Exam 2 Complex

Pneumothorax

-Collapsed lung -Collection of air in the pleural space -Pleural space is exposed to positive pressure (normally negative) Types: •Open Pneumothorax •Closed Pneumothorax •Simple Pneumothorax •Traumatic Pneumothorax •Tension Pneumothorax •Spontaneous Pneumothorax (Primary or Secondary) Simple pnemothorax: •Closed •Clinically stable •Idiopathic •Can evolve into a tension pneumothorax Spontaneous Traumatic pneumothorax: •Open, sucking chest wound •Trauma •Iatrogenic - caused by medical procedure (Central Line) •Penetrating chest or abdominal wound •Stab/gunshot wounds •Scuba diving Primary (spontaneous): •Mostly asymptomatic •Tall, thin, males in their 20's •Idiopathic •If stable f/u with X-Ray in 48 hours •Will likely reoccur withing 2 years Secondary (spontaneous): •Complication of lung disease •COPD, Emphysema, Cystic Fibrosis, Lung Cancer, infection •>50 years of age •Men >Women Bleb rupture Tension: •Air in the pleural space builds up enough pressure to interfere with venous return to the heart •Medical Emergency •Rapid progression to: Shock (cardiogenic), Cardiac Tamponade (squishing of the heart), Cardiac Arrest •Cardiovascular collapse •Must have EMERGENT needle decompression Diagnostic: •CXR •If tension pneumo - skip the x-ray and get straight to the needle decompression •CT Scan/Ultrasound •EGK/ECHO •CBC, Cardiac Troponins •ABG Medical managment: •Depends on the type of Pneumo & Stability of the Patient •Oxygen Therapy -> Mechanical Ventilation if needed •Needle Decompression (tension) •Chest Tube •Treat underlying lung disease Nursing care: Dx: •Acute Pain •Ineffective breathing pattern •Ineffective peripheral tissue perfusion •Anxiety Interventions: •Administer pain medications •Incentive Spirometry, administer oxygen, elevate bed semi-fowlers •Assess vital signs, encourage turning every 2 hours •Reassure patient

What is sepsis

-Consequence of dysregulated inflammatory response to infection. -Infection->bacteremia->sepsis->septic shock->multiple organ dysfunction syndrome->death -All patients with bacteremia and or infection is at risk for developing sepsis.

Diagnostics sepsis

-Cultures: blood, wound, urine (within 1hr, Asap from two different sites) -WBC -Hemoglobin, hematocrit -Platelets -Coags: PT/INR,aPTT -Procalcitonin, CRP, Lactic Acid -BUN, creatinine -Serum albumin -ABG's - acidosis

Gerontologic considerations for septic shock

-Decreased physiologic reserves -Aging immune system -Comorbid conditions -Nonspecific presentation of infection (Older immune system doesn't respond like younger) -Increasingly older population

Early Warning Scoring System

-Designed to identify early signs of sepsis -Used as a predictive tool to warn providers - not a diagnostic tool -Contains 6 simple physiologic parameters: -Respiratory Rate -Oxygen Saturation -Systolic Blood Pressure -Pulse Rate -Level of Consciousness or New Confusion -Temperature -Scores = (0-4 low risk; 5-6 medium risk; 7 or more high risk) -Early Recognition and a quick response is the key to survival

Surviving Sepsis Campaign (Septic shock)

-Early recognition and intervention are essential for the survival of patients with this syndrome. -Surviving Sepsis Campaign (SSC) to reduce overall patient morbidity and mortality from sepsis and septic shock by driving practice initiatives based on current best evidence. -The new guidelines have increased the focus On early identification of infection, risks for sepsis and septic shock, rapid antibiotic administration, and aggressive fluid resuscitation to restore tissue perfusion.

Septic shock (Cold stage)

-Elevated SVR -Low CO -Hypotension -Cold, clammy, mottled skin -Hypothermia -Hypermetabolism glucose & insulin resistance -GI failure -Urine Production Ceases -Multiple Organ Failure

Medical treatment (septic shock)

-Fluid Replacement Therapy (aggressive fluid resuscitation) Pharmacologic Therapy: -Vasopressor agents, specifically norepinephrine or dopamine - Antibiotic broad spectrum within one hour of diagnosis - Sedation - reduce metabolic demands, provide comfort - Deep vein thrombosis prophylaxis (low molecular weight heparin, lovenox) -PUD prophylaxis (pantoprazole) Nutritional Therapy: -Initiated within 24 to 48 hours of ICU admission -Malnutrition further impairs the patient's resistance to infection -Enteral over Parenteral (MAP needs to be greater than 65 if not give NE and if still not given than give dopamin

Fluid and Blood Replacement (Hypovolemic shock)

-Fluid placement is the primary concern -2 large bore IV's •IF PIV not assessable insert intraosseous -Simultaneous administration of fluid, medications, and blood component therapy

Never do this for cardiogenic shock

-Give a fluid bolus, because rapid fluid administration in patients with cardiac failure may result in acute pulmonary edema.

