CCA/ PCA Final Study Guide revised 6/13 BEHAVIORAL: 1.

Know what hypoactive delirium is: Characterized by psychomotor slowing demonstrated by a calm appearance, inattention and decreased mobility 2. Contributing factors to development of delirium Age > 70 years Transfer from nursing home History of stroke, epilepsy Alcohol abuse with a month admission Drug overdose or illicit use within a week History of HF, RF, or liver failure HIV Sepsis, hypoxemia, hypothermia or fever, cardiogenic shock, high severity of illness Metabolic disturbances, enteral feeding, rectal or bladder catheters, malnutrition, restraint use, visual or hearing impairment, anticholinergic medication use Sedatives and analgesic medications 3. Definition of addiction Addiction is a primary, chronic disease of brain reward, motivation, memory and related circuitry. Dysfunction in these circuits leads to characteristic biological, psychological, social and spiritual manifestations. This is reflected in an individual pathologically pursuing reward and/or relief by substance use and other behaviors. Addiction is characterized by inability to consistently abstain, impairment in behavioral control, craving, diminished recognition of significant problems with ones behaviors and interpersonal relations hips, and a dysfunctional emotional response. Like other chronic diseases, addiction often involves cycles of relapse and remission. Without treatment or engagement in recovery activities, addiction is progressive and can result in disability or premature death.

CARDIAC: Major hemodynamic effect of CAD Initial treatment of angina EKG, O2, NTG, Morphine EKG changes with acute MI St segment elevation (1mm) Hyperacute T waves (early sign of ST elevation) Loss of St segment Cardiac enzymes Proteins that are released as a result of cardiac cell inury or death Help quantify the amount of tissue injury or damage CK, CK-MB, myglobin, LDH, troponin I, troponin T Goal in treatment of cardiogenic shock Goals of treatment include identifying and correcting the underlying cause of the shock, increasing the effectiveness of the heart (vasodilators and diuretics, inotropes, Mechanical devices)and improving tissue perfusion (thrombolyctics, angioplasty, and surgery), decreasing myocardial O2 demand (sedatives and analgesics, activity restriction and supplemental O2) Effects of vasoactive drips EKG changes with hypokalemia

 Flattened or inverted T waves, U wave, St depression, wide PR interval Cause to discontinue TPA in MI Uncontrolled HTN, suspected aortic dissection, active bleeding Significance of elevated CVP Hypervolemia forced exhalation Tension pneumothorax Heart failure Pleural effusion Decreased cardiac output Cardiac tamponade Mechanical ventilation and the application of positive end-expiratory pressure (PEEP) Pulmonary Hypertension Pulmonary Embolism Antidote for Heparin Protamine sulfate Identification of dysrhythmias Medications to treat dysrhythmias Treatment for PEA Epi, CPR, Hs and Ts Treatment for SVT Stable Unstable Treatment for chest pain unrelieved by NTG Morphine Defibrillation vs. cardioversion Defibrillation is used in V fib Cardioversion is synchronized with pts intrinsic heart beat and used for unstable SVT Signs of cardiac tamponade Narrowing pulse pressure Pulsus paradoxus Muffled heart sounds Equalizing cardiac pressures Mechanism of MI Development of atherosclerosis, in which a plaque is formed within the arterial lumen Plaque contains a lipid core, which is encapsulated by fibrous cap. Disruption of the fibrous cap initiates a cascade of events that result in thrombus formation Patients experience ischemic discomfort due to the reduction in blood to the myocardium from wither a total or subtotal occlusion Advantages of minimally invasive valve surgery less pain, blood loss, and risk of infection. You will also recover faster than you would from open heart surgery. Most common arrhythmia in post op open heart patients Afib due to irritability of heart Whats considered excessive drainage S/P thoracic surgery A sudden increase in drainage or drainage volume exceeding 100ml per hour. Signs of aortic aneurysm dissection Tearing and ripping chest pain, laryngitis, pain beigns without provocation and is not relieved at rest. EKG may show changes if ischemia

 Signs of pericarditis sharp, pleuritic type pain or a dull, oppressive pain, which is difficult to differentiate from MI. Pain is oftern anterior in nature and may radiate. Pain is often exacerbated by inspiration. ST changes may be present throughout the EKG but there are no reciprocal changes Clinical manifestation of right heart failure Jugular vein distention, abdominal swelling, peripheral edema. Third heart sound and hepatic tenderness. Medical management of hypertrophic cardiomyopathy st Beta blockers (1 line therapy) Calcium channel blockers (verapamil is CCB of choice) Amiodarone for arrhythmias Diuretics (used cautiously) Percutaneous Alcohol septal ablation Ventricular septal myectomy Identify 12 lead EKG abnormalities with different MIs Leads I, aVL, V5, and V6 lateral Leads I and aVL- high lateral II, III, aVF- inferior V1 and V2- septal V3 and V4- anterior Ischemia T wave inversion, ST depression Injury ST elevatiom, lost St segment, hyperacute T waves Infarct- Pathological Q waves BP management of left sided heart failure Pts with CHf may have a lower than normal BP and therefore, the hold criteria for these medications may be lower than in pts w/ o HF Beta blockers are not initiated when the pt is fluid overloaded or in a decompensated state. Know actions of ACE inhibitors Prevents the conversion of angiotensin I to angiotensin II which is a potent vasoconstrictor agent. Decreased angiotensing II results in a reduced vasopressor activity and aldosterone secretion from the adrenal cortex Management on sinus tachycardia Side effects of Amiodarone Pulmonary toxicity, HF, QT prolongation Complication of Dopamine Gangrenous disorder Symptons of digoxin toxicity Confusion Irregular pulse Loss of appetite Nausea, vomiting, diarrhea Palpitations Vision changes Symptoms of Lidocaine toxicity Lightheadedness, dizziness, HA, visual disturbances, ringing in the ears (tinnitus); nausea; muscle twitching; tingling of the tongue; tremors; and mood swings Electrolyte disturbances predisposing to v-fib Hyperkalemia - increased automaticity with ventricular ectopy Hypomagnesemia- Dysrhythmias such as ventricular ectopy and ventricular fibrillation What medications cause significant bradycardia BETA BLOCKERS

 Atrial contraction occurs during what portion of ECG complex P wave What causes loud systolic murmur with MI Papillary muscle tear leading to acute mitral regurgitation Positive effect of temporary pacing will deliver electrical stimulus through two large patches placed on the chest wall. Can be placed in the same positions as when defibing or on the anterior and posterior thorax. Targets only the ventricle. Often used emergently. The negative electrode is placed on the anterior surface of the chest Know what different modes of pacing mean(eg VVI) nd th th 1st Letter 2 letter 3rd letter 4 letter 5 letter Chamer Chamber Response to Programmability Antitachycardia paced sensed sensing fx O= none O= none O= none R= rate O= function N/A A= atrium A= Atrium (fixed rate) modulation P= V= ventricle V= ventricle I= inhibited which means the antitachycardial D= dual D= dual T= triggered HR will increase pacing is (if PR with the pts enabled interval is activity S= ability to too long) shock D= Dual D= both fx are active Definition of sensing threshold What is stimulation threshold? the lowest amount of energy or the lowest amount of output required to cause the heart to respond to electrical impulse. What is sensitivity and how is it measured? Sensitivity is the ability of the pacemaker to sense the intrinsic cardiac activity. Measured in millivolts (mV) the lower the mV the more sensitive the pacemaker is Indications for temporary pacemaker therapy rd nd Bradyarrythimias- congenital or acquired 3 drgree and 2 degree AV blocks, sinus node dysfunctions(sinus node arrest, SSS, brady-tachy syndrome), Afib Tachyarrythmias- Afib/ aflutter, SVT, Junctional tachycardia Prophylaxis- Prior to anesthesia of there is a concern of exacerbations of an existing block, Prior to cardiac cath, During EPS studies, As a bridge to permanent pacemaker implantation, during cardiac surgery due to the high risk of postoperative arrhythmias or conduction disturbances. Identify rhythm strips Identify pacing problems in rhythm strips Failure to pace when the pacer fails to deliver and electrical stimulus at the programmed interval. Often equipment related (rate settings too low, low battery, loose leads, damage or dislodgement) or a sensing problem ( inappropriate sensitivity settings oversense non cardiac activity Failure to capture- when the pacer delivers the pacing stimulus but no complex is produced. Equipment related causes: low battery, output set too low, loose lead connections, disconnection, damage, dislodgement) Physiologic causes : fibrosis at the catheter tip, nonresponsive ischemic tissue, electrolyte imbalance,, acid-base imbalances, hypoxia, hypercarbia

Failure to sense (undersensing)- the pacer is not sensitive to or does not see the intrinsic activity and sends out pacing energy through the pts heart. Oversensing- pacer interprets non cardiac activity as intrinsic activity. May be due to large P or T waves, artifact on the ECG signal. Or inappropriate sensing levels.

