Acute Respiratory Failure Hypercapnic Respiratory Failure

Respiratory System  PaCO2 above normal (>45 mm Hg)

 Acidemia (pH <7.35)
Consists of two parts:
Hypoxemic Respiratory Failure
 Gas exchange organ (lung): responsible for
Etiology and Pathophysiology
OXYGENATION
 Pump (respiratory muscles and respiratory Causes:
control mechanism): responsible for
 Ventilation-perfusion (V/Q) mismatch
VENTILATION
 Shunt
NOTE: Alteration in function of gas exchange unit  Diffusion limitation
(oxygenation) OR of the pump mechanism (ventilation)  Alveolar hypoventilation
can result in respiratory failure
V-Q Mismatching
Results from inadequate gas exchange
1. V/Q mismatch
Insufficient O2 transferred to the blood: Hypoxemia  Normal Ventilation is 4 L of air per minute
 Normal Perfusion is 5 L of blood per minute
Inadequate CO2 removal: Hypercapnia
 Normal ventilation of alveoli is comparable to
Acute Respiratory Failure amount of perfusion
 Normal V/Q ratio is 0.8 (more perfusion than
 Not a disease but a condition
ventilation) or 4/5
 Result of one or more diseases involving the
lungs or other body systems Mismatch d/t:
Note: Acute Respiratory Failure: when oxygenation  Inadequate ventilation
and/or ventilation is inadequate to meet the body’s  Poor perfusion
needs
Range of V/Q Relationships
Classification:

Hypoxemic respiratory failure (Failure of oxygenation)

Hypercapnic respiratory failure (Failure of ventilation)

Causes V/Q mismatch

 COPD
 Pneumonia
Hypoxemic Respiratory Failure  Asthma
 Atelectasis
 PaO2 of 60 mm Hg or less  Pulmonary embolus
 (Normal = 80 - 100 mm Hg)
 Inspired O2 concentration of 60% or greater
 2. Shunt Effects of hypoxemia

An extreme V/Q mismatch  Build up of lactic acid → metabolic acidosis →

Blood passes through parts of respiratory system that
receives no ventilation
 d/t obstruction OR fluid accumulation
 Not Correctable with 100% O2
cell death
 CNS depression
 Heart tries to compensate → ↑ HR and CO
 If no compensation: ↓ O2, ↑ acid, heart fails,
shock, multi-system organ failure

Hypercapnic Respiratory Failure

3. Diffusion Limitations
Etiology and Pathophysiology
 Distance between alveoli and pulmonary
capillary is one- two cells thick  Imbalance between ventilatory supply and
 With diffusion abnormalities: there is an demand
increased distance between alveoli (may be d/t  Occurs when CO2 is increased
fluid)
Causes Hypercapnic Respiratory Failure
 Correctable with 100% O2
1. Alveolar Hypoventilation and VQ Mismatch:
Causes Diffusion limitations
 Ventilation not adequate to eliminate CO2
 Severe emphysema  Leads to respiratory acidosis
 Recurrent pulmonary emboli  Eg. Narcotic OD; Guillian-Barre, ALS, COPD,
 Pulmonary fibrosis asthma
 Hypoxemia present during exercise 2. VQ Mismatch:
 Leads to increased work of breathing
 Insufficient energy to overcome resistance;
ventilation falls; ↑PCO2; respiratory acidosis

Hypercapnic Respiratory Failure

Categories of Causative Conditions

1. Airways and alveoli

 Asthma
 Emphysema
4. Alveolar Hypoventilation  Chronic bronchitis
 Cystic fibrosis
Is a generalized decrease in ventilation of lungs and
2. Central nervous system
resultant buildup of CO2
 Drug overdose
Causes Alveolar hypoventilation  Brainstem infarction
 Spinal cord injuries
 Restrictive lung disease
3. Chest wall
 CNS disease
 Flail chest
 Chest wall dysfunction
 Fractures
 Neuromuscular disease
 Mechanical restriction
Hypoxemic Respiratory Failure  Muscle spasm
Etiology and Pathophysiology 4. Neuromuscular conditions
 Muscular dystrophy
Interrelationship of mechanisms
 Multiple sclerosis
 Hypoxemic respiratory failure is frequently
caused by a combination of two or more of
these four mechanisms Respiratory Failure
Tissue Oxygen Needs
Major threat is the inability of the lungs to meet the  Headache
oxygen demands of the tissues  Restlessness
Clinical Manifestations Nursing and Collaborative Management

