Acute Biologic Crisis

Prepared by:
Joanalain C. Cortez, RN
 CRITICAL CARE NURSING

Nurse licensed professional who

provides care to meet the patient s
individualized needs in response to
potentially life-threatening
conditions in an environment
supportive of highly technological,
collaborative and holistic care.
 Common Problems Seen in
Critical Care Setting
1. Anxiety
2. Impaired communication
3. Sleep deprivation
4. ICU psychosis

Common procedures
1. Hemodynamic monitoring
2. Circulatory assist device * IABP
3. Airway maintenance adjuncts
 Complications
1.Sepsis
2.MOSF Multiple
Organ System Failure
3.Shock
Nursing Interventions
1.Anxiety related to fear of death, unknown patients
and significant others; ineffective coping
mechanism .
Tx: Family participation, biobehavioral
intervention

2. Impaired communication related to barriers :

ET, new TT, or trauma
Tx : Acknowledge patient’s concern ;
reassurance ;
alleviate common difficulties; family feedback
3. Sleep deprivation : lack of consistent REM and
NREM
Tx: Meds ;Family visits ; rest periods; decreased
environmental stimulation ; biobehavioral
intervention

4. ICU psychosis
-acute confusional state sec.to CNS stimulants,
narcotics, depressants, steroids/ sleep deprivation,
sensory overload, F/E imbalance, dec. Oxygen,
infection, head trauma, brain disorders
 Hemodynamic Monitoring
1.Cardiac Output – volume of blood that is
ejected from the heart in 1 minute.
- determined by the HR x SV expelled per
heart beat.
- NV- 4-8L/min.

2. Pre-load – amount of stretch in the LV just

before ventricular contraction at the end of
diastole.
3. Afterload – tension the ventricle must
overcome to eject the blood into the
arterial systems (pulmonary and aortic);
measured by the systemic vascular
resistance.

4. Cardiac index – is the CO by the BSA

- better indicator of the body’s ability to
perfuse the tissues effectively than CO.
- - NV- 2.5 – 4.0 L/min/m 2
PCWP-BP in the most distal peripheral
capillariesof the PA. (Left Atrial
Pressure)

PAP-pressure exerted on the PA walls

being pumped out of the RV

MAP-average of S &D BP- DBP+2SBP

-------------------
3
CVP- blood within the heart & great
vesselsof the thorax
Types of Hemodynamic Monitoring
A. Arterial lines – provides a direct, intra-
arterial measurement of BP; assist in the
continuous measurement of SBP, DBP
and MAP.

Method : a 20 g arterial catheter inserted into

the radial, brachial or femoral artery
connected to high pressure tubing leading to
a pressure transducer and amplifier.
Nursing Management : Same mechanics
in CVP reading
1.Drawing a – blood sample – flush A line
with valve flush device to allow return
of sharp arterial waveform thru a 3 way
stopcock.

2. Change dressings 24-48 hrs., IV

solutions and IV tubings per hosp.
policy 48-72 hrs.
3. Watch out for complications : bleeding
from insertion site , hemorrhage,
infection- systemic , air embolus,
thrombosis, occlusion of circulation with
loss circulation distal to insertion site.

4. Perform Allen Test prior to radial artery

insertion and freq. monitor distal pulses
to decrease A/E.
B.Swan-Ganz Catheter –
Pulmonary Artery
Balloon Flow provide
indirect measurement of
LV function for detection
and treatment of CP
changes.
Method : a 5 lumen, balloon tipped ,
flow directed catheter connected to a
pressure transducer and pressurized
heparin flush system is inserted thru a
percutaneous or cutdown venous site
and directed into the RA.

Site : subclavian vein most common

Indications :
a. a need to monitor PAP and or
PCWP- indirectly reflect LV
function.
b. provide information about CO,
tissue perfusion and BV.
c. Obtain venous blood specimens
d. Proximal orts used for continuous
fluid or medication infusion.
Nursing Management :

1.Level and secure transducer at the

phlebostatic axis – 4th ICS, MAL – serves
as a reference point for the RA.

2. Taking readings – record PA Systolic and

Diastolic Pressures to obtain a PCWP or
LVEDP , then inflate the catheter balloon
slowly, watch for waveform changes-
dampening indicates wedging.
 3. After reading has been recorded, allow
the balloon to deflate passively and
lock it out to prevent accidental
wedging- take all reading at the end of
expiration.

