Med Surg Final Exam Study Guide

White coat hypertension.

When a pt has elevated BP at the physician's office, due to anxiety or nervousness about being at the appointment

How many IV catheters should the nurse anticipate inserting in a patient who may be experiencing hypovolemic shock?

2 Large Bore 18 gauge

Triage priorities after mass casualty incident

Class 1 Resuscitation/RED: Airway/Cardiovascular (Can be saved) Class 2 Emergent/YELLOW: Immediate Treatment, but not life threatening (fracture) Class 3 Urgent/GREEN: Minor, not immediate (laceration) Class 4 Urgent/BLACK: Expected to die, revert to RED/YELLOW

What is the compensatory stage of shock? Be sure to not just write the definition, understand what is occurring in this stage in regard to your body as a whole.

4 Stages · Initial · Compensatory · Progressive · Refractory Compensatory: The body activates neural, hormonal and biochemical compensatory mechanisms in an attempt to overcome the increasing consequences of anaerobic metabolism and to maintain homeostasis. The patient's clinical presentation begins to reflect the body's responses to the imbalance in oxygen supply and demand · Neurologic System o Restless, apprehension, confusion, change in LOC · Cardiovascular System o SNS Response: release of epinephrine and norepinephrine (vasoconstrictors) o Increased HR/Contractality o Coronary Artery Dilation o Narrowed Pulse Pressure o Decreased BP · Respiratory System o Decreased blood flow to the lungs o Tachypnea o Hyperventilation · GI System o Decreased Blood supply o Increased risk for paralytic ilieus · Renal System o Decreased renal blood flow o Increased Renin o Increase in Aldosterone o Increased in ADH · Temperature o Normal or abnormal · Skin o Pale/cool or warm/flushed

Type 1 and type 2 diabetes pathophysiology.

DM is a metabolic disorder resulting from either inadequate production of insulin (type 1) or inability of the body's cells to respond to insulin that is present (type 2) • Type 1 Patho: Autoimmune destruction of the pancreatic B cells, the site of production, eventually resulting in a total absence of insulin production. A genetic predisposition and exposure to a virus are factors that may contribute to the pathogenesis of immune related type 1 diabetes • Type 2 Patho: The pancreas usually continues to produce some endogenous(self made) insulin, however the insulin that is produced is wither insufficient for the needs of the body or is poorly used by the tissues or both. Most powerful risk factor is obesity, especially abdominal and visceral adiposity

Will a patient with septic shock have decreased or increased SVR? (Systemic vascular resistance)

Decreased Systemic Vascular Resistance

Disaster Triage Nursing (Color Tagging & START Method Review)

Disaster Triage Nursing Triage means to group or rank. In the emergency room (ER), patients are triaged based on their presenting signs and symptoms. The patients who have severe symptoms are seen immediately, while patients who don't will have to wait to be seen. In this review, we will be concentrating on triage related to a disaster situation. This is where there are many wounded individuals, but the personnel and resources available to treat those wounded are limited. Therefore, personnel and resources should be used wisely, and this is where the disaster color-coded triaging tagging system and START method can be helpful. Disaster Triage Color Tags There are four colors and a wounded individual will be tagged one color based on their health status. The four colors include: Red Yellow Green Black To help you keep the meaning of the tag colors red, yellow, and green separated, think of a traffic light and what you do at the traffic light when it turns certain colors. The reason I include this is because many students get confused about these three colors on exams. The black tag color is easy to remember because black is most commonly associated with death, which is the meaning of this tag color. Red Tag: Immediate What do you do at a traffic light when it turns red? You stop! Therefore, when a patient is tagged red, STOP and get them treatment because they have first priority in receiving care. Seen 1st Injuries are life-threatening but they could possibly survive if they are immediately treated. Severe alteration in breathing, circulation, and neuro/mental status Conditions that would cause a wounded individual to be tagged red (think of conditions or systems of the body that if severely damaged could majorly alter the breathing, circulation, and neuro system)Spinal cord injuries: remember various areas of the spinal cord control breathing, brain and heart function...shock can occur like neurogenic, cardiogenic etc.Severe bleeding (internal or external): if the patient is treated immediately so the bleeding could be stopped and transfused with blood products they may liveMajor burns that affects a high percentage of the body: burns can affect the circulation and the respiratory system (depending on the burn type and where it's located)Some types of major respiratory trauma: pneumothorax etc. Yellow Tag: Delayed What do you do at a traffic light when it turns yellow? You slow down or delay because you're about to stop. Therefore, when a patient is tagged yellow their treatment is delayed but for only about an hour or so because they could turn critical based on their presenting injuries. Seen 2nd (second priority) Significant injuries BUT at this point their breathing, circulation, and mental status is within normal range but this could change. Conditions:Bone fractures: major fractures that require medical treatmentIntegumentary damages: open wounds, deep lacerations etc. Green Tag: Minor What do you do at a traffic light when it turns green? You go! Many times these wounded individuals are termed the "walking wounded". Therefore, these patients can get up and GO (move around). Their injuries are minimal. Treatment can be delayed for several hours and some can treat themselves. Breathing, circulation, mental status not expected to change Black Tag: Expectant Wounded is dying or expired. Injuries are deadly to the point the individual will not survive. Absence of breathing, circulation, mental status. START Method This method can help determine what tag color a wounded victim is assigned. START stands for "Simple Triage And Rapid Treatment". This particular method is for the adult. It's very easy to use and quick. First, you want to look at the wounded individual and ask yourself "what is the wounded victim doing?" Are they able to walk around? OR Are they unable to walk or move? If the wounded individual can walk around and move, their breathing, circulation, and mental status are within normal range. Therefore, they are tagged GREEN. Walking? GREEN TAG Unable to move or walk? Check these three things in this order: Breathing, Circulation, and Mental Status/Neuro. The wounded individual that cannot walk will be tagged either RED, YELLOW, or BLACK. Breathing? Yes, rate is greater than 30: RED TAG Yes, rate is less than 30: check circulation No, reposition airway:Still not breathing: BLACK TAGYes: RED TAG Circulation? (radial pulse present or less than 2 seconds capillary refill) Yes: check mental status No: RED TAG Mental Status? (can they obey your commands?) Yes: YELLOW TAG No: RED TAG

Medications to know

Dobutamine · Adrenergic Agonists/Beta 1 · Mechanism of Action: Stimulates Beta 1 selective receptors of the heart muscle, increases cardiac output by increasing contractility (positive inotropy), which increases the stroke volume · Indications: HF · Side Effects: chest pain, dysrhythmias, headache, restlessness, excitement, insomnia Furosemide · Loop Diuretic · Mechanism of Action: Blocks reabsorption of Na, CL and water in the ascending loop of henle, causing rapid diuresis · Indications: Pulmonary edema, edema(r/t HF, liver disease, and kidney disease), HTN · Side Effects: Dehydration, electrolyte imbalances (hyponatremia, hypokalemia), hypotension, ototoxicity, hyperglycemia Epinephrine · Adrenergic Agonist/Acts directly on alpha and beta receptors · Mechanism of Action: In low doses it stimulates Beta 1 receptors increasing the force of contraction and HR. Also used to treat acute asthma and anaphylactic shock at these dosages because it has significant bronchodilator effects on the lungs. At high doses , it stimulates mostly alpha adrenergic receptors causing vasodilation, which increased BP · Side Effects: Tachycardia, nervousness, shakiness, headache, weakness methylprednisone · Glucocorticosteroid · Mechanism of Action: Inhibit or help control the inflammatory and immune response. They do so by stabilizing the cell membranes of inflammatory cells called lysosomes, decreasing permeability of the capillaries to the inflammatory cells, and decreasing the migration of WBC into already inflamed areas · Indications: Inflammatory diseases, respiratory flareups, dermatologic diseases, opthalamic disorders, organ transplants, GI disorder · Side Effects: fluid retention, moon face, hyperglycemia, psychosis hydrochlorothiazide · Thiazide Diuretic · Mechanism of Action: Blocks reabsorption of NA, Cl, water at distal convoluted tubule · Indications: HTN (often in combination with antihypertensive meds), edema (r/t HF, lover disease, and kidney disease · Side effects: dehydration, hypokalemia, hyperglycemia, NO OTOTOXICITY pancuronium · Neuromuscular Blocking Agent - Long Acting · Mechanism of Action: · Indications: Maintaining skeletal muscle paralysis to facilitate controlled ventilation during surgical procedures · Side Effects: muscle spasms, hyperkalemia due to injury of muscle cells and release of potassium into circulation, bronchospasm, , hypotension, excessive bronchial and salivary secretions glipizide · Sulfonylureas · Mechanism of Action: Bind to receptors on beta cells in the pancreas to stimulate the release of insulin. · Indications: Type 2 diabetes, may be used in conjunction with metformin and thiazolodinediones. Sulfonylureas should not be used in patients with advanced diabetes dependent in insulin administration · Side Effects: Hypoglycemia, weight gain due to stimulation of insulin secretion, skin rash, nausea, heartburn atropine · Cholinergic Blocking Agent (anticholinergic) · Mechanism of action: Blocks acetylcholine at parasympathetic neuroeffector sites, increases cardiac output and heart rate, decreases sweating and salivation · Indications: Bradycardia, reversal of anticholinesterase agents (insecticide poisoning), decreases secretions before surgery · Side Effects: Tachycardia, dry mouth, urinary retention, photophobia, nasal congestion adenosine · Unclassified Antidysrhythmic · Mechanism of action: Slows electrical conduction time through the AV nose and is indicated for conversion of PSVT to sinus rhythm. Half life less than 10 seconds, only available IV · Indications: PSVT · Side Effects: Chest pressure, facial flushing, SOB, dizziness, headache, blurred vision

What are indications a patient maybe experiencing hypovolemic shock?