 Sudden or gradual onset Nursing Diagnoses

 A sudden  in PaO2 or rapid  in PaCO2 is a
 Ineffective airway clearance
serious condition
 Ineffective breathing pattern
 When compensatory mechanisms fail,
 Risk for imbalanced fluid volume
respiratory failure occurs
 Anxiety
 Signs may be specific or nonspecific
 Impaired gas exchange
 Severe morning headache
 Imbalanced nutrition: less than body
 Cyanosis : Late sign
requirements
 Tachycardia and mild hypertension: Early signs
Planning
Consequences of hypoxemia and hypoxia  Overall goals:
 Metabolic acidosis and cell death  ABGs and breath sounds within baseline
 Decrease Cardiac output  No dyspnea
 Impaired renal function Prevention
Specific clinical manifestations  Thorough physical assessment
 Rapid, shallow breathing pattern  HistoryEffective cough
 Sitting upright Respiratory Therapy
 Dyspnea
 Pursed-lip breathing  Oxygen therapy
 Retractions  Mobilization of secretions
 Change in Inspiratory: Expiratory ratio  Effective coughing and positioning
 Mobilization of secretions
Respiratory Failure  Hydration and humidification
Diagnostic Studies  Chest physical therapy
 Physical assessment  Airway suctioning
 ABG analysis  Mobilization of secretions
 Chest x-ray  Hydration and humidification
 CBC  Chest physical therapy
 ECG  Airway suctioning
 Serum electrolytes  Positive pressure ventilation (PPV)
 Urinalysis Drug Therapy
 V/Q lung scan
 Pulmonary artery catheter (severe cases)  Relief of bronchospasm
 Bronchodilators
Nursing and Collaborative Management  Drug Therapy
Nursing Assessment  Relief of bronchospasm
 Bronchodilators
 Past health history  Reduction of pulmonary congestion: IV diuretics
 Medications  Treatment of pulmonary infections: IV
 Surgery antibiotics
 Tachycardia  Reduction of severe anxiety, pain, and agitation:
 Fatigue Benzodiazepines, Narcotics
 Sleep pattern changes
 Nursing and Collaborative Management

Medical Supportive Therapy

 Treat the underlying cause

 Maintain adequate cardiac output and
hemoglobin concentration
 Monitor BP, O2 saturation, urine output

Nutritional Therapy

 Maintain protein and energy stores

 Enteral or parenteral nutrition Etiology and Risk Factors
 Supplements
 Precipitating factor:
Acute Coronary syndrome
rupture of atherosclerotic plaque and subsequent
 an emergent situation thrombus formation
 characterized by an acute onset of myocardial
ischemia that results in myocardial death (ie,  Interruption in blood flow
MI) if definitive interventions do not occur Risk Factors
promptly
Modifiable
Unstable Angina
 Smoking
 there is reduced blood flow in a coronary artery  Hypertension
 often due to rupture of an atherosclerotic  Obese
plaque
 High blood cholesterol (LDL, Triglycerides)
 but the artery is NOT completely occluded
 Chronic kidney disease
AMI  Diabetes Mellitus

 Formation of localized necrotic areas within the Non modifiable

myocardium
 Age over 65
 Myocardial cell death resulting from decreased
 Male
blood flow
 Family History
Most common Cause:
Pathophysiology
 rupture of atherosclerotic plaque resulting to
Atherosclerosis
subsequent thrombus formation
 Gradual process
 Involves cholesterol plaque formation
 Subsequent thrombus formation
 Decreased blood flow
 Ischemia, prolonged
 Infarct

’
 Clinical manifestations

CHEST PAIN

T – Tight/Squeezing

H – Heavy/Crushing

R – Radiates (neck, arm, jaw, back)

O – Occurs without cause

W – “with something on my chest”

N – Not relieved by rest

Other signs and symptoms

D – DIZZINESS, VOMITING

I – INDIGESTION feeling

Zone of infarct (infarct) E – EXTRA HEART SOUND

-Presence of Q wave S – SWEATING

Zone of injury (hypoxic) or penumbra

-ST elevation w/ or w/o loss of R wave H – HYPOTENSION

Zone of ischemia A – ARRHYTHMIAS

-ST depression w/ or w/o T wave inversion R – RATE OF PULSE ALTERED (brady/tachy)

D – “DOOM” FEELING/ANXIETY

DIAGNOSTICS

ECG

 Inverted T-wave
 ST elevation
 Pathologic Q wave

Cardiac Biomarkers

 Creatine Kinase MB (CK-MB)

 Troponin I or Troponin T
 Myoglobin
IMAGING STUDIES Q wave

ECG changes

Inverted T wave (peaks first before inverting): Zone of

ischemia

Elevated ST segment: Zone of injury

Pathologic Q wave (develops in 1 to 3 days): Zone of

infarction

Normal ECG
LAB FINDINGS

INCREASED CARDIAC ENZYMES

 TROPONIN I (HEART SPECIFIC)