Contraindication of intra-aortic balloon pump therapy Absolute contraindication in acute aortic regurgitation Drug of choice for VT with prolonged QT interval Drug most effective in hypertensive crisis Nitroprusside Aortic stenosis causes what pressure changes in the heart THE AORTIC VALVE OPENING BECOMES SO NARROWED IT IS ESSENTIALLY IMPOSSIBLE TO INCREASE CARDIAC OUPUT BECAUSE OF THE RESTRICTION OF THE VALVE. THE MORE NARROE THE VALVE OPENING, THE HIGHER AFTERLOAD THE VENTRICLE MUST OVERCOME TO EJECT THE BLOOD Major side effect of therapeutic hypothermia Vasoconstriction, dieresis, electrolyte changes, decreased platelets, immunosupression, arrythimias Cooling and warming therapy with therapeutic hypothermia ENDOCRINE: Risk factors for and symptoms of diabetic ketoacidosis Polyuria, polydipsia, polyphagia N/V HA Dehydration Fatigue Increased BG blurred vision Hypotension and tachycardia Kussmauls respiration and fruity breath Dry, flushed skin, dry mucous membranes and poor skin turgor Confused and unresponsive. Fluid deficit of about 4-5L Labs Glucose >350 K Na BUN/ Cr Serum osmolality pH HCO3 Diagnostic indicator of efficacy of insulin administration HGBA1C Hallmark of HNNS Serum glucose> 650 Serum osmolality> 350 Severe dehydration No ketones >5.5 <125 Elevated In proportion to glucose <7.3 < 15

 No kussmauls No metabolic acidosis, normal anoin gap Physiological effect of SIADH ADH is produced from sites other than the posterior pituitary, resulting in excess hormone resulting in water retention by inhibiting the renal tubules from excreting water. In addition, aldosterone is suppressed and normal NA regulation is interrupted. Urine output will be diminished but highly concentrated because of excess Na excretion. And dilutional hyponatremia is induced. Know about the treatment of hyperkalemia with dextrose and insulin Emergency management of hyperkalemia: Administering IV glucose D50 bolus, and IV insulin, NaHCO3 Symptoms and treatment of hypoglycemia Clinical presentation Sx start when sugar drops below 60 Nervousness, sweating, intense hunger, trembling, weakness, palpitations, trouble speaking (neurogenic symptoms) When BG drops in the 45 range, patients progress to neuroglycopogenic stages (brain not getting enough glucose) confusion, drowsiness, changes in behavior coma, seizure, and death. Management 10-15 grams of glucose recheck BG in 10 min if no improvement another 115 grams should be given (can be repeated up to three times) Glucagon- (If NPO) Given IM. Causes a rapid release of glucose stores from the liver. Response seen in minutes and lasts about 90 minutes D50- usually 25-50mL. Close monitoring of sugar level is necessary in case rebound hypoglycemia occurs S/S ketoacidosis

Diabetic ketoacidosis occurs most commonly in pts with type 1 diabetes. It is often the presenting factor in newly diagnosed diabetic. Insulin deficiency - the inherent insulin deficiency in the diabetic patient triggers the cascade of events that results in DKA. In the absence of insulin, tissue cells are unable to utilize the glucose that is delivered and a false hypoglycemia is sensed. Glucacon is released in response and gluconeogenesis results. Fat metabolism increases, producing fatty acids, and increased ketones. The serum pH drops and metabolic acidosis results. Protein metabolism is also accelerated in an effort to produce more glucose. Amino acid production climbs and eventually the patient enters a negative nitrogen balance. In the mean time, the increasing hyperglycemia results in glycosuria and massive osmotic diuresis. The patient becomes severely dehydrated and electrolyte imbalances occur. As dehydration worsens, the blood becomes more concentrated, sludging in the capillaries. Tissue hypoxia

results and lactic acid begins to build up adding to the already acidotic state of the patient. Hypotension leads to decreased renal blood flow and eventually oliguria. Potassium is not excreted and hyperkalemia results. Left untreated the patient will experience shock, coma, and eventual death.

CLINICAL PRESENTATION The symptoms of DKA occur over several hours and include polyuria, polydipsia, polyaphagia, nausea, vomiting, headaches, dehydration, and fatigue. Blood sugar increases affect the eye sight and vision becomes blurred. These symptoms progress to confusion, delirium, coma, and death. The objective signs of DKA include hypotension, tachycardia, and kussmauls respirations (compensating for the acidosis). They may have dry, flushed skin, as well as dry mucous membranes and poor skin turgor. They will probably be confused, or unresponsive. Patients frequently have an acetone or fruity smell on their breath. LABS: Serum glucose > 350mg/dL (may increase to 1000mg/dL) Potassium > 5.5mEq/L Sodium < 125mEq/L BUN - elevated Cr - elevated Serum Osmolality in proportion to serum glucose pH < 7.30 serum bicarbonate < 15mEq/L DKA PATIENT MANAGEMENT The management of DKA begins by reversing the acidosis 1. Insulin a rapid bolus of regular insulin is administered followed by an regular insulin gtt. Most hospitals have sliding scale standing orders 2. IV saline The fluid deficit in these patients is usually around 4-5 liters. NS is given initially, at 1000ml per hour for 2 hours, then 1/2 NS is given at a rate of 300-400ml per hour. This will help with both dehydration and hyponatremia. 3. When the blood glucose level reaches 200-250mg/dL, the IV fluid is switched to add 5% glucose. An extremely rapid decrease in blood sugar levels may lead to hypoglycemia and the potential for developing cerebral edema. 4. As the acidosis is corrected and the potassium goes back into the cells, hypokalemia can result. Monitoring the electrolyte levels

closely is therefore necessary. Bicarbonate may be administered in severe acidosis. Strict I/Os is important, replacing IV fluids using a volumetric pump.
Treatment of diabetic ketoacidotic coma Rapid insulin bolus followed by drip NS at 1000mL per hour for 2 hours, then NS @ 300400mL per hour When BG reaches 250 IVF changed to ass 5% glucose in order to prevent hypoglycemia and cerebral edema Electrolyte replacement Peak actions of different insulins Type of Insulin Fast-acting Regular Lyspro/ Aspart/ Glulisine Intermediate-acting NPH Long-acting Detemir Glargine 1 hr. 1.5 hr. Flat, Max effect in 5 hrs. Flat, Max effect in 5 hrs. 12-24 hr. 24 hr. clear clear 1-2 hr. 6-10 hr. 12+ hr. cloudy -1 hr. <15 min. 2-4 hr. 1-2 hr. 6-8 hr. 4-6 hr. clear clear Onset Peak Duration Appearance

Know symptoms of diabetes insipidus Clinical presentation Polyuria, urine output in excess of 300ml/hr, polydipsia, alteration in bowel habits, and signs of dehydration Labs Serum Osmolality >300 Urine osmolality Urine specific gravity Serum Na Vasopressin <300 <1.005 >145 Positive

Management Fluid replacement with hypotonic fluids and water PO Desmopressin acetate nasal spray and vasopressin to increase water reabsorption in the kidneys I/o daily weights, skin assessment, electrolyte monitoring

