Adult Health III Exam#3

what are the different forms of shock?

• hypovolemic

• cardiogenic

• distributive

• obstructive

What is a shock state?

• inadequate tissue perfusion—> derangements in cellular, metabolic, hemodynamic function

• imbalance between cellular oxygen supply and cellular oxygen demand

• decreased delivery of oxygen with decreased oxygen uptake in tissues

hypovolemic shock

• intravascular volume depletion

• ex: third-spacing, blood loss

Cardiogenic shock

• inadequate myocardial contractility

distributive shock

• inadequate vascular tone (vessels dilate)

• ex: anaphylactic, neurogenic (spinal cord injuries), septic

Obstructive shock

• blocked blood flow

• pulmonary embolism ect.

What are the different stages of shock

• initiation

• compensatory

• progressive

• refractory

initiation stage

• subclinical hypo perfusion

• inadequate extraction of oxygen

• usually no clinical signs indicating hypo perfusion

Physiological events

• decreased intravascular volume (hypovolemic)

• decreased myocardial contractility (cardiogenic)

• obstruction of blood flow (obstructive)

• decreased vascular tone (distributive)

• mediator release (sepsis)

• histamine release (anaphylactic)

• suppression of SNS (neurogenic)

Compensatory Stage

Neural compensation by SNS

• increased HR and contractility

• vasoconstriction

• redistribution of blood flow to essential organs

• bronchodilation

Endocrine compensation—> RAAS, ADH, glucocorticoid release

• renal reabsorption of sodium, chloride, and water

• vasoconstriction

• glycogenolysis and gluconeogenesis

• chemical compensation —> V/Q mismatching

Symptoms apparent in this stage!! (still reversible)

• increased heart rate (except in neurogenic shock)

• narrowed pulse pressure

• thirst

• cool, moist skin

• oliguria

• diminished bowel sounds

• restlessness progressing to confusion

• hyperglycemia

• increased urine specific gravity and decreased creatinine clearance

• rapid, deep respirations causing respiratory alkalosis

impulses relayed to medulla oblongata, SNS releases epinephrine and norepinephrine release (adrenal medulla)

Progressive Stage

• profound hypo perfusion

• shunting of blood to vital organs

• ischemia in extremities

• metabolic acidosis develops

• anaerobic metabolism with lactic acidosis

• failure of your sodium potassium pump

• cellular edema

• coronary artery perfusion is decreased

• classic S/S of shock

• poorly responsive to fluid replacement

• reversal requires aggressive interventions

S/S

• decreased BP with narrowed pulse pressure

• tachypnea

• cold, clammy skin

• decreased capillary refill

• mottling

• anuria

• absent bowel sounds

• lethargy progressing to coma

• hyperglycemia resistant to insulin

• increased BUN, creatinine, potassium

• respiratory and metabolic acidosis

Refractory Stage

• blood pools in capillaries

• BP is too low to perfuse vital organs

• severe tissue hypoxia with ischemia and necrosis

• worsening acidosis

• SIRS (widespread inflammation)

• multisystem organ dysfunction syndrome

S/S

• life-threatening dysrhythmias

• severe hypotension despite vasopressors

• respiratory and metabolic acidosis

• acute respiratory failure

• ARDS

• DIC

• hepatic dysfunction or failure

• AKI

• myocardial ischemia, infarction, or failure

• cerebral ischemia or infarction

Central Nervous System changes in shock

• most sensitive to changes in oxygen and nutrient supply

• usually, the first system that sees changes in cellular perfusion

• restless, agitatoin, and anxiety are typical first symptoms

• confusion, lethargy can develops as worsen

• ultimately becoming unresponsive

Cardiovascular System changes in shock

• BP essential assessment!

• compensatory phase: SNS stimulation increases myocardial contractility and vasoconstriction

• narrowing pulse pressures precede tachycardia

• close attention to OP meds—> may blunt response to shock beta-blockers)

Cardiovascular Assessment in shock

• volume status can be supported by jugular vein assessment ( distended or flat)

• capillary refill

• fluid responsiveness (i.e passive leg raise)

• pulmonary artery catheter (Swan Ganz catheter) may be beneficial in assessing fluid status

• mixed venous saturation (SvO2) reflects the difference between delivery and consumption of oxygen

• high SVO2= tissues not taking oxygen

• low SVO2= tissues needing more O2

Respiratory System Changes in shock

• early stage: breathing is rapid and deep

• goal is to decrease CO2 to change acidosis

• metabolic wastes increased as shock progresses leading to generalized muscle weakness, leading to shallow breathing and poor gas exchange