Anxiety Tachypnea Increase in CO/HR Decrease in stroke volume, PAWP (Pulmonary artery wedge pressure), Urinary output ****If loss > 30%, blood volume is replaced****

What is the main vital sign a nurse must check before administering Digoxin?

Apical Pulse: Be aware of physician parameters, typically not administered HR < 60 Monitor potassium levels, low potassium levels cause digoxin toxicity. S/S Dig Toxicity: Visual changes, GI upset, fatigue, weakness, vomiting Anecdote: Digoxin Immune Fab - Digiband Normal 0.8-2.0 toxic : >3.0

What will be one of the nurse's main priority when caring for a patient with elevated potassium well beyond the normal range?

Cardiac Dysrhythmias

Chest tube management (Where should chest tubes be placed, what does the different types of bubbling in the water seal chamber signify etc).

Drains fluid, air from pleural space. Chest tube tip positioned UP for Pneumothorax and DOWN for hemothorax or pleural effusion Drainage collection Chamber: Report drainage > 70ml/hr to provider Water Seal Chamber: Add sterile fluid up to 2cm line, check Q2H. Chamber must be kept upright and below chest tube insertion site. TIDALING EXPECTED. Lack of tidaling = lung re-expansion or obstruction. CONTINUOUS BUBBLING INDICATES AIR LEAK Suction Control Chamber: CONTINUOUS BUBBLING EXPECTED Nursing Care tidaling Chest Tubes • Assess chest tube insertion site for erythema, pain, crepitus • Position pt in semi/high fowlers • Obtain chest xray for placement • Keep 2 hemostats, sterile water, occlusive dressing at bedside • Only clamp when ordered, do not strip/milk tubing Chest Tube Removal • Tell pt to take a deep breath, exhale, and bear down during removal. Apply petroleum jelly gauze dressing over chest tube site Chest Tube Complications • If drainage system becomes compromised, place end of tube in sterile water • If chest tube is accidently removed, apply dry sterile gauze over area - taped only on 3 sides • TENSION PNEUMOTHORAX: Can result from kink in tubing or obstruction. o Symptoms: Tracheal deviation, absent breath sounds on affected side, respiratory distress, asymmetry of chest

HIV (Patient teaching, modes of transmission, initial signs and symptoms etc).

HIV targets CD4+ lymphocytes, also known as T-Cells or T-Lymphocytes Modes of Transmission: Contact with body fluids, blood, semen, vaginal secretions, and breast milk Initial S/S: Flu-like symptoms, weakness, night sweats, headache, weight loss, rash Normal CD4+ T-Cells 800-1200 Stage 1: CD4+ T-Cells 500 or more Stage 2: CD4+ T-Cells 200-499 Stage 3 (AIDS): CD4+ T-Cells < 200 Symptoms: Kaposi's sarcoma. TB, pneumonia, wasting syndrome, candidiasis of the airways, Herpes, and other infections Diagnosis: ELISA TEST-Used to detect HIV Antibodies/Western Blot Test-Used to confirm diagnosis (Viral Load) Patient Teaching Practice good hygiene Avoid raw foods Don't clean cat litter box Avoid sick people Practice safe sex Ongoing monitoring of CD4+ T-Cells

Revisit types of stroke.

Ischemic Stroke: Inadequate blood flow to brain form partial or complete occlusion of an artery. Treatment: TPA - Tissue Plasminogen Activator • Thrombotic o Occurs from injury to a blood vessel wall and formation of a blood clot. Presence of built up plaque in the vessel o Results in narrowing of blood vessel o Most common cause of stroke: often associated with HTN and DM and many times are preceded by TIA o Extent of stroke depends on rapidity of stroke, size of damages area, presence of collateral circulation • Embolic o Occurs when an embolus lodges in and occludes a cerebral artery o Results in infarction and edema of area supplies by involved blood vessel o 2nd most common cause of stroke o Sudden onset with severe clinical manifestations Hemorrhage Stroke: Results from bleeding into the brain tissue Treatment: Stop the bleeding and treat the HTN • Intracerebral Hemorrhage o Bleeding withing the brain caused by a rupture of a vessel o Sudden onset of symptoms, progression over minutes to hours due to ongoing bleeding.....Poor prognosis with a 30 day mortality rate of 40 - 80% o HTN is the most common cause o Extent of symptoms varies and depends on amount location and duration of bleed o Manifestations: neurologic deficits, headache, N/V, decreased LOC, HTN • Subarachnoid Hemorrhage (SAH) o Intracranial bleeding into the cerebrospinal fluid - filled space between arachnoid and pia mater o Commonly caused by rupture of cerebral aneurysm, trauma or drug abuse • Cerebral Aneurysm o Majority are in Circle of Willis o Incidence increase with age, higher in women o Silent killer

What are the risk factors for CAD (Coronary Artery Disease)?

Nonmodifiable • Age, gender. Ethnicity, family hx, genetic predisposition Modifiable • Cholesterol, hypertension, tobacco use, physical inactivity, obesity

A patient experiencing a massive pulmonary embolism will experience respiratory failure by way of interference with which of the two, oxygenation or perfusion? Why?

Perfusion

Know classification categories for hypertension. Ex. 120/80 is classified as prehypertensive

Prehypertension: 120-139/80-89 Stage 1: 140-159/90-99 Stage 2: 160-179/100-109 Hypertensive Crises: Above 180/Above 110

What is MONA?

Protocol for patients presenting with chest pain, and suspected MI Morphine Oxygen Nitrates Aspirin

What are the manifestations of left sided heart failure?

Pulmonary Congestion: dyspnea, crackles, orthopnea, fatigue, pink/frothy sputum

What is the first thing the nurse should do when the patient is suspected to be having an infusion reaction to PRBC's?

STOP THE INFUSION, keep the line open and send all blood products back to the lab/pharmacy S/S of reactions