 Know about acute adrenal insufficiency Addisons Results from inadequate adrenal function and cortisol secretion Primary Addisons is due to an autoimmune or idiopathic process that destroys the tissue of the adrenal cortex Secondary Addisons is often the result of prolonged use of medication containing glucocorticoids being abruptly discontinued. Often detected when physical or emotional stress occurs because the adrenal gland is unable to keep up with the bodys needs during a stressful event. Cortisol levels are inadequate to maintain glycogenesis and hypoglycemia results Aldosterone secretion is also decreased and the renal tubules are not longer able to conserve NA resulting in hypokalemia and hyperkalemia. Hypotension results from the massive fluid loss. Sx: Early signs: Anorexia, weakness, malaise, electrolyte imblanace, hyperpigmentation of the skin(classic sign), irritability and depression Addisonian crisis Hypotension hyperkalemia, and hypoglycemia (classic triad), severe pain in back legs and abdomen, severe N/V/D dehydration and hypotension shock Tx: IVF with salt and glucose (D5NS) Vasopressors 100mg of cortisol Why we wean off cortisone In order to prevent secondary addisons GI: Method of measuring intra abdominal hypertension (IAP) Risk factors for IAP Symptoms of mesenteric ischemia Function of the colon What does the liver synthesize Leading cause of GI hemorrhage What is pancreatitis Proteins serve what function Goal of nutritional support Nutritional needs of head injured patient Lab indicator of nutritional status Nutritional support for pancreatitis When to use low intermittent suction Method to check NGT placement Intervention for coffee ground emesis from NGT Effect of malnutrition on respiratory failure Drug used to control variceal bleeding HEMATOLOGY: What is DIC occurs when the normal coag and fibrinolytic mech are altered. DIC occurs secondary to major illnesses. (Sepsis, OB, Tissue, Liver, Transfusion, CA,

Leukemia, Viral fevers, Envenomation) Pt will develop epistaxis, bleeding from conjunctiva, hematuria, or intracranial bleeding. Excessive or prolonged bleeding following venipuncture or from existing IV sites or wounds may be seen. Unexplained petechiae, ecchymoses, and hematomas may be present upon assessment of skin. What is HIT is uncommon immune reaction to heparin therapy. Note that heparin is made from bovine or porcine proteins. Pts immune system might produce antibodies to the antigens on the animal protein that leads to platelet destruction and might lead to thromboemboli development also. Thrombus development occurs in 35-58% of pts with HIT. Clots can be venous, arterial and have presented as DIC, CVA, MI, renal infarction, or at surgical graft sites. Causes of thrombocytopenia Etiologic causes can be due to 1.decreased platelet production, 2.decreased platelet survival, 3.excessive consumption of platelets, 4.splenic sequestration of platelets, or 5.platelet dilution (massive fluid administration). End result of all is insufficient number of platelets available to maintain hemostasis leading to hemorrhage. In some disorders such as excessive platelet consumption, thrombosis production can develop and the outcome is the potential for increased clotting not bleeding. Interventions for fever with blood transfusion MULTISYSTEM: Clinical manifestations of SIRS Temp >38 degrees C or < 36 degrees C Heart rate > 90 BPM RR >20 BPM or a PACO2 >32mmHG WBC >12000 cell/mm3, < 4000 cells/mm3, or the presence of >10% immature neutrophils. Measure to enhance large fluid volume Aggressive fluid and blood replacement Crystalloids and colloids are given Transfusions Monitor for overload (lung sounds, JVD, increased CVP and PAOP) Main cause of cardiogenic shock Results from hearts failure to pump blood resulting ina dequate delivery of oxygenated blood to the periphery Hemodynamic values with septic shock Hyperdynamic phase and is a direct attempt to maintain O2 delivery to the tissues in the presence of autoregulatory failure of the peripheral vascular bed. A decrease in systemic vascular resistance. Increase in capillary permeability and a loss of vascular tone resulting in relative hypotension. Hypotension develops because of the fall in preload and decreased SVR Increase in HR in response to the fall in blood pressure and the SNS stimulation. RAP and PAOP are low because of a decrease in venous return CO will increase as a result of increased HR and low SVR Ventricles dilate to help maintain an increased CO

 Indication of DIC with sepsis - Increased PT, PTT, FSP, D-dimer and decreased platelets, and fibrinogen Pt will develop epistaxis, bleeding from conjunctiva, hematuria, or intracranial bleeding. Excessive or prolonged bleeding following venipuncture or from existing IV sites or wounds may be seen. Unexplained petechiae, ecchymoses, and hematomas may be present upon assessment of skin. Pathological mechanism resulting in septic shock Vasodilation- acts to allow increased O2 and glucose delivery to the area, while increased vascular permeability allows these nutrients to pass more easily into the injured area. Vascular permeability- as the vessel becomes more permeable to larger molecules, proteins and antibodies will also be able to move from the vessels into the tissues Cellular activation- is initiated by the release of mediator. WBC will migrate to the injured area in response to certain mediators and adhere to the vascular wall. From there the WBCs will move through the vessel walls and into the tissues where they start to phagocytize bacteria and other cell debris. In addition, platelets are activated to protect the integrity of vessel walls and enclose the area of injury Coagulation- fibrinolytic system is also activated to check the coagulation system and maintain hemostasis. Difference between primary and secondary MODS What is primary MODS Occurs as a direct result of injury to an organ or organ system and any resuscitation measures. Ex. Pulmonary contusion or aspiration causing pulmonary dysfunction, ingestion of poisonous mushrooms resulting in liver dysfunction What is shock syndrome Difference between SIRS, localized infection, severe sepsis, septic shock SIRS o Temp >38 degrees C or < 36 degrees C o Heart rate > 90 BPM o RR >20 BPM or a PACO2 >32mmHG o WBC >12000 cell/mm3, < 4000 cells/mm3, or the presence of >10% immature neutrophils Sepsis o Systemic host response to SIRs plus a documented infection Septic shock o Sepsis with hypotension and inadequate tissue perfusion Response to cytokine release Increase the production of adhesion molecules that support coagulation, becoming a prothrombotic state Treatments based on Hemodynamic parameters Managing preload (measured by the RAP/CVP or the PAOP will guide the therapy) Increasing preload The PAOP may be low (< 8mmHg) when there is a volume deficit

Mechanism to increase preload is to increase circulating volume o Administer crystalloid or colloids NS or LR (crystalloids) Albumin, dextran, Hespan (colloids) Blood products o Main goal is tissue perfusion o Follow changes in PAOP, CO, and tissue perfusion Fluid challenge o Fluids are administered over 10-15 min in predetermined increments (50-250ml) and the change in PAOP is monitored. o An increase in PAOP (>7mmHg) or the development of pulmonary congestion suggests excessive preload and a position on the steep portion of the ventricular portion curve o Moderate increases in the PAOP are not too dangerous if pressure decreases within 10 min to within 3mmHg the original value o If the PAOP does not increase at least 3mmHg and perfusion remains inadequate, additional challenges are necessary until systemic perfusion returns. o If the volume has been optimized and tissue perfusion remains inadequate, further intervention is required. ( Inotropic support, afterload reduction, and chonotropic modification) o In pulmonary dysfunction If PAOP is decreased is CI/ SWI elevated? administer fluid challenge until PAOP is 1518mmHg Preload reducers a) Lasix a. Loop diuretic- blocks absorption of Na and water in the loop of Henle b. Can help reduce the PAOP within minutes by venous dilation and further reduction continues after diuresis begins. c. May not be adequate in pts with renal insufficiency d. Adverse side effects: hypotension, hypokalemia, and hypochloremia leading to alkalosis and hypomagnesemia. The electrolyte disturbances can lead to SVT and ventricular ectopy e. Dose : 40-60mg IV b) Nitroglycerin a. Reduces preload through nitric oxide mediated vasodilation. b. At doses 100-150mcg/min results in venous dilation (preload reduction) in doses >150mcg/min results in arterial vasodilation resulting in a slight reduction of afterload c. Usually started at 5-10mcg/min and titrated every 5-10min to desired CI/SVI and PAOP d. Tachyphylaxis occurs at doses higher than 300mcg/min when given for greater than 24hours. e. Should not be given within 24 hours of phophodiesterase inhibitors c) Morphine a. Produces a vasodilation that leads to peripheral pooling of blood, reducing blood return to the heart and relieving pulmonary congestion b. Can produce a positive inotropic action that is attributed to the release of adrenal catecholamine. In pts receiving Beta blockers, it reduces the negative inotropic effects c. Can decreased O2 consumption in large doses due to decreased O2 demand

