Assessment of Critically Ill PatientsWeek 1-2

Michael Haines, MPH, RRT-NPS, AE-C

Introduction/Objectives

• This will be a difficult class, reading and studying is a expectation NOT a suggestion!• Please try your hardest and give your best effort• Objectives of this class are to gain critical

assessment skills of the critical patient• 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

Week 1• Neurologic Monitoring• Cardiovascular monitoring• We will be covering this in several lectures, including a review of ECG

interpretation• Renal Function• We will review renal failure and labs

• Liver Function• Nutritional Assessment

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…

ConsciousnessReticular 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

ConsciousnessCortex• 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:• 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 linenLocalizing 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: • 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 cmH2OBe 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• 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.

VitalsHyperthermia • 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.

Arrhythmia Review

Electrocardiographic (ECG) Assessment• Indications For Obtaining an ECG

• Chest Pain• Dyspnea on Exertion• Palpitations• Pedal Edema• History of Heart Disease/Cardiac Surgery• Unexplained Tachycardia at Rest• Hypotension• Diaphoresis• Jugular Venous Distension• Cool, Cyanotic Extremities

Standard Monitoring Leads Lead 1

Standard Monitoring Leads Lead 2

Standard Monitoring Leads Lead 3

Initial Approach—Analysis4 Questions

• Rate?• Normal• Bradycardia, Tachycardia

• Rhythm?• Regular or Irregular

• Are there P waves?• Is each P wave related to a QRS with 1:1

impulse conduction?• QRS normal or wide?

Systematic Approach to ECG Interpretation

• Identify Rate

• Evaluate The Rhythm (Spacing Between QRS Complexes ≤ 0.04

Seconds Normal)

• Determine Presence of Waves

• Measure The P-R Interval (Normal: 0.12 to 0.20 Seconds)

• Measure Width of QRS Complex (Normal: ≤ 0.12 Seconds)

• Inspect The ST Segment

• Identify The Mean QRS Axis

Systematic Approach to ECG Interpretation

Variable Normal Interpretation

Rate 60 – 100 Beats/Minute Rate > 100 = TachycardiaRate < 60 = Bradycardia

PR Interval 0.12 – 0.20/Second > 0.20 = Heart Block

QRS Interval < 0.12/Second > 0.12 = Ectopic Foci

ST Segment Isoelectric Elevated or Depressed = Myocardial Ischemia

T wave Upright And Round Inverted With Ischemia; Tall And Peaked With Electrolyte Disturbances

VF

VF• Ventricular fibrillation is an irregular rhythm resulting from a

rapid discharge of impulses from one or more foci in the ventricles. The ventricular contractions are erratic and seen on the ECG as bizarre patterns of various sizes and configurations. No P waves are seen.

Some causes of VF include myocardial ischemia, hypoxia, hypothermia, electrocution, electrolyte and acid-base imbalance, and drug effects. Due to the absence of any effective cardiac output, life must be sustained by artificial means - i.e. external cardiac massage and defibrillation is "the" treatment.

VT

Polymorphic VT• TX without pulse:• CPR• DEFIB• EPI/Mg 2g

Premature Ventricular Contractions (PVCs)

• Causes

• Congestive Heart Failure

• Myocardial Infarction

• Hypoxia

• Single PVC is no Threat

• Warning Signs of Complications From PVCs

• Increase in Frequency (Multiple PVCs in One Minute)

• Multifocal PVCs

Warning Signs of Complications From PVCs

• Couplets – Paired PVCs (If Regular, Bigeminy)

• Salvos – Three or More PVCs in a Row

• R-on-T Phenomenon – PVC Occurs on T Wave; Can Lead to

Ventricular Tachycardia And/or Fibrillation

PVC Morphology—Match the Name

• Unifocal PVCs

• Multifocal PVCs

• Bigeminy• Ventricular

Tachycardia• Torsades

Common Dysrhythmias• Ventricular Tachycardia

• Series of Broad QRS Complexes

• Rates of 140 to 300 Beats/Min

• No Identifiable P Wave

• Sustained Ventricular Tachycardia – Lasts More Than 30 Seconds

• Non-Sustained Ventricular Tachycardia – Terminates Spontaneously After a

Short Burst

• May Become Hypotensive And Lethargic

• If Significant Deterioration of Cardiac Output, Patient Becomes Unresponsive

• Without Treatment, May Lead to Ventricular Fibrillation

VT• Ventricular tachycardia is a rapid, regular heart rhythm that

originates in the lower chambers of the heart. • May be monomorphic or polymorphic (Torsades De Pointes),

may or may not produce a pulse; in either case it is typically an emergent situation

Ventricular TachycardiaMonomorphic*

Atrial rate normal Onset tachycardia abruptRegularPresent—obscuredBlocked—fusion complexes possibleAntiarrhythmic agent, cardioversion, high-energy (defibrillation dose) shock