Septic Shock NCLEX Review

Septic shock occurs due to sepsis and leads to a major decrease in tissue perfusion to organs and tissues. So, in other words, shock (which is where cells are deprived of oxygen due to the lack of perfusion) occurs because of an invasion by a microorganism (septic). According to CDC.gov, "1 in 3 patient who die in a hospital have sepsis." This is a very alarming statistic! Therefore, as nurses we must be able to recognize the early signs and symptoms of this condition and know what patients are at risk for developing it. What is sepsis? It's the body's response to infection. In sepsis the response to the infection is amplified and a system-wide inflammatory response is activated. Unfortunately, what occurs throughout the small vessels in the body during sepsis is what leads to the decrease in blood flow (hence tissue perfusion) to organs/tissues. Therefore, septic shock is really the end result of sepsis if it's not treated promptly and effectively. Septic shock is characterized by the following (this is how you can know if your patient with sepsis is entering into shock territory): Persistent hypotension (<90 SBP) that doesn't respond to IV fluids Needs vasopressors (example Norepinephrine) to maintain perfusion (a MAP >65 mmHg)MAP (mean arterial pressure): this number tells us how well vital organs are being perfused. If it's lower than 65 mmHg, the organs aren't being perfused very well. Serum Lactate >2 mmol/LRemember from our video on "stages of shock" we talked about how when cells start to struggle (hence not receiving enough oxygen due to a decrease in tissue perfusion) they will switch from aerobic to anaerobic metabolism. The result of anaerobic metabolism is the buildup of lactic acid in the blood. Therefore, due to a decrease in tissue perfusion the serum lactate will be elevated. In septic shock, hypotension is NOT occurring due to a low cardiac output like with some of the other types of shock (ex: cardiogenic shock). It's occurring due to a drastic decrease in systemic vascular resistance due to the vasodilation occurring in the small vessels along with an increase in capillary permeability and micro-clot formation in the vessels. These phenomena are occurring due to the body's exaggerated response to the infection present in the body. Now, let's talk about the specifics of why we have persistent hypotension, a decrease in system vascular resistance, vasodilation, increased capillary permeability, micro-clot formation etc. First, it's important to know that septic shock is a distributive form of shock. Anaphylactic and neurogenic shock are the other two types of distributive shock. What does this mean? It means there is an issue with the distribution of blood flow in the small blood vessels of the body. The alteration in how blood is distributed leads to a limited supply of blood (hence oxygen) to the body's tissues and organs. It's much different than cardiogenic shock because with this type of shock the heart's cardiac output decreases. Cardiac output is how much blood the heart is actually able to pump per minute. If it can't pump enough blood per minute, the amount of blood flowing to the cell's organs and tissue falls. The cells can experience hypoxic injury and die. But here in septic shock there is a different reason for this DECREASE in tissue perfusion and drop in blood pressure: It stems from how the systemic vascular resistance is greatly diminished due to: MAJOR vasodilation that is altering tissue perfusionVessels become so large that blood is pooling and not flowing to tissues/organs Hypovolemia (relative): due to leaking vessels and this causes increased capillary permeabilityFluid moves from the intravascular space to the interstitial space, so there is a decrease in circulating blood volume Clot formation in microcirculation: this blocks blood flow throughout the vessels so blood can't flow to the tissues, hence decreasing tissue perfusion. All of this together majorly diminishes tissue perfusion (hence the development of shock and organ death). Let's analyze how this happens: A microorganism enters the patient's body. It can be a bacteria (most common causes of sepsis and it can be either gram positive or negative), virus, parasite, or fungus. This invasion can cause sepsis. Sepsis leads to an amplified activation of the body's systemic inflammatory response system to fight that infection and this is SYSTEM-WIDE! In sepsis the body thinks it is helping to attack the microorganism that has entered the body, but really it's failing and causing dysfunction to organs, which leads to septic shock. During this process, chemicals are releases by the microorganism and immune cells that will lead to vasodilation, increase capillary permeability, clot formation, and decreased myocardial function. How? The microorganism releases toxic substances that will damage the surrounding tissues. The presence of these substances leads the body to release cytokines and pro-inflammatory mediators to fight and clean up this mess from the microorganism, which makes sepsis worst. These substances will cause the following effects throughout the WHOLE body: The chemicals will leads to changes in capillary permeability (blood vessels will leak), vessels will widen (vasodilate), and coagulation issues will occur (clots will form within vessels and clotting factors will be depleted). Also to be released due to this process taking place will be "platelet activating factor". PAF leads to platelet aggregation, which will lead to clot formation in the microcirculation. Remember these vessels are damaged and this is SYSTEM-WIDE, so many small clots will form throughout the vessels. This will further block blood flow and lead to a further decrease in tissue perfusion. The problem with this is that it will use up clotting factors and DIC (disseminated intravascular coagulation) can occur. Watch for oozing of blood out of body orifices. And if it can't get any worst the heart's function will become depressed due to the presence of these cytokines in the body, especially tumor necrosis factor and interleukin-1. The heart will have a decreased ejection fraction (this is the percentage of blood leaving the heart with each contraction). Due to all of this, organs will have difficulty functioning because their blood supply will be limited. Risk Factors for developing Septic Shock "Sepsis" Suppressed immune system: AIDS/HIV, immunosuppressive therapy, steroids, chemo, pregnancy, malnutrition Extreme age (infants and elderly) People who've received an organ transplant Surgical procedures (anything invasive) Indwelling devices: Foley, central lines, trachs etc. Sickness (chronic conditions): diabetes, hepatitis, alcoholism, renal insufficiency *** Most common sites of sepsis: GI (abdomen), respiratory (lungs), GU (urinary tract) Signs and Symptoms of Septic Shock Early stages "warm phase" (patient is hyperdynamic and compensation is occurring): warm/flushed skin due to vasodilation (cool/clammy in late stage) decreased blood pressure hyperthermia high cardiac output (to help maintain tissue perfusion and compensation....remember it's not a CO problem so heart can pump at this point but it will fail later on) decreased systemic vascular resistance due to massive vasodilation tachycardia increased respirations lethargic/anxiety Late stage "cold phase" (patient is hypodynamic and decompensation is occuring): skin pale, cold, clammy severe hypotension increased heart rate hypothermia depressed heart function results in: low cardiac output and increase systemic vascular resistance (vasoconstriction) oliguria (less than 30 mL/hr of urine) coma When a patient is having persistent hypotension that isn't responding to fluid, needs vasopressors to maintain MAP >65, and lactate >2 mmol/L and altered tissue perfusion is occurring, the patient is in septic shock! Nursing Interventions and Treatment for Septic Shock Goal Summary: increase tissue perfusion (fluid replacement and then vasopressors if not working), oxygenate (>95%: tissues need oxygen and respiratory failure occurs due to ARDS, which will require mechanical ventilation), fight infection (cultures, antibiotics), decrease inflammation (some patients are candidates for Drotrecogin Alpha and corticosteroids), nutrition (helps body fight infection, prevent stress ulcers and heals), control glucose (this helps body fight infection...hyperglycemia leads to the altered function in the immune system) To help us remember all the treatment goals and nursing interventions remember: "Septic Shock" Start antibiotics: need to be started within the 1st hours of septic shock....broad-spectrum used until microorganism identified....CULTURES first but don't delay antibiotics Enteral Nutrition: early...this helps maintain gut integrity, helps with healing/fighting infection and prevent stress ulcers (may need prophylactic drugs like Famotidine as well) Protein activated C: "Drotrecogin alpha": has anti-inflammatory and antithrombotic effects....needs to be started within the first 24-48 hours....watch for BLEEDING (NOTE: Drotrecogin alpha "Xigris" is no longer on the market and used in the treatment of Septic Shock) Titrate Vasopressors to keep MAP >65 mmHg: Norepinephrine (1st choice) Causes vasoconstriction, which INCREASES systemic vascular resistance (this is majorly needed due to the vasodilation occurring in septic shock) USED when fluid replacements are not helping (fluids replacement is first). The mean arterial pressure is the amount of pressure in the arteries during one cardiac cycle and shows how well vital organs are being perfused (if it is less than 65...organs are not being perfused very well). Inotropics may be added with the vasopressors (Dobutamine), if there is still low tissue perfusion Crystalloids or Colloids fluids: FIRST, if not working then vasopressors The large amounts of fluid will fill those dilated vessels and refill the depletion of circulating volume. Needs at least 2 IV sites...warm fluids to prevent hypothermia Successful: increased blood pressure and/or increasing CVP (8-12 mmHg) Monitor urinary output 30 mL/hr or greater...needs a Foley! Steroids low dose (corticosteroids): used in SOME patients to help decrease the amplified inflammation, especially if the patient is not responding to vasopressors Hemodynamic monitoring: central venous/arterial cath to assess tissue perfusion and filling pressures in the right side of the heart (right atrium: CVP), (PAWP: filling pressure of left side of the heart) Oxygenate: keep oxygen saturation >95%...tissues need oxygen. Many patients will experience respiratory failure (ARDS) and will need intubation with mechanical ventilation. Cultures: blood, wound, urine etc. obtain BEFORE antibiotics Keep glucose <180 mg/dL....may need insulin drip...the immune system is affected by hyperglycemia Other: Check lactate levels: if patient needs vasopressors to keep MAP >65 mmHg even though fluid replacement has been given and lactate level is >2 mmol/L think SEPTIC SHOCK! Foley insertion: strict intake and output. UOP will help you assess tissue perfusion and if kidneys are being perfused well.... UOP should be > 30 mL/hr

Please know the differences between the four types of shocks. In other words what is the pathophysiology of them all? Know clinical manifestations as well.

Shock · Syndrome characterized by decreased tissue perfusion and impaired cellular metabolism · Imbalance in supply/demand for 02 and nutrients Cardiogenic Pathophysiology · Occurs when either systolic or diastolic dysfunction of the hearts pumping action results in reduced cardiac output. Systolic dysfunction is the hearts inability to pump forward and diastolic dysfunction is ineffective filling. (Structural problems, MI, Dysrhythmias) *****Cardiogenic shock is the leading cause of death from acute MI***** Clinical Manifestations Early Manifestations · Tachycardia, hypotension, narrowed pulse pressure, increased myocardial oxygen consumption Physical Assessment · Tachypnea, pulmonary congestion, pallor, cool/clammy skin, anxiety, confusion, agitation, increased pulmonary wedge pressure, decreased renal perfusion and urinary output Hypovolemic Pathophysiology · Absolute: loss of intravascular fluid volume. Hemorrhage, GI loss, fistula, drainage, DI, hyperglycemia, diuretics · Relative: results when fluid volume moves out of vascular space into extravascular space (third spacing) Clinical Manifestations · Anxiety, tachypnea, tachycardia, hypotension decrease in SV, PAWP, and urinary output Obstructive Pathophysiology · Develops when physical obstruction to blood flow occurs with decreased cardiac output (PE, tension pneumothorax, cardiac tamponade) Clinical Manifestations · Decreased cardiac output, increased afterload, variable left ventricular filling pressure Distributive (Neurogenic, Anaphylactic, Septic) Neurogenic: can occur in response to spinal cord injury or spinal anesthesia · hemodynamic phenomenon, · can occur within 30 min of spinal cord injury at 5th thoracic (T5) vertebrae or above · can last up to 6 weeks · *****results in massive vasodilation, leading to polling of blood vessels, tissue hypoperfusion, ultimately impaired cellular metabolism***** Clinical Manifestations · HYPOTENSION, BRADYCARDIA, inability to regulate body temp, dry skin, poikilothermia (taking on the temp of the environment) Anaphylactic: Acute life-threatening hypersensitivity (allergic) reaction, massive vasodilation, release of vasoactive mediators, increased capillary permeability Clinical Manifestations · anxiety, confusion, dizziness, sense of impending doom, chest pain, incontinence, selling of lips/tongue, angioedema, wheezing, strider(due to laryngeal edema), flushing, pruritis, urticaria, respiratory distress and circulatory failure Septic: Presence of sepsis with hypotension despite fluid resuscitation, presence of inadequate tissue perfusion resulting in hypoxia · *****3 major pathophysiologic effects: vasodilation, maldistribution of blood flow, myocardial dysfunction ( decreased EF and ventricular dilation)***** · Sepsis: systemic inflammatory response to documented or suspected infection · Severe Sepsis: sepsis complicated by organ dysfunction Clinical Manifestations · Tachypnea/hyperventilation, (results in respiratory alkalosis, respiratory failure developed in 85% of patients), decreased urine output, altered numerological status, GI dysfunction, GI bleeding, paralytic ilieus

What are right sided heart failure signs and symptoms?

Systemic Congestion: JVD, peripheral edema, ascites, hepatomegaly

Signs of Fluid Overload

Tachycardia, tachypnea, hypertension, bounding pulse, weight gain, edema, ascites, dyspnea, crackles, distended neck veins

What are manifestations of hypoglycemia?

Too much insulin in proportion to glucose in blood......blood glucose level < 70 Clinical Manifestations · Shakiness, palpitations, nervousness, diaphoresis, anxiety, hunger · Altered mental status: difficulty speaking, visual disturbances, stupor, confusion, coma · Untreated hypoglycemia can progress to loss of consciousness, seizures, coma, and death

What are manifestations of hypoglycemia?

Too much insulin in proportion to glucose in blood......blood glucose level < 70 Clinical Manifestations • Shakiness, palpitations, nervousness, diaphoresis, anxiety, hunger, pallor • Altered mental status: difficulty speaking, visual disturbances, stupor, confusion, coma • Untreated hypoglycemia can progress to loss of consciousness, seizures, coma, and death

If a patient has heart disease that escalates to an MI, what is the best lab test to determine if the patient has had an MI?

