, chikungunya, rickettsial infections, leptospirosis
• other viral hemorrhagic fevers: Ebola, Marburg, yellow fever, or
bunyaviruses
• measles in a returned febrile traveler with a rash
• Diagnostic Testing:
• IgM assay
• viral RNA detection with RT-PCR
• Other laboratory findings: leukopenia, thrombocytopenia, elevated
hematocrit (due to hemoconcentration from fluid loss), and
abnormal liver function tests
• In DHF: coagulopathy can be present
Management
• No specific antiviral agents that treat dengue
• Treatment: supportive
• Dengue fever is usually a self-limited illness and can be treated with
• rest, antipyretics, analgesics, and fluid replacement therapy
• Avoid NSAID and aspirin due to bleeding tendencies
• Px with DHF and DSS  close monitoring
• IV fluid replacement therapy and organ support as indicated
• Hemorrhage: blood product transfusions
ACUTE KIDNEY INJURY
Tintinalli
AKI
• Prerenal failure
• Tubular & glomerular function are maintained
• Restoration of circulating blood volume usually sufficient to restore function
• Postobstructive renal failure / postrenal failure
• Results in an increase in tubular pressure -> decrease the driving force for flitration
• Intrinsic renal failure
• occurs with disease of glomerulus, small vessels, interstitium / tubule & associated with release of renal
vasoconstrictor
• Common cause : ischemic injury / ischemic tubular necrosis
• Clearance of tubular toxin & initiaton therapy for glomerular disease -> decrease vasoconstriction & help
restore blood flow
• Cause of injury resolved -> remaining functional nephrons increase filtration & hypertrophy
• Depending size of remnant nephron pool -> GFR proportionately recover
• If remaining nephrons below critical number -> continued hyperventilation -> progressive glomerular sclerosis -> nephron
loss
Clinical Features
• Has few symptoms until severe uremia develop
• Nausea, vomiting, drowsiness, fatigue, confusion & coma – findings in
uremia
• Prerenal acute renal failure
• Develop thirst, orthostatic light-headedness & decreased urine output
• Excessive vomiting, diarrhea, urination, hemorrhage, fever / sweating -> reduce
circulating volume -> precipitate acute renal failure
• Endothelial leak & 3rd spacing -> sepsis, pancreatitis, burns & hepatic failure
• Decreased fluid intake from physical / cognitive disability -> hypovolemia
• Anticipate ischemic acute kidney injury – after cardiac arrest, severe sepsis /
with other cause of systemic hypotension
Clinical features
• Renal failure from crystal-induced nephropathy, nephrolithiasis & papillary necrosis
-> flank pain & hematuria
• Suspect pigment-induced renal failure in rhabdomyolysis / hemolysis after recent
blood transfusion
• Darkening urine and edema +/- constitutional symptoms (fever, malaise & rash) ->
acute glomerulonephritis -> may preceded by pharyngitis / cutenaeous infection
• Fever, arthralgia & rash -> common in acute interstitial nephritis
• Acute renal arterial occlusion -> severe flank pain
• Cough, dyspnea & hemoptysis -> Goodpasture’s syndrome / wegener’s
granulomatosis
• Anuria –> obstruction
Physical Examination
• Assess & correct volume status
• Evaluate mucous membrane, jugular vein distention, lung
auscultation, peripheral edema & tissue turgor -> identify dehydration
• Base deficit, lactate level, CVP & oxygen saturation & US -> indicator
of hypovolemia
• Cardiac exam -> check atrial fibrillation, abdominal aortic aneurysms
& signs of HF & assess extremity pulses
Diagnosis
• Determine if kidney injury is prerenal, postrenal / intrinsic
• Obtain CBC, electrolyte level (incl Mg & phosphorus) & hepatic function test & blood culture if
clinically appropriate
• Obtain urinalysis, urine osmolality & urine culture
• ECG : fastest screening for hyperkalemia
• 83% abnormal ECG -> 34% peaked T waves
• Chest radiography – evaluate increased volume, effusions & pneumonia -> can result from /
