CRITICAL CARE NURSING

Encoded by/Property of: Ryan Mendoza Ecunar, SLU SN IV

The critical care environment o If widening pulse P,  Increased ICP

 Fast-paced o If narrowed pulse P, shock  compensation
 Highly specialized o Pulse Pressure= BP Systole - Diastole
 Technical  Cardiac Monitoring
o Technologically advanced o A non-invasive procedure that poses minimal risk
o Skilled nurses to pt
 Requires various types of equipments o Placing conductive electrodes on the pts chest
 Necessary supplies must be easily and quickly accessible that recognizes the electrical activity of the heart
o Nurse patient ratio is 1:1 or 1:2 and relay it to a video display screen
o In RP, 1:4 o Review placement of electrodes
 Pts. Are cared for individually and uniquely o NOTE: if status post op, c breast CA, okay
 In life and death situations electrodes at the back
 c supportive devices  Hemodynamic M
 c multiple complications o Invasive M of the arterial or venous system
 in intensive ttt for specific dysfxs o M is accompanied through catheters that measure
changes in air and fluid P
Assessment o Can also be used to administer IVFs and certain
1. Nursing history arterial and/or venous blood for lab analysis
 May have direct admission o 2 types commonly used:
 CC nurse integrates data for pt and family, written hx and
 Intraarterial M
the transfer report
o E.g. HPN- HPI  Catheter is inserted into an
artery
 Diet
 radial or
 Smoking
 femoral connected
 ROH use
to a high P flush
 Stress
system filled c
2. Diagnostics
either
 ECGs
non/heparinized
 Respirations
saline solution
 Intraarterial P
 Intraarterial systems display a
 Pulmonary artery P
continuous reading of the pts
 Venous O2 sat
 Body temp BP
 Continuous Airway P M  Transducers are connected to
o Non-invasive technique that uses a transducer the system that interprets the
air and fluid P readings and
cable, ↑d P tubing & a display monitor
display results as waveforms
o The waveforms produced by the system enable
on cardiac monitoring
the clinician to continuously M the pts. Response
equipment
to various modes of mechanical ventilation
 Pulmonary artery M
o ↑d P- kinks and destructions
 Involves inserting a catheter
 Sources of obstructions: phlegm
via the
 NR:
 subclavian
 Look for kinks  or internal jugular
 Suction the pt vein and advancing
o ↓d P- cause by detached tubing, leak from the it into the
mechanical ventilator pulmonary artery
 CVP M
o Maybe used in lieu of a pulmonary artery catheter Teaching in the CCU is focused on the short term. The nurse
when evaluation of pulmonary artery P and L communicates to the pt and the family
sided heart failure are nor req’d
o Unit in cmH20 1. rationale for the ttts, procedures and medications
o 0-25 calibrations 2. plans for ongoing care
o Normal: 4-l2 cmH20 other books, 4-10 0r 6-12 3. goals for ttt
cmH20 4. interpretations of the dx, dx tests and expectations
o If below: hypervolemia 5. resources available foe financial, coping, support and other
o If above: hypovolemia personal needs
 Intracranial P M
o Involves placing a catheter through the skull into Abdominal aortic aneurysm (AAA
either the subarachnoid space or the cerebral  assoc c atherosclerosis (most common cause) and
ventricle to M changes in P within the cranial HPN
cavity  common to adults 70 y/o and above
o A transducer and tubing system gather the data cc  ↑ng age and smoking contributes as well
are displayed on the M screens  90 % develop below the renal arteries, usually
o In RP,  Cushing’s triad where the abdominal aorta branches from the
iliac arteries
Risk factors  Pain may range from mild discomfort to severe (depending
 HTN (more than ½ have HTN) on the size)  severe pain may indicate impending rupture
 Genetic predisposition
 Caucasian race
ALERT: No deep palpation!!!