d) Nitroprusside a. Direct acting vasodilator that is metabolized to nitric oxide and cyanide b. BP reduction is seen within seconds with duration action of less than 10 min once ots d/cd c. Dilates both arterioles an venules resulting in reduction of preload and afterload. d. Dose is 0.5-10mcg/kg/min (start infusion at 0.1-0.2mcg/kg/min and titrate every 5 minutes ti the endpoints of increased CI, reduced PAOP and SVR) e. Accumulation of cyanide will likely happen in pts with renal or liver dysfunction or with patients receiving greater than 23mcg/kg/min for linger than 72 hours e) Milrinone a. Reduces preload and afterload and causes an increased in CI and SVI Managing Afterload The two determinants of afterload are volume and mass of blood ejected from the ventricle and the compliance of the vascular space into which the blood is ejected. Right ventricular afterload is measured by the PVR and left ventricular afterload is measured by the SVR Reducing PVR o Simplest way to lower PVR is to ensure adequate oxygenation. If this does not improve PVR and the pt is exhibiting signs of right sided failure a more aggressive therapy is warranted. Reducing SVR 5 o A high SVR (> 1200dysen/sec/cm ) may reflect physiologic stress of left ventricular failure. o Medications that reduce SVR are Nitroprusside and hydralazine. And to a lesser extent Nitroglycerine Increasing SVR 5 o A low SVR (<800 dysenc/sec/cm ) may reflect septic shock or excessive administration of afterload reduction medications. o Medications that increase SVR include dopamine, epi, norepi, phenylephrine, and vasopressin. o Epinephrine Potent Alpha and Beta adrenergic receptor agonist. At a low dose (0.1mcg/kg/min) the greatest effect is stimulation of the beta receptors resulting in increased HR and contractility causing an increase in CI. You will also see a beta 2 stimulation seen by bronchodilation and increased blood flow to the mesenteric vasculature At doses higher than 0.1mcg/kg/min there is peripheral vasoconstriction and an increased in HR and contractility. Resulting in and increased PAOP, CI, and SVR Adverse effects are tacyarrythmias, MI, mesenteric ischemia, renal ischemia, and hyperglycemia. o

Norepinephrine Potent alpha agonist with minimal beta agonist effects. When administered, even at a low dose, the primary effects is vasoconstriction. Resulting in an increased

afterload. Has a positive inotropic effect and minimal effect on HR First line drug in management of septic shock that has not responded to fluid resuscitation. Dose is 2-20mcg/min: titrate to increase MAP and improved tissue perfusion o Phenylephrine Selective alpha 1 receptor agonist that causes arterial vasoconstriction. Leading to a rise in BP and redirects blood flow to essential organs. Because it is directed to alpha receptors, it does not cause an associated increase in HR. As a reflex response to increased resistance, it actually causes a slowing of the HR. Result can be reversed with atropine. There will be a rise in SBP and DBP, a slight decrease in CI and considerable increase in SVR. Adverse effects include HA, reflex bradycardia, excitability, restlessness, and rarely arrhythmias, Dose is 20-200mcg/min o Vasopressin (ADH) is a hormone synthesized in the hypothalamus from the posterior pituitary in response to hyperosmolality, hypotension, and hypovolemia. Activates receptors V1, V2, V3 Dose 0.1-0.4units/min. At high doses vasopressin can cause severe ischemia, altered platelet functioning, and decreased CI and cardiac arrest. It is important to monitor for signs of water intoxication which leads to a decreased LOC and increased risk for seizure activity. In High PAOP and low CO, nitroprusside can improve ventricular function by reducing the force the left ventricle has to generate to eject blood. It is reflected by an increased CO, reduction of SVR, and increased systemic BP In the failing heart, CO might be augmented with dobutamine or dopamine and nitroprusside. Dobutamine/dopamine will increase CO by the positive inotropic effects and Nitroprussside will reduce the afterload. In contrast, patients with right ventricular infarction may require elevated right filling pressures via volume resuscitation. Managing contractility Indirect measures of contractility are AVI, RVSWI and LVSWI Patients with poor contractility may also have a decreased CI, elevated filling pressures (RAP and PAOP) and a low SvO2 Conditions that usually present with low contractility are MI, CHF, and cardiomyopathy Increasing Contractility o Dobutamine Potent inotrope with moderate vasodilatory properties. Produces a stron inotropic response without a significant increase in HR making it the preferred agent for management of low output states (such as acute decompensated CHF and cardiogenic shock)

Dose is 5-20mcg/kg/min (Usually started at 5mcg/kg/min and titrated up to 2.5-5mch/kg/min every 5-10 minutes until the desired effect is produced. Doses higher than 20mcg/kg/min are not advised because of increased risk of hypotension, tachyarrythmias (Vtach and Vfib) o Dopamine Immidate precursor of norepinephrine and epinephrine. At low doses (0-5mcg/kg/min) dopaminergic receptors are activated leading to vasodilation of renal, mesenteric, and coronary beds. Hemodynamic effects at this range include tachycardia an hypotension (Especially in patients with low preload) At midrange doses (5-10mcg/kg/min) beta adrenergic receptors are activated leading to increased CO, decreased PAOP, and variable SVR. At high doses (10-20mcg/kg/min) causes the release of nrepinehprine, which stimulates the alpha 1 receptors resulting in vasoconstriction. Leading to and increase in SVR Regardless of the dose it results in an increase in HR. Use with caution in pts with ischemic heart disease. o Milrinone Phosphodietrerase inhibitor Type 3. Properties similar to dobutrex. Referred to as inodilator. Does not exert through beta adrenergic stimulation, therefore an increased HR is not seen. Will cause decrease in mean pulmonary artery pressure, PAOP and SVR. Dose is 50mcg/kg over 10 minutes followed by a continuous infusion of 0.25-0.75 mcg/kg/min. Eliminated by the kidney, so use with caution in RF. Side effects include hypotension and thrombocytopenia. Baseline PLT should be drawn prior to administration. Decrease contractility o Negative inotropic effects can be seen with hypoxia, acidosis, and hypercapnia o Drugs that decrease contractility are beta blockers, calcium channel blockers, Class I antidysrhythmics and barbs.

Stroke volume variation Variation in arterial pulsations caused by heart-lung changes during positive pressure ventilation <13 % Know hemodynamic profiles for different types of shock Shock type CVP PAOP SVR CO Hypovolemic Down Down Up Down Cardiogenic Up Up Up Down Distributive Anaphalactic Down Down Down Down Neurogenic Down Down Down Down Septic (hot or Down Down Down Up hyperdynamic) Septic cold or Up Up Down down hypodynamic

 Most important treatment for burn pts Fluid resucitation NEURO: Symptoms that mimic acute stroke Seizures (post ictal) Systemic infections Brain tumors Toxic metabolic conditions (hyponatremia, hypoglycemia,hyperglycemia, hypercalcemia) Diagnostic study necessary for ischemic stroke Plain CT brain Nursing care of acute stroke Goal: stabilizing the patient and minimizing the complications Airway patency: Most common cause of inadequate oxygenation in stroke pts are Airway obstruction Hypoventilation Aspiration PNA Atelectasis Normocapnia should be maintained. Hypercapnia leads to diversion of blood from ischemic region through steal effect and increased ICP Supplemental O2 for O2 sat > 94% Elevate Hob at least 30 degrees GCS <8, intubate Thrombolytics? Symptoms less than 3 hours Older than 18 Ct negative for hemorrhage IF TPA Admit to ICU Dose is 0.9mg/kg with max dose of 90mg. Infuse over 60 minutes with 10% of the dose given as bolus Neuro checks every 15 minutes during infusion, then 30 minutes for the next 6 hours, then hourly until 24 hours after treatment BP q 15 min X 2 hours, q 30 min X 6 hours, then hourly until 24 hours Maintain BP <180/105 If pt develops severe HA, acute HTN, nausea, vomiting call MD, stop infusion, and get STAT CT No NG, foley or ART lines. Obtain f/u CT in 24 hours BP management Maintain 220/120 for first 24 hours If need to lower BP (TPA, MI, dissection, RF, etc) lower BP gradually and the MAP should not be lowered more than 20mmHg Labetolol, Nitropaste, Cardene Temperature management Elevated temp is associated with increased metabolic demands, enhanced release of neurotransmitters, and increased production of free radicals. Tylenol, ASA, and hypothermia Glucose monitoring Supplemental glucose if less than 50 Treat hyperglycemia due to detrimental effects such as increasing tissue acidosis, lactic acidosis, and free radical production, and it

alters the blood brain barrier promoting the development of cerebral edema. Thrombectomy Thrombus is removed directly via cath