Nutriton AKI

-High carb meals initially -Restrict foods containing high amounts of K+ and phosphorus (bananas, citrus fruits and juices, coffee) -After the diuresis phase diet changed to High-Protien, High- Calorie Diet

Electrolyte abnormalities in AKI

-Hyperkalemia, hyperphosphatemia, hypocalcemia, anf hypinatremia

Signs and Symptoms of Shock

-Hypotension, weak thready pulse -Tachycardia - Confusion, Disorientation -Cool clammy skin or red, flushed skin -Polyuria (Some times) -Oliguria (All the time)

Etiology of AKI

-Hypovolemia -Hypotension -Decreased cardiac output and CHF -Obstruction of the kidney/ lower urinary tract. (tumor, blood, clot, and kidney stone) -Bilateral obstruction of the renal arteries or veins.

Medical care cardiogenic shock

-Identify underlying cause and correct it Initiation of first-line treatment : -Oxygenation -Pain control (Morphine helps with oxygen and pain) -Hemodynamic monitoring (CVP, PA line, swan, ballon pump, and arterial line) -Laboratory marker monitoring -Fluid therapy

Phases of AKI

-Initiation (Initial insult, end when oliguria develops) -Oliguria (increase in serum contractions of substance usually excreted by the kidney (urea, create, uric acids, intraxellular ions K ans mg) minimum amount of urine needed to clear the body within 24 hours is 400 ml -Diuresis (gradual increase in urine output, GFR getting better- watch fro dehydration) -Recovery (Improvement of renal function takes 3-12 months; lab values return to normal)

Hyperkalemia AKI

-Intracellular -Greater than 5.0 = EKG changes (tall, tented, or peaked T-waves) -Life threating -Can lead to deadly arrhythmias (V-Tach) -S/sx: irritability, abdominal cramping, diarrhea, paresthesia (numbness/ tingling extremities), generalized muscle weakness Treament: -Kayexalate (flushes K+ (dirrhea) (exchanging sodium ions for potassium ions in the intestinal tract) -Sorbitol- may be given with Kayexalate to induce diarrhea (increase water into the colon) -If hemodynamically unstable (hypotensive, changes in mental status, dysrhythmias) IV dextrose 50%, insulin (shift K+ into the cell), Calcium causes K+ to shift into the cell reducing serum potassium

Risk factors for sepsis

-Invasive procedures -Indwelling medical devices -Emergent and/or multiple surgeries -Intensive care unit admission > nosocomial infection -Bacteremia + blood cultures, 95% develop sepsis or septic shock -Community acquired pneumonia -Previous hospitalizations -Antibiotic-resistant microorganisms

Lab and diagnostic test for cardiogenic shock

-Labs (CBC, CMP, Cardiac enzymes, BNP (Raised level associated with CHF) -Echo (Priority) -EKG (Priority) -ABG (Metabolic acidosis) -Chest xray

Diagnosis of AKI

-Labs (electrolytes, serum creatinine, BUN, GFRm CBC, serum phosphorus, and calcium) -Urine (sodium, sediment, osmolality, and specific gravity) -Ultrasonography -ABG (metabolic acidosis) -EKG (dysrhythmias)

Diagnostic Abnormalities seen in Sepsis

-Leukocytosis >12,000 or -Leukopenia <4000 -Normal WBC -Hyperglycemia >140 (Immune system response) -Plasma CRP > 2x normal -Hypoxemia (No perfusion to the cell) -Acute Oliguria Elevated Creatinine •Coagulation abnormalities -INR>1.5, aPTT>60 seconds -Thrombocytopenia <100,000 -Hyperbilirubinemia -Adrenal Insufficiency -Hyponatremia, Hyperkalemia -Elevated serum lactate >2 (Bacteria nitirc oxide. Nitrate oxide make lactic go up) -Procalcitonin 2 x normal value

Pharmacologic Therapies hypovolemic shock

-Medications are given to reverse cause of intravascular depletion -Vomiting = antiemetics -Diarrhea = antidiarrheals -Hyperglycemia = insulin -Diabetes Insipidus = desmopressin

