Transcript Assessment of Critically Ill Patients Week 1

Assessment of Critically
Ill Patients
Michael Haines, MPH, RRT-NPS, AE-C
Introduction/Objectives
• Being able to assess a patient beyond surface
data is a critical aspect in becoming a qualified
clinician and will help to set you apart from
mediocre therapists
Components of a Neurological Assessment
• 1. Interviewing the patient
• 2. Determining level of consciousness
• 3. Pupillary Assessment
• 4. Cranial Nerve Testing
• 5. Vital Signs
• 6. Motor Function
• 7. Sensory Function
• 8. Tone
• 9. Cerebral Function
Interviewing your patient
• Purpose: gather information, either from the family or patient. It
also established a baseline sensorium
• READ THE PATIENTS CHART FIRST, KNOW PAST HX
• Identify the following when assessing neuro status:
• Headache
• Difficulty with speech
• Inability to read or write
• Altered level of consciousness or memory
• Confusion or change in thinking
• Decrease in sensation, tingling, pain
• Motor weakness or decreased strength
• Vision problems, diplopia
• Difficulty swallowing
• Tremors, twitches…
Consciousness
Reticular Activating System (RAS)
• Network of neurons and fibers in the brain stem which
receive input from the sensory pathways and project to
the entire cerebral cortex
• Arousal is dependent on adequate functioning of RAS
• Arousal is a function of the brain stem, it does not have
anything to do with the thinking parts of the brain
(basically it allows for physical reaction)
• If a patient opens their eyes when called upon, they have
an intact RAS for example but does not tell you if they
are cognitive, awake or aware
Consciousness
Cortex
• Modulates incoming information via connections to the
RAS
• Requires functioning RAS
• Awareness means that the cerebral cortex is working and
that the patient can interact with and interpret his
environment
• We evaluate awareness in many ways but tend to focus
on four areas of cortical functioning:
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Orientation
Attention span
Language
Memory
Level of Consciousness
• Consciousness is defined as the state of being
aware of physical events or mental concepts.
Conscious patients are awake and responsive to
their surroundings
• The level of consciousness has been described as
the degree of arousal and awareness.
• A manifestation of altered consciousness implies
an underlying brain dysfunction.
• Its onset may be sudden, for example following
an acute head injury, or it may occur more
gradually, such as in hypoglycemia.
Causes of Altered Level of Consciousness
• Profound hypoxemia
• Hypercapnia
• Cerebral
hypoperfusion
• Stroke
• Convulsions
• Hypoglycemia
• Recent administration
of sedatives or
analgesic drugs; drug
overdose
• Tumors
• High Ammonia levels
from liver failure
• Renal failure
• Encephalopathy
(hepatic, anoxic,
metabolic)
• Brain lesions, swelling
• subarachnoid
hemorrhage
• alcohol intoxication
• Severe shock
• Infection
ALOC
• The clinician must determine the cause of the ALOC and
suggest appropriate exams such as:
• CT of the brain (to rule out bleeding, swelling…)
• ABG to assess Co2, Pao2
• Blood Glucose levels with an Accucheck
• Pupil dilation to assess drugs
• Physical exams to determine significance
• Electrolytes, liver and renal panels, Infection
Assessment of LOC
• Observe patients response to verbal or motor stimuli
• No response to voice or light touch, then attempt painful
stimuli such as:
• Sternal rub
• Supraorbital pressure
• Pinching upper arms
Localizing is when a patient does a purposeful gesture,
such as picks up tubing, pulls at linen
Localizing is purposeful and intentional movement
intended to eliminate a noxious stimulus, whereas
withdrawal is a smaller movement used to get away
from noxious stimulus.
Assessment of Awareness
• The Glascow Coma Scale (GCS) helps us to
decrease the subjectivity of our responses
• GCS is a neurological scale that aims to give a
reliable, objective way of recording the
conscious state of a person for initial as well as
subsequent assessment.
• A patient is assessed against the criteria of the
scale, and the resulting points give a patient
score between
• 3 (indicating deep unconsciousness) and 15
(most awake/alert)
LOC
• GCS
• Individual elements as well as the sum of the score are
important.
• Generally, brain injury is classified as:
• Severe, with GCS ≤ 8
• Moderate, GCS 9 - 12
• Minor, GCS ≥ 13.