4. W/O for complications: dysrrhythmias,

infection, air embolism,catheter
occlusion, pneumothorax, thrombus
formation.
C. Circulatory Assist Device – Intra-
Aortic Balloon Pump a counterpulsation
device that assists to augment CO and to
provide adequate rest and recovery

Indications :
•cardiogenic shock
•heart failure
•support before heart transplantation
• unstable angina
• failure to wean from CP bypass after coronary
bypass surgery
Nursing Management :

1.Assist with placement as needed and

maintain sterility with dressing
changes.
2.Monitor and record effectiveness –
inc. CO, inc. BP, inc. U.O., inc. LOC,
palpable peripheral pulses, improved
ischemic EKG changes.
3. Monitor circulation, sensation and motor
function in leg of insertion , keep the affected leg
straight at all times.

4. Keep HOB elevated at least 30 degrees to

prevent migration of the balloon.

5. Monitor Sx:
hematuria ( excessive anti coagulants)
excessive oozing from catheter insertion sites
positive guiac in the stool
abnormal PT,PTT and platelet counts
6. Complications :

• air/foreign body embolus if balloon

should rupture
• thrombus formation at insertion site
• loss of distal circulation
• migration of catheter
• dissection of aorta
• sepsis
• complications of immobility
Common Complications in the ICU :
SEPSIS

-a diffuse, inflammatory systemic response to

a chemical, mechanical, bacterial or microbial
assault if untreated leads to shock.

-Severe sepsis : hypoperfusion,organ

dysfunction, hypotension, septic shock, multi
organ systemic failure, death.
Management : adeq. CO

1. ABC
2. D- disability/ drugs : Inotropics, Vasodilators
3. E-expose : V/S : CVP, ECG
4. F-fluids , nutrition
5. Cooling blankets/anti pyretics/antibiotics
MOSF-Multi Organ/ System Failute

Cause : failure of one or

more body systems after a
major insult to the body
such as infection, trauma,
severe illness, persistent
hypotension and hypoxia.
4 Major Systems :
1. Pulmonary dysfunction
2. Renal dysfunction
3. CV dysfunction
4. Coagulation system failure
S/Sx: per organ dysfunction leads to
dec. LOC then coma with bleeding and
fibrinolysis.
Dx: 1. ABG- severe acidosis
2. WBCs – dec. platelet less than
80,000/mm 3
3. dec. fibrinogen
4. inc. PT,PTT, hgb, hct , severe
anemia
5. inc. urea, BUN
6. inc. cardiac, hepatic enzymes
7. inc. serum K
8. CXR – interstitial edema and
hypoperfusion
Tx:
1. V/S,CVP 8-10 mmHg
2.ABC
3. Hemodialysis/hemofiltration
4.Nutritional suspport
5. Antibiotics
6.Bleeding control
7.Limit activities
SHOCK
-a state of imbalance between O 2
supply and demand in the body
that leads to inadequate blood
flow to organs, poor tissue
perfusion- possibly fatal cellular
dysfunction.
Classification:
1.Loss of CBV – hypovolemic
2.Dec. pump function – cardiogenic
3.Spinal cord injury – Neurogenic
4.Overwhelming presence of endogenous
mediators causing inflammatory response–
septic

Compensatory Mechanisms :
1. SNS- massive release of NE
2. Endocrine -ADH
3. RAAM
S/Sx :
Early Stage: normal BP, slightly increase CR,
normal to slightly dec.U.O., slight
restlessness,anxiety, thirst

Next Stage: progressive shock state – claasic

shock sx ; cool clammy pale skin, dec. capillary
refill, tachycardia, tachypnea, dec. BP, CO, temp.,
U.O., LOC, metabolic acidosis

Later Stage: Sx of specific organ failure :

anuria, slow thready pulse, ARDS, bleeding,
coagulation dysfunction, coma.
Dx:
1. dec. hgb/hct
2. ABG- acidosis
3. inc. serum lactate and K
4. inc. cardiac hepatic GI enzymes
5. inc. BUN crea – RF
6. initially increase glucose to decrease
glucose stores
7. dec. sp. grav. urine
8. depletion of clotting studies
9. ST ischemic changes ECG
Management :
1. ABCDEFGH
2. BT, IV NSS, LR, O 2, Vasopressors,
vasodilators,inotropics
3. Correct acidosis- anaphylactic and septic
shock
4. Comfort measures
5. V/S,UO,,peripheral circulation, titrate
meds., thorough assessment
6. Cardiac dysrythmias, coagulation
dysfunction, I&O, hemodynamic status
7. dec. external stimuli, family teaching
ARDS Acute RDS
-a syndrome char. by a non-cardiac
type of pulmonary edema and
increasing hypoxemia despite
administration of tx measures
formerly known as adult resp.
distress syndrome.
S/Sx :
1. labored respirations
2. restlessness
3. dry, non productive cough
4. cyanosis
5. pallor
6. adventitious breath sounds with
used of accessory muscles with
retraction
Dx :