 TROPONIN T
 CK-MB
 MYOGLOBIN
 LDH
 AST/SGOT

ELEVATED WBC

 IMAGING STUDIES
 CHEST XRAY (TO RULE OUT OTHER CAUSES)
 2D ECHOCARDIOGRAM
 PET SCAN (POSITRON EMISSION TOMOGRAPHY)
 MRI
 TEE (TRANSESOPHAGEAL ECHOCARDIOGRAPHY)
 LEFT HEART CATHETERIZATION WITH
ST segment elevation
CORONARY ANGIOGRAPHY (GOLD STANDARD
IN ASSESSING FOR CAD)

Angiogram

Unstable angina:

The patient has clinical manifestations of coronary

ischemia, but ECG and cardiac biomarkers show no
evidence of acute MI.
 Nitrates
 Causes vasodilatation thereby increasing blood
STEMI:
flow to the heart therefore increasing oxygen
The patient has ECG evidence of acute MI with supply
characteristic changes in two contiguous leads on a 12-  Given IV for MI
lead ECG. In this type of MI, there is significant damage  E.g. Nitroglycerine, isosorbide dinitrate (Isoket)
to the myocardium.
Nursing consideration
NSTEMI:
 Watch out for BP (may cause hypotension)
The patient has elevated cardiac biomarkers but no  Usually only 1 kind of nitrate is given at a time
definite ECG evidence of acute MI.
ANTIPLATELET/anticoagualants
MEDICAL MANAGEMENT
 ASA/ASPIRIN
 M – MORPHINE  CLOPIDOGREL (PLAVIX)
 – OXYGEN  TICLOPIDINE (TICLID)
 N - NITRATES  PRASUGREL (EFFIENT)
 A – ASPIRIN/ANTIPLATELETS - Used post PTCA
 R – REVASCULARIZATION  Ticagrelor
 ETC.
(Thombolytics/CABG/PTCA)
 Unfractionated Heparin
 C – CARDIAC REHAB  Low molecular heparins:
 H – Heart Rhythm Monitoring (for arrhtyhmias)
- Enoxaparin Na (Clexane)
MORHPINE
- Fondaparinux Na (Arixtra)
 TO DECREASE SEVERE CHEST PAIN
REVASCULARIZATION
 USUALLY AT 4 MG IV PUSH INITIALLY
 ALSO CAUSE MINOR BLOOD VESSEL THROMBOLYTICS
DILATATION INCREASING BLOOD FLOW TO THE
 e.g. Streptokinase, r-tPa, Urokinase
HEART
 Observe Bleeding precautions
Nursing consideration  Dissolves blood clots

 Monitor BP (may cause hypotension) PTCA- PERCUTANEOUS TRANSLUMINAL CORONARY

 Latest studies show increased mortality for
increased doses, so do not give more than
prescribed
Oxygen
Supports oxygenation in the heart
Nursing consideration
 Oxygen supplementation for COPD patients is
minimal (to prevent respiratory drive
depression)
 Assist in intubation if needed
 Rate of oxygenation is based on symptoms and
clinical manifestations
 Generally, high influx of oxygen may be needed
ANGIOPLASTY
 Invasive, consent needed
 Opens up coronary arteries
CABG (Coronary Artery Bypass Graft)
 Secure consent
 Secure blood products
Heart Rhythm Monitoring
 Observe for Cardiac Dysrhythmias
 Inform physician immediately for presence of
arrhythmias (esp. vent tachycardia, vent. Fib)
 Give anti-arryhthmics as ordered: Lidocaine or
Amiodarone
 Record and document
 ECG Diagnosis

 Ineffective cardiac tissue perfusion related to

reduced coronary blood flow
 Risk for imbalanced fluid volume
 Risk for ineffective peripheral tissue perfusion
r/t decreased cardiac output from left
ventricular dysfunction
 Death anxiety r/t cardiac event
 Deficient knowledge about post-ACS self-care