• interstitial. edema secondary to capillary leaking

• decreased peripheral circulation —> decreases the accuracy of the pulse ox monitor

• ABG analysis ensures accuracy of the laboratory data

Renal System changes in shock

• oliguria (UOP less than 0.5 mL/kg/hr

• RAAS is activated

• This causes Na+ and water retention and decreases the urine output because of hypotension

• acute tubular necrosis secondary to prolonged hypoperfusion

Gastrointestinal system changes in shock

• hypo perfusion decreases intestinal activity (decreased bowel sounds, increased gastric residual, distention, nausea, constipation

• paralytic ileus and ulceration develop (increased risk of GI bleeding secondary to prolonged hypoperfusion)
  hypoperfusion to the liver (elevated liver function, clotting factor production, drug toxicities develop, elevated ammonia and bilirubin

Hematologic changes in shock

• inflammation and coagulation enhances clotting and inhibits fibrinolysis

• increased microcirculatory system clotting and increased bleeding

• consumptive process for platelets and clotting factors

• liver fails to manufacture clotting factors

• Patient can have PE’s

What are the signs and symptoms of a Pulmonary Embolism

• petechiae

• ecchymosis

• hematuria

• melena/hematochezia

• hemoptysis

Disseminated Intervascular Coagulopathy (DIC)

• elevated D-dimer

• Platelets decreased

• used up clotting factors

• fibrin spilt to increased breakdown of existing clots

• micro clots lead to PE, CVAA, and /or bowel infarct

• nursing actions: limit venous sticks, watch for bleeding, transfusion administrations, level of consciousness and orientation for cerebral bleeds

Integumentary System changes in shock

• assess: color, temp., texture, turgor, moisture level

• observe for cyanosis (usually late)

• decreased elasticity in older adults may be unreliable

• mottling

Normal Lactate

• 0.6-2.2

• measure within an hour of presentation

Normal hematocrit

• female: 37-47%

• male: 42-52%

Management of shock

• identify source

• volume replacement, increased contractility (inotropic medications), remove source of shock (tamponade compression, clots, PTX, drug)

• ventilation and oxygenation and O2 support as needed

• prevent infection in the first place

What is the treatment for hypovolemic shock

• hypotonic: 0.45% NS—> can leave vessels rapidly causing interstitial and intracellular edema

• hypertonic: 3% saline to pull fluid from interstitial to vascular space

• colloid: albumin, hetastareh

• isotonic: NS, LR, plasmanate

• blood and blood products

What is the treatment for Obstructive Shock

• eliminate source of obstruction or compression

• pericardiocentesis for cardiac tamponade

• fibrinolytic, anticoagulants for PE

• emergency decompression for tension pneumothorax

Neurogenic shock treatments

• eliminate and treat the cause

• maintain MAP

• maintain adequate heart rate

• VTE prophylaxis

Septic shock treatments

• obtain blood cultures

• administer abx within 1 hr of diagnosis

• obtain lactate level

• administer fluid bolus

• administer vasopressors is systolic less than 90 or map less than 65

• good hand-washing techniques

• avoid invasive procedures

• oral and airway care

• initiate and maintain enteral nutrition

What are the functions of the pancreas?

• endocrine—> islets of langerhans produce insulin, glucagon, and somatostatin

• exocrine—> acinar fcells produce pancreatic enzymes (lipase—> more specific + amylase)

What is Acute Pancreatitis

• inflammatory process that delays the release of enzymes allowing then to “attack” pancreatic cells and leak into surrounding tissue

• also known as “autodigestion”