precipitate renal failure
• Obtain bedside US to assess urinary bladder volume
• Large postvoid bladder residual volume (>125 mL) -> bladder outlet obstruction -> place urethral catheter
• Anuria = 100 mL / day – be present with prerenal, postrenal / intrinsic kidney disease
• Alternating oliguria & polyuria – pathognomonic of obstruction
Laboratory Evaluation
• Creatinine & Glomerular Filtration Rate :
• Creatinine – to measure renal function
• In ps with no renal function (GFR = 0), serum Cr level increase
1-3 mg/dL/day
• Lesser increase in Cr – residual renal function
Stages of kidney disease
• Fastest increase – rhabdomyolysis
characterized by GFR :
• Elevation of serum Cr may take 48 hrs to accumulate after • Stage I - GFR
onset of decreased function 90/mL/min/1.73m2
• Cr clearance -> used to estimate GFR • Stage 2 – GFR 60-89
• Stage 3 – GFR 30-59
• Glomerulonephritis – increase tubular secretion of Cr,
• Stage 4 – GFR 15-29
• Trimethroprim, cimetidine & salicylate – decrease tubular • Stage 5 – GFR < 15 ->
secretion of Cr dialysis / transplant needed
• Normal kidney function is GFR > 90 mL/min/1.73m2
Laboratory Evaluation
• BUN : Cr Ratio • Fractional Excretion of Sodium
• Ratio of BUN to Cr can suggest • Indicator commonly used to
hypovolemia identify hypovolemia
• In setting of avid sodium retention –
• Tubular injury – ischemic acute
urea clearance 30% GFR; in setting of
adequate volume & sodium – urea tubular necrosis -> dilute urine ->
clearance can increase to 70-100% GFR fractional excretion of sodium >1%
• Prerenal failure – BUN : Cr >10
• BUN level :
• Depressed : malnutrition & hepatic
synthetic dysfuntion
• Increased : setting protein loading, GI
hemorrhage / trauma
• Urinalysis
• Acute glomerulonephritis – RBC
enter filtrate a glomerulus
• Microscope : casts & dysmorphic
cells
• In acute tubular necrosis – tubular
epithelium breaks down -> protein
leak into filtrate & tubular
epithelial cell may be seen in
sediment
• Hyaline cast - common in prerenal
failure
• Pigmented granular casts –
common in hemoglobinuria /
myoglobinuria
• Finding of Hb on urine dipstick +
no red cells in microscope ->
myoglobinuria
Imaging
• Renal US –
• Test of choice for urologic imaging in acute
kidney injury
• 90% sensitivity & specificity for detecting
hydronephrosis due to mechanical obstruction
• Kidney dimension <9 cm suggest chronic renal
failure
• Hyperechogenicitiy in renal parenchyma ->
diffuse parenchymal disease
• Color flow Doppler US -> assessment of renal
perfusion & allow diagnosis of large vessel
causes of renal failure
Treatment
• Critically ill patient – resuscitation
• Treat hypovolemia & identify & treat sepsis, MI & occult GI /
retroperitoneal hemorrhage
• Correct intravascular volume deficit – crystalloid
• Ps with GFR <30 mL/min/1.73m2 -> avoid IV contrast studies
• Avoid Gadolinum fro GFR <30 mL/min/1.73m2
• Prerenal Failure
• Causes of prerenal azotemia :
• Volume loss
• Hypotension
• Disease of large & small renal
arteries
• Prerenal failure -> common
precursor to ischemic &
nephrotoxic condition -> intrinsic
renal failure
• Postobstructive Renal Failure
• RF : extreme of age, male sex,
malignancy, nephrolithiasis,
retroperitoneal disease, GU surgery &
indwelling urinary catheters
• Timely relief of obstruction essential
return of normal renal function
• Permanent loss develops over 10-14 D
of complete obstruction
• Risk of permanent renal failure increase
significantly if obstruction is
complicated by UTI
• Intrinsic Renal Failure
• Can result from injury to the
glomerulus, tubule, interstitium &
vasculature
• In community acquired -> drugs &
infection (common precipitants)
• In hospital -> toxic & ischemic
insult
• Radiocontrast-induced
nephropathy provoked by imaging
with IV contrast agent
• Typical course : increasing Cr level,
25% above baseline, over 3-5 D ->
complete resolution
• RF : chronic renal insufficiency,