• Tracheal intubation and severe facial/eye swelling or damage
make it impossible to test the verbal and eye responses. In
these circumstances, the score is given as 1 with a modifier
attached
LOC
• The AVPU scale is a quick and easy method to
assess level of consciousness. It is ideal in the
initial rapid ABCDE assessment:
• Alert
• Responds to voice
• Responds to pain
• Unconscious
LOC terms
• Awake/Alert (responds in a meaningful manner to verbal
instructions or gestures)
• Confused (disoriented to time, place, or person, memory
difficulty is common, difficulty with commands, exhibits
alteration in perception of stimuli, may be agitated)
• Combative
• Stuporous (generally unresponsive except to vigorous
stimulation, may make attempt at verbalization to
vigorous/repeated stimuli, opens eyes to deep pain)
• Lethargic (drowsy, oriented when awake but if left alone will
sleep)
• Obtunded (decreased interest in their surroundings, slowed
responses, and sleepines)
• Comatose (unarousable and unresponsive, some localization
or movement, does not open eyes to deep pain)
States of ALOC
• Brain Death
• Persistent Vegetative State
• Locked-in Syndrome (muscle paralysis, involving voluntary
muscles, while there is full cognitive function)
• Progression from coma to full consciousness is often a gradual
occurrence (especially in the case of head trauma)
• Recovery from ALOC dependent on:
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Age (under 20 better prognosis)
Type of injury (reversible)
Premorbid health
Longer the coma the worse the prognosis
Absence of gag, pupillary reflexes = poor prognosis
Permanent flexion or flaccidness of extremities = poor prognosis
Pupillary Assessment
• Pupil dilation/constriction
• Certain drugs cause constriction of the pupils, such as alcohol and
opioids. Other drugs, such as atropine, LSD, MDMA, mescaline,
psilocybin mushrooms, cocaine and amphetamines may cause
pupil dilation.
Pupillary Assessment
Pupillary Assessment
• Pinpoint: opiate overdose or pontine hemorrhage
• Small: Bright room, Horners syndrome, pontine hemorrage
,ophthalmic drops, metabolic coma
• Large: dark room, some drugs, orbital injury
• Dilated: Always an abnormal finding, terminal stage of anoxia
ischemia or at death, anti-cholinergic drugs can dilate pupils
• SHAPE:
• Ovoid: intracranial hypertension
• Keyhole: post Cataract surgery
Ovoid shape
Keyhole shape
Pupillary Assessment
• Pupils can also react in the following manner:
• sluggish:
• found in conditions that compress the third cranial nerve, such
as, cerebral edema and herniation
• nonreactive or fixed:
• seen in conditions that compress the 3rd cranial nerve such as
herniation, severe hypoxia and ischemia
• hippus phenomenon:
• with uniform illumination of the pupil, alternating dilation and
contraction of the pupil occurs. This is often associated with early
signs of transtentorial herniation or may indicate seizure activity.
Intracranial Pressure
ICP kept below 20 cmH2O
Be mindful of things that
can increase ICP such as
suctioning, stimulation,
excessive PEEP levels, high
CO2 levels
Vital Sign Changes
• Changes in vital signs are not consistent early warning
signals. Vitals are more useful in detecting progression to
late symptoms. Both respiratory and cardiac centers are
located in the brainstem.
• Therefore, compression of the brainstem will cause
changes in vital signs. This is usually a late sign and
impending herniation/death will occur if the problem is
not resolved. The respiratory centers in the brainstem
control rate, rhythm, inspiration/expiration.
• The cardiac centers also play a part in cardiac
acceleration/inhibition e.g. controlling heart rate and
rhythm as well as hemodynamic stability/instability
Respiratory Rate
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Biots Breathing
Cheyne Stokes
Apneustic
What can cause changes in respirations from a neurological
standpoint?
• Increased Intracranial Pressure
• Initially with increased ICP you should expect to see a slowing
of respirations but as the ICP increases so will the rate of
respirations. The rhythm of respirations will also become more
irregular
Spinal Cord Injury
• Cervical spine trauma can cause alteration in respiratory
effort. If the injury is at level C4 (phrenic segment) or above,
total respiratory arrest can occur.
Pulse
• 1. Assess rate, rhythm, and quality of pulse
• 2. Assess tissue perfusion, cardiac output, activity intolerance
• 3. Assess for causes of cardiac instability and intervene appropriately
• What can cause changes in pulse from a neurological standpoint?
Tachycardia
• 1. If a patient has tachycardia related to neurological impairment it
can mean that they are reaching a terminal phase in their disease
process.