Troponin T • Normal < 0.1 ng.ml o Detectable: 2-3hrs o Duration: 10-14days Troponin I • Normal < 0.3 ng/ml o Detectable: 2-3hrs o Duration: 7-10days

Seizures

Uncontrolled electrical discharge of neurons • Epilepsy = chronic seizures, 2 or more Risk Factors • fever, cerebral edema, infection, toxin exposure, brain tumor hypoxia, alcohol/drug withdrawal, fluid/electrolyte imbalance Triggering Factors • Stress, fatigue, caffeine, flashing lights, metabolic disorder, electrolyte imbalance, etoh abuse or withdrawl, infection, trauma During Seizure • Turn pt to side. loosen restrictive clothing, do not insert airway, document onset/duration of seizure Post Seizure • check vitals, neurologic checks, reorient pt, seizure precautions, determine possible trigger

Anaphylactic Shock NCLEX Review

What is anaphylactic shock? It occurs due to the introduction of an allergen in the body. This leads to mast cells or basophils to release histamine and other chemicals system-wide. This will decrease tissue perfusion causing shock to occur. Anaphylactic shock is a form of distributive shock. The other types distributive shock are neurogenic and septic shock. How does an allergen enter the body to cause anaphylactic shock? An allergen can enter various ways such as via an: injection, inhalation, oral, or contact with the skin. Known Substances that can cause Anaphylactic Shock: Foods (shellfish, peanuts, eggs, milk) Medications (vaccines, contrast dye, NSAIDS, antibiotics...Penicillin) Insect venom Latex Physical exercise Unknown cause: "idiopathic" Now, let's talk about what is occurring during anaphylactic shock, and to do this we need to talk about the two types of reactions that can lead to anaphylactic shock. Anaphylactic shock can occur either due to an immune response where IgE antibodies are created or due to a non-immune response. Regardless of the reaction, both cause the same signs and symptoms, and occur because mast cells or basophils release histamine and other mediators. Anaphylactic reactionIgE related (immunological):Patient has to experience sensitization for reaction to occur!Sensitization is where the patient has a first-time exposure to an allergen that causes the creation of IgE antibodies. The antibodies attach to the mast cell or basophil and hang out waiting for the second exposure. When the second exposure to the allergen occurs, it causes the mast cells or basophils to release histamine and other substances. This leads to the anaphylactic reaction.It's a Type I Hypersensitivity Reaction: This means the allergen attaches to immunoglobulin E (IgE) antibodies (these antibodies are created due to this allergen) on mast cells and basophils. This leads to a system-wide release of histamine and other mediators.....this is illustrated below. Anaphylactoid reactionNon-IgE related (non-immunological):The patient doesn't have to be sensitized for the reaction to happen....but can happen with the first-time exposure.Causes same reaction as anaphylactic, but it's not via the immunoglobulin IgE antibodies on the mast cells or basophils.Allergens for this type of reaction include: contrast dyes, chemotherapy agents, NSAIDS, etc.These agents directly cause the mast cells and basophils to breakdown and release histamine. Effects of Histamine on the Body during Anaphylactic Shock Histamine will cause: Dilatation of vessels (lowers blood pressure and tissue perfusion) Bronchoconstriction (narrow airways and respiratory failure) Increases heart rate Increases the permeability of vessels (leads to swelling and depletes intravascular space of fluid that shifts to the interstitial space) Itching Increases contraction of GI stomach muscles and increases gastric secretions (leads to nausea, vomiting, diarrhea, and GI pain) It affects the following systems of the body: Cardiac, Respiratory, GI, and Skin Signs and Symptoms of Anaphylactic Shock The signs and symptoms of anaphylactic shock occur mainly due to histamine. So if you remember the effects of histamine on the body during anaphylactic shock, the signs and symptoms are easy to recall. Respiratory: dyspnea, wheezing (bronchoconstriction), swelling of upper airways due to edema "tightness", can't speak, coughing, stuffy nose, watery eyes Cardiac: tachycardia, hypotension (vasodilation)...may lose consciousness or become dizzy GI: vomiting, nausea, diarrhea pain Skin: red, swollen, itchy, hives (vasodilation) Nursing Interventions and Treatments for Anaphylactic Shock Prevention! Know your patient's allergies (assess, document, and AVOID patient's allergens). Anytime the patient is started on a new mediation or needs a procedure that requires something that is known as an allergen, always go back and review the patient's allergies! Implement your hospital's prevention measure system for allergens by using signs or bracelets for the patients with allergies. This will help make sure other members of the health care team aware of the patient's allergies as well. Remember anaphylactic shock can start occurring with seconds to minutes of the exposure. Recognize the signs and symptoms and ACT FAST! Allergen (remove it) & Airway (manage airway with high flow oxygen and continuous vital sign monitoring) Call Rapid Response (start CPR, if needed, until help arrives) Trendelenburg Position: this is the supine position with the legs elevated (unless vomiting (lay on side) or having major airway issues). This position will help increase venous return to the heart and increase cardiac output and blood pressure. First-line Drug is Epinephrine: This medication can administered IM or Subq (dose may be repeated, if needed per MD order). It may needed IV if severe hypotension persists. Epinephrine causes vasoconstriction which will increase the blood pressure, reduce swelling, and cause bronchodilation. Administer other medications per MD order (these medications may be ordered depending on the patient's status): IV fluids, breathing treatment of Albuterol, Antihistamines to target H1 (Diphenhydramine) and H2 (Ranitidine), Corticosteroids to prevent a recurrent attack Stay and monitor patient very closely: at risk biphasic anaphylaxis (signs and symptoms occur again even if not exposed to allergen...can happen hours after initial attack...may be less, worst, or the same as initial attack) TEACH!!! Patient education:Importance of avoiding allergen (may need allergy tests)Wearing medical alert bracelets and letting others know about allergen. Example: a child's caregiver, teacher, friends etc.ALWAYS carry an Epi-Pen! It's administered in the middle of the outer thigh.Replace when expired.Have patient demonstration how to use (there are Epi-Pen Trainer devices that can assist with this teaching):It's an auto-injector.Administered in the middle of outer thigh (can do this through clothes, if needed).After injecting the needle, hold the device in place for 3 seconds, so medication is fully injected and then remove.Massage the injection site for 10 seconds after injection. This will increase absorption.Seek medical attention immediately!