diabetes, HF, liver disease & HT
• Angiotensin-Converting Enzyme
Inhibitors
• ACE-inhibitor can simultaneously
decrease GFR & increase renal
blood flow
• Result : modest (10-20%) increase
in serum Cr
• Common complication : mild
hyperkalemia
• NSAID
• Cyclooxygenase inhibitors (most :
NSAID) -> can also cause renal
failure
• RF for adverse reaction : older age,
chronic renal insufficiency, CHF,
diabetes, volume depletion & use
of diuretic / ACE-inhibitors
• Antibiotics
• Antibiotics (esp aminoglycosides) -
important cause of iatrogenic
renal injury
• Vancomycin dosing for severe
sepsis & septic shock – increased
rate of AKI
• Floroquinolones may predispose
condition
• Pigments
• Hb & myoglobin from hemolysis /
rhabdomyolsis are deposited &
concentrated in renal tubules
• Large volume crystalloid infusion –
cornerstone of treatment for
rhabdomyolisis & hemoglobinuria
Treatment of intrinsic renal failure
• Fenoldopam = potent dopamine • Venodilators (nitrates) & dialysis
D1-selective receptor agonist –> best th/ for volume overload
that increases blood flow to the
renal cortex & outer medulla
while lowering systemic blood
pressure
• Agent of choice for HT
emergencies + renal dysfunction
SEPSIS
Rosen’s
• Sepsis syndrome: body’s
host response to an
infection
• The causative agent and
host’s activated
inflammatory cascade
overwhelm the body’s
defenses and regulatory
systems  disruption in
homeostasis
• Common manifestation:
tachycardia, tachypnea,
fever, and immune system
activation
Symptoms and Signs
• presence of a systemic infection and localization of the source of the
initial infection
• septic patient: tachycardia, tachypnea, hyperthermia or hypothermia
and, if severe, hypotension
• Flushed skin with warm, well-perfused extremities secondary to the early
vasodilation and hyperdynamic state
• Severely hypoperfused patient with an advanced shock state: cyanotic
• tachycardia and tachypnea: first indicators of sepsis
• Physical examination should also include a detailed evaluation for
focal infection, such as exudative tonsillitis, sinus tenderness,
tympanic membrane injection, and crackles or dullness on lung
auscultation
Diagnostic Testing
• Laboratory Testing:
• Hematology: WBC count, Hb and Hematocrit, platelets
• Blood Chemistry: Electrolyte abnormalities, serum creatinine, lactate, liver function tes
• Microbiology: Proper blood, sputum, urine, cerebrospinal fluid, and other tissue culture
samples, Gram staining
• Special Procedures:
• central venous pressure (CVP) line: guiding fluid resuscitation in sepsis patients
• Radiology
• to identify the source of infection
• chest radiograph considered in px with suspected sepsis syndrome: infiltrate, sign of
ARDS
• Soft tissue plain radiographs of infected areas: CT scan, MRI
MANAGEMENT
• Initial resuscitation, appropriate airway management, IV access,
oxygen, early and appropriate antibiotics, fluid resuscitation, and
vasopressor support
• Respiratory Support:
• rapid airway protection
• Indication for intubation: hypercapnia, persistent hypoxemia, airway
compromise, and profound acidosis
• positive-pressure ventilation
• low tidal volumes (6 mL/kg) in mechanically ventilated patients with acute
lung injury to prevent iatrogenic lung damage
• Cardiovascular Support
• Fluid Resuscitation: 2 L of isotonic crystalloid
• Fluid replacement should be titrated to clinical parameters such as heart rate, blood
pressure, change in mental status, capillary refill, cool skin, and adequate urine output
(0.5–1 mL/kg/hr)
• Normal saline (0.9%) and lactated Ringer’s solution are equally effective and neither
worsens lactic acidosis
• watching for fluid overload in patients who are predisposed: older adults, those with
congestive heart failure (CHF), renal impairment
• Vasoactive Drug Therapy
• If appropriate fluid resuscitation has failed  vasopressor
• Healthy px, MAP 65 mmHg  vasopressor