V-fib Collaborative Problems/ Potential Complications

 Acute pulmonary edema

 Heart failure
 Cardiogenic shock
 Dysrhythmias and cardiac arrest
 Give Thrombolytics 3 to 6 hours after onset  Pericardial effusion and cardiac tamponade
of symptoms
Planning and Goals
 Door to needle time: 30 minutes
 Thrombolytics must be given within 30  relief of pain or ischemic signs (eg. ST-segment
minutes after the patient arrived in the changes) and symptoms
hospital  prevention of myocardial damage
 Door to balloon time: 60 minutes  absence of respiratory dysfunction
 Emergent PCI (percutaneous coronary  maintenance or attainment of adequate tissue
ontervention) should be done w/in 60 perfusion, reduced anxiety
minutes from the time the patient is in  adherence to the self-care program
brought to the hospital  and absence or early recognition of
complications
Top Nursing Management
Interventions
Assessment
Relieving Pain and Other Signs and Symptoms of
 get hx, allergy, other diseases, hx of bleeding
Ischemia
 Ax for s/sx, monitor v/s, sat O2, ECG
 Bed rest
Intervention
 Elevate head
 Maintain on bedrest, prevent overexertion  Oxygen
 Maintain on O2 therapy and patent airway  Give medicines (e.g. nitrates, morphine, etc.)
 Alleviate anxiety
Improving Respiratory Function
 Give medicines (nitrates, blood thinners, etc) as
prescribed  Avoid fluid overload
 Get consent for treatments  Change position frequently (prevents fluid from
 Inform physicians for complications, accumulating in the lung bases)
arrhythmias  Monitor breathing, sat O2
 Oxygen therapy
Assessment
Promoting Adequate Tissue Perfusion
 Each sign or symptom must be evaluated
 IV lines must be present (usually at least 2  Bed rest
 Limit mobility until pain free and stable
 Check skin temp and tissue perfusion
Reducing Anxiety
 Establish rapport, trusting and caring
relationship
 Patient as partner in care
 Relaxation techniques
 Health education
 Facilitate calm environment
Monitoring and Managing Potential Complications
 Continuous monitoring including physical
status, hemodynamics and ECG
 Provide health education
 Promote independence
Expected Outcomes
 Experiences relief of angina
 Has stable cardiac and respiratory status
 Maintains adequate tissue perfusion
 Exhibits decreased anxiety
 Adheres to a self-care program
 Has no complications
Complications
 Dysrhythmias (V-fib, A-fib, etc.)
 Cardiogenic shock
 Pulmonary edema
 Heart Failure
 Pericarditis
 Dressler’s syndrome (self limiting, no known
prevention)
Cardiac Rehab
 Rehabilitation is started from the time of
admission but…
 an active rehabilitation program is initiated
 after the patient with an MI is free of symptoms
 An important continuing care program for
patients with CAD that targets risk reduction by
means of education, individual and group
support, and physical activity.
 It is considered to be an important part of
continuing care for patients with CAD
Goals of Cardiac Rehab
 Extend life
 Improve quality of life
 Throughout all phases of rehabilitation, the
goals of activity and exercise tolerance are
achieved through gradual physical conditioning.
 Cardiac efficiency is achieved when work and
activities of daily living (ADL) can be performed
at a lower heart rate and lower blood pressure
 thereby reducing the heart’s oxygen
requirements and reducing cardiac workload
Monitoring
 BP: SBP or DBP more than 20 mmHG increase
 Heart Rate: increase above the target
 ECG: for worsening/presence of arrhythmia
 Any of those is not a good sign
 Also, if other signs or symptoms occur, the
patient is instructed to slow down or stop
exercising.
Target heart rate
 +10% of resting heart rate or 120 bpm
 Following discharge, the target heart rate is
based on the patient’s stress test results,
medications, and overall condition
Phase I
 begins with the diagnosis of atherosclerosis
- which may occur when the patient is admitted
to the hospital for ACS
 In-hospital mobilization and health education
(focus on essentials of care NOT behavior
change for risk reduction)
 Reassure patient that although CAD is lifelong,
patients may resume a normal life after MI
 Use positive reinforcements to encourage
patient
 Recommended activities depend on patient
status
Phase II
 Occurs after discharge
 sessions are three times a week for 4 to 6 weeks
(may continue up to 6 months)
 Outpatient program consists of supervised,
often ECG-monitored, individualized exercise
training
 Teaching and counseling for lifestyle
modification for risk reduction is included
  Short-term and long-range goals are
collaboratively determined based on the
patient’s needs.
 Inform physician of any complications
 Family may be included in the support programs
Phase III
 Long term outpatient
 Focus: maintaining cardiovascular stability and
long-term conditioning
 usually self-directed and does not require a
supervised program
- Although it may be offered
The goals of each phase build on the accomplishments
of the previous phase
When can a patient resume sexual activities?
 Patients who are able to walk at 3 to 4 miles/h
can usually resume sexual activities.
 Some books would say that 2-3 months is
needed before sex may be resumed or…
 …when a patient can go up to flights of stair
witout difficulty.
Sex and M.I.
 Patient should be well rested
 Be in a familiar setting
 wait at least 1 hour after eating or drinking
alcohol
 use a comfortable position