• 2. In a patient with multiple trauma, hemorrhage must be ruled out
(intra-abdominal).
Bradycardia
• 1. Bradycardia is seen in the later stages of increased intracranial
pressure. As BP rises to overcome the increased ICP, reflex inhibition
causes a slowing of the HR.
• 2. Bradycardia can also be seen with spinal cord injury and
interruption of the descending sympathetic pathways
Vitals
Cardiac Arrhythmias
• Cardiac arrhythmias may occur in several neurological
conditions. Subarachnoid hemorrhage patients with blood in
the CSF and patients who have undergone posterior fossa
surgery tend to have an increased incidence of arrhythmia.
Blood Pressure
• 1. Assess for hypertension, hypotension, and pulse pressure
• 2. Assess tissue perfusion, cardiac output
Hypertension
• Increases in blood pressure are usually associated with rising
ICP.
• An increased systolic pressure, widening pulse pressure,
bradycardia and apnea are advanced stages of increased ICP
and are known as Cushing's response.
Vitals
Hypotension
• 1. Decrease in blood pressure is rarely seen as a result of
neurological injury. If it is present it is usually
accompanied by tachycardia and is terminal.
• 2. Hypotension and bradycardia can be seen with cervical
spine injuries as a result of neurogenic shock.
Temperature
• The hypothalamus is the regulatory center for
temperature. Regulation of heat is monitored by blood
temperature and is controlled through impulses to sweat
glands, dilation of peripheral vessels and shivering of
skeletal muscles.
Vitals
Hyperthermia
• Temperature elevation in the neurological patient can be
caused by direct damage to the hypothalamus or traction on
the hypothalamus as a result of increased ICP, CNS infection,
subarachnoid hemorrhage etc. Temperature elevations may
become very high, very rapidly. They need to be treated
aggressively as fever will cause an increase in cerebral oxygen
requirements, increased metabolic rate, and increased carbon
dioxide production. Increased carbon dioxide production can
lead to cerebral vasodilation. Cerebral vasodilation can
increase the ICP, leading to more cerebral ischemia.
Hypothermia
• Can occur with spinal shock, metabolic or toxic coma, or
lesions of the hypothalamus.
Kidney Disease
Terminology
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CRF: Chronic Renal Failure
ARF: Acute Renal Failure
ESRD: End stage renal disease
ESRF: End stage renal failure
GFR: Glomular filtration rate
Azotemia: Retention of nitrogenous waste products as renal
insufficiency develops
The Kidney
• Three of the biggest jobs that the kidneys have are:
• (1) to cleanse the blood,
• (2) to regulate and maintain an appropriate fluid and
chemical balance in the body, and
• (3) to produce the urine.
• Each of these functions is closely related to the other
two, not only because each involves the removal or
addition of fluid and chemicals from the blood, but also
because each of these functions takes place in the
kidney's nephrons. The starting point in the nephron for
each of these functions is the glomerulus. It is the
"gateway" that the blood must pass through in order to
be cleansed by the kidneys.
The Kidney
• There are 1 million nephrons in each kindey
• The kidney has an innate ability to maintain GFR by
hyperinfiltration and compensatory hypertophy of the
remaining healthy nephrons
Acute Renal Failure
• is a rapidly progressive loss of renal function, generally
characterized by oliguria (decreased urine production,
quantified as less than 400 mL per day in adults, less than
0.5 mL/kg/h in children or less than 1 mL/kg/h in
infants); and fluid and electrolyte imbalance. AKI can
result from a variety of causes, generally classified as
prerenal, intrinsic, and postrenal. An underlying cause
must be identified and treated to arrest the progress,
and dialysis may be necessary to bridge the time gap
required for treating these fundamental causes
Causes of ARF
• Prerenal causes of AKI are those that decrease effective blood flow
to the kidney. These include systemic causes, such as low blood
volume, low blood pressure, and heart failure, as well as local
changes to the blood vessels supplying the kidney (clots, stenosis…)
• Sources of damage to the kidney itself are dubbed intrinsic. Intrinsic
can be due to damage to the glomeruli, renal tubules, or
interstitium. Common causes of each are glomerulonephritis, acute
tubular necrosis (ATN), and acute interstitial nephritis (AIN),
respectively
• Postrenal is a consequence of urinary tract obstruction. This may be
related to benign prostatic hyperplasia, kidney stones, obstructed
urinary catheter, bladder stone, bladder, ureteral or renal
malignancy
Chronic Renal Failure
• The most common causes of CKD are diabetes mellitus,
hypertension, and glomerulonephritis.Together, these cause
approximately 75% of all adult cases
• http://www.youtube.com/watch?v=ikGl7DPXUK0&feature=rel
ated
• Presence of markers of kidney damage for three
months, as defined by structural or functional
abnormalities of the kidney with or without
decreased GFR, manifest by either pathological
abnormalities or other markers of kidney
damage, including abnormalities in the
composition of blood or urine, or abnormalities
in imaging tests.