• previously uncontrolled hypertension, MAP 75 mmHg or even higher
• NE should be the initial vasopressor
• Dobutamine: if myocardial dysfunction is evident
• After an initial stabilization period  titrate vasopressor
ACID BASE DISORDER
Tintinalli
Acid Base Disorders
• Acid-base homeostasis, maintained by :
• Respiratory control of Pco2 through change in alveolar ventilation
• Control of HCO3- reabsorption
• H+ excretion by kidneys
• 2 methods to analyze acid-base disorder
• Traditional bicarbonate-centered method
• Commonly use in bedside, but failed to identify acid-base abn due to alteration in
plasma free water / complex case of mixed acid-base disorder
• Stewart / strong ion method
• Accuracy in identify acid-base disorder, difficult of application at the bedside
Pathophysiology
Measurement of plasma
acidity
• Plasma hydrogen ion
concentration (H+)
normally 40 nmol/L
when pH 7.4
• When pH values 7.20 –
7.50, relation between
(H+) & pH nearly linear
• pH change of 0.01 = 1
nmol/L change in (H+)
Plasma Acid-Base Homeostasis
• Plasma (H+) = influenced by the rate of endogenous production, rate
of excretion, exogenous addition (e.g., acetylsalicylic acid ingestion)
and buffering capacity of body
• Buffer that are effective at physiologic pH:
• Hb
• Phosphate
• Proteins
• Bicarbonate
Plasma Acid – Base Homeostatis
• Henderson Hasselbach equation :
• Specify relationship between carbonic acid, bicarbonate & pH

• Kassirer-Bleich equation
• Great clinical utility
• To estimate concentration of any component of bicarbonate buffer system
Acid Production & Excretion
• Quantity of HCO3- is not fixed, varies according to physiologic need
• Provided by pulmonary exhalation of carbon dioxide (CO2)
• Renal Influence on Acid-Base Balance
• Kidney regulates excretion & formation of new HCO3-
• Renal response to pulmonary acid-base disturbance begin within 30 min of onset, but
requires hours to days to achieve equilibrium
• If tubular disease inhibits H+ extrusion -> proximal renal tubular acidosis results -> (HCO3-)
decrease to a steady-state level
• H2CO3 -> (HCO3-) + (H+)
• New HCO3- can also be created by kidney
• Formation increased during acidosis
• May require 4-5 days to reach equilibrium
• Drugs that alter uptake / delivery of Na+ to distal tubule can significantly alter HCO3- synthesis
Acid Base Disorder
• Acidosis = increased (H+) • Classification of acid base
• Endogenous production disturbance :
• Decreased buffering capacity • Respiratory
• Decreased excretion • Due to primary change in pCO2
• Exogenous addition • Metabolic
• Alkalosis = decreased (H+) • Due to primary change in (HCO3-)

• Acidemia & Alkalemia = net • Normal values :

imbalance of (H+) in blood • pH : 7.35 – 7.45
• E.g., ps has both acidosis & alkalosis • pCO2 : 35-45 mmHg
-> normal pH (has neither • HCO3- : 21-28 mEq/L
acidemia / alkalemia)
Anion Gap
Anion Gap
• AG may rise when (unmeasured) cations decrease – hypomagnesia,
hypokalemia & hypocalcemia
• Increase in AG = metabolic acidosis
• May be seen in metabolic & respiratory alkalosis -> elevate of AG by 2-3
mEq/L due to elevation in lactate (unmeasured anion) by enhancement of
glycolysis
• AG > 30 mEq/L usually caused by lactic acidosis / diabetic ketoacidosis
Parameters required for clinical acid-base
evaluation
• Events that may result in gain / loss of acid / base –
• vomit, diarrhea, medication / ingestion of toxin
• Dysfunction of organs of acid-base homeostasis – liver, kidneys & lungs
• Lab evaluation need blood sample for determination of :
• Blood gases (pH , pCO2, (HCO3-))
• Electrolytes ((Na+), (K+), (Cl-) & (HCO3-))
• Factors that affect ps acid-base status (albumin, lactic acid, creatinine, BUN)
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Metabolic Acidosis
• Result from : HCO3- loss, administration / ingestion of acid,
endogenous production & accumulation of acid
• Loss of HCO3-