Complications of AKI

-Metabolic Acidosis (Cant excrete hydrogen ions) -Fluid and electrolytes imbalances (Hyperphosphatemia and hypocalcemia (kidney no longer produces calcitriol; reducing calcium absorption from the gastrointestinal tract ) -Hyperkalemia (LIFE THREATENING) -Increased catabolism -Chronic Kidney Disease

Caution hypovolemic shock

-Monitor for s/sx of volume overload - rales, crackles, dyspnea, hypoxia -Transfusion reaction with blood products

Nursing care cardiogenic shock

-Monitor vital signs, oxygenation, cardiac rhythm, urine output, LOC, skin -Monitor EKG -Have resuscitation medications and equipment readily available -Explain all procedures or patients - the patient may be anxious and scared

Prerenal AKI

-Most common - Caused by reduced blood flow to the kidneys -Decreased perfusion (Reversible once renal perfusion is stored) -Leads to decreased GFR (Glomerular Filtration Rate) - Reversible- treated with volume replaces, restoration of perfusion to the kidneys (IVF, blood products, colloids) -No damage to the kidney itself -Pre-renal kidney injury above the kidney. Patho: -Decreased blood flow to the kidneys -Kidneys sense that it is volume deficient -Kidneys reabsorb Na+ -H2O follows Na+ -This results in dilution hyponatremia and decreased urine output Causes of decreased perfusion: -Volume depletion (GI losses, vomiting, diarrhea, nasogastric suction, hemorrhage, renal losses (diuretic, osmotic diuresis) -Impaired cardiac efficiency (cariogenic shock, HF, and MI) -Vasodilation (Anaphylaxis, antihypertensive medications or vasodilators, and sepsis) Labs: -Serum creatinine (Slow rise) -Urine osmolality (High) (More consintuated (dehydration state) - Urine volume (due to increase in both sodium and water reabsorption) -Fractional excretion of sodium (FENa) (Less than 1% = Na retention) -UA- normal may see hyaline cast -RESPONSE TO FLUID REPLETION (GOLD STANDARD)- serum creatinine will return to baseline within 24-72 hrs

Mechanism of chest trauma

-Most common cause = Motor Vehicle Accident (MVA) -Acceleration/Deceleration (Type of chest trauma) -Blunt force trauma (chest hitting something) -Penetrating trauma - gunshot, knife wound

Hypovolemic Shock

-Most common type of shock -Occurs when there is a 15-30% loss of intravascular blood volume (750-1500 mL) -Decrease in preload = decrease cardiac output = decrease perfusion & oxygenation = cellular death -The decrease in preload impairs cardiac output which ultimately leads to inadequate delivery of oxygen and nutrients to the tissues and organs (shock).

Vasopressors (septic shock)

-Norepinephrine remains the initial guideline recommended vasopressor for patients in whom hypotension persists after adequate fluid resuscitation -If norepinephrine alone does not maintain adequate blood pressure and tissue perfusion, vasopressin is used as a secondary agent. -Norepinephrine may lead to higher incidences of AKI than vasopressin

Postrenal AKI (obstruction)

-Obstruction distal to the kidneys (BPH and kidney stones) -Leads to backflow of urine into the kidneys= hydronephrosis -Reversed by removal of obstrucion Causes: -BPH -Blood clots -Kidney stone -Strictures -Tumors Gerontologic considerations: - >50% of hospitalized patient are >60 years of age -Prone to dehydration, decreased thirst, decreased mobility -Polypharmacy- nephrotoxic agents

Desired outcome of chest trauma

-Optimize oxygenation and gas exchange -Promote full lung expansion -Prevent complications

Nursing care hypovolemic shock

-Place patient in Trendelenburg -Increases venous return to the heart -Oxygen

Categories of AKI

-Pre-renal (hypo-perfusion) -Internal (actual damage to the kidney itself) -Post-renal (obstruction)

AKI

-Rapid loss of renal function due to damage of the kidneys. -Widespread and very common (Can occur over days or weeks) -50% or greater increase in serum creatinine above (<1mg/dL) -Accumulation of nitrogen broods in the blood = azotemia

Overview (pre- hypovolemic shock info)

-Remember: Heart Rate x Stroke Volume (preload, afterload, contractility) = Cardiac Output. -When preload is decreased, there are three compensatory mechanisms that can be possibly altered. The three compensatory mechanisms are increased HR, increased afterload, and/or increased contractility. -If compensatory mechanisms fail and hypotensive shock develops, the chances of survival and recovery are significantly decreased. -Oxygen delivery to vital organs is unable to meet oxygen demand. -Cells switch from aerobic metabolism to anaerobic metabolism, resulting in lactic acidosis -pAs sympathetic drive increases, blood flow is diverted from other organs to preserve blood flow to the heart and brain - peripheral tissue necrosis