• Rate• Rhythm

• P waves• P → QRS• Therapy

*Sustained—requires intervention for >30 seconds

Polymorphic VT*

Atrial rate normal (obscured)Onset tachycardia abruptIrregularPresent—obscuredBlocked—fusion complexes possibleUnsynchronized high-energy shock,magnesium (beneficial with baseline QTC

prolongation)

• Rate• Rhythm

• P waves• P → QRS• Therapy

*Torsades de pointes—QT prolonged

Ventricular Fibrillation

Chaotic, uncountable Onset abruptIrregularAbsent; no normal QRS complexesNot applicableImmediate shock(s)

• Rate• Rhythm

• P waves• P → QRS• Therapy

Coarse VF

Ventricular Fibrillation

Chaotic, uncountable Onset abruptIrregularAbsent; no normal QRS complexesNot applicableImmediate shock(s)

• Rate• Rhythm

• P waves• P → QRS• Therapy

Fine VF

Asystole

Absent None—“flatline”AbsentNot applicableCPR, vasopressor

• Rate• Rhythm• P waves• P → QRS• Therapy

Agonal ComplexesPulseless Electrical

Activity

ASYSTOLE

Pulseless Electrical Activity (PEA)

Variable—depends on baseline rhythm PEA is not a single rhythm but anyorganized rhythm without a pulseIdentify and treat underlying causeCPR, vasopressor

• Rate• Rhythm

• Therapy

ARTERIAL PRESSURE

A

B

A B

C

Self-AssessmentWhat are the rate and rhythm?

Bradycardia

Bradycardia• Bradyarrthmia: heart rate less than 60 BPM as in

conditions such as third degree heart block, AV block or bradycardia• Symptomatic bradycardia may have multiple

causes; trained athletes (need no intervention), or shock, blocks…• Managing symptomatic bradycardia• First ensure patent airway; assist breathing as

needed; give oxygen; monitor ECG (identify rhythm); obtain blood pressure, SPo2• Establish IV access

Bradycardia

• If patient has symptoms of poor perfusion caused by the bradycardia such as acute altered mental status, ongoing chest pain, hypotension or other signs of shock; syncope, chest pain, SOB, dizziness…You must intervene• If adequate perfusion continue to monitor• If poor perfusion: Prepare for Transcutaneous

Pacing. Without delay for high degree block (type II second degree block or third degree AV block)

Bradycardia• Consider ATROPINE 0.5 mg IV while awaiting pace

maker. May repeat to a total dose of 3 mg. If ineffective begin pacing.• Consider epinephrine (2-10 ug/min) or Dopamin (2-10

ug/min) infusion while awaiting pacer or if pacing is ineffective• Prepare for transvenous pacing• Treat contributing causes• Consider expert consultation• remember if pulseless arrest develops begin CPR• Always search for possible contributing factors (H’s and

T’s)

60

AV NodalTissue

AV Node

His-Purkinje System

P

QRS <0.12

>0.20 seconds

Sinus Node

• Underlying sinus rhythm• One P wave • PR interval >0.20

second• One P wave for each

QRS

First-Degree AV Block

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• Underlying sinus rhythm• P wave fails to

periodicallyconduct

• PR interval prolonged• One P wave for each

QRS until block

PR interval

AV NodalTissue

His-Purkinje System

>0.20 seconds

Sinus Node

QRS

X

P

Second-Degree AV Block—Mobitz IWenckebach Phenomenon

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• Underlying sinus rhythm• One P wave • PR interval usually

normal, no prolongation• One P wave for each QRS

until sudden block and dropped QRS

Second-Degree AV Block—Mobitz II

PR intervals unchanged

AV NodalTissue

AV Node

His-Purkinje System

P

Often normal QRS complex

Often Normal

Sinus Node

Block

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• Underlying sinus rhythm (usual)

• Escape junctional rate 40-60 • PR interval variable• P waves unrelated to QRS• Narrow QRS = block above

His junction

AV Node

His Purkinje System

P

QRS <0.12

Sinus Node

QRS fromAV-His escape

Third-Degree AV Block—Junctional EscapeP waves unrelated to QRS

AV Block—Which Type?

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• Transcutaneous• Transvenous − Ventricular− Atrial− Dual Chamber

Pacemakers

–

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–• Transcutaneous

Pacemakers

• Transvenous — Ventricular

Pacemakers

Sinus NodePacemaker Malfunction

Tachycardia: Unstable • Unstable Tachycardia: Altered mental status,

ongoing chest pain, hypotension or other signs of shock.• Rhythms include: A-Fib, A-Flutter, SVT,

Monomorphic and Polymorphic VT and Wide complex tachycardia• Immediate cardioversion recommended for

unstable tachycardias• Heart rate is usually greater than 100; there are

many causes and may be symoptomatic or asymptomatic

Tachycardia: Unstable• First establish presence of a pulse. If present; assess

and support ABCD’s and give Oxygen• Monitor EKG to identify rhythm, obtain blood

pressure and SPo2• Identify and treat possible causes• If patient is Unstable: Perform immediate

cardioversion; establish IV and give sedation if patient is conscious, do not delay cardioversion!