 Sexual dysfunction or cardiac symptoms should
be reported to the health care provider
Angina Pectoris “Chest Pain”
 is a clinical syndrome
 usually characterized by episodes or paroxysms
of pain or pressure in the anterior chest
 Caused by insufficient coronary blood flow
resulting in a decrease oxygen supply when
there is increased oxygen demand
Cause
 INSUFFICIENT CORONARY BLOOD FLOW
 resulting in a decreased oxygen supply when
there is increased myocardial demand for
oxygen
 There is MORE DEMAND for OXYGEN
 But LESS SUPPLY
Types of Angina
 Stable angina
 Unstable angina (also called preinfarction
angina or crescendo angina)
 Intractable or refractory angina
 Variant angina (also called Prinzmetal’s
angina)
 Silent ischemia
Stable angina: predictable and consistent pain that
occurs on exertion and is relieved by rest and/or
nitroglycerin
Unstable angina (also called preinfarction angina or
crescendo angina): symptoms increase in frequency and
severity; may not be relieved with rest or nitroglycerin
Intractable or refractory angina: severe incapacitating
chest pain
Variant angina (also called Prinzmetal’s angina): pain at
rest with reversible ST-segment elevation; thought to be
caused by coronary artery vasospasm
Silent ischemia: objective evidence of ischemia (such as
electrocardiographic changes with a stress test), but
patient reports no pain
What can trigger Angina?
Physical exertion- which can precipitate an attack by
increasing myocardial oxygen demand
Exposure to cold- which can cause vasoconstriction and
elevated blood pressure, with increased oxygen
demand
Eating a heavy meal- which increases the blood flow to
the mesenteric area for digestion, thereby reducing the
blood supply available to the heart muscle; in a severely
compromised heart, shunting of blood for digestion can
be sufficient to induce anginal pain
Stress or any emotion-provoking situation- causing the
release of catecholamines, which increases blood
pressure, heart rate, and myocardial workload
Unstable angina is not associated with these factors
Pathophysiology
  Risk Factors: Smoking, hypertension,
hyperlipidemia
 Injury to the vascular endothelium
 Endothelium undergoes changes and stops
producing the anti-thrombotic and vasodilating
agent
 The presence of inflammation attracts
inflammatory cells such monocytes
(macrophages).
 The macrophages ingest lipids into the arterial
wall forming fatty streaks.
 Activated macrophages also release
biochemical substance that can further damage
the endothelium and oxidation of the low
density lipoprotein.
 Following the transport of lipid into the arterial
walls smooth muscle cells proliferates and form
a fibrous caps called atheromas or plaque into
the lumen of the vessel causing narrowing and
blood obstruction
 Decrease blood supply to the coronary arteries
 Ischemia of the coronary arteries
 CHEST PAIN
Clinical Manifestations
 varying in severity from mild indigestion to a
choking or heavy sensation in the upper chest
 Ranges from discomfort to agonizing
 Chest Pain
Chest Pain
- often felt deep in the chest behind the sternum
(retrosternal area)
- Typically, it is poorly localized (can’t be
pinpointed)
- may radiate to
 Neck
 Jaw
 Shoulders
 Inner aspects of the upper arms, usually the left
Clinical Manifestations
 The patient often feels tightness or a heavy
choking or strangling sensation: that has a
viselike, insistent quality
 A feeling of weakness or numbness (arms,
wrists, hands)
 Shortness of breath
 Pallor
 Diaphoresis
 Dizziness or lightheadedness
 nausea and vomiting
 Anxiety
 In many patients, anginal symptoms follow a
stable, predictable pattern.
 Unstable angina is characterized by attacks that
increase in frequency and severity and are not
relieved by rest and administering nitroglycerin.
 Patients with unstable angina require medical
intervention
Geriatric considerations
The elderly person may not exhibit the typical pain
profile because of the diminished responses of
neurotransmitters that occur with aging. Often, the
presenting symptom in the elderly is dyspnea
N> Help the older person recognize the symptoms
Diagnostics
 ECG- Ischemic changes like T wave inversion
may be noted
 Cardiac Biomarkers- to rule out ACS
 Coronary Angiogram- To see if there are
blockage in the coronary arteries
 Perfusion imaging (like nuclear scan)- To see
how well the myocardium is perfused with
blood
Medical Management
 Bed rest
 PTCA-Percutaneous transluminal coronary
angioplasty
 Atherectomy: An atherectomy is a procedure
that utilizes a catheter with a sharp blade on
the end to remove plaque from a blood vessel.
The catheter is inserted into the artery through
a small puncture in the artery, and it is
performed under local anesthesia.
 CABG (coronary artery bypass graft)
- A form of bypass surgery that can create
new routes around narrowed and blocked
coronary arteries, permitting increased
blood flow to deliver oxygen and nutrients
to the heart muscle
- The cardiac surgeon makes an incision
down the middle of the chest and then saws
 through the breastbone (sternum). Bypass
grafting involves sewing the graft vessels to
the coronary arteries beyond the narrowing
or blockage. The other end of this vein is
attached to the aorta.
 NTG sublingual should be taken immediately
as ordered.:
- Up to three (3) doses only
- 5 minutes apart
- Go to hospital or call ambulance if not relieved