Internal AKI (Damage to the kidney itself)

-Actual damage to filtration systems of the kidneys its self. -Can be caused by untreated prerenal AKI -Acute Tubular Necrosis (ATN) is the most common and can develop secondary to prolonged or untreated pre-renal disease -Decreased GFR, progressive azotemia (build up of nitrogen levels), fluid and electrolyte imbalances. -Kidney Biopsy is needed to confirm diagnosis Causes: -Prolonged renal ischemia (Transfusion reaction, hemolytic anemia, rhabdomylosis (tramua, crush injuries, burns) Lack of blood flow) -Nephrotoxic agents (amino-glycosides, ACE inhibitors, heavy metal, NSAIDS, IV dye) -Infectious process (Acute glomerulonephritis or pyelonephritis) Labs: - UA- muddy brown casts (due to damaged kidneys) or renal tubular epithelial cells -Fractional excretion of sodium (FENa)- 2 percent or greater -Serum creatinine (Progressive rise daily) -Urine osmolarities (will almost always be low) -Urine volume- may be oliguric/ nonoliguric

Hemorrhage (hypovolemic shock)

-Administer blood products -Hemoglobin to assist with oxygen transport -Reverse coagulopathy (platelets or plasma may be given)

Stroke volume

-Amount of blood pumped by the left ventricle with each beat, 50-100 ml, determined by 3 factors: preload, afterload, and contractility increase stroke volume increase cardiac output

Cardiac Output (CO)

-Amount of blood the heart pumps per minute, 4-8 liters per min, determined by HR x stroke volume

Clinical presentation and assessment of cardiogenic shock

-Angina -Tachycardia -Fatigue -Express feelings of doom -Hypotension -Distend neck vein -Diminshed pulse -Peripheral edema -Dyspne

Sympathetic Nervous System (hypovolemic shock)

-Antidiuretic Hormone -(vasopressin) released by the posterior pituitary reabsorbs water (in response to an increase in blood osmolarity) -Aldosterone - adrenal cortex - reabsorbs sodium -increases water volume intravascularly -Catecholamines- adrenal gland - norepinephrine, epinephrine

Common causes of sepsis

-Bloodstream (bacteremia) -Lungs (pneumonia) -Kidneys (urosepsis) -Bacteria -Fungi -Virus -Nosocomial infection have a greater mortality rate than community acquired infections.

Physiology/pathophysiology of cardiogenic shock

-Cardiac output is compromised -Blood supply for tissues and organs is inadequate resulting in impaired tissue perfusion.

Renin-angiotension aldosterone system

-Renal blood flow reduced -> juxtaglomerular cells in the kidneys convert prorenin into renin ->plasma renin carries out the conversion of angiotensinogen (released by the liver) to Angiotension I -> Angiotension 1 is converted into Angiotension II by the angiotension-converting enzyme. Angiotension II is a POWERFUL vasoconstrictor -> Angiotension II stimulates aldosterone to be released from the adrenal cortex which causes the reabsorption of sodium thus increasing reabsorption of water in the blood.

Systemic Inflammatory Response Syndrome (SIRS) (Sepsis)

-Results from a clinical insult that initiates a systemic inflammatory response -Can be provoked for many reasons: trauma, infection -Interrupts the coagulation system which results in clots forming even though there is no bleeding or injury. -This results in microvascular occlusions that disrupt cellular perfusion and inappropriate consumption of clotting factors. -The imbalance of inflammatory response and clotting and fibrinolysis cascades are critical elements of the devastating physiologic progression in patient's with sepsis.

Septic shock (warm stage (early)

-SVR decreased d/t peripheral vasodilation -CO increase -Tachycardia -Tachypnea -Confusion -Normal BP -> if low responds to fluids

Medical priorities septic shock

-Secure the airway - intubation, mechanical ventilation -Oxygen administration -IV access- central line -Early administration of IVF (Use isotonic crystalloid NS) -Broad Spectrum antibiotics within one hour (Zosion) -Hemodynamic monitoring - arterial line, central venous pressure monitor -Blood pressure support with vasopressors -ICU admission -Tight control of blood glucose <180mg/dl (insulin gtt)

What is septic shock?