 Cystic medial necrosis Diagnostics
 Athero/arterisclerosis 1. CT scan/ MRI
 Immunologic conditions 2. Angiography- uses contrast dye solution injected into the
 Male four times than women aorta or involved vessel to visualize the precise size and
 Advancing age location of the Aneurysm
 Pregnancy 3. abdl UTZ- to dx AAA
 Congenital defects of the aortic valve 4. transesophageal achocardiogram- to differentiate
 Coarctation of the aorta 5. CXR
 Inflammatory aortitis
 Syphilis Nursing Responsibilities
 Trauma 1. in aortic dissection
 Local infection (pyrogenic or fungal) mycotic aneurysm a. IV beta blockers (Esmolol)
b. Na nitroprusside (similar c Dep patch)
Aneurysm- abN dilation of the BVs c. CCBs
- commonly affects aorta and peripheral arteries d. Avoid giving direct vasodilators further
- may also develop in the ventricles destruction injury
- forms due to weakness of the arterial wall e. Post-operative anticoagulants
- HTN is a major contributing factor i. Heparin
- destruction of the collagen and elastin ii. Low dose ASA tx
- Collagen- ↑s tensile strength of the 2. Surgery
vessel- preventing dilation a. Post-op care
- Elastin- allows recoil b. M u/o
1. primary component of the c. M FE imbalance
intimal wall and medial d. M graft leaks
layers i. Ecchymosis of the scrotum and
Types: perineum (penile area)
1. True Aneurysm ii. ↑ng abdominal girth
a. brought abt by the eroding effects of iii. Weak and absent peripheral pulses
atherosclerosis and HTN iv. Fall in Hgb and Hct
b. affects the 3 layers of the vessel wall and most v. Pain over the pelvis, back and groin
are Fusiform or circumferential vi. Decreasing u/o
i. Fusiform- spindle shape and taper at vii. Decreasing hemodynamic M
both ends
ii. Circumferential- involves the entire Nursing Diagnoses
diameter of the vessel  risk for ineffective tissue perfusion
2. False Aneurysm  risk for injury
a. also known as the traumatic Aneurysm bec of  anxiety
traumatic break in the vessel wall rather than
weakening Acute Respiratory Distress Syndrome
b. usually are saccular- like small outpouchings Pathophysiology
i. Berey Aneurysm- type of saccular Pulmonary insult
Aneurysm but relatively small (2 cm in ↓
diameter) Chemical mediators released
ii. Dissecting Aneurysm ↓
1. develops when a break or Damage to alveolar capillary membrane
tear in the tunica intima and ↓ ↓ ↓
media allows blood to invade Interstitial edema  alveolar edema  damaged surfactant-
or dissect the layers of the ↓ producing cells
vessel wall Dilution ↓
2. blood accumulates in the of surfactants ↓d surfactant production
adventitia and thus form a ↓ ↓
saccular or a longitudinal
aneurysm ↓d lung compliance, atelectasis,
Aortic Dissection - a life- threatening condition hyaline membrane formation
- a tear in the artery inner layer allows
blood to dissect or split in the vessel ↓
wall ↑d work of breathing impaired gas exchange
- manifestation is epigastric pain ↓ ↓
RESPIRATORY FAILURE
Clinical manifestations
 Asymptomatic Acute Respiratory Failure
 Pulsating abdominal mass in the middle and upper abd  consequence of severe respiratory dysfx
when lying down, bruit is heard  defined by arterial blood gas values
 Intermittent and constant pain over the midabdominal area o an arterial 02 level of <50-60mmHg
region and lower neck (if pain is present) o an arterial CO2 level of >50mmHg
 4. radiation
 in COPD  usually assic c unburn and radiation fr
o acute drop in blood O2 levels ttt of cancer
o increased CO2 levels  usually superficial involving the
 failure of O2- hypoxemia s a rise in CO2 levels epidermis
hypoventilation- hypoxemia and hypercapnia  e.g. solar, x-rays, radioactive agents
 acute lung injury
 Mortality due to multiple organ system dysfx Factors Affecting Burns
 AKA adult hyaline membrane dse  Depth of the burn (layers of underlying tissue affected)
 charac by noncardiac pulmonary edema and refractory o Det by the elements of the kin that have been
hypoxemia damaged or destroyed
Characs of Burns by Depth
Manifestations  Superficial (epidermis): skin maybe pink to red and dry
 dyspnea - usually heals in 3-6 days
 tachypnea - peeling of the skin is evident
 anxiety - e.g. sunburn
 restlessness - redness, mild edema, pain and
 apprehension increased sensitivity to heat
 impaired judgment - desquamation is 2-3 days