Medications: Acute Glomerulonephritis

Calcium Channel Blocker: Amlodipine (Norvasc),  An inflammation of the glomerular capillaries

Diltiazem. (Cardizem) membranes caused by immunologic reaction
that results in proliferative and inflammatory
- To patient not responsive to beta blockers
change in glomerular structure.
and treatment for vasospasm
 Acute Glomerulonephritis: begins suddenly
Anticoagulants: Heparin, Enoxaparin (Lovenox)  Chronic Glomerulonephritis: develops gradually
over years
- Prevention of thrombus formation
Infectious causes
Beta Adrenergic Blocking Agents (Beta blockers)
 Staph, klebsiella, group A beta-hemolytic
- Metropolol (Lopresor), Atenolol (Tenormin)
streptococcus infection
- Reduction of myocardial oxygen consumption
 The most common is the streptococcal infection
by blocking beta adrenergic stimulation of the
from throat or elsewhere in the body.
heart

Nitroglycerin (NTG) (Nitorstat, Nitro Bid)

- Indicated for short and long term reduction of

myocardial oxygen consumption through
selective vasodilation

Nursing management

Assess and monitor patient

 Assess for PQRST of chest pain

 May exhibit worsening of symptoms
 ECG monitoring

Bed rest
Clinical Manifestations of acute glomerular nephritis
Reduce stress/anxiety
 Hematuria
 Allow verbalization  Edema
 Guided imagery/Music therapy  Azotemia-accumulation of nitrogenous wastes
 Provide spiritual needs  Urine appearance may be cola colored due to
Drugs as ordered (e.g. NTG) rbc’s
 Hypertension
Nursing care  Hypoalbuminemia
 Hyperlipidemia
 Teach the patient to identify the symptoms
 Rising BUN and creatinine
 Tell the patient to report them if noted
 Instruct that when chest pain occurs, rest
immediately

Complications
  Hypertensive encephalopathy: symptoms
include: headache, vomiting, visual damage and
epileptic attack
 Heart failure: dyspnea, pulmonary edema
 Rapid decline in renal function can occur to
ESRD; oliguria and anuria

Management

 Treat s/s such as elevated BP

 Diuretics
 Monitor daily weight, monitor edema, lungs
sounds and blood pressure
 Check GFR by 24h urine for creatinine clearance
 Treat streptococcal infection with antibiotics,
preferably PCN
 Corticosteroids
 Restrict sodium
 May progress to chronic glomerulonephritis,
will treat as in CKD

Nephrotic Syndrome

 Is a type of renal failure characterized by

increased glomerular permeability and Complications of nephrotic syndrome
manifested by massive proteinuria.
 Massive proteinuria
 Is not a specific glomerular disease
 Hypoalbuminemia
 Is a syndrome with a cluster of findings that
 Edema: periorbital, peripheral, ankle, abdomen
include:
 Lipiduria
 Marked increase in protein (proteinuria) in
 Hyperlipidemia
urine (especially albumin)
 Increased coagulation
 Hypoalbuminemia: decrease albumin in the
 Renal insufficiency
blood
 Edema Treatment of nephrotic syndrome
 High serum cholesterol and LDL
 Diuretic
 A condition of increased glomerular
 ACEIs can decrease proteinuria
permeability
 Cholesterol lowering agents
 Results in massive protein loss
 Heparin to reduce coagulability
 Often linked genetically or r/t
 Limit sodium intake
immune/inflammatory process
 Caused by chronic glomerulonephritis, diabetes Acute Renal Failure
mellitus with glomerulosclerosis, amyloidosis,
lupus, multiple myeloma and renal vein  Reversible clinical syndrome whereby there is
thrombosis sudden and pronounced loss of kidney function
 Major manifestation is edema  Occurs over hours to days
 Hallmark is albuminuria exceeding 3.5g/day  Results in kidneys failure to excrete nitrogenous
waste

Categories of Acute Renal Failure

Intrarenal actual parenchymal damage
 Prolonged renal ischemia from myoglobinuria
(rhabdo, trauma, burns), hemoglobinuria
(transfusion reaction, hemolytic anemia)
 Nephrotoxic agents like aminoglycosides,
radiopaque contrast, heavy metals, solvents,
NSAIDs, ACEIs, acute glomerulonephritis
Prerenal-hypotension, tachycardia, decreased CO,
decreased urinary output, lethargy
intrarenal and postrenal—oliguria or anuria,
hypertension, tachycardia, SOB, orthopnea, n/v,
generalized edema and weight gain, lethargy, confusion
Nonoliguric form also exists. Phases are similar.