1. CXR – white out due to bilateral diffuse

infiltrates
2. PFT – dec. in compliance , lung capacity
3. Increase peak inspiratory pressures
4. ABG- initially resp. alkalosis due to
hyperventilation then acidosis.
5. Inc. hemodynamic monitoring – PA
Systolic and Diastolic Pressures with
normal PCWP and LVEDP
Pathology :
1. Primary Insult
2. Chemical mediators released
3.Interstitial edema
4. Alveolar edema
5. Damaged surfactant producing cells
6. Dec. lung compliance
7. Atelectasis, hyaline membrane formation
8. Inc. work of breathing
9. Impaired gas exchange
10. Respiratory failure
Tx :
1. O 2
2. Neuromuscular blocking agents
3. Sedation to tolerate mech.
Ventilation
4. Fluid therapy- crystalloids,
colloids – IVC volume
5. Hemodynamic monitoring
6. Treat underlying cause of ARDS-
antibiotics
7. Provide nutritional support – CHON
balance
8. Steroid therapy – stabilize cellular
membrane and dec. fluid shifts
9. Diuretic therapy
10. Comfort, positioning HOB elevated
11. V/S, EKG, Neuro
12. Conserve energy-schedule
activities/family teaching
 She sails on the sea shore/ coz she
sells/ sea shells / by the sea shore.

 Peter piper/ picked a pack of pickled

pepper/ How many packs / of pickled
pepper / did Peter Piper picked?
 Beta Bota/ bought a bit of butter
 He said/ his butter was bitter, and
 It will make/ my butter better
 So, Beta Bota / bought a bit of butter.
 CARDIOPULMONARY RESUSCITATION

BCLS – to recognize cardiac or resp. arrest and re establish

or provide airway breathing pattern and effective
circulation until the client responds or until another
type of life support is initiated.
HT / CL maneuver, jaw thrust maneuver LLF
M-M/ ambu bag
Closed CC
Adult one rescuer: 15:2 for 4 cycles : 1 minute
1 ½ inches compression lower 1/3 sternum at a rate of 100
times per minute.
ACLS – manages the airway thru ET intubation
or use of an advanced airway device.
- ET placement check
- Venous access peripheral IV g 16-18

Drugs:
Asystole: pulseless electrical activity
1. Epinephrine
2. At SO 4
3. CPR/ transcutaneous pacing
Bradycardia
1. At SO 4
Fibrillation, Pulseless Vtach :

1.Epinephrine 1mg repeated 3-5 min, IV; tracheal

adm. 2-2.5mg in 10 ml NSS
2. Vasopressin –Pitressin 40 U or ET single dose
once only
3. Amiodarone- Cordarone 300mg IV
4. Lidocaine-Xylocaine-1-1.5mg/kg IV
5. Lidocaine drip 1-4 mg/min for maintenance
infusion
6. Procainamide 20mg/min IV
7. Na HCO3- 1 MEQ/kg/IV bolus
Ventricular fibrillation
-chaotic rhythm, rapid disorganized
depolarization of ventricles

Tx: defibrillation – 200-300-360

joules / O 2 / CPR / Epinephrine
lidocaine amniodarone
Ventricular Tachycardia
-rapid ventricular contraction 100bpm
above VR – 150-250 bpm QRS more than
.12 sec. wide, bizarre

Tx : hemodynamically stable: O 2 /
lidocaine amniodarone to dec. irritability
PVC
-ectopic beats occur earlier than expected
followed by a compensatory pause.
Salvos:
1. more than 6/min PVC
2. paired
3. multifocal –differing shapes
4. R on T

Tx: Lidocaine
SVT
-more than 100 bpm originating above the
ventricle but not in the sinus node.
-AR more than 140 bpm VR depends on
degree of block

Tx :
1. Attempt vagal nerve stimulation
2. Adenosine 6 mg rapid IVP
3. Verapamil– Isoptin 2.5-5mg IV over
2mins.
4. Synchronized Cardioversion
Nursing Role During a Code :
Call Code
CPR, paraphernalia
Determine team leader
Serial assessments and
documentation
Crowd control
Psychosocial needs of family,
room mates and staff
Diabetic Ketoacidosis
-a complication of IDDM, a condition
arising from a lack of insulin resulting in a
derangement of CHO, CHON and fat
metabolism with DHN and electrolyte
imbalance.