 motor impairment  Partial thickness (epidermis and dermis):maybe superficial
 tachycardia and deep partial thickness
 HTN  Superficial: involves the dermis and the papillae
 Cyanosis of the dermis
 Dysrhythmias - Burn is often bright red but has a
 Hypotension moist glistening appearance c blister
 Decreased cardiac output formation
 Tissue hypoxia - Burnt area will blanch when P is
 Metab acidosis applied; touch and pain sensation
 Develop within 24-48hourss p initial insult remain intact
 Progressive respiratory distress - Heals in 21days c minimal or no
 Cyanosis does not improve c O2 admin scarring
- Upper 3rd of the dermis
Medications - Good blood supply
 Nitric oxide reducers (nitrous oxide a free radical) - Blisters
 Surfactants - Nerve endings are exposed painful
 Inflammatory blockage utilizing steroids  Deep partial thickness: involves entire dermis but
 Mech vent extends further
 Nutrition – eat PO, enteral and parenteral feeding - Sebaceous glands and epidermal
sweat glands remain intact
Review arachidonic acid pathway!!! - Surface of the skin appears pink and
waxy and may be moist or dry
Burns - Capillary refill is decreased and
 An injury resulting fr exposure to heat, chemicals, radiation secretions to deep P is present
or electric current - Requires more than 21 days to heal
 A transfer of energy fr a source of heat to the human body (3-6 weeks) c scar
initiates a sequence of physiologic event in the most severe - Can proceed to full thickness due to
cases leads to irreversible tissue destruction infection, hypoxia or ischemia
- Contactures, hypertrophic scarring
Types of Causative agents of Burns  Full thickness: epidermis, dermis, underlying
1. thermal tissues: skin appears waxy, dry, leathery, charred
 most common injury - Involves all layers of the skin,
 dryheat: open flame including the epidermis, dermis and
 moist heat: steam, hotliquids the epidermal appendages
2. chemical - It can extend to the SQ, connective
 caused by direct skin contact c acids, tissues, muscle and bone
strong alkali, organic compounds - Hard, dry, leathery eschar
 chemicals destroy tissue CHON leading - Eschar- dead tissue, must be
to necrosis removed
 e.g. inhalatory (cement)  burns - Grafting to heal
3. electrical  Deep full thickness wounds
 depends on the type and duration of - Extend beyond the skin to
current and amount of voltage underlying tissues and fascia,
 difficult to assess because the muscles, bones and tendons
destructive processes are concealed - Complete absence of sensation
 entry and exit wounds tend to be small,
masking a widespread tissue damage  Extent of the burn (percentage of body surface area
underneath the wound involved)
 eg. Direct and alternating current, o Expressed as a % of the total body surface area
lightening (TBSA) use rule of nines (prehosp)
 i. Is an overgrowth of dermal tissue that
Extent of Burns- expressed in % of the TBSA remains within the boundaries of the
 Rule of Nines- emergency outside the hospital; rapid wound
 Lund and Browder method- det surface area measurement f. Keloid- a scar that extends beyond the boundaries
for each body part accdg to cts. Age of the original wound
 Parkland’s Formula = 4 mL x TBSA x wt kgs.
 ABLS formula = 2- 4mL x TBSA x wt kgs.pt Burn Stages
 Curling’s Ulcer- brought abt by stress 1. Emergent/Resuscitative stage
a. Fr onset of the injury through successful fluid
Classification of Burn Injuries by Extent resuscitation
 Minor burn injuries b. HCWs estimate the extent of burn injury
i. excludes electrical and c. Institute 1st aid measures
inhalational and complicated d. Ct may be intubated
injuries such as trauma 2. Acute stage- start of the diuresis and ends c the closure of
ii. partial thickness burn of less than the wound, either by natural healing or by using skin grafts
1% of TBSA 3. Rehabilitative stage
iii. full thickness burn of less than 2% a. Begins c wound closure and ends when the ct
of TBSA returns to highest level of H restoration, cc may
iv. e.g take years
1. sunburn- exposure to b. CT and PT may be needed
UV light; most common i. ROM exercises
2. scalding burns ii. Splints to prevent contracture
deformities and compartment syndrome
Zone of hyperemia
Pathophysiologic Effects of a Major Burn