Cardiogenic Shock NCLEX Review

What is cardiogenic shock? It's where the heart can NOT pump enough blood to meet the perfusion needs of the body. Therefore, the heart does not pump enough blood throughout the body, which will decrease cardiac output and this leads to a decrease in tissue perfusion and oxygen supply to the organs/tissue's cells. Note: In cardiogenic shock, there is NOT an issue with a loss of blood volume like in some of the other types of shock. Blood volume is normal. However, because the heart has experienced a decrease in its ability to function properly, that blood volume starts to back up and leads to congestion in the lungs and the right side of the body (keep this in mind for when we review the signs and symptoms). Let's break down the heart's role: The heart is the PUMP of the body. It takes blood to the right side of the heart that has been used and depleted of oxygen by the cells of the body and pumps it to the lungs. The lungs oxygenate and remove carbon dioxide from the blood and sends it back to the heart via its left side. The left side is very strong, especially the left ventricle, which is the main pumping chamber of the heart. The left side shoots the fresh oxygenated blood into the aorta. The aorta branches off into many arteries that go into this complex network of vessels to feed the organs oxygenated blood. Therefore, the heart is the main center piece in the body that plays a role in tissue perfusion, and everything in the body depends on the heart for its survival. If the heart can't pump blood efficiently, the organs don't receive fresh oxygenated blood and the cells that make up that organ start to die. Therefore in a nutshell, when the heart can't pump, cardiac output falls, which decreases tissue perfusion and the cells that make up our organs don't receive enough oxygen to work. They start to panic and eventually die. When cardiac output falls (hence the blood pressure drops), the patient begins to enter the stages of shock (we talked about the stages of shock in the previous lecture: initial, compensatory, progressive, and refractory). Cardiac Output and Cardiogenic Shock First, let's talk about cardiac output because it's a very important term you should know when taking care of a patient with cardiogenic shock: Cardiac output is the amount of blood the heart pumps per minute. The heart's cardiac output should be anywhere from 4-8 liters of blood per minute. Cardiac output is determined by the person's heart rate times the stroke volume. Stroke volume is the amount of blood pumped from the left ventricle each beat (50-100 ml). Stroke volume is determined by the preload, afterload, and contractility of the heart. Preload is the amount the ventricle stretches at the end of diastole (hence it's the amount the ventricles stretch once their filled with blood....so it's the end-diastolic volume). Remember diastole is the relaxation/filling phase of the heart. Afterload is the pressure the ventricle must pump against to squeeze blood out. Therefore, it's the force the heart has to pump against to get blood out of the ventricle. Contractility is how well the muscle cells are contracting. Therefore, it's how well the heart is contracting to pump blood. If the stroke volume falls (meaning the heart muscle is NOT pumping blood very well), the cardiac output decreases and this leads to a fall in tissue perfusion. So, in other words, cardiac output tells us how well the heart is pumping and perfusing the cells that make up our organs. When we talk about treatment for cardiogenic shock it will include medications that will affect preload, afterload, and contractility via drugs like vasopressors, inotropes, vasodilators, and diuretics. Examples: if the afterload is decreased (which is the resistance the heart must pump against to get blood out of the heart....if you decrease this, it makes it easier for the heart to pump blood forward) the stroke volume will increase hence delivering a higher cardiac output....vasodilators can achieve this. if contractility is increased (which is how strong the muscle cell contracts) it will increase stroke volume and cardiac output....positive inotropic medications can achieve this. if preload is increased (which is the amount the ventricle stretches at the end of diastole) the stroke volume will increase hence delivering a higher cardiac output... vasopressors can achieve this by causing vasoconstriction, which will increase venous return to the heart. Another term you may see, especially when talking about cardiogenic shock, is Cardiac Index. This is a more specific cardiac output measurement based on the patient's body size. It's calculated by taking the cardiac output and dividing it by the patient's body surface area. Patients with cardiogenic shock will have a CI (cardiac index) less than 2.2 L/min/m2. Normal CI is: 2.5-4 L/min/m2 Causes of Cardiogenic Shock What can cause the heart's cardiac output to fall (hence cardiogenic shock)? Issues that cause the heart to have problems: contracting (systolic dysfunction)...the heart can't successfully pump blood out of the heart and to the body filling (diastole dysfunction)....the heart's chambers don't fill properly so blood really can't be pumped to perfuse the body Examples: ****Main cause: Acute myocardial infarction (contracting issue): this is known as a heart attack. It occurs due to a blockage in the coronary arteries. The coronary arteries supply the cells of the heart muscle with oxygen. When blood flow is dramatically decreased or blocked completely to the cells that make up the heart muscle, they start to die. When majority of the blood flow to the left coronary is diminished, the muscle cells that make up the left ventricle die. Remember the left ventricle is the main pumping chamber of the heart. It pumps the blood to the aorta which then goes to the body. If a patient has an acute myocardial infarction that affects the left ventricle, the patient is at high risk for developing cardiogenic shock.Why? When the heart cells die, the heart doesn't contract (pump) like it should, especially the left ventricle. Preload, afterload, contractility are all going to be affected along with the heart rate. Cardiac output falls (can't pump much blood per minute) and tissue perfusion is decreased to the body's cells. Pericardial tamponade (filling issue): too much fluid is around the heart, so it can't fill properly. Other causes: dysrhythmias, myocarditis, endocarditis, pulmonary edema, structure issues with valves and/or septal walls etc. Quick Patho on what happens during cardiogenic shock Cause (ex: acute myocardial infarction) -> major cell damage to the heart muscle -> can't pump efficiently.....ability to pump blood out of the heart and to the body has decreased -> decreases stroke volume -> decreased cardiac output -> decreases perfusion to the body's cells that make up our organs and tissues -> cell injury (signs and symptoms of body systems struggling due to low oxygen) Signs and Symptoms of Cardiogenic Shock When trying to recall these signs and symptoms, think about what happens in the body due to decreased cardiac output and when blood starts to back flow into the lungs and the right side of the heart. Let's break down the signs and symptoms by body systems: Heart: it's weak and not pumping blood forward or filling efficiently.....this leads to: Back flow of blood from the left side to the lungs (pulmonary congestion, crackles, dyspnea, increased respiratory rate, low oxygen, increased heart rate) As it progresses, blood will back flow from the lungs to the right side of the heart (neck veins become distended due to an increase in venous pressure and there will be a high CVP...central venous pressure) Chest pain (decrease perfusion to heart muscle via the coronary arteries) Hypotension: Systolic blood pressure less than 90 mmHg or 40 mmHg from baseline for at least 30 minutes Weak peripheral pulses If on hemodynamic monitoring may have:Decreased cardiac index <2.2 L/min/m2Increased pulmonary capillary wedge pressure (PCWP) >18 mmHgIncreased central venous pressure Brain: cells are not being perfused due to low cardiac output and the build-up of waste in the body (liver and kidneys are failing to filter out toxic substances).....leads to confusion, agitation, restlessness Kidneys: decreased blood flow to the kidneys activates the renin-angiotensin system. This leads to the release of angiotensin II, which leads to the release of aldosterone and ADH (antidiuretic hormone). These substances will cause the kidneys to keep sodium and water (aldosterone) and cause the body to retain water (ADH).....leads to oliguria <30 mL/hr urinary output WHY? These substances are naturally released by the body to help increase blood volume so cardiac output can be increased. Other signs and symptoms will be associated with renal failure like an increased BUN and creatinine. Skin: decreased perfusion to the skin....leads to decreased capillary refill, cool, pale, and clammy skin Nursing Interventions for Cardiogenic Shock To understand the nursing interventions, we need to know the goals of medical treatment for a patient with cardiogenic shock. Goals include: reperfusion to the heart muscle if there is a decreased blood flow to the heart muscle via the coronary arteries. The can be performed via a heart catheterization, and if a blockage is found, a stent can be placed. increase cardiac output via cardiac medications (most meds are titrated and the patient is on hemodynamic monitoring to assess certain pressures in the heart) decrease fluid overload, if present (via diuretics) maintain oxygen status due to pulmonary edema (will need mechanical ventilation) Nurse's Role: Hemodynamic monitoring (more about this below), maintain mechanical ventilation (will need to help with respiratory failure), central line placement for medication, monitoring, assessing for signs of adequate tissue perfusion: mental status, blood pressure, heart rate, rhythm, urine output, skin color and capillary refill, lung sounds etc. Monitoring labs: high cardiac markers ex: elevated troponin (this substance is released if there is injury to heart cells), increased BNP (this substance is released by the cells that make up the ventricles when they stretch due to high blood volume), pulmonary edema on chest x-ray, echocardiogram (show a low ejection fraction), acid-base level that demonstrate acidosis serum lactate >4 mmol/L (cells will switch from aerobic to anaerobic metabolism which will produce lactic acid), drop in blood ph <7.35 Hemodynamic monitoring: Pulmonary artery wedge pressure/pulmonary capillary wedge pressure (increased in cardiogenic shock): a pulmonary artery catheter (Swan-Ganz catheter) is inserted through the right side of the heart via a vessel and the catheter is wedged in the pulmonary arterial branch and a balloon is temporarily inflated to measure left atrial filling pressure. Normal 4-12 mmHg >18 mmHg in cardiogenic shock....blood is backing up in the heart and lungs (hence not being pumped out and creating a high pressure in the left atrium) Central venous pressure (CVP): catheter used to measure the pressure in the right atrium and superior vena cava. INCREASED in cardiogenic shock (Normal CVP is 2 to 6 mmHg or 8-12 mmHg depending on source). WHY? The back flow of blood to the right side of the heart (right atrium into venous circulation) leads to venous congestion, which increases the central venous pressure. Medications: a combination of medications can be given and medications vary depending on the cause of the cardiogenic shock and the patient's response. Diuretics: cardiogenic shock is one of the two types of shock that doesn't have a decrease in blood volume (the other is neurogenic shock). Patients with cardiogenic shock have a backup of fluid in the lungs from an injured heart that is failing to pump blood forward. Diuretics (ex: furosemide....watch potassium level "hypokalemia"....normal level is 3.5-5 mEq/L) will help remove extra fluid volume via the kidneys. This will decrease the preload (amount ventricles stretch at the end of diastole), which will help the relieve the workload of the heart. However, watch the fluid status of the patient, renal function, and for worsening hypotension. Vasopressors: causes constriction of vessels and increases preload (venous return) and cardiac output Norepinephrine (vasoconstrictor) sometimes used over dopamine because it doesn't cause tachydysrhythmias: it increases tissue perfusion by increasing blood pressure Vasopressors that create a positive inotropic effect: increases the strength of the heart's contraction (increases contractility) and stroke volume Dobutamine (increases contractility and cardiac output BUT can cause vasodilation due to the way it acts on receptors and may make hypotension WORSE. If this occurs that patient may be started on norepinephrine or dopamine. Dopamine (increase contractility, causes vasoconstriction: increases blood pressure and MAP (want >60 mmHg), but watch out for tachydysrhythmias) Vasodilators: decreases preload and afterload: increases stroke volume because it decreases the afterload, so it's easier for the heart to pump blood forward so cardiac output increases. The workload on the heart decreases by dilating the coronary arteries....causes hypotension and may not be used if the patient is severely hypotensive (monitor blood pressure very closely). Ex: Nitroglycerin or Sodium Nitroprusside IV Fluids: Normal saline (if even used) is used with extreme caution due to pulmonary edema that may be present. A fluid challenge is majorly used for the other types of shock when blood volume is the issue...remember in cardiogenic shock blood volume is not the issue. Intra-aortic balloon pump It's a device placed to help improve coronary artery blood flow and increase cardiac output. How? A catheter is inserted through a vessel (ex: femoral artery) up through a section of the aorta. A balloon attached to the catheter will inflate and deflate during systole (contraction) and diastole (relaxation). When the balloon deflates during systole. it creates a suction-like pressure that will draw blood out of the weak heart and into the coronary arteries and systemic circulation (hence increasing cardiac output and blood supply to the heart muscle). When the balloon inflates during diastole. it will create pressure that will push blood into the coronary arteries (hence further increasing blood supply to the heart muscle).

