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121 Cards in this Set
- Front
- Back
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Carbon monoxide poisoning |
- d/t Fire -increased inhaled CO2 displaces O2 on Hg molecule (the O2 can go anywhere then) - therefore, if less O2 delivered to tissues=hypoxia
*cherry red skin* Treatment: 100% humidified O2 |
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Mucosal Burns of oropharynx
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From smoke or steam inhaled above glottis = thermal below glottis = chemical |
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Burn process |
-inflammation -vasodilation -edema -decreased BP and perfusion -decreased intravascular volume -increased Hct (fluid in tissues increased [Hct] in blood *can cause burn shock |
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Electrical burns can cause |
-injury - fall -dysrythmias - electrical current disrupts hearts electrical current -acidosis - inflammation causes cells to rupture releasing K into ECF -renal failure - muscle damaged released myoglobin |
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Full thickness Burn |
-depth of damage has destroyed nerve endings -dry wound -waxy, white to black -decreased sensation (lack of pain) |
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Partial Thickness Burn |
-nerves & blood vessels surrounding wound are intact -serous exudate in wound -pink-cherry red -painful with exposure to air |
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Risks of burns |
-infection -decreased resp function or blockage -compartment syndrome |
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Burns injuries increase demands on what systems in the body? |
-Cardo system and Renal system because of fluid and electrolyte shift (changes to fluid status, lytes, and pH) -Resp system (d/t edema or eschar formation or increased O2 for healing) -increased circulation needs (increased challenge for pt's with DM or PVD, leading to decreased circulation and gangrene, necrosis, and amputation) |
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Phases of Burn Management |
Emergent Phase (24-48hr)
-mobilization of ECF -reestablish perfusion Acute Phase (weeks-months) -burn covered by skin graft heals Rehab Phase -increase in ability to perform ADLs, reconstructive surgery, or cosmetic surgery |
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Burn immunological changes |
-inflammation impairs WBCs -decreased skin barrier = easier for pathogen to enter *infection risk |
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Topical Dressing burns |
antimicrobial dressing |
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escharotomy |
-incision through necrotic tissue to restore circulation -decreases circumferential pressure and increased circulation to area |
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Tx for burns |
-fluid resuscitation -O2 -analgesics -enteral feedings (increase calorie and protein) -reposition limbs to prevent contracture -monitor labs |
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Managing airway with occlusive edema |
-intubate within 1-2 hours -extubate once edema subsides (3-6 days) |
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treatment for patient with >30% TBSA (total body surface area) burned |
-central venous line -artery line (continuous BP and blood specs) |
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Burn wound care |
-debride and then skin graft |
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Why shouldn't a burn patient bathe? |
-water is hypotonic so it draws electrolytes out of fluid -cross contamination (in tub of water) -may cause hypothermia after bath |
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Why we wouldn't give IM and PO meds for burns |
IM - med pools in edema and then pt overdoses once fluid mobilizes; you wouldn't want to jab this patient with a needle either! PO - not absorbed fast enough or enough due to decreased GI perfusion; possibility of paralytic ileus, so GI tract would be stopped. **IV (or topical) meds are preferred choice for these patients |
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Burns - hypermetabolic state |
Large burn -increased resting metabolic expenditure -increased catecholamine -increased glucongeagenesis = increased BG - maybe needs insulin -increased protein breakdown = increased lactic acid = acidosis |
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Why are burn patients at risk for contractures? |
-pain = decreased movement and flexion -scar tissue shortens tissue at joints *splints and reposition |
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5 types of shock |
-cardiogenic - low blood flow
-neurogenic - maldistribution of blood -hypovolemic - low blood flow -anaphalaxis- maldistribution of blood -septis- maldistribution of blood |
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What is the main cause of shock related to low blood flow? |
-heart failure |
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Maldistribution of blood flow main cause |
-vasodilation causes fluid shift into tissues and is in the wrong place |
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Cardiogenic shock |
-pump impaired -SV and CO decreased = decreased tissue perfusion -congestion of pulm vessels = pulm edema -decreased O2 in blood = decreased perfusion *heart can't pump blood out of heart so hydrostatic pressure increases |
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Cardiogenic shock S/S |