Babinski sign positive indicates a pyramidal tract or upper motor neuron problem Contraindication to TPA Severe uncontrolled HTN Active internal bleeding Hx of CVA Recent (within 2 months) intracranial or intraspinal surgery or trauma Past or present bleeding disorder Seizure at onset of stroke Recent major surgery within 10 days Recent GI or GU bleeding within 10 days Recent trauma Arterial puncture Retinopathy Traumatic CPR > 75 years Pregnancy Current use of anticoagulation Hx of uncontrolled HTN Know about Guillian-Barre syndrome (GBS) Infectious polyneuritus, is a demyelination of lower motor neurons affecting the spinal and crania nerves (PNS)It is an ascending paralysis and is usually symmetric with no alteration of consciousness. It may occur after viral infection, usually of the upper respiratory tract. The most serious complication is respiratory arrest. Signs are decreased vital capacity and increased protein in CSF. UTIs are a common complication Condition that results in increased ICP Increased brain volume (cerebral edema) Increased blood volume (vascular congestion and hyperemia) Increased CSF volume (hydrocephalus) Space occupying lesions (tumors, hematomas, abscesses Measures to prevent ICP Maintain normocapnia Prevent straining No hip, or neck flexion Prevent Noxious stimuli Maintain bed at 30 degrees Maintain normothermia Interventions to manage ICP Hyperventilation Possible in patient who are mechanically intubated Hyperventilating CO2 lessened cerebral vasoconstriction General goal is to maintain PaCO2 around 35mmHg In acute cerebral hypertension hyperventilate to achieve PaCO2 values of 20-30mmHg Osmotic Diuresis Mannitol or hypertonic saline Creates a water gradient and causes water to shift from the brain tissue into the vascular bed. As vascular volume increases, the kidneys will increase filtration and urinary output should rise. General goal is to keep the osmolality less than or equal to 320.

Enhancing Venous return Optimal head elevation is >30 degrees. Neck should remain midline without constriction of the neck veins. Avoid hip flexion or 90 degrees in order to avoid elevations of blood volume on the abdominal region Minimization of stimuli. Space nursing care and evaluate need for activities. The goal od for the ICP to return to baseline within 3-5 minutes after the activity and elevation. Minimize verbal and tactile stimulation from staff and visitors. Adequate pain control and prevention of straining. Induced coma Utilizes barbiturates or propofol to induce a come in order to reduce ICP Used only when all other efforts have failed Goal is to create a rapid decrease in cerebral metabolism, which decreases cerebral volume and blood flow, and theoretically decreases ICP. Leads to hypotension, GI paralysis, hypothermia Surgical intervention Burr holes are made to relieve pressure caused by bleeding or hematoma Craniotomy to remove blood clots, masses, or foreign objects such as bullets or sharp objects that have penetrated the brain. Decompressive craniotomy- a large portion of a patients skull and dura are removed with skin closure over the exposed brain. This allows space for the brain to swell Pharmacological interventions Anticonvulsants- if used, unless the patient develops seizure activity, they will be stopped after injury. Vasoactive medications- may be needed to elevate or lower mean arterial pressure to enhance cerebral perfusion pressures (Keep MAP >60) Sedation- used to decrease metabolic activity and control ICP. Neuromuscular blockade- may be used in patients who are very restless and cannot be controlled with sedatives.

Signs of increased ICP Early sigs of increased ICP- progression in LOC, agitation, HA and vomiting Late signs- pupillary dilation from cranial III compression and loss of reflexes Risk factor for neurogenic shock Causes: spinal cord injury above T6, high levels of anesthesia, and ganglionic or adrenergic blocking agents. Stress, pain, CNS dysfunction and medications are other causes Compensatory response to control increased ICP Shunting CSF into the subarachnoid space Increased CSF absorption in the venous sinus Decreased CSF production in the choroid plexus of the ventricles Decreased blood volume by altering cerebral blood flow Skull expansion can only occur in infants before the skull sutures have closed ICP waveform components

The waveforms originate from pulsations in the choroid plexus of the ventricles and corrensponds to each heartbeat. P1- the percussion wave (highest initial peak) P2- the tidal wave- when ICP increases P2 will be higher than P1 or P3 and the waveform will become more rounded. As P2 becomes equal or greater than P1, compliance within the brain is decreased P3- the dicrotic wave Monitor trends A wave- sudden elevation in pressure that occurs in a patient with an ICP that is already greater than 20mmHg and who has decreased brain compliance. Can be anywhere from 50-100mmHg and will cause some transient symptoms or pressure signs caused by a variety of things such as cerebral ischemia. Also called plateau waves because of their distinctive shape on a trended wave analysis. B waves- sharp spikes that occur at intervals of 30 seconds to two minutes. ICP will peak at 20-50mmHg, but does not stay at that level. These changes are usually related to the respiratory cycle, and are not considered clinically significant. C waves- relate to normal arterial pressure variations and will occur four to eight times per minutes. The pressure may be elevated to 20mmHg, but no other changes will be seen.

How to assess sensory function Sensory Stimulation Light touch Joint position change Pain- sharp vs. dull Vibration Dermatome chart Most important part of neuro check consistency Clinical criteria to establish brain death Fixed pupils without response to light Absent corneal reflexes Absent oculocephalix reflex (dolls eyes) Absent oculovestiublar reflex (cold calorics) Absent gag reflex Absent cough reflex No spontaneous respirations indicated by PaCO2 > 60 during apnea test No motor function to deep stimuli No presence of complicating conditions such as temp >90 degrees F, severe hypothermia No presence of mood altering drugs, SBP >90 What is compliance measure of the brains adaptive capacity to maintain cerebral equilibrium despite system challenges. It is a measure of stiffness What is autoregulation ability to maintain adequate cerebral blood flow by constricting or dilating cerebral arteries in response to pressure changes. The SNS assists in autoregulation by releasing chemicals such a catecholamines that effect vessel diameter. If autoregulation is lost, not enough blood flow reaches the brain leading to cell death, necrosis, and edema. What factors is cerebral blood flow dependent on CO and MAP.

The ability of cerebral blood vessels to constrict and dilate in response to pressure changes within the brain. PaCO2- when levels rise, the cerebral vessels dilate, and when levels are low they constrict. As the level of O2 in the brain decreases, blood vessels dilate, then the O2 levels increase, vessels constrict. Cause, symptoms of SAH Explosive HA, patients will briefly lose consciousness, have nausea, vomiting, and focal neurological deficits such as hemiparesis, hemiplegia or aphasia, photophobia and nuchal rigidity, and may have seizures Causes: ruptured aneurysm/ AVM symptoms of subdural hematoma sleepy, decreased LOC, pupil on side of lesion is usually dilated, onset of symptoms are slow Artery assoc with larger artery atherosclerotic stroke MCA is the most frequent location to develop Diagnostic test for visualizing ischemia CT brain Diagnostic test for visualizing AVM/s CTA & MRI *In echo under the diagnostic test section in ischemic and hemorrhagic stroke slide #9: AVMs are imaged best by using MRIs. Diagnostic angiography is a standard for evaluation. Diagnostic test for intra-cranial hemorrhage CT brain Symptoms assoc with intracerebral hemorrhage Partial or total loss of consciousness, vomiting or severe nausea, numbness or paralysis on one side of the body, seizures, and sudden severe HA Different types of seizure activity Partial seizures Simple- occurs without impairment to consciousness so the patient is awake. Focal changes in motor or sensation occur such as flashing lights, hallucinations, or twitching of the face. Complex- occurs when consciousness is impaired. May or may not inclide other features of seizure activity Evolving- progress to generalized seizures Generalized Absence- may go unnoticed as the only noticeable symptom occurs when the patient stares off into space and is unresponsive Myoclonic- generally confined to one area and are associated with sporadic jerks Clonic- rhythmic and repetitive with bilateral movements of the extremities Tonic- include a stiffening of the musculature Tonic- Clonic- most common. There is an alteration of muscle contraction with rhythmic flexion. Bowel and bladder continence is generally lost during this type Atonic- sudden loss of muscle tone called drop attacks Cause of brain abscess Major sources of infection are the middle ear (40%), or mastoid sinus (10%), and IV drug use