Edematous Pancreatitis

causes fluid accumulation and swelling'; usually mild and self-limiting

Necrotizing pancreatitis

more severe, causes cell death and tissue damage; involves serious complications

• pancreas starts dying

Describe the inflammatory process of Pancreatitis

• build up of pancreatic enzymes

• cytokine storm creating vasodilation and leaky capillaries

• platelet-activating factor multi-organ failure; release of histamine

Ranson’s Criteria

At admission

• Age> 65

• WBC > 16

• Glu > 200

• AST > 250

• LDH > 350 —> marker of anaerobic metabolism

At 48 hours out

• Ca < 8

• HCT fall > 10%
  PO2 < 60

• BUN increases > 5

• Base deficit (low bicarb) > 4

• sequestration of fluids > 6L

What is the mortality chart related to Ranson’s Criteria for Pancreatitis

• 0-2 = 2%

• 3-4 = 15%

• 5-6 = 40%

• 7-8 = 100%

Causes of acute Pancreatitis

• alcohol consumption

• Biliary disease—> common bile duct obstruction, ERCP procedure, gallstones

• heredity

• hypercalcemia

• hypertriglyceridemia

• idopathic

• infections

Medications

• azathioprine—> immune suppressant

• corticosteroids

• estrogen

• furosemide

• octreotide —> treat GI bleeds

• pentamidine—> prevents pneumocystic pneumonia

• sulfonamides

• thiazide diretics

tramatic injusry

tumors of pancreatic duct

why can high triglycerides cause pancreatitis?

• When levels exceed 1000 mg/dL, lipase binds triglycerides to albumin

• pancreas releases extra triglycerides as free fatty acids which damages acinar cells

• High triglycerides cause red blood cells to become sluggish in circulation; capillaries plug up leading to stasis of blood flow and endothelial damage

How does various infectious agents cause pancreatitis?

pathogens trigger trypisongen to become active in the pancreas instead of the duodenum resulting in autodigestion

Systemic complications of Pancreatitis

Cardiovascular

• cardiac dysrhythmias

• hypovolemic shock

• myocardial depression

Metabolic

• hyperglycemia

• hyperlipidemia

• hypocalcemia

• metabolic acidosis

Gastrointestinal

• GI bleeding

• abscess

• pseudocyst

Hematologic

• coagulation abnormalities

• disseminated intravascular coagulation

Pulmonary

• Acute respiratory distress syndrome (ARDS)

• atelectasis, pneumonia, pleural effusion

• hypoxemia

Renal

• acute renal failure

• azotemia

• oliguria

What laboratory data would indicate pancreatitis to the nurse?

• decreased albumin

• alkaline phosphate increased with biliary disease

• increased bilirubin, AST, LDH

• decreased calcium

• increased glucose

• increased hematocrit with dehydration and decreased hematocrit with hemorrhagic pancreatitis

• decreased potassium

• increased serum and urine amylase

• increased serum lipase

• increase WBC count

What are S/S of pancreatitis

• Severe nausea and vomiting

• Upper abdominal pain

• abrupt onset

• pain in the periumbilical area (knawing epigastric pain)

• abdominal distention and rigidity

• hypoactive bowel sounds

• tachycardia

• tachypnea

• hypotension

What signs would be seen with hemorrhagic pancreatitis

• Cullen sign

• Grey Turner sign

Treatment for Pancreatitis

• NPO and NG tube

• strict I&O

• replace fluids and electrolytes

• monitor for hypocalcemia, hypomagnesemia, hypokalemia

• relieve pain with opioids (NO MORPHINE)

• give TPN with NO LIPIDS through central line

• Lopid (gemfibrozil)

• Imipenem-cilastin (Primaxin)

What are the side effects of Lopid (gemfibrozil)

• elevated liver enzymes

• myalgia

• rhabdomyolysis

What does Imipenem-cilastin (primaxin) do to help with pancreatitis?

diffuses into pancreatic tissue giving best chance of killing any invading bacteria

Peptic Ulcer Disease risk factors

• smoking—> stimulates acid secretion

• Helicobacter pylori infection

• NSAIDS

• alcohol consumption

Causes of upper GI bleeds

• duodenal ulcer

• gastric ulcer

• esophageal or gastric varices

• Mallory-Weiss tear

Causes of Lower GI bleeds

• polyps

• inflammatory disease

• Diverticulosis

• cancer

• vascular ectasias

• hemorrhoids

S/S of upper GI bleeding

• Hematemesis

• Melena

• Hematochezia

• abdominal discomfort

• signs and symptoms of hypovolemic shock

GI bleed laboratory data

• decreased H/H

• increased WBC

• decreased platelet count

• K+ decreased then increased

• decreased Na+

• BUN and Creatinine increased

• hyperglycemia

• increased lactate

• increased prothrombin time

• respiratory alkalosis

• metabolic acidosis

GIB treatment

• colloids, crystalloids, blood or blood products

• gastric

• antacids

• H2-histamine blockers

• PPI

• mucosal barrier enhancers—> sucralfate

What kind of ulcer is nocturnal pain common?