-changes in LOC -confusion -cyanosis -cool and clammy skin -pallor -increased cap refill -increased GFR -decreased UO -increased RR, HR -decreased SBP -decreased Bowel sounds -N&V |
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Hypovolemic shock |
-decreased venous return to heart -decreased preload -decreased SV =decreased CO = decreaed perfusion *impairs cellular metabolism |
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DIC |
Disseminated Intravascular Coagulation |
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DIC process |
Shock -coaggulation mechanisms enhanced -microemboli form - use up clotting factors -decreased blood flow = risk of organ failure -bleeding risk *hard to treat |
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Vasodilators(drugs)
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-excessive constriction -decreases perfusion -increased workload of heart -decreases CO and BP = decreased perfusion |
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Goals for hypovolemic shock |
-fluid replacement -Tx cause |
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Glucose during early and late sepsis |
early - BG is high late - BG is low |
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Goals for shock |
-halt shock process -restore circulation - increase BP with fluids -correct pH imbalance |
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Why might GFR decrease during shock? |
-vasodilation = decreased perfusion to kidneys -liver failure - decreased albumin = edema -microemboli(DIC) block vessels and decrease blood flow to kidneys |
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SIRS |
systemic inflammatory response syndrome -inflammation = vasodilation |
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Fluid resuscitation for shock
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-hypovolemic -sepsis(corticosteroids) -anaphalaxis (epi and corticosteroids) -maybe neurogenic -may overwork the heart if HR is decreased and increase in fluids -vasocontricotrs and bolus may cause fluid overload |
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Neurogenic Shock |
SCI at T5 or above (T1-T5 supply heart and blood vessels with nerves) -SNS stimulation decreased *decreased BP and HR (only form of shock where BP and HR are decreased right away) |
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Anaphylactic shock |
Exposure to antigen -vasodilation -fluid moves to tissues -laryngeal edema and pulm edema (crackles) -bronchospasms (wheezes) |
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Septic Shock |
-infected blood -vasodilation |
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Stages of Shock |
1. Compensatory Stage -reversible stage -compensatory mechanisms effection -HR increased 2. Progressive Stage -compensatory mechanisms need more O2 - become ineffective -vital organ perfusion decreased -increased capillary permeability 3.Refractory Stage -vasoconstriction = decreased perfusion = anearobic metabolism |
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vasopressors for shock |
-peripheral vasoconstriction -shunt blood to core from extremities |
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Vasodilators for shock |
-decrease workload of heart = increase output |
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nitrates for shock |
dilate coronary arteries and systemicly |
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diuretics for shock |
-decreased preload |
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Beta blockers for shock |
-inhibit SNS -decrease HR and improve contractility |
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Definition of hepatitis |
inflammation of the liver |
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some causes of hepatitis |
- virus - bacteria - drugs - alcohol - chemicals |
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Etiology (set of causes) for types of Hepatitis
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Hep A: from orally consuming contaminated foods, water/other drinks, blood, stool & direct contact; overcrowding/poor hygiene & risk of contamination with fecal matter (acute: 2 month incubation period) - Hep B: Blood/bodily fluids; increased risk of liver cancer or being chronic - Hep C: Blood exposure; long-term liver damage without cancer, chronic |
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Signs & Symptoms of acute hepatitis |
- increased PT/INR
- Increased liver enzymes - anorexia - N/V - RUQ discomfort - fatigue - decreased albumin |
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unconjugated bilirubin |
- lysed RBCs produces this - cannot be renally excreted |
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conjugated bilirubin |
- by liver - may be renally excreted |
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What is an optimal diet for someone with acute hepatitis? |
- increased calories - increased carbs - decreased fat (d/t lack of bile) - decreased protein - decreased alcohol (ETOH) **Also encourage +++rest for patient with acute hepatitis** |
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How long until you will see detectable serum levels of hepatitis antigens & antibodies appear for diagnosis? |
2 month window period |
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How does the medication lamivudine help chronic hep B patients if its chronic? |
- with someone presenting with a decrease in liver enzymes (GGT; AST; ALI), this lamivudine decreased the viral load and also helps with decreasing liver damage |