Zone of Stasis- with (Refer to Lippincott Manual of Nsg Practice 8th ed, start pp1122)
inflammatory by-products  Skin Changes
 Moderate burn injuries o Epidermis- outer layer
i. excludes electrical and o Dermis- 2nd layer
inhalational and complicated  Made up of collagen, fibers, CTs and
injuries such as trauma elstic fibers
ii. partial thicknessof 15-25%  Within it are BVs, sensory nerves, hair
iii. full thickness burns of less than follicles, sebaceous and sweat glands
10% TBSA  Functional Changes
 Major burn injuries o Evaporation
i. includes all burnsa of the hands, o Skin can tolerate up to 40degs
face, eyes, ears, feet and o 71deg C and above will cause cell destruction cc
perineum, all electrical injuries, is so rapid
multiple traumas, and all cts. That  Vascular Changes
are considered high risk o Fluid shifts
 3rd spacing due to extravasation
Burn Wound Healing  Edema
1. Inflammatory  Hypovolemia
a. Immediately ff the injury, plts. Coming in contact  Hyperkalemia
c the damage tissue aggregate  Hyponatremia
b. Fibrin is deposited, trapping further plts. And  hemoconcentration
thrombus is formed (clamping)  Fluid remobilization
c. Hemostasis is maintained by the thrombus and o Diuretic stage- 48 to 72 hours
vasoconstriction o Hyponatremia
d. Vasodilation occurs and increases vascular o Hypokalemia
permeability o Hemodilution
e. Neutrophils infiltrate (24 hours) then is replaced o Metabolic acidosis
by the monocytes and converted to macrophages o GIVE: colloids (Zenalb- in 5% or 25 % prep) –
that consumes the pathogens and dead tissue albumin maintains Oncotic pressure pulling P
f. Also stimulates the proliferation of fibroblasts  Cardiac changes
g. Angiogenesis – promoted by VEGF apoptosis ↓Cardiac Output (CO)  ↓d circulation  vasomotor rxn (vasocons)
2. Proliferation ↓
a. Within 2-3 days p burn Baroreceptors stimulated
b. Granulation tissue begins c complete stimulus ↓ stimulus
reepithelialization Adrenalmedulla Medulla oblongata
c. Epithelial cells cover the wound ↓ ↓ impulse
3. Remodelling Release of catecholamines PNS
a. Lasts for years (Epinephrine and Norepi) ↓
b. Collagen fibers laid down ↓ Effect of sympathetic response
c. Scars contact and fade in color Increased Heart rate
d. Hypertrophies scar and keloid may appear
e. Hypertrophic scar  Pulmonary changes
 o Cause of death (CO poisoning) more than 60 %  Open- apply antimicrobial and expose
CO  DEATH  Close- allocate P dressings to prevent
o Upper airway affected by inhaled smoke that scar and keloids
causes edema then obstruction  10% is o Positioning, splints, exercise and contractures
confusion, delirium, etc, 40%  comatose o Support garments
Injury  Applied 5-7d p grafting
↓  Maintaining 10-20 mmHg to control
Increased histamine production scarring
↓  Eg. Jobst support garment
Increased VP  Used for 6 mos to a year
↓EV
Alveolus Shock
↓  state which develops where there is inadequate tissue
Congestion perfusion causing the cells to be deprived of adeq 02,
↓ convert to anaerobic metabolism resulting in the production
CO and CO2 exchange impairment of lactate and acidosis
 GI Changes  500 cc is adeq volume to manifest shock
o Decreased perfusion to the GI tract
o Sympathetic response Classification of Shock
o Curling’s Ulcer- due to ↓ BV  (compensation) 1. Hypovolemic shock- extremely lowered ciculating blood
increased Cardiac output  epinephrine release volume (due to hemorrhage, internal andextravascular loss)
 Increased GI mobility  Increased HCl 2. Cardiogenic shock
release  invitation a. inability of the myocardium to pump an adeq
cardiac output to maintain tissue perfusion
Compensatory Mechanisms b. happens when myocardial fx is depressed, several
 Inflammatory compensation compensatory mechanism are activated
 Sympathetic nervous system stimulation c. sympathetic stimulation increases heart rate and
contractility, and renal fluid retention increases
Nursing Diagnoses preload (tachycardia and effects of RAA
 Decreased cardiac output r/t altered stroke volume fr an mechanism) and cause selewctive
increased capillary permeability vasoconstriction
 Body image disturbance d. Renin-angiotensin-Angiotensinogen System
 Pain
 Impaired tissue perfusion ↓Cardiac output  kidneys (↓ perfusion)  juxtamedullary nephrons
 FVD/FEI ↓