• The presence of GFR <60 mL/min/1.73 m2 for
three months, with or without other signs of
kidney damage as described above.
Am J Kidney Dis 2002; 39:S1
Chronic Renal Failure
Diabetes
• A group of metabolic diseases in which a person has high blood
sugar, either because the body does not produce enough insulin, or
because cells do not respond to the insulin that is produced. This
high blood sugar produces the classical symptoms of polyuria
(frequent urination), polydipsia (increased thirst) and polyphagia
(increased hunger).
• There are three main types of diabetes:
• Type 1 diabetes: results from the body's failure to produce insulin,
and presently requires the person to inject insulin.
• Type 2 diabetes: results from insulin resistance, a condition in which
cells fail to use insulin properly, sometimes combined with an
absolute insulin deficiency.
• Gestational diabetes: is when pregnant women, who have never had
diabetes before, have a high blood glucose level during pregnancy. It
may precede development of type 2 DM.
GFR
• Volume of fluid filtered from the renal glomerular capillaries into the
Bowman's capsule per unit time.
• Glomerular filtration rate (GFR) can be calculated by measuring any
chemical that has a steady level in the blood, and is freely filtered
but neither reabsorbed nor secreted by the kidneys. The rate
therefore measured is the quantity of the substance in the urine
that originated from a calculable volume of blood
• The GFR test measures how well your kidneys are filtering a waste
called creatinine, which is produced by the muscles. When the
kidneys aren't working as well as they should, creatinine builds up in
the blood.
Stages of CKD
• Stage 1*: GFR >= 90 mL/min/1.73 m2
• Stage 2*: GFR 60-89 (mild)
• Stage 3: GFR 30-59 (moderate)
• Stage 4: GFR 15-29 (severe; pre-HD)
• Stage 5: GFR < 15 (kidney failure)
Am J Kidney Dis 2002; 39 (S2): S1246
• Normal or elevated GFR
Signs & Symptoms
• General
• Fatigue & malaise
• Edema
• Ophthalmologic
• AV nicking
• Cardiac
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HTN
Heart failure
Hyperkalemia
Pericarditis
CAD
• GI
• Anorexia
• Nausea/vomiting
• Dysgeusia
• Skin
• Pruritis
• Pallor
• Neurological
• MS changes
• Seizures
Uremia
• Is the clinical and laboratory syndrome, reflecting dysfunction
of all organ systems as a result of untreated or undertreated
acute or chronic renal failure
Changes in the blood
• The kidneys work to filter toxins and waste products out of the
blood. When kidney function declines, waste products begin
to build up within the blood. Creatine and urea build up.
Phosphate also accumulates in the blood. A build up of
hydrogen ions may also occur, leading to acidosis.
Changes in electrolytes
• Because of the resulting changes to the blood chemistry, the
electrolyte balance of the blood and cells is disrupted. Fluid
retention also results. Often fluid retention is the first
noticeable sign that the kidneys are beginning to shut down.
The resulting water weight gain and edema in the hands and
feet signal that the kidneys are not removing waste products
and fluids as they should.
Pulmonary Edema
• as acute renal failure worsens, fluids continue to
build within the body and may begin to collect in
the air sacs of the lungs. This condition, known
as pulmonary edema, can result in difficulty
breathing, restlessness, anxiety and wheezing.
Untreated pulmonary edema can ultimately lead
to respiratory failure. Most deaths that occur in
cases of renal failure are due to either a systemic
infection or respiratory failure that results from
the initial failure of the kidneys.
Why does edema occur in
patients with kidney
disease?
• Edema forms in patients with kidney disease for two reasons:
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a heavy loss of protein in the urine, or
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impaired kidney (renal) function.
Heavy loss of protein in the
urine
• The heavy loss of protein in the urine (over 3.0
grams per day) with its accompanying edema is
termed the nephrotic syndrome. Nephrotic
syndrome results in a reduction in the concentration
of albumin in the blood (hypoalbuminemia). Since
albumin helps to maintain blood volume in the
blood vessels, a reduction of fluid in the blood
vessels occurs. The kidneys then register that there
is depletion of blood volume and, therefore, attempt
to retain salt. Consequently, fluid moves into the
interstitial spaces, thereby causing pitting edema.