 Catalyst of secondary brain injury Catalyst for secondary brain injury is an imbalance in the exchange of O2 and waste products, which leads to anaerobic metabolism, abnormal protein and lipid metabolism, breakdown of cell walls, and finally cell death Know cranial nerves I OLFACTORY II OPTIC III OCCULOMOTOR- PEERLA IV TROCHLEAR V TRIGEMINAL VI ABDUCENS VII FACIAL VIII ACOUSTIC IX GLOSSOPHARYNGEAL X VAGUS XI SPINAL ACCESSORY XII HYPOGLOSSAL What is an AVM Masses of abnormal vessels which grow in the brain They consist of a nidus through which arteries directly connect to veins instead of through capillaries. Treatment for cerebral vasospasm Nimotop (calcium channel blocker) Hemodilution Hyperventilation hypervolemia Speech interpretation center of brain Wenickes area of the temporal lobe BP management of aneursyms Prior to definitive aneurysm treatment, medical approaches involve control of hypertension, administration of calcium channel blockers, and prevention of seizures. Following surgical or endovascular aneurysm treatment, blood pressure is maintained at higher levels to diminish complications associated with vasospasm Know about vasospasms Vasospasm ( narrowing of the cerebral artery resulting in ischemia and infarction) Develop 5-8 days after initial hemorrhage. Detected through cerebral angiogram Treat with Triple H therapy (hypervolemia, hypertensive, hemodilution) Risk factor for acute stroke Risk factors: Modifiable: Afib Cardiac diseases Carotid and other vessel diseases Smoking Cocaine abuse DM

ETOH abuse Elevated chol HTN Polycythemia Metabolic syndrome Physical inactivity Obesity Non-modifiable Sickle cell Hx. of TIA, CVA, or MI African American Age > 65 Male

What does F.A.S.T. stand for Facial drooping Arm weakness Speech slurring Time Know which cerebral arteries assoc with what type of stroke Lacunar: small cavity infarct usually less then 15mm wide and is usually associated with untreated HTN and smoking. They can be silent or can present as either pure motor or pure sensory deficits Middle Artery: Result in loss of movement and sensation on the contralateral side. Gaze preference on the ipselateral side. If on the pts dominant side, it will produce receptive, expressive or global aphasia. If on the nondominant side there will be neglect syndrome Posterior Artery: If the midbrain, subthalmic, and thalmic regions of the brain are affected, the patient will present with third nerve palsy, weakness, and ataxia. If the infarct is extensive in this region, coma unreactive pupils and deceberate rigidity will be seen. If the injury occurs to the medial temporal and occipital lobes, the symptoms include memory loss, and disturbances or loss of vision on the contralateral side. Basilar Artery A TIA will produce dizziness or a feeling of lightheadedness. Total occlusion causes total quadriplegia and locked in state Cerebellar Artery Occlusions of the superior cerebellar artery cause cerebellar ataxia, partial deafness, nausea, vomiting, and loss of pain and temperature on the contralateral extremities. Cranial nerve deficits are common and include nystagmus, dysphagia, dysarthria, and decreased cough reflexes Anterior Artery: ipsilateral deafness, facial weakness, and vertigo Symptoms of different areas of stroke o develops when the normal flow of CSF is obstructed Communicating- the mechanisms for absorbing CSF in the arachnoid villi is obstructed by something like meningitis of blood Noncommunicating- the circulation is obstructed at some point (ie. Tumors) Management of Cerebral perfusion pressure

Normal ICP= 0-15mmHg >20mmHg= treatment is started to decrease the pressure >40mmHg= medical emergency CPP= MAP- ICP Normal CPP= 60-90mmHg If below 60= cerebral ischemia

BP management in neuro pts Maintain 220/120 for first 24 hours If need to lower BP (TPA, MI, dissection, RF, etc) lower BP gradually and the MAP should not be lowered more than 20mmHg Labetolol, Nitropaste, Cardene Symptoms of meningitis Similar to encephalitis (Fever, increased WBC, HA, seizures, stiff neck, photophobia, changes in LOC that may progress to coma) Positive Brudzinki sign: occurs when you flex the pt.s neck and there is involuntary flexion of both knees and hips. Positive Kernig sign: bend the patients thigh up to a 90-degree angle toward the abdomen. If the patient is unable to completely extend the knee when you do this maneuver, it is positive Cranial nerve dysfunction is a result of inflammation or vascular changes. Common deficits can be ocular palsies (CN III, IV, VI) facial palsies (CN CII), hearing loss and dizziness (CN VIII Treatment for status epilepticus Ativan, Dilantin, Phenobarbital If above dont work Propofol or versed coma Protect airway Know what Cushings reflex indicates When CSF pressure and the pressure within the intracranial cerebral arteries start to equilibrate, the cerebral arteries become compressed and begin to collapse. This compromises cerebral blood flow. Cushings reflex is activated and the arterial pressure rises to a level higher than the CSF pressure, allowing cerebral blood flow to be reestablished and ischemia to be relieved. The pressure is maintained at a new higher level, and the brain is protected from further loss of adequate blood flow. Cushings reflex causes the symptoms of Cushings triad Cervical spinal cord injury management Support ABCs Intubation Neurogenic shock can occur when injury to the spinal cord causes impairment to the SNS resulting in hypotension and bradycardia. Fluid resuscitation with vasopressors will be required. Hypothermia may also occur Steroid infusion Surgical repair Later treatment: Pulmonary, toilet, bladder and bowel regimes Skin care and evaluation PT/ OT, rehab Contracture prevention devices OB: Treatment for pregnancy induced hypertension

There is no specific treatment, but is monitored closely to rapidly identify pre-eclampsia and its life-threatening complications (HELLP syndrome and eclampsia). Drug treatment options are limited, as many antihypertensives may negatively affect the fetus. Methyldopa, hydralazine, and labetalol are most commonly used for severe pregnancy hypertension. OB causes of DIC HELLP, Ecclampsia, retained placenta ORGAN PROCUREMENT: When to notify life alliance GCS= or < 5 and ventilator dependent Brain death testing to be initiated Prior withdrawl of life sustaining therapies on mechanical ventilated patients Upon cardiac death/asystole PACU: Pain assessment and management Opioids bind with specific receptors in the central nervous system. The action of each receptor type varies but all provide some level of analgesia and the main use of narcotics during conscious sedation is to provide the patient with some level of pain relief. Additionally, narcotics can produce sedation, and in higher doses, all will produce a profound decrease in the patients level of consciousness and a risk of respiratory arrest Antagonist of benzodiazepines Flumazenil (Romazicon), synthesized in 1979 by Roche Laboratories, is a reversal agent that competes with benzodiazepines for the same receptor sites Management of laryngospasms Racemic epinephrine PULMONARY: ABG interpretation pH < 7.35 acidosis > 7.45 alkalosis PaCo2 >45 acidosis < 35 alkalosis HCO3 < 22 acidosis > 26 alkalosis Purpose and Complications of PEEP positive end pressure maintains a preset pressure within the system at the end of expiration. The goal of this technique is to prevent closure of the small airways and terminal alveoli, maintaining functional residual capacity and improving hypoxemia. Used in conjunction with most ventilator modes. Positive pressure ventilation also impairs cerebral venous return which causes increased ICP in pts with impaired autoregulation Risk factors for DVT What causes act of inspiration negative pressure that causes air to rush in and inflate the lung the increase in negative pressure is created when the parietal pleural pulls outward during chest expansion and the elastic visceral pleura pulls inward trying to collapse the lung What is ventilation the process of moving air in and out of the lungs Vacuum pressure for suctioning