• Externalization of intestinal contents – vomiting, enterocutaneous fistulae
• Renal wasting of bicarbonate – renal tubular acidosis, carbonic anhydrase
inhibitor therapy
• Endogenous acid – accumulate in renal tubular acidosis, ketoacidosis
& lactic acidosis
• Dilutional acidosis – acidosis from rapid infusion of normal saline ->
endogenous accumulation from CO2 hydration
Metabolic Acidosis
• Respiratory compensation
• Attempt to lower the (H+) by reduction in Pco2 through increased ventilation
• Limit of respiratory compensation during metabolic acidosis
• Respiratory minute volume declines when pH decrease 7.10 -> bicarbonate therapy
• Clinical Features & Physiologic consequences of acidosis
• Abdominal pain, headache nausea +/- vomiting – generalized weakness, dyspnea (acidosis
stimulate respiratory symptoms)
• Cardiac contractile function is reduced
• Hepatic & renal perfusion & systemic blood pressure decline & pulmonary vascular resistance
increases
• Severe acidosis -> vascular collapse
• Catabolic state develops – generalized increase in metabolism, resistance to insulin &
inhibition of anaerobic glycolysis
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Differential Diagnosis of Wide AG Acidosis
• DD/ :
• Renal failure – uremia
• Acidosis seen in initial stages of renal failure, may be severe but tend to be stable -> HCO3- 15mEq/L in case
of chronic renal failure
• Ketoacidosis – diabetic ketoacidosis, alcoholic ketoacidosis, starvation ketoacidosis
• Positive ketones
• Major ketone in serum of a patient with untreated diabetic / alcoholic ketoacidosis -> β-hydroxybutyrate ->
specific test : nitroprusside tests
• Lactic acidosis
• When lactate production > lactate metabolisms
• Type A : Tissue hypoxia & elevated lactate production
• Type B : Normal tissue oxygenation & impairment of lactate metabolisms
• Causes of lactic acidosis : renal failure, shock, sepsis, cardiac arrest, trauma, seizure, tissue ischemia, DKA,
thiamine deficiency
• Ingestion – methanol, ethylene glycol, salicylates
Treatment
• Restoration of normal tissue perfusion & oxygenation
• If there’s inadequate respiratory compensation -> 1st th/ correct
respiratory problem
• Buffer therapy in acidosis
• Slow replacement of sodium bicarbonate in ps with sodium bicarbonate loss
due to diarrhea / renal tubular acidosi is useful
Metabolic Alkalosis
• Metabolic alkalosis results from :
• Gain of bicarbonate
• Loss of acid
• Clinical features & physiologic consequence of alkalosis :
• Generalized weakness, dizziness, myalgia, palpitations, nausea +/- vomiting,
paresthesia & possibly muscle spasm / twitching
• Physiologic effects of alkalemia -> neurologic abn (tetany, neuromuscular
instability & seizure)
Cause of metabolic Alkalosis
• Bicarbonate & chloride -> major serum anions easily altered
• Chloride loss – vomit (also acid loss), diarrhea, diuretic therapy, chloric-wasting
disease (cystic fibrosis)
• Serum chloride concentration & extracellular volume reduce -> increase mineralocorticoid
activity -> enhance Na reabsorption & potassium & hydrogen ion secretion in distal tubule
-> increase HCO3- exceeds tubule maximum ability to reabsorb filtered bicarbonate ->
alkaline urine, free of chloride (<10mEq/L) -> hypokalemic, hypochloremic alkalosis that
respond to normal saline
• Excess mineralocorticoid activity
• Not associated with hypovolemia -> urine chloride normal / elevated –> alkalosis can’t be
reversed with normal saline
• “Chloride-unresponsive alkalosis” & HT -> renal artery stenosis, renin-secreting
tumor, adrenal hyperplasia, hyperaldosteronism, Cushing’s syndrome
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Metabolic Alkalosis
• Compensation for metabolic alkalosis : Alveolar ventilation
• pCO2 in ps with significant metabolic alkalosis should rise by 0.7 mmHg for
each milliequivalent increase in (HCO3-)
• Treatment :
• Treatment of underlying cause