duodenal ulcer

What kind of ulcer hold a food-pain pattern

gastric ulcer

List the functions of the Liver

• blood storage

• blood filtration

• production of bile

• conjugation of bilirubin

• carb metabolism

• fat metabolism and storage

• protein metabolism

• synthesis of prothrombin, fibrinogen, factors VII, IX, and X

• removal of activated clotting factors

• detoxification of drugs, hormones, and other substances

S/S of Acute Liver Failure

• hyperexcitability

• insomnia

• irritability

• lethargy

• decreased LOC, coma

• convulsions

• sudden onset of high fever

• N/V

• chills

• jaundice

Lab Alterations in Liver Failure

• increased albumin

• increased ammonia

• increased cholesterol

• prolonged prothrombin and partial thromboplastin time

• increased APT, AST, ALT

• increased bilirubin

What percentage of damage to the parenchyme must take place before liver function tests are elevated?

70%

What is the msot specific indicator of hepatocellular damage?

ALT

Normal ammonia levels

35-65

What is ammonia?

byproduct of protein metabolism

what is the relationship between ammonia and BUN levels

as ammonia levels rise, BUN levels will drop

Lactulose

• MOA: increases H2O content and softens stool; lowers pH of colon which inhibits diffusion of ammonia from colon into blood= lowers ammonia levels

• Adverse effects- belching, cramps, flatulence, diarrhea

• should not be used with other laxatives

• monitor NH4 levels, BG levels

• give on empty stomach; administer with 8 oz of juice or water

What is a normal bilirubin

0.5 mg/dL

What bilirubin would indicate significant liver failure?

15-20 mg

What is bilirubin

from the breakdown of hemoglobin; fat soluble and binds to albumin for transport to liver

What is the relationship between the liver and bilirubin

conjugates bilirubin making it water soluble soo it can be excreted by the kidney and in bile

Why might someone have an increased “conjugated” or Direct bilirubin

due to a blockage in he hepatic duct, bile duct, or collecting channels of liver

Why might someone have an increased “unconjugated” or indirect bilirubin?

liver no longer able to function and can no longer change “fat soluble” form of bilirubin into a “water-soluble” form

What is the pathophysiology behind Ascites?

• increased pressure in the Liver causes an increased resistance to blood flow; liver is less able to detoxify and transport nutrients

• as blood flow decreases through liver ; less protein is filtered by liver into the lymphatic system

• increased protein causes protein to “sweat” through the liver into the peritoneal cavity

• intravascular protein diminishes severely and abdomen becomes distended

Hepatic Encephalopathy

• subtle behavioral abnormalities

• marked stupor and confusion

• deep coma and death

• rigidity

• hyperreflexia

• asterixis—> nonrhythmic, rapid extension-flexion movements of the head and extremities, best seen when the arms are held in extension with dorsiflexion of the wrists

Laënnec’s Cirrhosis

• long-term alcohol abuse

• fatty liver; fibrotic tissue replaces liver cells

• Acetaldehyde (toxic metabolite of alcohol ingestion) causes liver cell damage and death

Biliary Cirrhosis

• long-term obstruction of bile ducts

• decrease in bile flow

• degeneration and fibrosis of the ducts

Cardiac Cirrhosis

• Severe long-term right-sided heart failure

• decreased oxygenation of liver cells

• cellular death

Postnecrotic Cirrhosis

• exposure to hepatotoxins or chemicals, infection, or metabolic disorder

• massive death of liver cells

• development of liver cancer

Patho and effects of Portal Hypertension

• fibrosis and scarring lead to distorted vessels in liver

• causes blood flow through liver to be impaired

• venous blood from GI tract has nowhere to go

• this causes a back-up into a low pressure system which results in esophageal varices

• Veins will eventually rupture that can lead to GI bleeding

Common Hepatotoxic drugs

• Acetaminophen (Tylenol)

• Salicylates (aspirin)

• Enflurane (Ethrane)

• Halothane (Fluothane)

• Methoxyflurance (Penthrane)

• Phenytoin (Dilantin)

• Phenobarbital (Luminal)

• MAOIs

• Amitriptyline (Elavil)

• Doxepin (Sinequan)

• Isoniazid

• Nitrofurantoin (Macrodantin)

• Rifampin

• Sulfonamides

• Tetracycline

• haloperidol (Haldol)

• Chlorpromazine (Theorazine)

• Fluphenazine (Prolixin)

• Prochlorperazine (Compazine)

• Promethazine (Phenergan)

• Thioridazine (Mellaril)

• antithyroid drugs

• contraceptives

• oral hypoglycemics

• Cimetidine

• valium

• librium

Nursing Management of Liver Failure

• monitor ammonia levels and conduct ongoing neurological assessment

• administer lactulose and neomycin, and monitor results

• restrict protein intake

• reduce the risk of GI bleeding through antacid and H2-blockers

• use sedatives and narcotics sparingly

• prevent and treat infection, dehydration, electrolyte and acid-base disturbances

• reorient the client and provide safety during periods of impaired mentation

Dobhoff Tube

• weighted placed in the duodenum

PEG Tube

percutaneous endoscopic gastrostomy

What are exclusions to enteral nutrition?