-Septic Shock is a type of vasodilatory or distributive shock. -Defined as sepsis that has circulatory, cellular, and metabolic abnormalities that are associated with a greater risk or mortality than sepsis alone. -Tissue Hypoperfusion and Organ Dysfunction -Clinically, these patients fulfill the criteria for sepsis, who despite adequate fluid resuscitation, require vasopressors to maintain a mean arterial pressure (MAP) greater than or equal to 65mmHg and have lactate >2mmol/L(>18mg/dL)

Cariogenic shock

-Shock resulting from impairment or failure of the myocardium -An inadequate pumping of the heart, resulting in decreased systemic blood flow and inadequate tissue perfusion. -This is not a volume issue; this is a pump issue .

Patho of sepsis

-Start with the initial insult (bacteria, fungi, and virus) -Immune system is then activated. -immune systems response is to activate biochemical cytokines and mediators that produce inflammatory response and a complex cascade of physiologic events that lead to poor tissue perfusion (increase lacate from cellular anaerobic to aerobic) -Increase capillary permeability (Leading to fluid seepage form the capillaries) -Vasodilation occurs (Bacteria realase nitride oxide) -The combination of vasodilation and capillary permeability interrupt the bodys ability to provide adequate perfusion, and nutrients to the cells. (like decreased vascular volume) (Gram negative bacteria was associated with sepsis but there has been in increase in gram positive bacteria as well.)

Septic Shock - distributive shock

-Starts with sepsis -> body's extreme response to an infection -Widespread vasodilation and increased capillary permeability caused by endotoxins -Hemodynamic Instability despite adequate fluid resuscitation -ICU ADMISSION -High Mortality Rate -Warm & Cold Stage

Identifying SIRS

-Temperature >38.3 C (>101 F) -Temperature <36 C (96.8 F) -Tachycardia -Tachypnea -WBC >12,000 or <4000 -Presence of Bands (CBC has baby white blood cells) Not helpful in diagnosing sepsis (Just lets us know inflammatory waring in the body.

Preload

-The amount the ventricles stretch at the end of diastole (relax)

Afterload

-The pressure the ventricle must pump against to get blood out of the heart.

Nursing Care AKI

-Through history-> medication reconciliation -Strict I/O -> may need foley or purewick catheter -Daily weights -Monitor for s/sx of fluid overload (JVD, crackles in lunges, dyspnea) -Reducing Metabolic rate (bed rest) -Promote pulmonary function (ICF) -Preventing infection -Providing skin care (nitrogous product cause dryness, and mositurize skin) -Provide psychosocial support -Promote pulmonary Function (TCDB) to prevent atelectasis and URI -Monitor invasive lines for infection, use aseptic technique -Foley- Monitor for CAUTI -Meticulous Skin Care (bathing with cool water, frequent turning, keep skin clean and moisturized, keep fingernail trimmed to avoid excoriation) -Psychosocial support

S/SX Tension Pneumothorax

-Tracheal Deviation & Mediastinal Shift are classic findings -Severe hypoxemia -Muffled heart sounds Think Cardiogenic: -Shock -Hypotension -Tachycardia -Central cyanosis (List and chest cyanosis)

Pulmonary contusion

-Trauma-induced lung hemorrhage and edema without laceration -Direct or indirect damage of the parenchyma of the lung that leads to edema or alveolar hematoma and loss of physiological structure and function of the lung Symptoms: •May be asymptomatic or impaired •Chest pain •Hypoxia •Wheezing •Crackles •Dx with X-Ray Treatment: -NSAID's (Ibuprofen or tordole) -Ice to affected area x 2 days (20 minutes on and then off) -incentive spirometer (Want lungs to expand to prevent pneumonia or atelectasis) -Supportive (typically resolves in 7 -14 days, improved pain 2-3 days -Some pts that are severely compromised may require mechanical ventilation Nursing care: •Support and Educate Return to the ER: -Acute increase in pain -difficulty breathing, -Hemoptysis - any concerning symptoms

Medical management AKI

-Treat the underlying cause -Maintain fluid balance, avoid fluid excess -Monitor and treat electrolyte imbalances -Treat electrolyte abnormalities - Hemodialysis, CRRT (Last resort, filter blood, remove excess fluid) -Reverse metabolic acidosis -> sodium bicarb -Phosphate binding agents (calcium or lanthanum carbonate) for hyperphosphatemia -Adjust medication -> avoid nephrotoxins -Diuretics- may be used to control fluid volume but do not improve recovery from AKI