Heavy loss of protein in the
urine
• The treatment of fluid retention in these patients is to reduce
the loss of protein into the urine and to restrict salt in the diet.
The loss of protein in the urine may be reduced by the use of
ACE inhibitors and angiotensin receptor blockers (ARB's). Both
categories of drugs, which ordinarily are used to lower blood
pressure, prompt the kidneys to reduce the loss of protein
into the urine.
Impaired kidney (renal)
function
• Patients who have kidney diseases that impair
renal function develop edema because of a
limitation in the kidneys' ability to excrete
sodium into the urine. Thus, patients with kidney
failure from whatever cause will develop edema
if their intake of sodium exceeds the ability of
their kidneys to excrete the sodium. The more
advanced the kidney failure, the greater the
problem of salt retention is likely to become. The
most severe situation is the patient with endstage kidney failure who requires dialysis
therapy.
Management
• Identify and treat factors associated with progression
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HTN
Proteinuria
Glucose control
Treat pulmonary edema (Bipap)
Hypertension
• Target BP
• <130/80 mm Hg
• Consider several anti-HTN medications with
different mechanisms of activity
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ACEs/ARBs
Diuretics
CCBs
HCTZ (less effective when GFR < 20)
Metabolic changes with CKD
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Hemoglobin/hematocrit 
Bicarbonate 
Calcium
Phosphate 
PTH 
Triglycerides 
Metabolic changes…
• Monitor and treat biochemical abnormalities
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Anemia
Metabolic acidosis
Mineral metabolism
Dyslipidemia
Nutrition
Anemia
• Common in CRF
• HD pts have increased rates of:
• Hospital admission
• CAD/LVH
• Reduced quality of life
• Can improve energy levels, sleep, cognitive function, and
quality of life in HD pts
Treating Anemia
• Epoetin alfa (rHuEPO; Epogen/Procrit)
• HD: 50-100 U/kg IV/SC 3x/wk
• Non-HD: 10,000 U qwk
• Darbepoetin alfa (Aranesp)
• HD: 0.45 g/kg IV/SC qwk
• Non-HD: 60 g SC q2wks
Metabolic acidosis
• Muscle catabolism
• Metabolic bone disease
• Sodium bicarbonate
• Maintain serum bicarbonate > 22 meq/L
• 0.5-1.0 meq/kg per day
• Watch for sodium loading
• Volume expansion
• HTN
Mineral metabolism
• Calcium and phosphate metabolism abnormalities associated
with:
• 14 of 16 ESRD/HD pts (20-30 yrs) had calcification on CT scan
• 3 of 60 in the control group
NEJM 2000; 342(20): 1478-83
• Renal osteodystrophy
• Calciphylaxis and vascular calcification
Lactic Acidosis
• Lactic acidosis is a physiological condition characterized by
low pH in body tissues and blood accompanied by the buildup
of lactate
• Considered a distinct form of metabolic acidosis.
• The condition typically occurs when cells receive too little
oxygen
• For example during vigorous exercise. In this situation,
impaired cellular respiration leads to lower pH levels.
Simultaneously, cells are forced to metabolize glucose
anaerobically, which leads to lactate formation.
• Therefore, elevated lactate is indicative of tissue hypoxia,
hypoperfusion, and possible damage.
• Lactic acidosis is characterized by lactate levels >5 mmol/L and
serum pH <7.35.
Lactic Acidosis
Causes, incidence, and risk factors
• The most common cause of lactic acidosis is intense exercise. However, it
can also be caused by certain diseases, such as:
• AIDS
• Cancer
• Kidney failure
• Respiratory failure
• Sepsis
Symptoms
• Nausea
• Weakness
• Signs and tests
• Blood tests to check electrolyte levels
• Treatment
• The main treatment for lactic acidosis is to correct the medical problem
that causes the condition. Oxygen
Lactic Acidosis
• Patients will require high levels of Oxygen, often requiring
mechanical ventilation. They will also demonstrate with
increase VA to compensate
Anion Gap
• The anion gap is the difference in the measured cations and
the measured anions in serum, plasma, or urine.
• The magnitude of this difference (i.e. "gap") in the serum is
often calculated in medicine when attempting to identify the
cause of metabolic acidosis. If the gap is greater than normal,
then high anion gap metabolic acidosis is diagnosed.