• bowel obstruction

• hemodynamically unstable

• GI bleeding

• bowel ischemia

• intraabdominal HTN

When can enteral nutrition be started?

24-48 hours after admission

Enteral feeding nursing considerations

• elevate HOB to 30 degrees

• do not crush sustained release meds

• flush tube if feedings are on hold

• stop feeding if intolerant (abd. distention, constipation, N/V)

• reduce complication associated with narcotics and sedatives

• flush tube with 30 mls before and after meds

• for elderly: physiologic stress increases caloric need to 35 kcal/kg/day

Jevity and Isosource

• fiber containing, average osmolality

• given to patient with minimal or no cormobidities

Osmolite

• no fiber; low osmolality

• given to surgical patient with GI conditions

Pivot

• partially hydrolyzed protein

• given to patient with the following: SIRS, ARDS,

• improves protein absorption

Glucerna

• low carb content; higher protein

• improves glucose control for diabetics or patient with hyperglycemia

Nepro

• lower in sodium, phosphorus and potassium

• high and low protein formulations available

• carb controlled

• used for: CKD patients or ESRD

• high protein for dialysis; low protein for non dialysis patients

Insoluble fiber

• added to provide prebiotics and add bulk to stool!

Arginine/glutamine

added to promote wound and pressure injury healing

Parenteral Nutrition

• form of nutrition that supplies protein, fat, minerals, electrolytes, and carbohydrates

• used when EN is contraindicated

• dedicated line without mixing with other drugs

• increased risk of hyperglycemia

• increased risk of infection/sepsis

• fluid and electrolyte imbalances

Lipids

• fatty acids

• monitor triglyceride levels

• watch for lipid emulsifiers (propofol)

• monitor electrolytes

• high risk for refeeding syndrome

What is the most sensitive indicator of protein synthesis and catabolism

• prealbumin

• 15-36 mg/dL

RAAS

• triggered by hypovolemia/ renal ischemia or decreased sodium ion concentration of blood

• renin production by specialized cells in the juxtaglomerular apparatus of the kidney

• renin + angiotensin (produced by liver)

• angiotensin I

• Angiotension I + cconverting enzyme in the lungs

• angiotensin II

causes:

• peripheral vasconscrition

• aldosterone release from adrenal glands (sodium and water reabsorption)

• all leads to increased blood pressure

Prerenal AKI

• intravascular volume depletion

• vasodilation

• decreased cardiac output

• medications that impair autoregulation and glomerular filtrate

Intrinsic/Intrarenal AKI

• ischemia

• azotemia

• hypotension

• hypovolemia

• obstetric complications

• contrast dye

• transfusion reaction

• tumor lysis syndrome

• rhabdomyolysis

• preexisting renal impairment

• DM

• hypertension

• volume depletion

• severe heart failure

• advanced age

Post-renal AKI

• benign prostatic hypertrophy

• blood clots

• renal stones or crystals

• tumors

• postoperative edema

• medications

• tricyclic antidepressants

• ganglionic blocking agents

• foley catheter obstruction

• ligation of ureter during surgery

Nephrotoxic Drugs

• aminoglycosides

• amphotericin B

• Acyclovir

• ACE inhibitors

• AARBs

• adefovir

• cephalosporins

• cyclosporine

• cisplatin

• daptomycin

• fluroouracil

• fluoroquinolones

• famotidine

• interferon

• indinavir

• methotrexate

• NSAIDs

• penicillins

• rifampin

• ritonavir

• tacrolimus

• vancomycin

Stage 1 Renal Disease

• 130 mls/min

• screen for risk factors: HTN, diabetes, obesity

Stage 2 renal disease

• 90 mls/min

• CKD risk factor reduction

• lower BP

• control diabetes

• wt. loss

Stage 3 renal disease

• 60 mls/min

• treat complications of CKD

• uraemia

• manage anemia

• prevent malnutrition