• Consult expert consultation and watch for pulseless arrhythmias

• If patient is stable; establish IV, obtain EKG and determine if QRS is narrow (less than 0.12 seconds)

Narrow QRS• Determine if rhythms is regular (consistent p waves and R-R interval)

or irregular. • IF IT IS REGULAR: Attempt Vagal maneuvars and/pr ADENSOSINE 6

mg rapid IV push, if no conversion give 12 mg rapis IV push may repeat 12 mg dose once

• If rhythm converts: Probable reentry SVT: observe recurrence and treat recurrence with adenosine or long acting AV nodal blocking agaent (beta blocker or diltiazem)

• If it does not convert: Probable A-Flutter, Ectopic arterial tachycardia or Junctional tachycardia. Control rate (beta blocker, use caution with COPD and CHF patients); treat underlying cause and consider expert consultation

IF IT IS IRREGULAR: Probable a-fib or possible a-flutter or MAT; consider expert sonsulatation and control rate with beta blockers.

WIDE QRS

• If it is REGULAR: if ventricular tachycardia or uncertain rhythm give AMIODARONE 150 mg IV over 10 minutes; repeat as needed to max of 2.2 g/24 hours• Prepare for elective cardioversion• If SVT with aberrancy give adenosine• IF IT IS IRREGULAR: if atrial fibrillation with

aberrancy do same things as narrow complex• Of pre-excited atrial fib (AF + WPW) consult

cardiologist

Cardioversion

• Synchronized• Transcutaneous

–

CardioversionEnergy Recommendations

Biphasic Waveform

• Atrial Fibrillation 120-200 J Initial• Atrial Flutter & SVT 50-100 J Initial• Monomorphic VT 100 J Initial• Increase the energy dose in a stepwise

fashion for any subsequent cardioversion attempts

• Use manufacturer-recommended doses

–

CardioversionEnergy Recommendations

Monophasic Waveform• Atrial Fibrillation 200 J• Atrial Flutter & SVT 200 J• Monomorphic, Unstable

With Pulse 100 J

• Polymorphic or Pulseless VT—Treat as VF with high-energy unsynchronized defibrillation doses

(Do not use low energy—high likelihood of causing VF in unsynchronized mode)

–

Junctional Rhythm• AV Junction Takes Over The Pace Making Role

• Follows Normal Pathways of Conduction

• Normal QRS Complexes

• P wave May or May Not be Present

• Causes

• AV Node Damage

• Electrolyte Disturbances

• Digitalis Toxicity

• Heart Failure

Renal Function

Kidney Disease

Terminology• 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=related

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Chronic Renal Failure

• 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.

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.

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Stages of CKD

• Stage 1*: GFR >= 90 mL/min/1.73 m2 • Normal or elevated GFR

• 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)

Signs & Symptoms• General• Fatigue & malaise• Edema

• Ophthalmologic• AV nicking

• Cardiac• 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:

1. a heavy loss of protein in the urine, or

2. 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 end-stage kidney failure who requires dialysis therapy.

Management• Identify and treat factors associated with progression• 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• ACEs/ARBs• Diuretics• CCBs• HCTZ (less effective when GFR < 20)

Metabolic changes with CKD• Hemoglobin/hematocrit • Bicarbonate • Calcium• Phosphate • PTH • Triglycerides

Metabolic changes…• Monitor and treat biochemical abnormalities• 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

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Mineral metabolism• Calcium and phosphate metabolism abnormalities associated

with:• Renal osteodystrophy• Calciphylaxis and vascular calcification

• 14 of 16 ESRD/HD pts (20-30 yrs) had calcification on CT scan• 3 of 60 in the control group

• 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• SepsisSymptoms• 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

Lactic Acidosis

• 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.

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

• Another frequently used mnemonic is KARMEL.• K-Ketoacidosis• A-ASA• R-Renal failure• M-Methanol• E-Ethylene glycol• L-Lactic acidosis

High Anion Gap

• 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

Metabolic ABGS

• 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.

Answer

• 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

Metabolic Acidosis

• 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 Henderson-Hasselbalch 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.

Answer

• 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)

Base Excess

• 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

BUN• 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

• 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

Renal Failure

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.

• Typically associated with CHF, depending on the patient often requires positive pressure for associated pulmonary edema. Typically non-invasive ventilation

Increased BNP

• 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.

Cardiac 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 Enzymes

Liver FailureAcites, decreased sensorium

• 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.

Albumin

• 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).

INR/PT

• 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

Metabolic encephalopathy

Disseminated intravascular coagulation (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.

DIC

Nutrition• Think about uremia• Catabolic state• Anorexia• Decreased protein intake

• Consider assistance with a renal dietician

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CV disease• 70% of HD patients have concomitant CV disease

• Heart disease leading cause of death in HD patients

• LVH can be a risk factor

• 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

Anion Gap

• 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)

CaO2

• 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

CvO2

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.