Anion Gap
• With potassium
• It is calculated by subtracting the serum concentrations of
chloride and bicarbonate (anions) from the concentrations of
sodium and potassium (cations):
• = [Na+] + [K+] − [Cl−] − [HCO3−]
• Without potassium (Daily practice)
• However, the potassium is frequently ignored because
potassium concentrations, being very low, usually have little
effect on the calculated gap. This leaves the following
equation:
• = [Na+] − [Cl−] − [HCO3−]
Anion Gap
• In normal health there are more measurable cations
compared to measurable anions in the serum; therefore, the
anion gap is usually positive.
• Because we know that plasma is electro-neutral we can
conclude that the anion gap calculation represents the
concentration of unmeasured anions.
• The anion gap varies in response to changes in the
concentrations of the above-mentioned serum components
that contribute to the acid-base balance. Calculating the anion
gap is clinically useful, as it helps in the differential diagnosis
of a number of disease states.
High Anion Gap
• "Mudpiles"
• The mnemonic MUDPILES is commonly used to remember the
causes of increased anion gap metabolic acidosis
• M-Methanol
• U-Uremia (chronic renal failure)
• D-Diabetic ketoacidosis
• P-Propylene glycol ("P" used to stand for Paraldehyde but substance
is not commonly used today)
• I-Infection, Iron, Isoniazid
• L-Lactic acidosis
• E-Ethylene glycol (Note: Ethanol is sometimes included in this
mnemonic as well, although the acidosis caused by ethanol is
actually primarily due to the increased production of lactic acid
found in such intoxication.)
• S-Salicylates
High Anion Gap
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Another frequently used mnemonic is KARMEL.
K-Ketoacidosis
A-ASA
R-Renal failure
M-Methanol
E-Ethylene glycol
L-Lactic acidosis
Metabolic ABGS
• A 23-year-old woman with gastroenteritis experiences nausea
and vomiting. Aterial blood gas analysis is done 1 hour after
the onset of symptoms. Which of the following sets of blood
gases is most likely.
• A pH 7.30; PCO2 50; HCO3- 24
• B pH 7.28; PCO2 40; HCO3- 18
• C pH 7.56; PCO2 40; HCO3- 35
• D pH 7.51; PCO2 50; HCO3- 35
Answer
• Choice D is the best answer.
• 1. Vomiting causes loss of stomach acid leading to metabolic
alkalosis.
• The rise in pH will inhibit the peripheral chemoreceptor for
pH located in the carotid bodies leading to hypoventilation
(increased PCO2), which is compensatory.
Metabolic Acidosis
• A 35-year-old man with type 1 diabetes is admitted to the
emergency department after being found unconscious and
unresponsive at home. His breath has a "fruity" odor. His
wife told the EMTs that his diabetes had been "out of control"
lately and that he has no other medical problems. His
breathing is deep and rapid. An arterial blood sample is taken
for analysis. Which of the following sets of arterial blood
gases is most likely.
• A pH 7.00; PCO2 50; HCO3- 12
• B pH 7.22; PCO2 30; HCO3- 12
• C pH 7.56; PCO2 40; HCO3- 35
• D pH 7.51; PCO2 45; HCO3- 35
Answer
• Choice B is the best answer. The presentation is consistent
with ketoacidosis (ketones are volatile acids that are
eliminated via both kidneys and lungs). The overutilization of
fats for metabolism leads to ketoacidosis, a metabolic
acidosis. The low pH stimulates the carotid pH receptor
leading to hyperventilation (lower PCO2) which is
compensatory. recall that according to the HendersonHasselbalch equation, pH = 6.1 + log [HCO3]/PCO2 x
αlpha. Compensation is always aimed at restoring the ratio
HCO3/PCO2 back to a normal value, so if HCO3 decreases,
PCO2 must decrease via hyperventilation to provide
compensation.
Base Excess
• Base excess is defined as the amount of strong acid that must
be added to each liter of fully oxygenated blood to return the
pH to 7.40 at a temperature of 37°C and a pCO2 of 40 mmHg
• A base deficit (i.e., a negative base excess) can be
correspondingly defined in terms of the amount of strong
base that must be added.