 ATR- initially, hyperthermia…late, hypothermia Renin secreted fr the kidneys
 Impaired skin integrity ↓ ↓
 High risk: infection (high risk- preventable, foreseeable Aldosterone Angiotensin 1
crisis, no s/sx yet ↓ ↓ACE in lungs
Na and water retention Angiotensin II
Interventions ↓ ↓
 fluid tx Increased BV VC
 plasma exchange tx ↓ ↓
 M o/u Increased BP Increased BP

Management Causes/Etiology of Cardiogenic shock

 pain control  most common cause is the loss of 40-50% of viable
 tetanus prophylaxis myocardial tissue
 nutritional support  Mechanical Px
 prevent gastric acidity to prevent Curling’s Ulcer o Valvular heart dses
o PPI’s, H2 receptor inhibitor, antacids, o Perforated intraventricular septum
 Antimicrobials o Papillary muscle dysfx/rupture
o silver sulfadiazine o Myocardial rupture
o silver nitrate o Syphilis a spirochete  destroys myofilaments
 Surgery  Shock and aneurysm
o Escharectomy o Cardiomyopathies
o Debridement o Hypovolemia
 Removal of wound debris and eschar o Metabolic dysfx
 Has 3 types o Vasomotor dysfx
 Mechanical o Microcirculatory dysfx
 Enzymatic 3. Extracardiac obstructive shock- physical condition to flow
 Surgical (ie. Tension Pneumothorax, dissecting AA and pulmonary
o Skin Grafting embolus)
 Autograft 4. Distributive shock
 Homograft/allograft (cadavers) a. abN distribution of intravascular vol.
 Heterograft/ xenograft (animal)- pigs b. includes the ff
 Wound Mx i. Septic shock
o Dressing the wound 1. more on G- bacteria
 a. blows off O2   ESR- if elevated- due to injury and inflammation, indicates
increased RR infection
resp alkalosis  BUN and Creatinine clearance- elevated due to ↓d renal
2. endogenous pyrogenes perfusion
↓  Lactate- elevated sec to anaerobic metabolism
EARLY/ WARM stage  Glucose levels- elevated due to release of glycogen sec to
↓ sympathetic response
Hypothalamus  ABGs
↓ o Resp alka in early stages assoc c tachypnea
progresses←Increased temp o Resp acidosis in later stages due to respiratory
↓ depression
LATE/ COLD stage  ↓ friction ability o Metabolic acidosis in later stages sec to anaerobic
↓ metabolism
Dilation, etc  Urinalysis- increased specific gravity due to effects of
↓ ADH
3rd spacing  CXR- pulmonary congestion latter stages
↓  ECG- dets MI (elevation of ST segment, widening of QRS
Decreased cardiac output complex, overriding U) heart rate and ischemic changes
↓
Metabolic acidosis Pathophysiologies of Shock
3. Coagulating fx 1
XI- Hageman factor Marked ↓d cardiac output
↓ ↓ ↓ ↓ ↓
Complement sys kinin sys fibrinolytic cascade clotting Cardiac index (% cardiac output dist to systemic circu) < 1.8 L/m/m2
↓ ↓ ↓ ↓
Interferons serotonin Protrombin and ↓d coronary blood flow
(natural antiviral) bradykinin thrombin ↓
histamine Compensatory mechanism occur
ii. Anaphylactic shock (increase VR and catecholamine)
iii. Neurogenic shock ↓ ↓
Increased pload inc contractility
Manifestations ↓
1. Compensatory Phase ISCHEMIA
a. tachycardia (compensation 2 sympathetic
stimulation and RAA system 2
b. bounding pulse L vent and diastolic P
c. tachypnea (compensation for hypoxia and ↓ ↓ ↓
excessive amounts of CO2) Pulmonary P s cavity distention dec pload
d. restlessness and irritability (resulting fr cerebral ↓ ↓
hypoxia) Pulmonary edema endocardial ischemia
e. decreased U/O, cool and pale skin ↓ ↓
(vasoconstriction) Increased arterial hypoxemia
f. epinephrine  SNS  tachycardia  ↑BP pulmonary artery P ↓
2. Progressive stage ↓ cellular acidosis
a. HPoN (failing compensatory mech) Ischemia and R Vent failure
i. MAP <60mmHg but manifestation of
HPoN reveals if arterial P is <40mmHg  fluid retention may increase volume to the pt where
b. Narrowed pulse P pulmonary congestion and hypoxemia occur
c. Dec stroke vol- weak, rapid and thready pulse  iscgemia also ↓s ventricular diastolic compliance, further
saused by decreased cardiac output elevating L atrial P worsening pulmonary congestion
d. Shallow resp
e. Weakness progresses Effects of Vasoconstriction
f. Dec renal output  vasoconstriction cc is the effect of systemic vascular
g. Respiratory acidosis resistances, increases myocardial pload, further impairing
3. Irreversible stage cardiac performance and increasing myocardial o2 demand
a. Unconsciousness reflexes (A_B/ Electrolyte further causing worsening ischemia and further to pts.