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What meds are administered for chronic Hep C? |
A combination therapy of Ribavarin & Interferon |
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How does alcohol abuse lead to cirrhosis and a decrease in optimal liver functioning? |
-it leads to fat deposits in the lever cells (this is reversable if pt stops using alcohol; if continued used of alcohol, cell necrosis occurs causing scar formation). -this condition leads to disorganized regeneration and decreased blood flow (which may cause hypoxia). -all this leads to a decrease in liver function |
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Toxic hepatitis |
heads straight for cell necrosis, leading to disorganized regeneration and decreased blood flow, ending at a decrease in liver function |
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Chronic Hep B & C |
there is chronic inflammation which leads to necrosis & fibrosis, all equaling a decrease in liver function |
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Manifestations of Cirrhosis |
- due to a decreased metabolism of carbs, fats, and proteins, this leads to weight loss, decreased energy, increased serum levels of albumin and GI symtpoms (N/V, diarrhea, etc.) - the blood flow through the liver is backing up, causing a host of things to happen (portal HTN, liver & spleen enlargement - leading to RUQ pain & heavy feeling) |
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Splenomegaly |
- abnormal enlargement of spleen - usually associated with portal hypertension |
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What is the function of the liver? |
1. metabolism (breakdown of nutrients) 2. storage of nutrients (carbs/fats; protein turns into albumin which circulates in bloodstream) 3. detoxification 4. bile production (needed for absorption of fats in our foods) |
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What are the two separate blood supplies that the liver receives? |
1. Portal Venous System (provides liver with nutrient-rich blood from small intestines) 2. Proper Hepatic Artery (arterial blood supplying O2-rich blood) |
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What is the vessel that carries blood from the liver? |
Hepatic Vein - this blood is nutrient & oxygen-poor, so it will circulate back to the heart and lungs, and then through the small intestines to collect O2 & more nutrients |
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How does bile leave the liver? |
Through the common hepatic duct. |
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Portal HTN |
- pressure in the portal vein is abormally high, much higher than in the systemic system - usually resulting from liver disease - structural changes in liver d/t fibrosis & scarring |
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Esophageal Varises |
- created from the amount of blood/pressure of that blood being shunted through the systemic portal system instead of going through the portal system d/t back up in the liver. - the vein walls become stretched and thinned, causing varises. - may be irritated by ingestion of ETOH, ASA, coarse food - can be given beta blockers to decrease portal venous pressure (BP & HR) **discourage coughing! Administer cough meds!** |
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internal esphageal varises |
- very dangerous as these swollen vessels may eventually rupture and release a substantial amount of blood - this bleeding is not immediately apparent, since the blood is swallowed and passed in the stool. Treatment: - administer PRBCs, plasma, Vit K (monitor PT/INR) |
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What is the goal in treating chronic hep B & C with medication management? |
to decrease the viral load. |
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What is the risk for having a low hemaglobin in a patient diagnosed with cirrhosis? |
- anemia d/t altered metabolism and inadequate RBC formation (d/t liver disease); - at risk for complications associated with decrease O2 delivery to tissues |
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What is the risk for having a low platelet count in a patient diagnosed with cirrhosis? |
- platelets low, secondary to overactive, enlarged spleen (d/t liver failure); - at risk for bleeding |
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what the is the risk for having a higher INR count in a patient diagnosed with cirrhosis? |
- INR high secondary to decreased production in clotting factors (d/t liver failure) - bleeding risk |
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Which blood products would a patient receive if their Hgb is low, platelets are low, and INR is up? |
- PRBCs (to increase Hgb) - Platelets (to increase platelets) - FFP - fresh frozen plasma (to increase clotting factors) |
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Which complication of cirrhosis would be most likely to necessitate the implementation of a soft diet? |
esophageal varises (coarse food may cause life threatening esophageal bleeding) |
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A lab finding of a decreased albumin would most likely be linked to a patient (diagnosed with liver failure) with peripheral edema and ascites why? |
- decreased albumin means less oncotic pull in vessels and fluids move to tissues and abdomen (peripheral edema is caused by impaired albumin synthesis) |
