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Multisystem Problems
Multisystem Problems
PROBLEMS
RHEALEEN V. VICEDO, MAN, RN
Assistant Professor IV
INTENDED LEARNING
OUTCOMES
01. 02.
Assess patients Identify Diagnostic
with multisystem studies
problems
• PROGRESSIVE / DECOMPENSATED
• IRREVERSIBLE / REFRACTORY
INITIAL / COMPENSATORY
STAGE
• BP remains normal
• SNS stimulation : “fight or flight response”
↓
Catecholamine release
↓
↑HR
↓
↑contractility
↓
Maintain cardiac output
INITIAL / COMPENSATORY
STAGE
• MAP= CO x PR
• Normal: > 65 mmHg (60-90mmHg)
• MAP= Mean Arterial Pressure
• CO = Cardiac Output (Stroke Volume x HR )
• PR = Peripheral Resistance (diameter of arterioles)
• MAP= SBP + 2 (DBP)
3
• SBP- systolic blood pressure
• DBP- diastolic blood pressure
INITIAL / COMPENSATORY
STAGE
↓ renal tissue
perfusion
renin
ANGIOTENSIN Aldosterone
release
↑ BP
INITIAL / COMPENSATORY
STAGE
↓ cardiac output
↓ hydrostatic pressure in
capillaries
Fluid shift
(ICS→ECS)
↑ circulating blood
volume
INITIAL / COMPENSATORY
STAGE
hypoxemia
hyperventilation
O2 supply to Respiratory
tissues Alkalosis
↑ tissue perfusion
INITIAL / COMPENSATORY
STAGE
↓ cardiac output
SNS stimulation
↑ cardiac output
STAGES OF SHOCK
• PROGRESSIVE / DECOMPENSATED
• IRREVERSIBLE / REFRACTORY
PROGRESSIVE/DECOMPENSATED
STAGE
• Compensatory mechanisms fail
• MAP ↓
• BP < 90 mmHg or ↓ 40mmHg from baseline
• ↓ mental status
PROGRESSIVE/DECOMPENSATED
STAGE
• Compensatory mechanisms fail
• MAP ↓
• BP < 90 mmHg or ↓ 40mmHg from baseline
• ↓ mental status
PROGRESSIVE/DECOMPENSATED
STAGE Impaired blood flow to tissues
↓ O2 supply
Anaerobic Metabolism
DECOMPENSATED / PROGRESSIVE
↓ glomerular filtration
D
N Acute tubular necrosis
E
Y Tubular epithelial cells slough off
S
Blockage of tubules
Loss of nephron
function
Renal Failure
DECOMPENSATED / PROGRESSIVE
↓ cerebral tissue perfusion
B
STAGE
R Accumulation of
Cerebral hypoxia toxic substance Acidosis
A
I
N
U
N Non cardiac pulmonary edema
G
S Destruction of type 2 pneumocytes
↓ surfactant production
DECOMPENSATED / PROGRESSIVE
L
Ventilation-Perfusion Mismatch
STAGE
U
N
G hypoxemia ↑ work of breathing
S
Paralytic ileus
STAGE
G
I
T
Release of endotoxins
↓ liver perfusion
I
V Bacteria enters the general circulation
E
R Toxin production
Septic Shock
DIC
• Acidosis
DECOMPENSATED / PROGRESSIVE • Blood stagnation
• Bacterial toxins
• Prostaglandins
• Procoagulation factors
Intavascular clotting
B
STAGE
↓ C.O.
↓ Circulation
STAGES OF SHOCK
• PROGRESSIVE / DECOMPENSATED
• IRREVERSIBLE / REFRACTORY
IRREVERSIBLE / REFRACTORY
STAGE
• Severe organ damage
• Patient does not respond to Tx
✓E.g
✓Hemorrhage
✓Dehydration
✓Burns
✓Trauma
✓ascites
HYPOVOLEMIC SHOCK
Massive Blood / fluid
loss
↓ coronary artery
↑ Venous pooling ↓ arterial BP
filling
Microcirculation
↓ venous return
damage
Cellular hypoxia
Vasoactive substance
release
↑ capillary
permeability
BURNS
• Burns are caused by:
• HEAT
• CHEMICALS
• ELECTRICITY
• RADIATION
• A critical burn can be life threatening and needs
immediate medical attention.
TYPES OF BURNS
• SUPERFICIAL - FIRST DEGREE
• Involves only the top layer of skin.
• The skin is red and dry and the burn is
usually painful.
• The area may swell.
• Most sunburns are superficial burns
• Usually heal in 5-6 days without scaring.
TYPES OF BURNS
• PARTIAL THICKNESS - SECOND
DEGREE
• Skin is red and has blisters that may
open and seep clear fluid making the
skin appear wet.
• Usually painful and the area swollen.
• The burn heals in 3-4 weeks
• Scarring may occur.
TYPES OF BURNS
•FULL THICKNESS -THIRD DEGREE
• Destroys all layers of skin and any or all of
the underlying structures – fat, muscle,
bones, etc.
• Look brown or black (charred) with the
tissues underneath sometimes appearing
white.
• relatively painless if the burn destroys the
nerve endings.