imbalance) demise
b. HPoN worsens (decreased cardiac output)  vasoconstriction to maintain BP can compromise
c. Slow, Cheyne-stokes respiration (2 to resp center multisystematically (renal, splanchnic and cutaneous
depression) perfusion)
d. Anuria (renal failure) Medical Mx
i. Diff: oliguria- 100-400 cc/24 hours vs.  id underlying cause if possible
ii. Anuria- 5-10 cc/24hours o Streptokinase and Urokinase  Thrombolytics
 Intubation, mech vent and suppl O2 to increase
Diagnostic Examinations oxygenation
 CBC- hct (concentration of compositions, plasma) levels  Improve O2 content (Hgb and arterialO2 sat)
may be ↓d due to hemorrhage  Continuous cardiac M- detects changes in heart rate and
o ↓d Hct nay mean DHN rhythm
o ↓d overload
  Two (2) IV lines c large gauge needles (g 14-16, in o Avoid trendelenburg position bec it increases
RPonly 18 is available) for fluid and drug admin respiratory impairment
 IV fluids (crystalloids) to maintain and Increase o Just position the pt to modified trendelenburg
intravascular volume position :
Medications PILLOW
 Inotropics- increases heart contractility and cardiac output o Promote adequate rest by using energy
o Dopamine (has Calcium) conservation measures and maintaining a restful
o Dobutamine and Epinephrine and quiet env’t.
 Vasodilators
o Given c vasopressors to decrease the ventricular
workload Mneumonic of Hormones and their Origin
o Only for cardiogenic shock  Adenohypophysis/ Anterior Pituitary Gland: FAT-LPG-Me
 Nitroglycerine and nitroprusside o F- Follicle-stimulating hormone
Has vasodilatory effects towards o A- Adrenocorticotropic hormone
peripheral circulation o T- Thyroid-stimulating hormone
↓ o L- Luteinizing hormone
Decreased vascular resistance o P- Prolactin
↓ o G- Growth hormones
Decreased stroke volume o M- Melanocyte stimulating hormone
 Thrombolytic Tx  Posterior hypophysis/ Posterior pituitary gland: Anti-Oxy
o For coronary revascularization to allow o A- Antidiuretic Hormone
restoration of coronary artery blood flow o O- Oxytocin
o Streptokinase/ Urokinase
o NOTE: If MI lasted already for 12 or 6 hours, Diabetic Ketoacidosis
don’t give T tx anymore because the myocardium
is already dead! Causes
 Diuretics- If c fluid overload to decrease ventricular  infection
workload  Illness
 For septic shock:  Surgery
o Give antibiotics  Stress
 Insufficient or absent insulin
o Antipyretics due to fever  vasodilatory effects
Assessment Findings
o BT whole blood and its by-products
 Kussmaul’s breathing
 PRBC  Fruity breath odor
 WB  3 P’s
 Plt. Concentrate  Wt loss
 FFP also has cryoppts and plt (for DIC-  Muscle wasting
cryoppts has clotting factors 10-20 cc  Leg cramps
to be used) Treatment
o Osmotic diuretic maybe needed to increase renal  rehydration PNSS
bloodflow and U/O  IV insulin
 M blood glucose
Nursing Management  Assess LOC and patent airway
 MVS q 15min  MVS – for DHN
o <80 mmHg usually results in inadequate  restoration of acid-base balance and electrolyte balance
coronary artey blood flow (incr in O2 flow if  control of glucose level (insulin drip) or sliding scale
blood P is <80 mmHg then notufy the physician  for Hyperkalemia:
immediately) o Kayexalate tx (Enema) – excretion of K
 M ECG tracings continuously o Gics solution – admin of hyperosmolar solution
 Hemodynamic M plus insulin in D50-50
o CVP, RV P, Pulmonary artery P, Pulmonary o Aerosol tx (salbutamol)- a sympatomimetic drug
wedge P, L atrial P and CO ↓
 M U/O Excretes K (no need for resting)
 Maintain patent airway and adequate ventilation ↓
 M serum levels Adequate contraction of the heart
 M skin color and temp and note changes ↓
o Cold clammy skin is maybe a sign of continuing Bronchodilation