• A further distinction can be made between actual and
standard base excess: actual base excess is that present in the
blood, while standard base excess is the value when the
hemoglobin is at 5 g/dl. The latter gives a better view of the
base excess of the entire extracellular fluid
Base Excess
• The predominant base contributing to base excess is
bicarbonate. Thus, a deviation of serum bicarbonate from the
reference range is ordinarily mirrored by a deviation in base
excess. However, base excess is a more comprehensive
measurement, encompassing all metabolic contributions.
• metabolic alkalosis if too high (more than +2 mEq/L)
• metabolic acidosis if too low (less than −2 mEq/L)
BUN
• A blood urea nitrogen test measures the amount of urea nitrogen
that's in your blood. Your liver produces ammonia — which contains
nitrogen — after it breaks down proteins used by your body's cells.
• The nitrogen combines with other elements, such as carbon,
hydrogen and oxygen, to form urea, which is a chemical waste
product.
• The urea travels from your liver to your kidneys through your
bloodstream. Healthy kidneys filter urea and other waste products
from your blood. The filtered waste products leave your body in
urine.
• If a blood urea nitrogen test reveals that your urea nitrogen levels
are higher than normal, it probably indicates that your kidneys
aren't working properly. Or it could point to high protein intake,
inadequate fluid intake or poor circulation.
BUN
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Typical Ref. Range: 5-25 mg/DL
Optimal Range: 12-20 mg/DL
Causes of Increased ("Azotemia")
Renal dysfunction (creatinine increases proportionately)
Pre-renal Azotemia (less proportional creatinine elevation)
Diabetes mellitus, uncontrolled
Starvation/dehydration/diarrhea
Congestive heart failure (decreased renal circulation)
GI hemorrhage and obstruction
Shock/Tissue necrosis/ Third degree burns
Renal Artery Stenosis (with hypertension)
Post-Renal
Renal vein thrombosis
Urinary tract obstruction
Non-Renal
Gout
Increased protein catabolism (Tetracycline, Addison's, excess glucocorticoids)
High protein diet
Renal Failure
• Patients with high BUN/Creatine associated with renal failure
may develop pulmonary edema from fluid overload.
• They will produce with increase WOB, decreased SaO2. often
require intubation
• Chronic anemia also associated with CRF, carrying capacity of
O2 will be decreased
BNP
• BNP is a substance secreted from the ventricles or lower
chambers of the heart in response to changes in pressure that
occur when heart failure develops and worsens. The level of
BNP in the blood increases when heart failure symptoms
worsen, and decreases when the heart failure condition is
stable. The BNP level in a person with heart failure – even
someone whose condition is stable – is higher than in a
person with normal heart function.
Increased BNP
• Typically associated with CHF, depending on the patient often
requires positive pressure for associated pulmonary edema.
Typically non-invasive ventilation
Cardiac Enzymes
• Cardiac enzyme studies measure the levels of the enzyme
creatine phosphokinase (CPK, CK) and the protein troponin in
the blood.
• Low levels of these enzymes and proteins are normally found
in your blood, but if your heart muscle is injured, such as from
a heart attack, the enzymes and proteins leak out of damaged
heart muscle cells, and their levels in the bloodstream rise.
• Because some of these enzymes and proteins are also found
in other body tissues, their levels in the blood may rise when
those other tissues are damaged. Cardiac enzyme studies
must always be compared with your symptoms, your physical
examination findings, and electrocardiogram (EKG, ECG)
results.
Liver Enzymes
• Elevated liver enzymes may indicate inflammation or damage to
cells in the liver. Inflamed or injured liver cells leak higher than
normal amounts of certain chemicals, including liver enzymes, into
the bloodstream, which can result in elevated liver enzymes on
blood tests.
• The specific elevated liver enzymes most commonly found are:
• Alanine transaminase (ALT)
• Aspartate transaminase (AST)
• Elevated liver enzymes may be discovered during routine blood
testing. In most cases, liver enzyme levels are only mildly and
temporarily elevated. Most of the time, elevated liver enzymes
don't signal a chronic, serious liver problem.
Liver Failure
Acites, decreased
sensorium
Albumin
• Albumin is a protein made specifically by the liver, It is the
main constituent of total protein; the remaining fraction is
called globulin (including the immunoglobulins).
• Albumin levels are decreased in chronic liver disease, such as
cirrhosis. It is also decreased in nephrotic syndrome, where it
is lost through the urine.
• Poor nutrition or states of impaired protein catabolism, may
also lead to hypoalbuminaemia.
INR/PT
• Since the Prothrombin time test or PT test evaluates the ability of
blood to clot properly, it can be used to help diagnose bleeding.