How Cardiac Medication increase CO

-Vasodilators in low doses acts as a venous vasodilator therefore reduces preload. At higher doses it causes arterial vasodilation which reduces afterload. -Vasopressors increase preload by vasoconstriction. By increasing the amount of blood coming into the heart, we increase the filling of the ventricles which increases preload resulting in increased stroke volume which increases cardiac output -Inotropes work by improving contractility, which increases stroke volume with results in increased cardiac output Most patients will be on a combination of these medications Most patients will be on combo drugs

patho of hypovolemic shock

-decreased intravascular volume= decreased venous return/ preload=decreased SV/CO/CI= decreased tissue perfusion

Cases of hypovolemic shock

-external fluid losses, as in traumatic blood loss -internal fluid shifts, as in severe dehydration, severe edema, or ascites Hemorrhagic: -Tramua -Sx -Child birth -GI bleeds Treatment: GIVE BLOOD Non-hemorrhagic: -Vommiting -Diarrhea -Skin (burns, heat strock) -Renal (diuretics) -Third space (Cirrhoses, DKA, CHF, Trauma) Treatment: -Isotonic (LR/NS) -Albumin

Medical management of hypovolemic shock

1.Restore intravascular volume to reverse the sequence of events leading to inadequate tissue perfusion 2.Redistribute fluid volume 3.Correct the underlying cause of the fluid loss as quickly as possible. (Ex. stop bleed or vomitting)

A client is admitted to the hospital with a prerenal disorder, a nonurologic condition that disrupts renal blood flow to the nephrons, affecting their filtering ability. One cause of prerenal acute kidney injury is: A.Anaphylaxis B.Myoglobinura secondary to burns C.Polycystic Disease D.Uretheral

A

Cardiac output is very important for determining if a patient is in cardiogenic shock. What is a normal cardiac output in an adult? A.2-5 liters/min B.1-3 liters/min C.4-8 liters/min 8-10 liters/min

C.

In severe sepsis, cardiovascular failure is typically manifested by: A.Increased peripheral artery resistance. B.Bradycardia C.Hypotension D.Increased cardiac output

C.

Pharmacologic Therapy for cardiogenic shock

Cardiac medication to improve CO: -Inotropic Agents (doubatimine and miltrope) -Vasodilators -Vasopressors (Levofed) -Antiarrhythmics -Vasopressin -Thrombolytics Pain control: - Morphine, decreases preload and afterload PUD prophylaxis (PPI) DVT prophylaxis (TEDs, SEDS, low molecular heaprin)

Causes of cardiogenic shock

Cardiogenic: -MI (Number one) -Dysrhythmias -Severe Congestive Heart Failure -Cardiac Tamponade Noncardiogenic: -Severe hypoxemia -Acidosis -Hypoglycemia -Hypocalcemia -Tension pneumothorax

Surviving Sepsis Campaign - CMS (Septic shock)

Complete within 3 hours of patient presentation/symptoms Rapid identification of the infectious source is a critical element in managing sepsis -Obtain serum lactate level -Obtain blood culture prior to administration of antibiotics -Administer prescribed broad-spectrum antibiotics -Initiate aggressive fluid resuscitation in patients with hypotension or elevated serum lactate (>4 mmol/L): (Minimum inital fluid bolus of 30 mL/kg using crystalloid solutions

Which of the following is the most sensitive indicator of renal function? A.Serum Creatinine B.BUN C.Creatinine Clearance Potassium

A.

The nurse is caring for a client's status after a motor vehicle accident. The client has developed AKI. What are the nurse's roles in caring for this client? Select all that apply. A.Providing emotional support for the family B.Monitoring for complications C.Participating in emergency treatment of fluid and electrolyte imbalances D.Providing nursing care for primary disorder (trauma) E.Directing nutritional interventions

A.,B.,C.,D.

Vasopression

Actions: -Pituitary hormone -Causes vasoconstriction -Increases SVR -Increases BP Nursing Actions: -Constant hemodynamic monitoring -Titrated to effect -Monitor urine output -Central line - extravasation

Vasopressors review

Actions: -Strengthens cardiac contractions -Increase preload -Increases cardiac output -Low dose increase kidney perfusion -High dose decrease kidney perfusion -Norepinephrine (levophed) Rapid onset/short duration Nursing Actions: -Use if IVF not effective -Administer w IVF -Constant hemodynamic monitoring -Central line - extravasation -Titrated to effect -Monitor urine output

A patient is being treated for cardiogenic shock. Which statement best describes this condition? A."The patient will experience an increase in cardiac output due to an increase in preload and afterload." B."A patient with this condition will experience decreased cardiac output and decreased tissue perfusion." C."This condition occurs because the heart has an inadequate blood volume to pump." D."Cardiogenic shock leads to pulmonary edema."