Causes of Acute Renal Failure

Prerenal 60-70% of cases (hypoperfusion of the kidney)

 Volume depletion as seen in hemorrhage, renal

losses from diuretics, GI losses from vomiting,
diarrhea
 Impaired cardiac output secondary to MI, heart
failure, dysrhythmias, cardiogenic shock
 Vasodilation from sepsis, anaphylaxis,
antihypertensive med
 Client becomes oliguric (urine less than
400ml/day)
 Anuria: urine less than 100 ml/day

Postrenal Urinary tract obstruction by calculi, tumors,

BPH, blood clots

Phases of Acute Renal Failure

1. Initiation Phase: occurs with the insult and ends

when oliguria develops
2. Oliguria Phase: with urinary output less than
400ml/24h .
- Increase potassium
- Increase BUN
- Increase creatinine

3. Diuresis Phase: lasts for 1-3 weeks.

- Increased in urine output from 1 to 3 liters/ day.
- Beginning recovery. Renal function gradually
improves
- Recovery—may take 3-12 months. May have
permanent reduction in functioning of 1%-3%.
- Watch out for dehydration
Clinical Manifestations

4. Recovery Phase: Begins when the glomerular Varies

filtration rate increases.
• May include S/Sx since many organs may be affected
- BUN increases
- Creatinine started to normalized • Altered urine output
- Renal function begins to improve for 3 to 12
months • Edema or dry skin

Key features of ARF • Patient may appear critically ill and lethargic
CNS S/Sx include:
• Drowsiness
• headache,
• muscle twitching
• seizures
Laboratory Profile of ARF
 Elevated BUN and creatinine
 Sodium retention but may be deceptive due to
water retention
 Potassium increased
 Phosphorus increased
 Calcium decreased
 Sp. Gravity decreased and fixed
Diagnostic Procedures
X- RAY- used to determine the size of the kidneys and if
there is obstruction
CT scan- to identify presence of tumors and
obstructions
Management
 Objectives: Restore normal chemical balance
and prevent complications until restoration of
renal function
 Identify and treat underlying cause
 Maintain fluid balance—wts, serial CVP
readings, BP, strict I&O
 May give Mannitol, Lasix or Edecrin
 May need temporary dialysis
 If prerenal, fluid challenges and diuretics to
enhance renal blood flow
 Oliguric renal failure, low dose dopamine.
Calcium channel blockers may be used to
prevent influx of calcium into kidney cells,
maintains cell integrity and increase GFR
 Hyperkalemia—closely monitor electrolytes
 Kayexalate/Sorbitol—may need Flexiseal
 IV dextrose, insulin and calcium may help shift
K+
 Cautious administration of any medication that
can be nephrotoxic
 Monitor ABGs and acid-base balance
 Monitor phosphate levels
Nutritional Therapy
 Azotemia and uremia are directly related to the
rate of protein breakdown
 Dietary proteins are individualized to each
patient. Is a catabolic state and if insufficient
intake, patient may lose up to 0.5-1 pounds
daily. Encourage high CHO. Protein needs for
non-dialysis patients need 0.6g/kg of body
weight
 Dialysis patients will need 1-1.5g/kg
 Fluid restriction=urine volume plus 500ml
Nursing Interventions
 Monitor fluid and electrolyte balance
 Reduce metabolic demands
 Promote pulmonary function
 Prevent infection
 Provide skin care
 Provide support
Chronic Renal Failure (End-stage renal disease)
 Progressive, irreversible deterioration in renal
function
 Causation: #1 diabetes mellitus, hypertension,
glomerulonephritis, pyelonephritis, polycystic
kidney disease, vascular disorders, others
 Uremia---collection of nitrogenous wastes
normally excreted by the kidneys. S/S include:
HA, seizures, coma, dry skin, rapid pulse,
elevated BP, scanty urine, labored breathing
Kidney changes
 Nephrons hypertrophy and work harder until
70-80% of renal function is lost
 Nephrons could only compensate by decreasing
water reabsorption thus:
 Hyposthenuria—loss of urine concentrating
ability occurs
 Polyuria—increased urine output
 Then isosthenuria—fixed osmolality
 Gradual decline in urinary output
Stages of Renal Failure
Stage 1: GFR greater than or equal to 90mL/min/1.73
m2. Kidney damage w/normal or increased GFR
Stage 2: GFR = 60-89, mild decrease in GFR
Stage 3: GFR = 30-59, moderate decrease in GFR
Stage 4: GFR = 15-29. severe decrease in GFR
Stage 5: GFR < 15. Kidney failure  Iron supplements
 Diet—CHO and fat, vitamins, restrict protein
Clinical Manifestations
Dialysis Therapies
Every system is affected
Indications:
CV—hypertension (RAAS), heart failure, pulmonary
edema, pericarditis, MI 1. Uremia
2. Persistent hyperkalemia
Pulm.—crackles, Kussmaul, pleuritic pain
3. Uncompensated metabolic acidosis
Derm—severe pruritus, uremic frost (urea crystals) 4. Fluid volume excess
5. Uremic encephalopathy
GI—n/v, anorexia, uremic fetor (ammonia odor to
6. Remove toxic substances
breath), constipation or diarrhea
Acute Dialysis Indication
Neurologic—LOC changes, confusion, seizures,
agitation, neuropathies, RLS  a high and increasing level of serum potassium
 fluid overload
Hematologic—anemia, thrombocytopenia
 Impending pulmonary edema increasing
Musculoskeletal—muscle cramps, renal acidosis, pericarditis, and severe confusion
osteodystrophy, bone pain, bone fractures  Medication overdose or poisoning
 Hepatic coma
Metabolic changes—urea and creatinine, sodium,
 Hyperkalemia
potassium, acid-base, calcium and phosphorus
 Hypercalcemia
Stages of Renal Failure  Hypertension
 Uremia
STAGE 1- DIMINISHED RENAL RESERVED
 An urgent indication for dialysis in patients with
 Gradual decrease in renal function. renal failure is pericardial friction rub.
 Nocturia and polyuria
Dialysis
 24-hour urine monitoring for creatinine level.
 Based on principles of diffusion, osmosis and
STAGE 2: RENAL INSUFFUCIENCY
ultrafiltration
 Metabolic waste begins to accumulate in the  Diffusion—removal of toxins and wastes. Move
blood from blood to dialysate.
 BUN, uric acid and phosphorus increases  Osmosis—excess water is removed. Goes from
 Decrease response to diuretics area of higher solute concentration (blood) to
lower concentration (dialysate)
STAGE 3: END STAGE RENAL DISEASE:  Ultrafiltration—water moves from high
 Excessive amount of nitrogen wastes such as pressure area to lower pressure. Applied by
urea and creatinine accumulate to the blood. negative pressure, more efficient than just by
 Kidney cannot maintain homeostasis osmosis
 Severe fluid overload and electrolyte Hemodialysis (HD)
imbalances occurs
 used for patients who are acutely ill and require
Medical Management short-term dialysis (days to weeks)
 Calcium and phosphorus binders—Calcium  And for patients with advanced CKD and ESRD
carbonate, calcium acetate who require long-term or permanent renal
 Antihypertensives replacement therapy
 Antiseizure—valium or dilantin  Prevents death but does not cure CKD
 Erythropoietin  Cannot replace endocrine function of kidneys
  May be done at home (expensive) with a
caregiver’s help
 At home, treatment time may be adjusted to
meet patient’s needs