When used in this instance, it is often used in conjunction with the
PTT to evaluate the function of all coagulation factors.
• Occasionally, the test may be used to screen patients for any
previously undetected bleeding problems prior to surgical
procedures.
• The International Normalized Ratio (INR) is used to monitor the
effectiveness of blood thinning drugs such as warfarin
(COUMADIN®).
• These anti-coagulant drugs help inhibit the formation of blood clots.
They are prescribed on a long-term basis to patients who have
experienced recurrent inappropriate blood clotting. This includes
those who have had heart attacks, strokes, and deep vein
thrombosis (DVT).
Metabolic encephalopathy
• Metabolic encephalopathy is temporary or permanent damage to
the brain due to lack of glucose, oxygen or other metabolic agent, or
organ dysfunction. Most cases occur when the liver cannot act
normally to remove toxins from the bloodstream during an acute
illness, but it can also be caused by a toxic overdose, or other
systemic disease.
• Causes
• Metabolic encephalopathy occurs during significant metabolic
derangements, after some types of poisoning, and during diseases
such as cirrhosis or hepatitis that slow or stop liver function, or
diabetes, heart or renal failure.
• It can also happen during medical conditions that cause blood
circulation to bypass the liver. These problems keep the liver from
removing toxins like ammonia, which build up in the blood as part of
normal metabolism. High levels of these toxins can temporarily or
permanently damage the brain, causing metabolic encephalopathy.
Metabolic encephalopathy
• Patients will require intubation for airway protection
• Risk for Sepsis
Disseminated intravascular
coagulation (DIC)
DIC
• Disseminated intravascular coagulation (DIC) is not a specific
diagnosis, and its presence always indicates another
underlying disease.
• Disseminated intravascular coagulation (DIC) is characterized
by a systemic activation of the blood coagulation system,
which results in the generation and deposition of fibrin,
leading to microvascular thrombi in various organs and
contributing to the development of multiorgan failure.
• Consumption and subsequent exhaustion of coagulation
proteins and platelets, due to the ongoing activation of the
coagulation system, may induce severe bleeding
complications, although microclot formation may occur in the
absence of severe clotting factor depletion and bleeding.
Nutrition
• Think about uremia
• Catabolic state
• Anorexia
• Decreased protein intake
• Consider assistance with a renal dietician
CV disease
• 70% of HD patients have concomitant CV disease
• LVH can be a risk factor
Kidney Int 1995; 47(1): 186-92
• Heart disease leading cause of death in HD patients
Anion Gap
• Anion Gap= the difference in the measured cations and the
measured anions in serum, plasma, or urine.
• Used to assess Metabolic Acidosis or alkalosis, normal around
8-16 mEq/L. Use MUDPILES to determine cause of metabolic
acidosis (high gap)
• = ( [Na+] ) − ( [Cl−]+[HCO3−] ) without potassium
• = ( [Na+]+[K+] ) − ( [Cl−]+[HCO3−] ) with potassium
CaO2
• CaO2: norm 20 vol%
• (Hbx1.34)SaO2 + (PaO2x.003) total amount of O2 carried in
100ml of blood, combined content of O2 carried on Hb and
dissolved in plasma,
• (can be reduced by <Hb, anemia or <CO)
CvO2
• CvO2: (Hb x 1.34)SvO2 + (PvO2 x .003)
• norm is 15 vol%, represents the value of O2 in blood returning
to the right side of the heart after tissues have oxygenated.
• C(a-v)O2 = arterial to mixed venous oxygen content
difference
• Determines how well the tissues take up O2
Nutritional Assessment
• Reciprocal Status Between Nutrition And Respiratory Status
• Necessary For Energy Utilization And Normal Organ Function
• Anthropometrics
• Usual Height and Weight
• History of Weight Loss
• Actual vs. Ideal Body Weight
Components of a Comprehensive
Nutritional Assessment
• Clinical Laboratory Tests
• Visceral Proteins
• Creatinine-Height Index
• Immune-Related Tests
• Nitrogen Balance
• Dietary Balance
• Usual Food Intake
• Food Likes and Dislikes
• Appetite
Components of a Comprehensive
Nutritional Assessment
• Total Caloric Requirements
• Resting Energy Expenditure Prediction x Stress Factor
• Indirect Calorimetry: The measurement of the amount of heat
generated in an oxidation reaction by determining the intake or
consumption of oxygen or by measuring the amount of carbon
dioxide or nitrogen released and translating these quantities into
a heat equivalent.