Ketoacidosis occurs when FA are broken

down to ketone bodies because of
absoloute or relative deficiency of insulin.
Etiology : As the need for cellular fuel grows more critical ,
the body begins to draw on its fat and CHON
stores for energy.
 Increase fatty acids are metabolized from
adipose tissue cells and transported to the liver.
 Liver in turn, accelerates the rate and produces
ketone bodies ( KETOGENESIS ) for catabolism
by other body tissues particularly muscle.
 As increase metabolism- increase ketone
bodies – accumulate in the blood
 ( KETOSIS ); spill into urine ( KETONURIA );
metabolic acidosis develops develops from
acidic effect of ketoacetoacetate and B-
hydroxybutyrate---- severe acidosis
Precipitating Factors :

1. taking too little insulin

2. omitting doses of insulin
3. failing to meet increased for insulin due
to surgery, trauma pregnancy puberty or
febrile illness.
4. developing insulin resistance owing to
insulin antibodies or severe emotional
stress.
4 Pathologic events in DKA

1.Incomplete lipid
metabolism
2. DHN
3. Metabolic acidosis
4. Electrolyte imbalance
 S/Sx :
 - hyperglycemia
 glycosuria
 polydipsia
 ketonemia
 ketonuria
 metabolic acidosis
 Kussmaul’s respiration
 acetone breath-dec. acetone combining power
 DHN
 dry skin
 sunken eyeballs
 flushed face
 electrolyte imbalance
 tachycardia
 Management : Prevent complications

1.Adequate ventilation
2.Fluid replacement NaHCO3,
NaCl,K
3.Insulin
4.Indwelling FC
5.IVF,D5050 IV
6.Hgt ,ABG,CXR,12 lead EKG
 HHNK-Hyperglycemic
Hyperosmolar Nonketotic Coma
-a condition resulting from elevated
concentration of blood glucose

- level which increases the osmolarity

of blood without significant
ketoacidosis.
Causes :
1. large NaHCO3 infusion as in CPR
2. marked hyperglycemia
3. uremia with increased BUN
4. Na retention from adrenal steroid

Tx:
1. Insulin
2. F/E
3. Dialysis
 THYROID STORM
-one of the 3 major complications of
Grave’s ds.: exophthalmos, heart ds.,
thyroid storm.

-Sometimes fatal, acute episodes of

thyroid overactivity char. By high fever ,
severe tachycardia, DHN and extreme
irritability.
Causes :
1.Increased amounts of thyroid
hormones
2.With Grave’s ds., undergoes sudden
stress or develops an infection
3.A pregnant woman enters labor
4.Individuals inadequately prepared
for thyroid surgery
5.Unrecognized hyperthyroidism
S/Sx:
1. increased temp. 41 C
2. DHN
3. irritability
4. frustration
5. cardiac dysrythmias
6. CHF
7. delirium
8. diarrhea/N/V
Tx:
1. hypothermic blankets,anti-pyretics
2. oral/parenteral anti thyroid drug PTU -to block thyroid
hormone secretion followed one hour later by K iodide.
3. corticosteroid prev. adrenal insufficiency- inhibit T4
(thyroxine)-T3(triiodothyronine) conversion rxn
decreasing fever and maintain BP
4. beta adrenergic blocking agents- Propranolol,Quinidine
– block the overactive sympathetic nervous functions
and relieve cardiac dysrthmias
5. barbiturates- agitation
6. antibiotics
7. caloric intake , B complex – inc. catabolic rate
HEPATIC ENCEPHALOPATHY

-encompasses a spectrum of
CNS disturbances such as
severe liver injury, liver failure
or portal shunt.
Pathology :
1.Increased NH3 levels in the blood and CSF-
many unusual cpds. Begin to form
Octopamines: false neurotransmitters
2. Failure of the liver to perform a function
due to liver cell damage and necrosis.
3. Shunting of blood from portal system
directly into the systemic venous circulation
bypassing the liver.
4. CNS disturbances- hepatic coma – death
S/S x :

1.impairs memory, attention, concentration and

rate of response
2.sleep pattern reversal
3. significant changes in handwriting and speech
4. flapping tremors- liver flap or asterixis
5. hyperventilation with resp. alkalosis
6. fetor hepaticus – presence of methylmercaptans
causing the odor char.
7. lab results : inc.NH3 and glutamine
8. dec. LOC- depressed—confused—coma
Dx:
1.Serum NH3 level, electrolytes,
CSF

2. ABGs,EEG, Hepatic Function

Tests – bilirubin, albumin,
prothrombin, enzymes
Management :
1.Reduce CHON in the intestine- CHON
restriction 20-40gms/day, assess GI
bleeding, cathartics/enemas
2. Reduce bacterial production of NH3 –
Neomycin and Lactulose Neomycin-not
absorbed into the circulation but exerts a
powerful effect on the intestinal bacteria
responsible for NH 3 production.