Hypovolemic Shock NCLEX Review

What is hypovolemic shock? It occurs when there is LOW fluid volume in the intravascular system. Hypo: low Vol: volume Emic: blood "low blood volume" The intravascular system is the space that contains the volume of blood in a person's circulatory system. Therefore, if there is a decrease in the volume of blood in a person's circulatory system, what does the heart have to pump? Hardly anything at all! If the amount of blood the heart pumps to the organ/tissues DECREASES, the cardiac output decreases. This will lead to decreased tissue perfusion, which will alter the function of cells. It will limit their access to oxygen and signs and symptoms of shock will occur. A person needs to lose about 15% or MORE of their intravascular volume for hypovolemic shock to occur. The average human blood volume is 5 L (exact amount depends on the person's size). So, if a person who has a blood volume of 5 L and loses 1 L of blood volume (1,000 mL), that would be 20% of their blood volume. This person would start showing signs and symptoms of hypovolemic shock. Causes of Hypovolemic Shock What can lead to a loss of fluid volume in the intravascular system? Any condition that leads to fluid leaving the body externally or there is shifting of fluid within the body that leaves the intravascular space. Relative hypovolemic shock: this is an INSIDE fluid shift from the intravascular system (this tends to be more concealed than absolute) Fluids or blood collecting or leaking inside the body from internal bleeding, third-spacing of fluid (severe burns due to increased capillary permeability), fracture of long bones, damage to organs like the pancreas...example: Cullen or Turner's Sign. Massive vasodilation from septic shock Absolute hypovolemic shock: this is an OUTSIDE fluid shift from the intravascular system that leaves the body (this tends to be more noticeable compared to relative) Massive bleeding from injury or surgery Excessive fluid loss from oral (vomiting), GI (diarrhea), GU (urine), integumentary (sweating).....many times this is caused by a disease process (diabetes or endocrine disorders) or illnesses Pathophysiology of Hypovolemic Shock What is happening in hypovolemic shock? There's major depletion of volume in the intravascular system (relative or absolute cause) -> this decreases the amount of venous return to the heart (this is the amount of blood draining back to the heart) -> this DECREASES preload (the amount the ventricles stretch once their filled with blood)...they won't be stretching very much because there isn't much fluid to fill them -> this decreases stroke volume (the amount of blood pumped by the left ventricle with each beat -> this DECREASES CARDIAC OUTPUT (this is the amount of blood the heart pumps per minute....4-8 Liters per minute...CO = HR x SV) -If cardiac output falls too low, the amount of blood that should be going to the organs/tissues cells per minute will drastically fall. And guess what important substance is in the blood that the cells of the organs and tissues rely on to survive? OXYGEN! But since the amount of blood that reaches them is low, the cells won't receive enough oxygen to function and hypoxic injury to the cell can occur. The body will attempt to compensate by activating the sympathetic nervous system, which will trigger the body's built-in survival system. Now, based on the percentage of fluid volume that is lost will determine the signs and symptoms the patient may present with and what stage the patient is likely in. Hypovolemic shock can be divided into four stages or classes, and these are like the stages of shock we just reviewed in this series, but these stages are based on the percentage of fluid volume loss. Remember the numbers: 15, 15-30, 30-40, 40% and what is happening to the blood pressure, heart rate, urinary output, mental status, and the skin. Class I : <15% of volume loss....up to 750 mL in an adult The body can maintain cardiac output with this volume loss. Patient is mainly asymptomatic with this class. Heart rate within normal limits (less than 100 bpm) Blood pressure, respiratory rate, within normal limits Skin pink, warm, and capillary refill normal (<2 seconds) Normal urinary output (greater than 30 mL/hr) Mental status: normal...may be a little anxious Class II: 15-30% of volume loss....750-1500 mL in an adult Cardiac output is starting to fall due to the volume loss. There is major body system compensation via the sympathetic nervous system, renin-angiotensin system, and the shunting of blood to vital organs. Heart rate will increase....tachycardia (greater than 100 bpm)....due to the effects of the SNS Blood pressure decreases but within normal limits (for now due to vasoconstriction) Respirations increase (mild)...due to low oxygen level in the body Urinary output will start to lower (20-30 mL/hr)....blood flow is shunted and body will start to keep water from aldosterone and ADH being released due to angiotensin II Skin: cool, clammy, increased capillary refill >2 seconds...blood flow diverted to vital organs Diminished peripheral pulses Mental status: mild anxiety Class II: 30-40% of volume loss....1,500-2000 mL in an adult The body can't compensate anymore....it's exhausted! Therefore, cardiac output falls so low that tissue perfusion is altered, which causes the cells that make up the organs to malfunction....heart, liver, lungs, kidneys, brain etc. Heart rate increased (significant tachycardia >120 bpm) Respiratory increased....progressing to respiratory failure Hypotension Oliguria (<30 mL/hr)....renal failure...high BUN and creatinine Poor peripheral pulses Skin: very cool, mottled, capillary refill >2 seconds Mental status: very anxious and confused.....acidosis, low oxygen, and low perfusion to the brain Class IV: >40% of volume loss......more than 2,000 mL in an adult Death is very near....needs very dynamic treatment! The body is shutting down....the fluid loss is SEVERE! Significant tachycardia (>140 bpm), increase respiratory (respiratory failure), severe hypotension, anuria (no urine production), mental status: lifeless, coma *Source: Class/Stage volume loss percentage and amount of volume loss modified from American College of Surgeons Guidelines Signs and Symptoms of Hypovolemic Shock Remember it depends on the percentage of volume loss, but in a nutshell: tachycardia, hypotension, cool/clammy skin, weak peripheral pulses, anxiety, decreased urinary output.....central venous pressure: low, PAWP/PCWP: low Nursing Interventions for Hypovolemic Shock Treatment goals: fluid resuscitation, correct underlying cause that is leading to the fluid loss....example: hemorrhaging: surgery (get the patient ready for surgery) Nursing Interventions Monitor oxygenation and perfusion status of patient: place on oxygen, may need intubation and mechanical ventilation, what is the patient's hemodynamic status? blood pressure, heart rate, rhythm, tissue perfusion to organs: mental status, urinary output (will need catheter insertion to closely monitor urinary output...UOP needs to be greater than 30 mL/hr) If bleeding, hold firm, direct pressure. If showing signs and symptoms of hypovolemic shock, place in modified Trendelenburg position (feet at 45' and head flat....increases venous return to heart and cardiac output). Obtain IV access (at least two IV sites that are large....18 gauge or bigger in a large vein like antecubital)...needed for rapid fluid delivery and other medications....many patients with severe hypovolemic shock (especially ones who are not responding to fluid treatment) will have a central line and hemodynamic monitoring to monitor cardiac output and fluid replacement. Collect labs: hgb, hct (blood level), lactate level (status of cell's metabolism), blood gases (acidosis?), electrolytes, bun, and creatinine Severe hypovolemic shock: Central Venous Pressure (low) and PAWP/PCWP (low) Fluids for Hypovolemic Shock Crystalloids and colloids Solution are two types of volume expanders used in hypovolemic shock: varies depending on the patient's status and volume loss Crystalloids: Normal Saline or Lactated Ringer's: Isotonic fluids that will add more fluid to the intravascular system...increasing preload, stroke volume, and cardiac output most commonly started out on a crystalloid solution watch for fluid volume overloadIf in fluid overload, hemodynamic monitoring may show: elevated CVP or PWCP/PAWPAuscultate for fluid in the lungs...cracklesEdema, jugular venous distention Remember the 3:1 rule for crystalloid solutions: For every 1 mL of approximate blood loss, 3 mL of crystalloid solution is given. **** Crystalloid solutions are able to diffuse through capillary wall, so there is less fluid that remains in the intravascular space compared to colloid solutions. Colloids: Albumin, Hetastarch: made up of large molecules (example: proteins) that can't diffuse through the capillary wall so more fluid stays in the intravascular space for longer more expensive patient can have an anaphylactic reaction monitor for fluid overload ***If giving large amount of fluids, need to WARM them. WHY? If not warmed, it can lead to hypothermia, and this will alter clotting enzymes. Keep the patient warm, but not to the point of sweating. Blood and Blood Products: Packed Red Blood Cells, Platelets or Fresh Frozen Plasma (FFP): PRBCS: helps replace fluid and provides the patient with hemoglobin, which will carry oxygen to deprived cells (crystalloids and colloids can't do this)....these types of fluid may be used when the patient is not responding to crystalloid fluid challenge, experiencing severe bleeding/severe hypovolemic shock etc. Platelets: for uncontrolled bleeding to help with thrombocytopenia Fresh Frozen Plasma: for when the patient needs clotting factors ****monitor for transfusion reaction with these products