B.

In septic shock, dysfunction and sometimes failure of one or more organs occur secondary to which of the following? A. Systemic vasculitis B.Decreased perfusion C.Hemorrhage D.Acute Coronary Syndrome

B.

A client with decreased urine output refractory to fluid challenges is evaluated for renal failure. Which condition may cause the intrinsic (intrarenal) form of acute renal failure. A.Poor perfusion to the kidneys B.Damage to the cells in the adrenal cortex C.Obstruction of the urinary collection system D.Nephrotoxic injury secondary to use of contrast media

D.

Assessment of chest trauma

Inspect: -Depth and symmetry of chest wall excursion (Look at chest for breathing, trama, or brushing) Auscultate: -Diminished breathe sounds -Absence of breathe sounds -Adventitious breathe sounds (Abnormal breathe sounds) Palpate: Crepitus, subcutaneous edema (rice crispy treats) Percuss: -Resonance (normal) -Dullness (fluid) •Chest Tenderness - worsens with breathings •Ecchymosis (bruising) •Respiratory Distress (tachypnea, hunched over trying to breathem use accessory muscle •Hypotension •Shock •Seatbelt Sign- admit to hospital

Complications of Sepsis

MODS - Multiple organ dysfunction syndrome: -Occurs from the release of toxic metabolites and destructive enzymes in response to inadequate oxygenation -Caused by severe hypotension Organ Failure -> the more organs failing chance of mortality: -Lungs - PaO2, FiO2 -Hematology - platelets -Liver - bilirubin -Kidneys - serum creatinine & urine output -Brain - Glasgow coma score -Heart - hypotension requiring vasopressor

BUN (AKI)

Measures the amount of nitrogen in your blood. Made from protein. Liver breaks down the protein and excretes it into the blood creating blood urea nitrogen. Which is eventually excreted by the kidneys.

Cardiac Index

More specific measurement of a patient's cardiac output based on the patient size (CO/body surface area) 2.5-4L.

Creatinine (AKI)

Muscle breakdown, filtered and excreted by the kidneys, not reabsorbed

Complication of sepsis

Overstimulation of clotting cascade: -Thousands of small clots form within the organ capillaries, creating hypoxemia and anaerobic metabolism -Platelets & fibrinogen are depleted ->hemorrhage -Treated with IV Heparin -> Heparin accelerates formation of antithrombin III, inactivates thrombin and prevents conversion of fibrinogen into fibrin (Prothrombin to thrombin/ Fibrinogen to fibrin (CLOT)) -Look for petechiae, ecchymosis, and blood leakage from IV sites -PT/PTT Increases -Fibrinogen decreases -Platelets decreases

Nursing responsibilities (septic shock)

Prevention of Sepsis: -Strict infection control (cleaning equipment and the patient environment) -Thorough hand hygiene -Aseptic technique and close monitoring of IV lines, arterial & venous puncture sites, surgical incisions, traumatic wounds and urinary catheters for infection. -Removal of invasive devices that are no longer necessary (catheters) -Timely débriding of wounds to remove necrotic tissue -Prevent ventilator associated Pnueumonia (Early ambulation)

Initial management think fast!

Primary survey -> Chest trauma -> airway breathing circulation

GFR (AKI)

Rate and level at which your kidneys filter

Hypovolemic shock rule

Restore intravascular volume. 3:1 rule: -Recommends administration of 3 mL of crystalloid (isotonic) solutions for each milliliter of estimated blood loss.

Vasodilators

Sodium Nitroprusside Actions: -Decreases afterlaod -Relax smooth muscles -Reduce SVR -Improve cardiac output Nursing Actions: -Continuous arterial blood pressure monitoring -Titrate -Administer with CAUTION- this is a potent casodilator -Protect from the light

Hemothorax

•Blood in the pleural space •Rapid accumulation >1000 ml •Penetrating or blunt trauma, aortic rupture •Myocardial rupture •Laceration of the lung, intercostal or internal mammary vessel •Can have hemopneumothorax (blood and air) •Sx - dyspnea, decreased breath sounds, dullness on palpation Nursing managment: •Prepare for chest tube set up •Provide Oxygen •Administer analgesics as ordered •Comfort/support patient and family •Surgical consents if thoracotomy is needed IVF & Blood administration Medical management: •CXR -> Diagnose •Chest Tube •Emergency Thoracotomy •Pain Control •Fluid Resuscitation Blood Administration