Lactulose – a combination of galactose and

fructose that passes through the intestine
 3. Eliminate :
a. hypovolemia- F/E imbalance
b. hypoxia
c. concurrent infection
d. hypokalemia-diuretics,I&O
e. depressants except phenobarbital

4. Maintain function in the unconscious

person- immobility/injury

Complication :
death
 RENAL FAILURE
-state of total or nearly total loss
of the kidney’s ability tomaintain
F/E balance and excrete waste
products.

-inability of the kidney to function

normally or effectively.
Renal Insufficiency
-designates significant loss of renal function
but with a function requiring to maintain a normal
environment provided no additional stress is added.

Azotemia
-accumulation of nitrogenous wastes within the
blood,not life threatening without a decreased output.

Uremia
-an azotemia progressing to a symptomatic
state.
 Types of Renal Failure :

A.Acute RF

-a sudden, complete or nearly complete loss of kidney

function which develops rapidly over a period of day or
few weeks. Output drops suddenly to less than 400ml/day.
3 Phases :

1.Oliguric Phase – begins shortly after injury and is char.

By gradually decreasing U.O.
2.Anuric Phase – there is total absence of urine production.
3. Polyuric Phase – recovery , there is marked diuresis,
there may be rather marked wasting of various
electrolytes, esp. Na, K, HCO3.
Causes :

1. Pre-renal – when the lesion or cause is before the kidney.

- shock, mismatch BT
2. Renal – when the lesion is found in the kidney itself.
- nephritis,nephrotoxic infection
3. Post renal – reached the kidney
- obstruction of the urinary tract : renal calculi.
 B. Chronic RF
-gradual deterioration of kidney function
occurring over months or years.

3 Stages:
1. Stage of diminished renal reserve- renal function is
impaired but metabolic wastes do not accumulate in
the blood and the BUN remains normal.
2. Stage of renal insufficiency – metabolic wastes begin
to accumulate in the blood and there is a slight increase
in BUN.

3. Stage of uremia – the kidney loses its ability to maintain

homeostasis.U.O. is usually scanty, electrolyte balance
is severely disturbed and nitrogenous wastes accumulate
in high concentrations.
3 Causes :

1. Pre-renal
-gout,DM,sub acute endocarditis
2. Renal
-SLE,pyelonephritis,GN
3.Post renal
-prostatic obstruction
S/Sx :
 alteration in U.O.
 weak,easily fatigued becomes increasingly drowsy
 HA and slight breathlessness and lethargic
 restlessness and insomnia
 dry, skin and mucous membrane
 halitosis- urineferous breath
 loss of appetite, intractable N/V
 CNS manifestation- anxiety, irritability, hallucination,
mental wandering, muscle twitching, coma
 HPN
 anemia
 edematous, tend to bruise easily
 Management :

1. Diet: Giordano Giovanetti Regimen- dec. CHON,

essential amino acid, -controlled K 1,500mg, 20g
very low CHON, minimal essential AA.
2. Tx of Infection : unnecessary surgery and instrumentation
are avoided; antibiotics
3. Tx of alterations in Body Chemistry
-limit CHON metabolism and K ;
-hyperkalemia –peaked T wave, depressed ST segment,
flaccid paralysis,slow respiration, anxiety, convulsions

Tx: Kayexalate –contain Na in a compound absorbed

by the GIT. While in the GIT, the Na exchange places
with serum K ; and K becomes part of the non absorbable
compound.
-Ca gluconate- as an emergency measure when the K level is
dangerously high and cardiac arrythmias are imminent.

-Glucose and insulin- insulin causes glucose to go into cell; as

glucose moves into the cell, it takes with it and reduce the
serum K.

-Na HCO 3 – treat acidosis.

Aggressive Mgmt :

1. Hemofiltration/Hemodialysis
2. Peritoneal Dialysis
Thank you!
Thantk ou!