CRITICAL BURNS
• Burns involving trouble in breathing.
• Burns covering more than one body part.
• Burns to the head, neck, hands, feet or genitals.
• Burns (other than a very minor one) to a child or an
elderly person.
• Burns resulting from chemicals, explosions, or electricity.
RULE OF NINES
FLUID RESUSCITATION IN
BURNS
FORMULAS
• Total fluid volume to be administered for the first 24 hours
• Parkland : LR 4 mL/kg / TBSA
• Modified Brook: LR 2 mL/kg / TBSA
• ½ of the total amount should be administered on the 1st 8
hours
• The remaining ½ is divided into 2 for the succeeding 16 hours
FLUID RESUSCITATION IN
BURNS
• EXAMPLE:
A 35 year old female patient has been burned by a chemical.
Burned parts are the following: anterior left arm, whole left leg,
and the anterior chest. The weight of the patient is 75kg.
E.g.
• Head injury
• Spinal cord injury
• General anesthesia
• Drug overdose (opiates, barbiturates, tranquilizers)
• Fainting / syncope
VASOGENIC/DISTRIBUTIVE
SHOCK
• SEPTIC / TOXIC SHOCK
• Wide spread infection
• Generalized vascular collapse from systemic infection
• Usually caused by gram-negative organisms
• Endotoxins → massive vasodilation
E.g.
• Bacteremia
SYSTEMIC INFLAMMATORY
RESPONSE SYNDROME (SIRS)
• Similar to sepsis but there is no identifiable
source of infection
• Stimulates an overwhelming inflammatory
immunologic and humoral response
SYSTEMIC INFLAMMATORY
RESPONSE SYNDROME (SIRS)
MANIFESTATIONS:
• Fever of more than 38°C (100.4°F)
• HR > 90
• RR > 20 ; PaCO2 < 32 mm Hg
• WBC >12,000/µL or <4,000/µL or >10%
immature [band] forms
VASOGENIC / DISTRIBUTIVE
SHOCK
• ANAPHYLACTIC SHOCK
• Severe allergic reactions
• Patients already produced antibodies (IgE) to foreign
bodies → systemic antigen-antibody reaction
• Large quantities of fluid may leak out of the capillaries
causing severe hypovolemia
VASOGENIC / DISTRIBUTIVE
SHOCK
• Trigger → mast cells
activated → release of
histamine, bradykinin,
cytokines, leukotrines,
prostaglandins →
widespread
vasodilation → airway
obstruction → death
VASOGENIC / DISTRIBUTIVE
SHOCK
Precipitating event
vasodilation
Activation of inflammatory
response
↓ venous return
↓ C.O.
↓ tissue perfusion
PARAMETERS FOR ASSESSING
STATUS OF CLIENT IN SHOCK
• HEMODYNAMIC MONITORING
• BP
• Pulse
• Central venous System
• pulmonary artery pressure, pulmonary capillary
wedge pressure
• Cardiac output
• ECG
PARAMETERS FOR ASSESSING
STATUS OF CLIENT IN SHOCK
• HEMODYNAMIC MONITORING
PULMONARY CAPILLARY WEDGE
PRESSURE (PCWP)
• Measured by inserting balloon-tipped,
multi-lumen catheter (Swan-Ganz
Catheter) into a peripheral vein
• Normal: 2-15mmHg
• Most accurate reflection pf left atrial
pressure, left ventricular end-diastolic
pressure (LVEDP), or preload
PARAMETERS FOR ASSESSING
STATUS OF CLIENT IN SHOCK
• NEUROLOGIC MONITORING
• alertness
• orientation
• confusion
• HEMATOLOGIC MONITORING
• RBC
• HCT, HGB Levels
• WBC
• Platelets
• PT, PTT clotting time
COLLABORATIVE MANAGEMENT
• PROMOTING FLUID BALANCE
• whole blood and blood products
• Colloid solutions (plasma expanders)
• Crystalloid solutions
• eg. d5%, PNSS, PLR’s
COLLABORATIVE MANAGEMENT
• ASSISTING WITH CARDIAC SUPPORT
• Modified Trendelenburg position
• Supine, head supported with pillow
• Legs extended and elevated at 20-30°
• Pelvis higher than torso
• Intra-aortic balloon pump
COLLABORATIVE MANAGEMENT
• ASSISTING WITH RESPIRATORY SUPPORT
• Oxygen therapy
• mechanical ventilation
• Deep breathing, coughing exercises
• Suction prn
COLLABORATIVE MANAGEMENT
• ASSISTING WITH RENAL SUPPORT
• monitor urine output q1
• Monitor BUN, Crea
• Diuretics: furosemide, mannitol
• Na+ Bicarbonate
• Antibiotics
• Heparin
• Steroids
• Antacids/ proton pump inhibitors
DRUG THERAPY
• Glucose 50% to meet energy demands
• Naloxone (Narcan) to block endorphin-mediated
hypotension
• Dyphenhydramine (Benadryl)
• Narcotics with great care
• Cardiogenic Meds:
• For dysrhythmias e.g. Lidocaine
• For bradycardia e.g. Atropine
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