Vacuum pressures should be kept low 60-150mmHg

PPE when suctioning Sterile gloves, mask Delivery of oxygen with bag mask ventilation 100% What is tidal volume the amount of air you breath in and out with each breath at rest Pulmonary circulatory system there are two vascular beds. Pulmonary and bronchial system pulmonary- forms a network around the alveoli and allows circulating blood to participate in gas exchange. Starts in the pulmonary artery and divides into the right and left pulmonary arteries. At the capillary level the blood downloads CO3 and picks up O2 from the alveoli. largest in the body bronchial- systemic blood supply for the tracheobronchial tree and other pulmonary structures. Left side of thorax supplied by aorta. right side supplied by arteries branching off the intercostals, subclavian, or internal mammary Anatomical shunt- small amount of blood return from the bronchial circuit into the right side of the heart mixing with oxygenated blood. Resulting in a O2 sat of 96-99% Assessment of positioning of ETT CXR Physical examination methods, such as auscultation of chest and epigastrium, visualization of thoracic movement, end-tidal carbon dioxide detection What is a ventilation/perfusion mismatch (V/Q) Ventilation/perfusion mismatch: Intrapulmonary shunting- blood coming from the right side of the heart circulates around to the left heart w/o ever picking up O2. (ie. septal defects, PDA, PNA, ARDS) Alveolar dead space- alveoli ventilated but not blood flow to pick up O2 (ie. PE) Low ventilation perfusion- adequate blood surrounds under ventilated alveoli. Similar to shunting. Know about the oxyhemoglobin curve reflects how O2 normally jumps off HGB when the body is at a normal Ph and temp Left shift: pt is alkalotic and or cold. HGB binds tightly and wont let go easily. pt will have good SaO2 but low PaO2 Right shift: the pt is acidotic and/or hot. HGB decreaes and it releases O2 very rapidly into the serum. SaO2 will drop but PaO2 will remain at an acceptable level. Know about pulmonary arterial hypertension Increased pressures in the pulmonary arteries of at least double the pressure :>25mmHg at rest and >30mmHg during exercise. Results in narrowing and stiffeing of pulmonary artery lumen walls ans causes an obstruction of blood flow, which over time leads to right sided heart failure. Gold standard for diagnosis is cardiac cath Know different breath sounds (crackles, wheezes)

Bronchovesicular heard over the areas where there is a transition between larger and smaller airways Bronchial are normally heard over the trachea down to the carina Vesicular are heard over the small airways and terminal respiratory units Crackles are heard during inspiration and expiration over the alveoli and small airways and indicated fluid or secretions. Rhonchi deeper sounds of fluid and secretions over the larger airways. Usually heard in expiration and may also clear when coughing Wheezing- high pitched whistling heard in airways that are narrowed by constriction or accumulation of secretions. Usually heard on expiration. Friction rubs- heard when two dry surfaces are rubbing together. Leathery dry course sound. Heard on both inspiration and expiration.

Know different types of pneumothorax Open pneumo: occurs when the outer chest wall is damaged and allows air to enter the lung . The air moving in and out inhibits lung expansion and increases WOB. Closed pneumo: occurs when the oouter chest wall is intact but damaged visceral pleura allow air to enter with no place to exit. Usually caused by the rupture of a small bleb on the surface of the lung, overdistention of alveoli or trauma during central line placement. Tension pneumo: occurs when air cannot be evacuated from the pleura, and the mediastinum is forced to the opposite side, sometime causing collapse of the opposite ung as well. There is decreased CO and venous return.Often related to PEEP > 15cmH20 if the Vt used is too large. Intra-thorasic versus atmospheric pressures Intrapleaural pressures becomes more negative a you breath. It is this negative pressure that causes air to rush in and inflate the lung the increase in negative pressure is created when the parietal pleural pulls outward during chest expansion and the elastic visceral pleura pulls inward trying to collapse the lung inflates the lung must overcome resistance What is intrapulmonary shunting Intrapulmonary shunting- blood coming from the right side of the heart circulates around to the left heart w/o ever picking up O2. (ie. septal defects, PDA, PNA, ARDS) What is ARDS The end organ response of the lungs to a syndrome of multisystem dysfunction or failure. The injury occurs at the level of the alveolar-capillary membrane and can be the result of a direct injury to the epithelium of the lung, or an indirect injury, that is the acute insult that happens elsewhere in the body, causing the release of mediators that effect the lung. Patients with sepsis, aspiration, diffuse pneumonia, or trauma are at high risk for developing ARDS. Pulmonary epithelial injury initiates the inflammatory response, which includes activation of neutrophils and macrophages. Damage to the alveolar-capillary membrane occurs as a result of the release of humoral medicators. Three phases are involved in the progression of ARDS Exudative Phase (24 hrs after injury) release of mediators leads to increased capillary permeability therefore to fluid leaking into the interstitium causing alveolar flooding and hypoxemia. Release of mediators also cause formation of microemboli in the pulmonary vasculature

Proliferative Phase (7-10 days after initial insult) because of alveolar flooding, damage is caused to both types of epithelial cells. Damage of the type II epithelial cells cause loss of surfactant, alveolar collapse and V/Q mismatch (perfusion indicator). Presence of microemboli leads to vasoconstriction and pulmonary HTN causing renal failure and decreased cardiac output. Fibrotic Phase (2-3 weeks after injury) loss of surfactant and decreased lung perfusion causes pulmonary fibrosis which leads to increased pulmonary hypertension and progression of hypoxemia. Diagnosis, management of PE Dx is based on physical findings The patient may present with a complaint of dyspnea, a pleuritic type of chest pain, dry cough, and anxiety will feeling of impending doom. As hypoxemia and hypercapnea increase, these symptoms may progress to an alteration in LOC. The patient may also develop hemoptysis, diaphoresis, and audible wheezing. Other common clinical presentations include tachypnea, crackles, tachypnea, nd and fever. On auscultation, the pulmonic component of the 2 heart sound may be heard easily, and a pleural friction rub may be heard over the lungs. Characteristic EKG changes are ST with T wave inversion in leads V1 to V4. ABG results: will show a low PaO2 and respiratory alkalosis or low PaCO2 and pH as a result of the tachypnea, V/Q lung scan, spiral CT angiography, or pulmonary angiogram. Heparin gtt titrated to keep aPTT 1.5-2.5 times control. Coumadin may be started concurrently. When the INR is 2-3, heparin may be discontinued. IVC filter placement below the renal arteries to prevent further migration of emboli from the LEs. Thrombolytic therapy is the standard of care for patients who are hemodynamically unstable. Of equal importance is the maintenance of oxygenation and ventilation and attempting to reverse the effects of pulmonary hypertension. Hemodynamic support in the form of inotropic agents and fluid administration to increase preload may be needed to overcome pulmonary hypertension and improve cardiac output. Management of chest tubes Drainage should be measured regularly noting the character and amount. If clots or other material obstructions are present preventing free flow of drainage you may attempt to milk the tubing according to your hospital policy. Observe for s&s of infection. Avoid kinks or long loops (fluid in loops are an excellent growth medium for bacteria) in the tubing by impeding drainage of air or fluid impedes the timely re-expansion of the lung or can contribute to the development of a tension pneumo. Maintain chest tube below the patient. Should the CT tube become dislodged, place petroleum gauze over insertion site (prevents/minimizes pneumothorax) Call MD, prep for reinsertion and f/u CXRY. If the drainage unit is damaged resulting in interruption of the water seal, the end of the CT can be placed in the bottle of sterile water until a new system can be assembled. Sudden cessation of drainage from a previously free-flowing system may indicate an impending emergency. If the patient is stable, systematically check the netire system for kinks or clots in the tubing, loss of suction, or a break in the system. If the patient is unstable, call MD and while monitoring the patient closely, attempt to milk the tubing according to hospital policy. If the collection chamber is full or the unit has fallen over causing drainage to leak into other chambers, they system will need to be replaced. Prepare the system, clamp the CT, and reconnect and secure the drainage tubing to the end of the CT. Unclamp the tube and ensure the resumption of drainage and proper function of the system.