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Why would a finding of decreased edema of the ankles and decreased abdominal girth be linked to a therapeutic benefit of a sodium restricted diet and an albumin transfusion? |
- a lowered sodium diet decreases H2O retention, thereby lessening hydrostatic push into tissues. - An albumin transfusion will draw fluid out of tissues and will keep fluid in the vessels. |
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A patient with ascites has returned from a parascentesis. What would a potential complication be of this procedure? |
- patient could present with light headedness and be drowsy, d/t too much fluid being drained too quickly, and suddenly decreasing pressure against walls of vessels (loses tone and BP drops) |
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albumin |
- large transport protein that helps move smaller molecules through the blood; - is synthesized by the liver - plays essential role in fluid balance (keeps fluids from leaking into tissues) **Remember: fluids will move from an area of lower concentration of solutes to an area of higher concentration of solutes.** |
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What is the goal of giving Lactulose to a patient with hepatic encephalopathy? |
- goal of 3-5 BMs/day (to rid the body of the build-up of ammonia via the GI tract) -monitor for decrease in K and fluids. |
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Ascites |
- Fluid in abdomen d/t portal HTN, lack of album in Treatment: - decrease Na in diet - albumin infusion - administer diuretics - parascentesis Nrg Responsibilities: - monitor serum K - monitor BP - daily weight - amount being drained - correct meal tray - albumin infusion (considered blood product), so monitor V/S and all considerations with blood products |
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S/S of hepatic encephalopathy |
- altered LOC - too much ammonia in the blood - +++confusion - decrease in LOO - neurological toxic signs & symptoms |
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What are some dignostic tests for cirrhosis? |
- liver enzymes (GGT; AST; ALT) - bilirubin - cholesterol - PT/INR - albumin |
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collaborative care for patient with cirrhosis |
- +++ rest (to decrease metabolic demands & increase cellular regeneration) - dietary requirements (d/t anorexia) - elevate edematous areas - monitor electolye/fluid balance - turn q2h to maintain skin integrity |
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Liver Cancer |
- Caused by Hep B or C, cirrhosis, high rate of heptatic blood flow Treatment: - palliative care similar to cirrhosis (+++ rest to decrease metabolic demands & increase cellular regeneration) |
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Pancreatitis |
- is a disease in which the pancreas becomes inflamed - Pancreatic damage happens when the digestive enzymes are activated before they are released into the small intestine and begin attacking the pancreas. - may be caused from ETOH, infection, drugs |
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S/S of pancreatitis |
- PAIN! - N/V - jaundice (if bile duct is obstructed) - LUQ pain, especially with eating - fever and increase in WBCs - hyperglycemia - decreased BP (d/t vasodilation) - shallow resps with crackles from pain (d/t inflammation of diaphram leading to atelectasis) |
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Treatment for pancreatitis |
NPO (to allow bowel rest to decrease enzyme release into small intestines) |
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What are the implications for the patient when the pancreas is removed? |
- diet modification (decrease in fats) - taking pancreatic enzymes with every meal - insulin dependent diabetic |
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What is the fundamental issue with shock? |
**decreased perfusion** **the need is to get oxygenated blood to the organs and tissues. |
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etiology of a burn |
1) A burn leads to increased vascular permiability, which leads to a decrease in intravascular volume, leading to increased hematocrit. This causes increased viscosity, increased peripheral resistence, ending in SHOCK. 2) A burn leads to increased vascular permiability, which leads to edema, a decrease in blood volume, leading to increased peripheral resistence, ending with SHOCK. |
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Why is H2O, Na, and albumin moving into the tissues from the blood vessels during the first 24-48hrs of a severe burn? |
- this is the period of acute inflammation - vessels are either damaged from the burn or highly permiable d/t the inflammatory process -H2O, Na, and albumin leak from vessels into the tissues (there is an increase in edema, a decrease in serum Na, and an increase in serum K) |
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What is the danger in having a circumferential burn? |
-compartment-like syndrome (d/t the constricting effects around the entire limb caused by the burn) -escharotomy will be performed by making an incision through the eschar to expose the fatty tissue below, releasing the pressure |
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What are the key features of the completion of the emergent phase of burn management? |
- establish perfusion (airway, circulation) - mobilization of ECF - re establishment of circulatory volume |
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What are the key features of the completion of the acute phase of burn management?