Objectives:

to extract toxic nitrogenous substances from the blood

and to remove excess water

Dialyzer

 DIALYZER (also referred to as an artificial

kidney)
 serves as a synthetic semipermeable membrane
 replacing the renal glomeruli and tubules as the
filter for the impaired kidneys.
AV Fistula

Preferred permanent access (longest useful life)

 created surgically (usually in the forearm)

 joining (anastomosing) an artery to a vein,
either side to side or end to side
 2 to 3 months to mature before it can be used
 Dilates since the veins thicken due to the
pressure from artery
Vascular Access  Once dilated, accommodates 2 large bore
needles (g.14-16)
• Vascular Access Devices (temporary)

• Arteriovenous Fistula (AVF/AV Fistula)

• Arteriovenous Graft (AV Graft)

Vascular Access Device

 Double Lumen Catheter, non-cuffed, large bore

Inserted:
 Subclavian
 Internal jugular
 femoral vein
 Involves some risk
 Removed when no longer needed
 Short term
 Double-lumen catheter, cuffed
 May be used longer
 Inserted in the internal jugular vein AV graft
 Still with some risk of infection
 created by subcutaneously interposing a
biologic, semibiologic, or synthetic graft
material between an artery and vein
 Usually created when the veins are not suitable
for fistula
 Usually in the arm (may also be in chest, thigh)
  Complications: Stenosis, infection, and
thrombosis
 Has higher rate of malfunction than AV fistula

Complications of Hemodialysis

 Altered lipid metabolism (hypertriglyceridemia)

 Heart failure, coronary heart disease, angina,
stroke, and peripheral vascular insufficiency
 Anemia
 Metallic taste and nausea (among uremic
patients)
 Malnutrition
 Sleep disturbances (early morning or late
afternoon HD)
 Double-lumen catheter, cuffed
 May be used longer
 Inserted in the internal jugular vein
 Still with some risk of infection

Dialysis Disequilibrium Syndrome

 Caused by rapid decrease in fluid volume and

blood urea nitrogen levels during HD
 Change in urea levels can cause cerebral edema
and increased ICP
 Neurologic complications include: vomiting,
restlessness, decreased LOC, seizures, coma or
death
 Can be prevented by starting HD for short
periods and low blood flows