peripheral vascular constriction, indicating
progressive shock Addison’s Disease
 M arterial blood samples
 primary adrenocortical insufficiency, hypofx of the adrenal
o to increase ABG levels
cortex causes decreased production of hormones
o ABG results are the determinant for O2
Assessment
manipulation  fatigue, muscle weakness
 Provide psychological support- reassuring ct. to relieve  anorexia, N/V, wt loss
apprehension and keep family advised  hypoglycemic reactions
 Minimize factors contributing to shock  hypotension, weak pulse
o Elevate lower extremities to 45 degs to promote  decreased capcity to deal c stress
venous return  low cortisol levels
  bronzelike pigmentation of the skin – common to 2o
Pancreatitis
Secondary:ACTH and low adrenal gland fx ↓Sugar ↓Sex ↓salt  inflame process c varying degrees of pancreatic edema
Primary: ACTH px  ↓AG fx  ↓Sugar ↓Sex ↓salt  inflame of the pancreas that may result to autodigestion of
the pancreas by its own enzymes leading to hemorrhage
Nursing responsibilities: and necrosis
 Hormone replacement  occurs most often in men in the middle ages
o Glucucorticoids  Alcoholism is the most common cause
 Decadron (dexamethasone)  Other causes:
 hydrocortisone o Biliary tract dse
o Mineralocorticoids o Trauma
 (fludrocortisones acetate) o Drugs
 MVS and I&O
 Decrease stress in the env’t
 Prevent exposure to infxn and heat (hot weather) Etiology and Risk factors
 Rest periods, prevent fatigue 1. ROH abuse- causes physiochemical alteration of CHON that plugs
 Weigh daily the pancreatic ductules (sphincter of Oddi)
 Provide small freq feedings (high in CHO, Na and CHON) 2. Gallstones- when a stone migrates through the ampulla of Vater
to prevent hypoglycemia and hyponatremia 3. abdl trauma
4. hyperlipedemia
Addisonian Crisis 5. hypercalcemia
 severe exacerbation of adddison’s dse caused by acute 6. familial causes
adrenal insufficiency 7. Pancreatic trauma
Precipitated by 8. pancreatic ischemia
o Strenuous activities
o Infxn (pneumonia) Assessment
o Trauma  LUQ pain mid-epi of the LUQ that radiates to the back and
L shoulder and L flank
o Stress and failure to take meds
 Pain is continuous and is worsened by lying down in supine
o Iatrogenic: surgery on pituitary gland or adrenal
position
glands, rapid cdrawal of exogenous long time  FETAL POSITION is the most comfortable position for
steroid use them
Assessment  Wt loss due to N/V
 severe generalized muscle weakness  Steatorhhea
 hypotension  Abdominal assessment
 hypovolemia o Generalized jaundice
 shock due to vascular collapse
o Cullen’s sign – grey blue discoloration of the
flank
Nursing responsibilities
o Low bowel sounds due to paralytic ileus
 admin glucucorticoids (hydrocortisone) and IVFs to
maintain hydration abt 3-5 liters of saline o Abdominal tenderness, rigidity and guarding the
 strict bedrest and eliminate all forms of stressful activities peritoneum
 MVS and I&O, weigh daily o VS – M impending shock
 Protect fr infxn
 Assess for fluid balance (increase in fluid intake during the Laboratories
hot weather due to increase in perspiration)  serum amylase-2-12 hours fr onset of the mainifestations
 serum lipase- on of the most specific indications bec it is
Thyroid Storm solely the Pancreatitis (7h-2d)
 WBC- above 10,000mm3
 uncontrolled life threatening hyperthyroidism caused by
 Hyperglycemia
excessive release of thyroid hormone
 hypocalcemia
 commonly caused by stress, infection and unprepared
thyroid surgery
Types of Pancreatitis
S/Sx
1. Acute Pancreatitis
o Apprehension
a. apigastric pain radiating to the back
o Restlessness b. Cullen’s Sign (purpura around the umbilicus)
o Extremely high temp of abt 40 deg C c. Turners sign (violet discoloration/ ecchymosis at