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- decrease perfusion (A-air is getting in; B-air is mixing with blood; C-blood is getting to vital organs) - completion of phase would be characterized by the acceptance of skin grafts |
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What are the key features of the completion of the rehab phase of burn management? |
- full body function (or what is expected to be fully mobilized) |
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How does the nurse know if a new skin graft is "adhering" successfully to the donor recipient? |
- is the colour of the graft flesh tone? Is it necrotic? - Are the edges well approximated? - Is there discharge at the edges? *Use the same principles you would for any wound. Don't remove any dressings unless there is a specific order to do so. |
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what are 3 psychosocial and/or spiritual needs of burn patient?
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1. To be able to talk about the traumatic experience that has happened to them 2. To know that there is a support system for them 3. Why has this happened to me? and other similar type questions |
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What type of solution is used for Fluid Resuscitation in burn patients? |
ringers lactate, Hartmann's solution and NS are used. |
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What type of medications will be used for a burn patient? |
-artificial tears -antidepressants/sedatives (to deal with anxiety) -opioids (IV analgesics) -topical antimicrobials (infused with silver) -IV antibiotics if sepsis occurs (but not for long term) -Tetanus (if not within 10 yrs) |
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What is an autograft vs. donor graft? |
Autograft: a graft of tissue from one point to another of the same individual's body; Donor graft: from a sibling, family member or tissue donation |
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What are the classifications of shock? |
1. Low Blood Flow 2. Maldistribution of Blood Flow |
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Low Blood Flow (for shock) |
happens d/t two types of shock: -cardiogenic shock (from heart failure) - hypovolemic shock (from anemia, dehydration, surgery) **Heart muscle is unable to pump the blood.** |
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Maldistribution of Blood Flow (for shock) |
happens d/t three types of shock: - septic shock (from UTI) - anaphylactic shock (from allergen/medication) - neurogenic shock (trauma to nervous system) **Lack of O2 systemically caused vasodilation to occur, leading to low HR and systemic vasodilation=pooling of blood, and decreased blood to the brain.** |
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Signs & Symptoms of cardiogenic shock |
- changes in LOC - confusion - cyanosis, pallor, cool/clammy skin - increased resps. - crackles - decreased BP, increased HR, narrowing pulse pressure - decreased bowel sounds, N/V - decreased GFR (increased Urea, creatinine, Na, decreased K) - decreased urine output - increased peripheral edema - chest pain (angina) |
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Neurogenic shock |
**Only type of shock that has bradycardia & low HR!** - a type of shock that results from peripheral vascular dilation. - occurs when the nervous system is no longer functioning properly d/t trauma (damaged or severed spinal cord). - the nervous system provides the blood vessels with tone, called sympathetic tone; this is disrupted by the trauma. |
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anaphylactic shock |
- a severe and sometimes fatal systemic allergic reaction to an allergen (drug;food;venum; chemical) - marked by resp distress & vascular collapse. |
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Signs & symptoms of anaphylactic shock |
-first symptoms are intense anxiety, weakness, feeling of impending doom - these are followed by pruritis and urticaria (itching & swelling) - other symptoms include: hypotension, shock, arrhythmias, resp congestion, edema of the glottis, N/V. **Treatment: Epinephrine first, then generally speaking, a bolus would be given.** |
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Cardiogenic shock |
- an abnormal condition often but not always characterized by a low cardiac output associated with acute MI and congestive heart failure **Therapy may include: diuretics, vasoactive drugs; be careful about giving extra fluids d/t cardiac issues you don't want the heart to be overloaded: don't be aggressive with bolus! |
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Hypovolemic Shock |