• Acetazolamide produce bicarbonaturia & effective for th/ of metabolic
alkalosis -> careful monitoring of potassium, mg & phosphate concentration
• If severe alkalosis (HCO3- > 45 mmol/L) -> use of IV hydrochloric acid 0.1
mmol/kg/h & < 0.2 mmol/kg/h
Respiratory Acidosis
• Definition : alveolar hypoventilation & diagnosed when pCO2 > greater than expected value
• Origins :
• Increased CO2 production (high-glucose diet)
• Abnormal gas exchange (pneumonia)
• Common path : inadequate ventilation
• Caused by : head trauma, chest trauma, lung disease / excess sedation
• Chronic hypoventilation in extremely obese ps -> pickwickian syndrome
• A rise in pCO2 -> stimulate respiratory center -> increase RR & minute ventilation
• If arterial pCO2 > 60-70 mmHg (5-10% ps with severe emphysema) -> respiratory acidosis depress respiratory center
• Stimulus for ventilation provided by hypoxemia -> giving o2 -> remove main stimulus to breathe -> pCO2 rise abruptly
• But don’t withhold O2 from ps with severe dyspnea
• Based on the change in (H+) compared with the change in pCO2, ratio :
• 0.3 – chronic respiratory acidosis
• 0.8 – acute respiratory acidosis
Treatment
• Th/ improve alveolar ventilation
• Generally if minute ventilation doubled -> pCO2 will be reduced by 50%
• COPD -> bronchodilator (β-agonists, anticholinergics, systemic sympathomimetic
agents) + careful administration of small amount of O2
• In chronic respiratory acidosis : reduction of pCO2 should proceed slowly
• Minute ventilation for normal 70 kg -> 6L/min ,in COPD -> <4L/min
• If indicated in ED -> start minute ventilation about 5L/min -> gradually increase
according to clinical response & change in pCO2
• In chronic respiratory acidosis – arterial pCO2 shouldn’t be reduced > 5 mm
Hg/h
• Rapid correction cause sudden development of severe combined metabolic &
respiratory alkalosis -> dysrhytmias
Respiratory Alkalosis
• Alveolar hyperventilation & exists when pCO2 < expected
• Caused by condition stimulate respiratory center
• CNS tumors / stroke
• Infection
• Pregnancy
• Hypoxia
• Toxins (e.g., salicylates)
• Acute reduction in pCO2 –> reduction in (H+) -> increase negative charge -> bind
calcium -> reduction in ionized calcium -> tetany & paresthesias
• Chronic respiratory alkalosis seen at high altitudes, among mountaineers climbing
over 3700m where partial pressure of O2 significant diminished
• Th/ acetazolamide
Clinical approach to acid-base problem &
mixed acid-base disturbance
1. Look pH
• Decrease – acidosis
• Increased – alkalosis
2. If pH indicate acidosis – predominant mechanism ascertained by
examine (HCO3-) & pCO2
• If HCO3- low (primary metabolic acidosis) -> examined AG -> correct AG for abn
albumin level
• If AG increased compared to steady state value / >15 -> wide AG metabolic acidosis present
• If AG unchanged -> disturbance is nonwidened / normal AG metabolic acidosis, typically
with hyperchloremia
• If change in AG = change in HCO2 -> pure wide AG acidosis
 • Examine whether ventilatory response is appropriate :
• If decrease in pCO2 = decrease in HCO3 -> appropriate respiratory compensation
• Decrease in pCO2 > decrease in HCO3 -> concomitant respiratory alkalosis
• Decrease in pCO2 < HCO3 -> concomitant respiratory acidosis
• If pCO2 elevated -> respiratory acidosis -> examine ratio of (H+) : pCO2 :
• Ratio is 0.8 = acute
• Ratio is 0.33 = chronic
• Ratio : 0.8 – 0.33 = acute exacerbation of chronic condition
• Ratio < 0.33 = metabolic alkalosis present
• If pH > 7.45 -> primary / predominant disturbance : alkalosis
• HCO3 Elevated : primary metabolic alkalosis -> check ratio pCO2 : HCO3 ->
• <0.7 – there’s also alkalosis respiratory
• 0.7 – compensatory ventilatory response
• > 0.7 – there’s also respiratory acidosis
• pCO2 low : primary respiratory alkalosis -> check ratio H+ : pCO2 ->
• 0.75 – acute respiratory alkalosis
• >0.75 - concomitant metabolic alkalosis