o Tachycardia the L flank)
o CHF d. Elevated pancreatic enzymes (lipase and
o Resp distress amylase)
o Delirium e. MX:
o Coma i. NPO
Nursing responsibilities ii. IVF
 maintain a patent airway and adequate ventilation iii. NGT
 O2 and IV tx iv. TPN as a last resort most common
 Admin anti thyroid drugs, sedatives and cardiac drugs compli of this is hyperglycemia
 Give INDERAL v. Avoid ROH
 Control fever c non ASA drugs (it competes c thyroxine 2. Chronic Pancreatitis
site  storm) a. Abdl pain or tenderness (LUQ)
 b. DM ↓
c. Mx: Liver
i. High calorie diet, low fat ↓
ii. Avoid ROH Urea
iii. Admin pancreatic enzymes ↓
iv. glucoseMx Kidneys
Pathophysiology ↓
Trypsin by HCl Ammoniacal odor of the urine
↓
Protelytic enzymes and lipolytic enzymes Management
↓  admin enemas c intestinal antibiotics eg. Aminoglycosides
Prematurely activated in the pancreas gentamicin and lactulose (increases the osmolality  incr
↓ fluid  soft stool … attracts the fluids to feces, absorbs
Tissue damage NH4 to be disposed in the feces) as ordered
Interventions  restrict dietary CHON in the diet: provide a high CHO
 Comfort Measures intake and Vit K supplements
o Knee chest position or side lying position c
pillow pressed against the abd Renal Failure and End-stage Renal Dse
 TPN  early sign is albuminuria (cloudy in appearance)
 During the recovery phase when food is tolerated give  N, K and CHON are absorbable in kidneys
small freq feeding mod to high CHO, high CHON, low fat
meals Acute Renal Failure
 Food shld be bland c liitle spice  is the rapid decline of renal fx c azotemia (presence of
 Caffeine (tea, etc._ shld be avoided GI irritants urine by-products in the blood) and fluid and electrolyte
 ENSURE (directly absorbed amino acids) imbalance
 AVOID ROH  onset is sudden (hours to days)
 Fasting- to rets the pancreas and dec Pancreatic enzyme  % of nephron involvement : 50 %
action  Duration is 2-4 weeks to less than 3 months
 IV- for rehydration  Prognosis- good if nephron of renal fx c supportive care,
 Meperidine- drug of choice high mortality in some situations
 Morphine- contraindicated because spasm of the sphincter Causes
of Oddi can potentiate parenchymal injury  Renal infection
 Ca and MgSO4 – IV replacement o take full course antibiotics and drink at least 3L
 Gastric decompression- prevents gastric digestive juices fr
of h2o everyday – prevents ARF (abt 8-10
flowing into the duodenum
glasses)
 NGT drainage and suction- for continuous V/ give
 NSAIDS
 DEMEROL
o vs COX1  dec BV dec CO  tissue hypoxia
(give Na and H20 tx)
Food in the duodenum
 DM
↓
o High glucose level inc tonicity of the
CCU cells PZ cells
Stimulated circulation  dec perfusion  formation of
↓ ↓ plaques in the intimal wall of glomerolus  dec
Gallbladder pancreas release enzymes GRF  RF
↓ ↓  HTN
Release bile Pancreatitis  Glomerulonephritis
↓
Bile salts Types of ARF
1. Pre-renal failure- inadequate kidney perfusion
Nursing Dx: imbalance nutrition: LTBR a. due to heart failure, etc
2. Intrarenal or intrinsic renal failure – damage to the
Hepatic Encephalopathy glomeruli, interstitial tissues or tubules
a. DM
 inability of the liver to convert ammonia to urea that b. Pyelonephritis (cloudy or whitish urine output)
accumulates causing neurologictoxic manifestations c. Presence of stones
 causes: 3. Post-renal Failure – obstruction in the urine flow
o liver cirrhosis a. Tumor in kidney bladder
o hepatitis b. Testicular carcinoma
o Pancreatitis c. Cystolithiasis
o gallstones
 ammonia (crosses the BBB blood brain barrier) Other lecture:, refer to brown paper…

CHON
↓
AA
↓
Intestine thru E coli
↓
Ammonia
RYAN M. ECUNAR, SLU SN IV
Saint Louis University
College of Nursing
Baguio City