Stages of Shock NCLEX Review

What is shock? This condition results from some type of cause (discussed below) that leads to decreased tissue perfusion, which causes cell hypoxia. If the cell hypoxia is severe enough it will cause organ dysfunction (MODS) and eventually lead to death. The cause of shock depends on what type of shock is presenting. The types of shock include: Septic shock: occurs due to a severe infection Hypovolemic shock: occurs due to severe fluid loss Neurogenic shock: occurs due to severe damage to the neuro system (example: spinal injury) Cardiogenic shock: occurs due to a weak heart Anaphylactic shock: occurs due to an allergic reaction Note: Distributive shock includes septic, anaphylactic, and neurogenic shock. Stages of Shock What are the stages of shock? Initial, compensatory, progressive, and refractory Initial Stage Big Takeaway from this Stage: Cardiac output is low enough to cause the cells to experience hypoxia. The cells will SWITCH from AEROBIC to ANAEROBIC metabolism. Anaerobic metabolism will create LACTIC ACID, which will accumulate in the blood and lead to lactic acidosis. Signs and symptoms of shock in this stage are very subtle compared to the next stages. Let's analyze this stage: A type of shock is presenting! Therefore, we have a cause that has led to DECREASED TISSUE PERFUSION. Hence, we're going to have LOW cardiac output. What is cardiac output? It's the amount of blood the heart pumps each minute. It is calculated by taking the heart rate and multiplying it by the stroke volume and this equals the cardiac output. In this stage, the cardiac output is just low enough where tissue perfusion is unable to support the oxygen demands of the cells that make up the tissues/organs. Remember the cells that make up our organs and tissues have to constantly be receiving fresh oxygen and other nutrients to survive. When they don't receive these substances, they start to take matters into their own hands by....... Switching the way they metabolize! The cells will switch to anaerobic metabolism (metabolism WITHOUT oxygen ) from aerobic metabolism (metabolism WITH oxygen). Why do they do this? Because they don't have any oxygen to use because they aren't receiving it...remember tissue perfusion is decreased. What's the downside of anaerobic metabolism? It produces a waste product called LACTIC ACID. Normally, our body can deal with lactic acid via the liver, but the liver is not functioning at an optimal level because of the low amount of oxygen its cells are receiving. In better circumstances when tissue perfusion is adequate, the liver takes lactic acid and convert it to pyruvic acid and then to glucose via gluconeogenesis. Therefore, lactic acid will start to accumulate in the blood (especially as the patient advances to the other stages of shock). The accumulation of lactic acid causes the blood's pH level to drop (hence acidosis occurs) and it further damages the cells. Important lab values to remember: Normal serum lactate level <1 mmol/L Abnormal indicating lactic acidosis >4 mmol/L Compensatory Stage Big Takeaway from this Stage: The body systems are coming to the RESCUE!! Hence, they are going to "try" to compensate by using the body's natural built-in survival team: the hormonal, neural, and biochemical processes in the body. Be sure to remember what substances are being released and how they affect the body during this stage. This built-in system will try to fight the results of anaerobic metabolism. In addition, it will attempt to increase the cardiac output and blood pressure via the stimulation of the sympathetic nervous system (SNS) and renin-angiotensin system (RAS), which will increase tissue perfusion (this is what the patient needs right now so the cells can receive oxygen and live). Let's analyze this stage: If the cause of shock is corrected during this stage (hence a patient with hypovolemic shock receives fluid replacements that correct the fluid status of the patient), this stage is REVERSIBLE and the patient can make a full recovery. However, if the cause is NOT corrected the patient will enter the next stage. The body will succeed at first with increasing cardiac output and blood pressure via the rescue team discussed above. This will result in an increase in tissue perfusion, BUT the body is limited on how long it can maintain this rescue effort. How does the body provide compensation? As the blood pressure drops (hence cardiac output becomes very low), the body will sense this and say "Okay, the amount of blood the heart is pumping per minute it WAY too low, especially for our vital organs (mainly the heart and brain), so we must ACT now!" One of the structures to sense this drop in blood pressure is the baroreceptors, specifically the receptors in the carotid sinus and aortic arch. This will stimulate the sympathetic nervous system to release the catecholamines: epinephrine and norepinephrine. What do these catecholamines do? They cause vasoconstriction! This will result in an increase in blood pressure and heart rate. When this occurs there is increased perfusion to the vital organs. Less blood will go to the non-vital organs (GI, renal, skin, lungs), while more will go to the vital organs (heart and brain). Furthermore, because there was a drop in blood pressure (hence arterial pressure), there will be a decrease in capillary hydrostatic pressure. What does capillary hydrostatic pressure mean? In a nutshell, it's the force of pressure the blood creates around the capillary wall. If the blood pressure and cardiac output are low, the force of pressure the blood creates around the capillary wall is definitely low. This will signal to the body to try to increase venous blood return by shifting fluid from the interstitial compartment to the intravascular compartment. Think of it this way: it's like the body is trying to give itself a natural IV fluid bolus. By doing this, the body is attempting to increase cardiac output and the blood pressure, which will increase tissue perfusion. Now let's talk about how other systems are affected and how they play a role in the compensatory stage: Kidneys: because blood flow is decreased to the kidneys they activate the renin-angiotensin system. What this system does? Renin stimulates angiotensinogen which creates angiotensin I. Angiotensin I turns into Angiotensin II. Angiotensin II is a very mighty vasoconstrictor. This substance will cause vasoconstriction in both the arterial and venous system. The constriction in the venous system will lead to more blood return to the heart, and the constriction in the arterial system will increase blood pressure. All this together will lead to an increase in tissue perfusion and the cells will receive more oxygen. The presence of angiotensin II will also trigger the release of ALDOSTERONE. What does aldosterone do? It makes the kidneys KEEP sodium and water. Why does this matter? It will increase blood volume! In addition, because the kidneys are keeping sodium, it will create the urine to contain a high amount of sodium, which leads it to have a high osmolality. The high osmolality signals to the posterior pituitary gland that the body is trying to keep water for some reason, so it releases ADH (antidiuretic hormone). What does ADH do? It prevents water from leaving the kidneys. Hence, further increases BLOOD VOLUME. By increasing blood volume, the cardiac output by the heart will be increased along with tissue perfusion. Notice that all the systems trying to rescue the body from shock are trying to release substances that will increase cardiac output or increase blood volume because it knows that if it can do this it will increase tissue perfusion. GI: perfusion is decreased to this system so it slows down. The patient is a risk for paralysis of the intestines in a condition called paralytic ileus. Skin: perfusion is decreased so blood flow is low, which leads the skin to be cold and clammy. Now, this is not the case during this stage in SEPTIC SHOCK. The patient's skin will be hot and flushed due vasodilation presenting. Lungs: perfusion is decreased so parts of the lung may not be perfused. Now, ask yourself what do the lungs do? They perform gas exchange. If some parts of the lungs are not being perfused, gas exchange is not going to occur in those parts. So, there is a ventilation and perfusion mismatch and oxygen levels will become low in the blood. This will lead the patient to hyperventilate (they are trying to compensate by increasing the rate and depth of breathing in an attempt to increase the oxygen level). Progressive Stage Big Takeaway from this Stage: the rescue effort in the previous stage has FAILED, and the body can't compensate anymore. The patient is progressing to MODS (multiple organ dysfunction syndrome). There is no more compensation in this stage. Therefore, cardiac output is low, tissue perfusion is low, and the cells are NOT receiving oxygen, which this leads to cell hypoxic injury. Think of this stage by body systems and how each system is failing because of cell hypoxic injury. The cells will start to swell (the ion pumps are failing) and CAPILLARY PERMEABILITY is increased. The patho in this stage really deals with capillary permeability. Literally, the flood gates have been opened from the intravascular space to the interstitial space. Fluids and proteins will be drawn into this space and this will lead to major edema throughout. In addition, this will deplete blood volume (therefore undo everything the body attempted to do in the previous stage). In other words, when the blood volume decreases it decreases the cardiac output and tissue perfusion. Let's analyze this stage: Brain: cells to the brain are not being perfused. The mean arterial pressure is < 60 mmHg. This means the cerebral perfusion pressure (CPP) is inadequate to maintain perfusion to the brain's cells. When this happens, you will start to see major mental status changes. The patient will be very slow in their speech, restless, anxious, agitated, and not respond to stimulation. Lungs: ARDS (acute respiratory distress syndrome) will develop. In a nutshell, this occurs due to increased capillary permeability in the alveoli sacs (this is where gas exchange occurs). The alveoli sacs will collapse due to the fluid surrounding them and the lung will lose its elasticity. The patient will need intubation and mechanical ventilation to breathe. The patient will have fluid in the lungs (crackles), increase respiratory rate, decrease oxygen level, and respiratory failure. Heart: the cells that make up the heart start to die. This includes the cells that play a role in the electrical conduction system of the heart and that help the heart contract/pump. So, cardiac dysrhythmias occur along with death to myocardial tissue. GI: cells that make up the gut start to die. For example, the cells that protect the lining of the gut from its own acid, start to quit working. Consequently, ulcers can develop which can turn into massive gastrointestinal bleeding (which isn't good because clotting abilities will be affected due to liver hypoxia). Liver: the decreased perfusion to the liver causes the cells that make up the liver to die. The liver is a very important organ that plays a role in filtering germs, waste products, and drugs from our body. In addition, it plays a role with clotting factors. Therefore, when the cells that do these jobs are malfunctioning there is a build-up of toxic waste (bilirubin, ammonia etc.), risk for infection, and bleeding problems. DIC (disseminated intravascular coagulation): small clots will form in the vessels (further compromising blood flow to organs). This depletes the body's platelets and clotting stores and leads to massive, uncontrollable bleeding. Watch for any type of oozing, especially around IV sites, central lines, blood puncture sites etc. Refractory Stage The word "refractory" means unmanageable. Therefore, once a patient enters this stage it cannot be reversed. All organs will shut down and fail. What was happening in the previous stage is going to be WORSE until the organs quits working. Death is inevitable.