Diagnostic of chest trauma

•CXR (1st, shows fractures and lung expansion) •CBC (bleeding) •Cardiac Enzymes (r/o cardiac injury) (will ris) •EKG - blunt chest trauma (shows conduction patway) •ECHO Ultrasound

Rib fracture

•Common injuries - (70-80% due to MVA) •Occur most often following blunt force trauma but can also occur from severe coughing, athletic injuries & abuse •Ribs 4-10 are the most vulnerable to blunt trauma •Blunt force trauma: MVA •Penetrating trauma: gunshot wound •Most fx resolve withing 6 weeks Types: •Open - overlying skin disrupted •Closed - skin intact •Pathologic Fracture: Cancers that metastasize to bone, infection, osteopathic •Stress Fractures: seen in patients with chronic cough Symptoms: •Localized pain •Pain on inspiration •Splinting of chest •Shallow respirations •Crepitus on palpation Treatment: •Conservative treatment for most •Depends on the number of ribs broken •Observation for elderly patients & children •Surgical Stabilization -> acute pain or resp compromise •Pain control -> avoid splinting (NSAIDs, Opioids, Nerve Blocks) Assessment: •Localized pain •Pain on inspiration •Splinting of chest •Shallow respirations •Crepitus on palpation Treatment: •Conservative treatment for most •Depends on the number of ribs broken •Observation for elderly patients & children •Surgical Stabilization -> acute pain or resp compromise •Incentive Spriometry - prevent atelectatsis & pneumonia •Pain control -> greatly affects mortality in patients, treat early (-NSAIDs, Opioids, Nerve Blocks) (Patients with 3 or more rib fractures, a flail segment, and any number of rib fractures with pulmonary contusions, hemopneumothorax, hypoxia, or pre-existing pulmonary disease should be monitored at an advanced level of care.) Gerontologic Considerations: •High risk -Hospital admission for observation •Increased mortality -Elderly patients with a single rib fracture have twice the mortality as their younger counterparts with the same injury. -Mortality increases by 19% for each additional rib and the risk of pneumonia by 27% Decreased lung capacity

Intropic agents

•Milrinone lactate, dobutamine Actions: -Strengthens cardiac contraction -Increases stroke volume -Increases cardiac output -Can cause vasodilation in some patients Nursing actions: -IV infusion -Continuous hemodynamic monitoring -Titrate to effect -Often used in combination with vasopressors

Flail chest

•Significant force is imparted on the chest •MVA, Ejection from a car, pedestrian struck by a car, assault with a blunt weapon (baseball bat) •Severe Injury •Causes pulmonary contusion •High risk for respiratory failure •A segment of the chest wall moves paradoxically (opposite direction from the rest of the chest wall) outward during expiration and inward during inspiration •Typically cased by a Pneumothorax or blunt trauma - example: chest hitting the steering wheel of a car •Multiple Rib Fractures - segment of the rib cage breaks and becomes detached from the chest wall •F =Frequent Rib Fractures (multiple) •F = Chest Fails to Fill with air •F = Fatal ->if left untreated •F = Fixation -> Surgery •F = Fluid overload -> Pulmonary Contusion, lungs are sensitive Assessment: •Ribs move independently of the rest of the chest wall and in the opposite direction = paradoxical respirations •Severe chest pain •Splinting •Dyspnea •Anxiety •Weak cough, use of accessory muscles •Diminished breath sounds •Subcutaneous emphysema causes a crackling or crunch when palpated Diagnostic and treatment: -CXR - initially -CT Scan - more effective -Mechanical Ventilation -Surgical Fixation & Stabilization of fracture -Fluid resuscitation -ABX -DVT prophylaxis -Chest Tube -Pain Control Nursing care: Adminster: •Oxygen (humidified) •Analgesics (pain control) Educate: •Pillow for coughing •Turn, Cough Deep Breathe •Incentive Spirometry •Avoid Air Travel & Scuba •Restricted Activity until healed! •Smoking Cessation

Red flag signs for chest trauma

•Worsening hypoxia •Use of accessory muscles •Paradoxical movements of the chest with respirations (Inhale lungs go down; exhale lungs go up supposed to be opposite) •Hemodynamic Instability •Tenderness over multiple ribs (fractured ribs) •Palpable depression or deformity of the sternum (Be careful heart is below it)

BLEB

•blister-like air pockets that form on the surface of the lung •When these blebs rupture or 'pop' inhaled air is able to travel from the airways to the thoracic cavity, creating a pneumothorax or lung collapse.