- a state of physical collapse caused by massive blood loss - may stem from GI blooding, internal or external hemorrhage or excessive reduction of intravascular plasma volume and body fluids. **Treatment would include: prompt replacement of blood (PRBCs, Platelets, FFP for coagulation factors), and fluid volumes (bolus), identification of bleeding sites (vomiting/internal or external trauma) & fluid loss sites (sweating/burns/vomiting) and control of bleeding.** |
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Signs & Symptoms of hypovolemic shock |
- low BP - thready pulse - clammy skin - tachycardia - rapid breathing - reduced urine output |
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Septic shock |
- a form of shock that occurs in septicemia when bacteria in the bloodstream release exotoxins - primarily caused by the increased diameter of blood vessels & increased permiability of the vessels (increased fluid in tissues) - these toxins cause vasodilation to occur, resulting in a dramatic fall of BP - low organ perfusion=low organ function - patient could go into ARDS |
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Signs & symptoms of Septic shock |
- fever - tachycardia - increased resps - confusion - coma - usually preceded with S/S of infection (often from GI/GU systems) **Treatment would include: 1)antibiotics & vasopressors; 2) IV fluids and volume expanders (but first you need to solve the vasodilation issue!); 3)corticosteroids to decrease inflammatory response |
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Sepsis |
decay or contamination caused from infection |
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systemic inflammatory response syndrome (SIRS) |
- is an inflammatory state affecting the whole body, frequently a response of the immune system to infection - It is the body's response to an infectious or noninfectious agent -your patient could present as hyperglycemic at first (because the body has large stores of glucose to use), then present as hypoglycemic later (as those stores have been used up). |
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multiple organ dysfunction syndrome (MODS) |
- also known as multiple organ failure, total organ failure or multisystem organ failure, is altered organ function in an acutely ill patient requiring medical intervention to achieve homeostasis
- is labelled MODS d/t >2organ failures/loss of homeostasis |
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Treatment for neurogenic shock |
- be very, very careful of giving IV fluids, because the parasympathetic system is happening - there is systemic vasodilation happening so fluids will leak into tissues: SOLVE VASODILATION ISSUE FIRST!! |
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What would some common lab results look like with septic shock? |
- increase OR decrease in WBCs - decreased platelets (d/t DIC) - Increased lactate (anerobic metabolism) - increased glucose (stress response) - increased urine specific gravity (concentrated d/t lack of fluid volume in urine) - decreased urine - increased serum Na & decreased serum K |
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Compensatory stage of shock |
- this stage is reversable - compensatory mechanisms are effective to maintain body homeostasis |
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Progressive stage of shock |
- compensatory mechanisms becoming ineffective - there is a decrease in vital organ perfusion - there is an increase in capillary permiability, leading to leakage of fluid & proteins into the interstium (++ edema) - DIC starts in this stage |
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Refractory stage of shock |
- vasoconstriction leads to decreased perfusion - decreased cardiac output - compensatory mechanisms not effective or not functioning any longer - Multiple organ dysfunction syndrome happening |
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What are two key problems with disseminated intravascular coagulation? |
1) there is profound embolic formation throughout the body, yeilding thrombic episodes 2) the usage of coagulation factors and platelets in forming microemboli now increases the bleeding risk (as PT/INR are elevated & platelets are decreased) |
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What is our main goals with a patient with shock? (3) |
1) halt the shock process! 2) restore circulation (BP) 3) correct pH imbalace |
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Explain the 3 causes for decreased GFR in SIRS |
1) Massive vasodilation 2) Liver Failure 3) DIC (micro-emboli can block renal vessels, causing decreased blood flow to kidneys) |