Neurogenic Shock NCLEX Review

What's neurogenic shock? This type of shock leads to the inability of the sympathetic nervous system to stimulate nerve impulses, which causes hemodynamic problems. This leads to a decrease in tissue perfusion where the cells that make up our organs and tissue don't receive enough oxygen. Hence, signs and symptoms of shock occur. Neurogenic shock is a type of distributive shock (anaphylactic and septic shock are the other types of distributive shock). This means that the vessels that deliver blood flow to the cells have an issue with distributing that blood flow. In neurogenic shock, it's due to massive vasodilation because the sympathetic nervous system has lost the ability to stimulate nerves that control vessel vasomotor tone (this is the ability to regulate the diameter of the vessels...discussed in detail below). What can cause neurogenic shock? Spinal cord injuries that are located at the cervical or upper thoracic locations (above T6) Drugs that affect the autonomic and sympathetic nervous system Spinal anesthesia Neurogenic shock is sometimes referred to as vasogenic shock. Pathophysiology of Neurogenic Shock Let's talk about what is occurring in neurogenic shock, but first let's do a quick review of the autonomic nervous system. The autonomic nervous system controls the functions we cannot consciously control like our heart rate, digestion, rate of breathing, pupil response, etc. It is divided into two systems called the: Sympathetic Nervous System (SNS) and Parasympathetic Nervous System (PSNS) The parasympathetic nervous system is known as the "rest and digest" system. It helps us relax by decreasing our heart rate and allows us to digest food, among other functions. The sympathetic nervous system is the "keep you alive or fight or flight" system! It increases the heart rate, blood pressure, dilates your pupils for better vision etc. Therefore, a HUGE role it plays is that it controls VASOMOTOR TONE. This means that the SNS regulates the diameter of our vessels. It will cause our vessels to constrict or dilate as needed, depending on the signals it receives from the body. Now, it's very important to note that the PSNS and SNS are always balancing each other out to keep things regulate in our body. For example, if the SNS had to kick in to save your life, eventually it would have to slow down and this is where the PSNS system would help. Therefore, if one system is not working (as the case with neurogenic shock...the SNS is malfunctioning), the other system will be UNOPPOSED and in a sense take over, which is why many patients with neurogenic shock will have bradycardia. How does the sympathetic nervous system regulate the diameter of our vessels? The nerve fibers of the sympathetic nervous system branch out and hang out on the layers of the vessels. When nerve signals are fired, it will cause the neurotransmitters epinephrine and norepinephrine to be released. These neurotransmitters will cause the vessel to constrict (narrow). However, if there is a low level of nerve firing or NO firing, these neurotransmitters are NOT released, so the vessel just relaxes....hence dilates. This is the problem with neurogenic shock. The nerves are not being stimulated, so they are relaxed. This causes major problems! Why? Dilated vessels affect the blood pressure. When vasomotor tone is lost, vessel dilation occurs and this lowers systemic vascular resistance (SVR), which causes a major decrease in blood pressure (hypotension). Due to the decreased SVR and low blood pressure, blood pooling will occur in the vessels. This will DECREASE the amount of blood draining back to the heart (remember there is not pressure/resistance helping to push it back so it just hangs out away from the heart). What does this leave the heart to pump? Hardly anything at all! This will cause a DECREASE in tissue perfusion. In addition, this blood pooling will lead to a risk of deep vein thrombosis (DVT) development and lower the body core temperature (hypothermia). Why hypothermia? The blood is just sitting in the extremities cooling down and not returning to the core body to be warmed. These patients will have warm/dry extremities but a cold body. Why does this lead to a decrease in tissue perfusion? There is venous pooling of blood and not much blood will be flowing back to the heart because there isn't any resistance making it go back. This will decrease cardiac preload (the amount the ventricle stretch at the end of diastole/filling phase) and cardiac afterload (resistance the ventricles must overcome to pump blood out of the heart and this is due to the decrease in SVR). Remember we discussed in our lecture on cardiac output that cardiac preload and afterload play a huge role with cardiac output because they affect stroke volume (the amount of blood the ventricle pumps with each BEAT), which affects cardiac output. CO is calculated by: CO = Heart Rate (HR) x Stroke Volume (SV) Cardiac output is the amount of blood the heart pumps per minute. When CO falls, so does the amount of blood that is rich in oxygen that flows to the cells that make up our tissues and organs. If cells don't receive enough oxygen they start to die, and the patient starts to experience the classic signs and symptoms of shock. Also, hypothermia can occur due to the body's inability to regulate the body temperature because of hypothalamus dysfunction. This is further complicated by the peripheral vasodilation and pooling of blood in the extremities (as discussed above). This will lead to heat loss because the blood isn't returning back to the body to keep it warm. So, extremities will be warm and dry, but the body will be cold (poikilothermic: loses the ability to regular core body temperature). Bradycardia will occur too! The heart rate is controlled by both the sympathetic and parasympathetic nervous system. SNS increases the heart rate and PSNS works to decrease the heat rate. Therefore, they are both balancing out the heart rate. If we lose the function of the SNS, the PSNS will be unopposed and bradycardia will occur. Recap of the pathophysiology and the signs and symptoms in neurogenic shock: The major signs and symptoms you will see with neurogenic shock are... hypotension, bradycardia, hypothermia, warm/dry extremities but cold body Patho: One major function that is lost in neurogenic shock is the ability to regulate the diameter of the blood vessels. Therefore, the vessels are just relaxed (dilated). This will decrease systemic vascular resistance and hypotension will occur. Also, since the SNS isn't working very well (which helps increase our heart rate) the parasympathetic system will take over (which decreases the heart rate)...so bradycardia will occur. Hypothermia occurs because of hypothalamus dysfunction and is further complicated by blood pooling in the extremities (remember this blood is sitting there and cooling off because it is not going back to the body). Warm/dry extremities can be found due to dilated vessels causing the blood to pool in the extremities. These signs and symptoms are slightly different than the other types of shock we have covered, especially in the early stages of shock. WHY? Remember during the early stages of shock in the other types of shock, the sympathetic nervous system kicks into gear to help "save" the body by causing vasoconstriction with the release of norepinephrine and epinephrine. This would increase the heart rate, blood pressure (in hope of increasing CO) etc. However, in neurogenic shock, this doesn't occur because the body has lost the ability to stimulate the sympathetic nervous system due to this injury. Neurogenic shock is different from spinal shock because neurogenic shock causes hemodynamic changes with hypotension and bradycardia related to its injury. Whereas, spinal shock causes changes with sensation, motor, and reflexes. Neurogenic Shock Nursing Interventions and Treatments Goal: Manage patient's ABCS (Airway, Breathing, Circulation & Spine) Protect the spine: Keep spine immobilized (don't want to cause any more damage and decrease perfusion to the spine) Example: cervical collar, log rolling patient during transport, using a backboard May need intubation and mechanical ventilation if respiratory failure present (respiratory issues can occur depending on the location of the injury) Maintain tissue perfusion: want MAP to be 85- 90 mmHg. This helps maintain perfusion to organs, specifically the spine. (Dave and Cho, 2018) How? Intravenous fluids: crystalloids (fills the dilated vessels, increases venous return to the heart which will increase cardiac preload and cardiac output) IVFs are used with caution because the patient usually has a normal blood volume. Therefore, monitor for fluid overload.Example: dyspnea, crackles, swelling, increased CVP or PAWP If no response with IVFs, then vasopressors may be used. Vasopressors: causes vasoconstriction (narrowing of vessels) which will increase SVR and increase blood pressure and cardiac output Positive inotropes: Dopamine (vasoconstriction and increases heart rate) Bradycardia? Atropine blocks the parasympathetic effects on the heart If severe, the patient may need temporary pacing Rewarming devices for hypothermia: slowing with rewarming and monitor body core temperature Foley (some patients lose bladder function).... Want urinary output 30 cc/hr or higher...this tells us how well the kidneys are being perfused Prevent DVT (blood is pooling) apply compression stockings, ROM (range-of-motion exercises), anticoagulants per MD order Avoid crossing patient legs or placing pillow under patient's knees because this further compromises circulation

What are some expected findings of hypovolemic shock?

· Anxiety, tachypnea, tachycardia, hypotension decrease in SV, PAWP, and urinary output

What are the characteristics of neurogenic shock?

· HYPOTENSION, BRADYCARDIA, inability to regulate body temp, dry skin, poikilothermia (taking on the temp of the environment)

What should a diabetic be counseled on before exercising?

· Only exercise when blood glucose between 80-250 · Do not exercise if ketones present in urine · If more than 1 hour has passed since eating and exercise is planned, consume a carbohydrate snack · Wear diabetic identification · Check glucose more often following vigorous exercise Don't work out the area insulin was most recently administered in

What are assessment findings of a patient who is in respiratory distress?

· Shallow increasing respiratory rate, progressing to decreased rate · Use if accessory muscles · Asymmetric chest expansion · Pleural friction rub · Abnormal breath sounds · Tachycardia progressing to bradycardia · Hypertension progressing to hypotension · Pulsus paradoxus, JVD, Pedal edema · Abdominal distention, ascites · Somnolence, confusion, delirium · Changes in pH, PaCO2, PaO2, SaO2

Post op management care

• Encourage early ambulation • Prevent DVTs: apply SCD, reposition frequently , administer anticoagulants • Treat pain and nausea • Monitor for S/S of infections at surgical site (redness, extreme tenderness, purulent drainage o Expected Findings: pink wound edges, slight edema, slight crusting on incision line • Teach patient to splint w/coughing and beep breathing • Assess airway: Check SpO2 (should be > 95% or at pre-op level, respirations, lung sounds. Suction secretions if needed • Assess circulation: Assess for signs of hemorrhaging (hypotension, tachycardia), skin color/temp, peripheral pulses, ECG readings • Assess vital signs (must be stable for D/C from PACU • Monitor I/O - Ensure urine output > 30ml/hr • Assess surgical wounds, incisions, dressings • Ensure return of gag and swallow reflex

What is DKA?

•DKA is an acute complication of diabetes and most likely to occur in Type 1 •Caused by a profound deficiency in insulin and characterized by uncontrolled hyperglycemia (greater than 300), ketosis, metabolic acidosis, and dehydration •When the circulating supply of insulin is insufficient, glucose cannot be properly used for energy. The body compensates by breaking down fat stores as a secondary source of fuel. Ketones are acidic byproducts of fat metabolism that can cause serious complications. Ketones alter pH causing metabolic acidosis.

What are important teaching points for diabetic patients regarding foot care?

•Inspect feet daily, cleanse feet daily with soap and water, dry thoroughly, no lotion between toes, apply corn starch-based powder on sweaty feet, don't use commercial remedies for removal of corns or calluses •Wear protective shoes, no open toes shoes, cotton or wool socks •Trim nails straight across, consult a podiatrist Get shoes in the afternoon

Main patient teachings when discussing CAD Prevention.

•Physical Activity: 30 minutes of moderate physical activity on most days of the week, 2 days of weight training •Nutritional Therapy: Lower LDL, by decreasing saturated fats and cholesterol. Increase complex carbs and fiber •Lipid Lowering Drug Therapy •Antiplatelet Therapy