Fluid in the water seal chamber should fluctuate with inspiration and expiration. If this fluctuation is absent, there may be a blockage somewhere in the system. Beginning at the insertion site on the patients chest, examine the entire system including the tubing, connections, and all three chambers. Excessive bubbling in the water seal chamber indicates a probable leak somewhere in the system.. using rubber shod clamps, begin gently clamping the chest tube as close to the patient as possible, moving downward along the chest tube and drainage tubing until the bubbling stops. The point at which the bubbling stops indicates that you have pinpointed the leak above the clamp. The fluid in the water seal chamber should remain level at approx 2cm. If this fluid begins to rise, negative pressure is building in the system. Most systems have a negative pressure release valve which, when held down, will release the pressure and return the water seal level to normal. If the suction control chamber is connected to wall suction, there should be a small amount of continuous bubbling present. If bubbling is absent, there is no suction. Confirm that the wall suction is on and set appropriately. The suction chamber control is marked and should be filled according the amount of suction desired. If the chamber is under or overfilled, take a syringe and add or remove to the desired level. CT removal: Premedicate for pain prior to physician pulling at end-expiration. F/u chest xray to ensure hyperinflation of the lung. Monitor for several hours for s&s indicating development of pneumothorax. What causes high and low pressure alarms on vent Low pressure alarms usually caused by ventilator disconnect or leak in the system. High pressure alarms occur when the amount of pressure needed to ventilate the patient exceeds the present pressure limit. Multiple patient factors triggering an alarm include excessive secretions, biting, coughing, gagging, attempting to talk, pulmonary edema, bronchospasm, pneumothorax, or hemothorax. Low volume alarms occur when the patient does not receive the preset tidal volume. Causes include vent disconnects, airway cuff leaks or displacement, increased airway resistance, or decreased lung compliance. High volume alarms can be caused by an increased respiratory rate or tidal volume which is usually caused by pain, anxiety, hypoxemia, or acidosis. Apnea alarm occurs when there is no spontaneous respiration within a preset interval. Virchows triad Three predisposing factors (collectively called Virchows Triad) have been identified as contributing to the development of pulmonary emboli: Venous stasis Altered coagulability of the blood Damage to the vessel walls Medication to treat laryngeal edema Respiratory treatments of racemic epinephrine. Given to patients after removal of ETT (Auscultate carotids to listen for stridor). Administered for the infant suffering from croup along with cool mist oxygen. Medication to treat bronchospasms In regards to patient with asthma due to inflammatory process caused by irritants contributes to bronchospasm. Bronchodilators, particularly beta 2 antagonists may be delivered by neb or metered dose inhaler. Systemic and inhaled

corticosteroids will be administered to decrease the bronchial inflammatory process. What is the significance of peak inspiratory pressure (PIP) PIP stands for peak inspiratory pressure is the maximum pressure that occurs during ventilation and is measured at end inspiration. Barotrauma is the result of high ventilator pressures that cause alveoli to expand beyond their limit, resulting in rupture of the alveoli and air leakage into the tissues or into the mediastinum. Alveolar rupture presents as subcutaneous emphysema (crackling sensation during palpation where air has leaked into tissues) Additionally, the air leak may result in a pneumothorax, requiring CT placement to decompress and facilitate lung re-expansion. Volutrauma describes the lung parenchymal injury which is a result of high ventilator volumes or distension. The lung damage is similar to early ARDS and is manifested by an increase in permeability of the a alveolar-capillary membrane, pulmonary edema, the accumulation of protein and neutrophils in the alveolar spaces and reduction of surfactant. Effects and characteristics of Acute Lung Injury (ALI) Acute lung injury (ALI) is a diffuse heterogeneous lung injury characterized by hypoxemia, non cardiogenic pulmonary edema, low lung compliance and widespread capillary leakage. ALI is caused by any stimulus of local or systemic inflammation, principally sepsis. The term acute lung injury has been abandoned in the 2012 Berlin classification of ARDS, and this state is now called mild ARDS. Prevention of VAP Perform oral care frequently. Keep HOB 30 degrees or higher unless contraindicated. ETT with continuous suction above the cuff; do not routinely change vent circuits. Keeping a closed circuit will prevent microbes from gaining entry. RENAL: Gold standard for measurement of renal function Creatinine clearance is the gold standard for the measurement of renal function. Creatinine clearance measures the amount of creatinine produced (serum creatinine) against the amt of creatinine secreted (urine creatinine). The creatinine clearance closely approximates the glomerular filtration rate. PROCESS: First draw a serum creatinine level. Then collect urine for 12-24 hrs and measure urine creatinine levels. The kidney tubules should be able to excrete close to 100% of the creatinine that is produced. The normal value for creatinine clearance is 110-120 ml/minute. Values of less than 50ml/min indicate significant renal dysfunction. Know different categories of renal failure The types of renal failure include acute kidney failure which includes prerenal, intra renal, and postrenal dysfunction. They are classified by the location of they dysfunction causing the decrease in the GFR. PRERENAL DYSFUNCTION Defined by conditions with normal tubular and glomerular function; GFR is depressed by compromised renal perfusion. INTRARENAL OR INTRINSIC RENAL FAILURE Disease of the glomerulus or tubule, which are associated with release of renal afferent vasoconstrictors.

POSTRENAL Postrenal or postobstructive failure initially causes an increase in tubular pressure, decreasing the filtration driving force. This pressure gradient soon equalizes and maintenance of a depressed GFR is then dependent upon renal afferent vasoconstriction. Prerenal Failure Acute Prerenal Failure or acute kidney failure is the most common type of acute renal failure seen in the acute care setting. This type of renal failure is due to a problem occurring before the blood enters the kidney, causing diminished renal perfusion and potentially resulting in ischemia. Initially, the nephrons are not significantly damaged. If the process is not reversed quickly, the ischemia results in intrarenal failure specifically - ATN acute tubular necrosis. Etiology of acute (prerenal) kidney failure includes any condition that decreases the blood flow to the kidneys i.e. a decrease in the intravascular volume from internal fluid shifts of external losses. AKF may also occur with cardiovascular failure due to a decreased cardiac output. Clinical examples include hemorrhage, severe dehydration, heart failure, and hypotension, and shock from any etiology. The Key to recognizing the clinical presentation of acute kidney failure is to understand the cause. It is important to obtain a thorough assessment and history. Also needed is an evaluation of the pts serum creatinine and UO. Monitor the pts creatinine, UO, I/Os. Prerenal failure may be due to hypovolemia or to low cardiac output Hypovolemia S&S Oliguria Hypotension Tachycardia Orthostatic BP changes CVP less than 5mmHG Dry Mucous Membranes Flat jugular veins Lethargy progressing to coma LOW CARDIAC OUTPUT S&S Hypotension Tachycardia Peripheral and Systemic Edema Clammy Skin Elevated Pulmonary Artery Diastolic Pressure (PADP) Pulmonary Wedge Pressure > 18mmHg due to the hearts inability to pump the blood out into the systemic circulation. Laboratory findings in AKF are the result of the reduced perfusion of the kidneys resulting in a decrease in the GFR The BUN is elevated and the serum creatinine is slightly elevated. If the failure is due to a problem with perfusion rather than function of the nephrons, the BUN-Creatinine ratio will be greater than 20:1. The urine specific gravity is greater than 1.015 because, as the body attempts to hold onto water, the urine becomes more concentrated. Urine osmolality is greater than 500mOsm/kg, which is due to concentrated urine.

Urine sediment remains normal because tubular structure remains intact. Urine sodium 10-15mEq/L Fractional excretion of sodium (FENa) is less than 1%. FENa is the ration between the amount of urine filtered and the amount excreted. It is one of the best tests for distinguishing the type of failure, because retention of sodium by the kidneys is one of the early signs of acute kidney failure. PATIENT MANAGEMENT Centers around the goal of reestablishing renal perfusion and preventing progression of the effects of reduced perfusion. It is important to restore effective blood volume. If hypovolemia is present, an IV fluid challenge or volume expander may be administered. A diuretic also may be administered to attempt to keep the kidneys functioning. If cardiac failure is the cause, enhancing the contractility and optimizing the filling pressures of the heart can led to an improvement in cardiac output, thus preventing further progression of renal failure. INTRARENAL (INTRINSIC) KIDNEY FAILURE Acute tubular necrosis is a common aspect of acute intrarenal kidney failure. It may result from nephrotoxic or ischemic insults to the nephrons or can involve an inflammatory process such as glomerulonephritis. NEPHROTOXIC DAMAGE may be due to certain antibx, chemotherapy, contrast media as well as other meds that may be toxic to the kidney. Know where your meds are cleared liver Vs. kidney in order to monitor for signs of potential problems. Chemical agents such as insecticides and heavy metals may also cause nephrotoxicity. Generally, nephrotoxicity without ischemia results in better outcomes because only the epithelial layer is affected. ISCHEMIC DAMAGE may be the result of prolonged failure, severe dehydration, shock, or sepsis or as a result of a transfusion reaction. Inflammatory damage occurs from acute pyelonephritis or glomerulonephritis. STAGES OF CHRONIC REANL FAILURE STAGE 1: DIMINISHED RENAL RESERVE 50% of the nephrons are damaged Although the serum creatinine level may be doubled from baseline, it may still be within the normal range. Thus, it is important to obtain a baseline level to monitor for trends. If there is an upward trend noted in the serum creatinine level, a urine creatinine clearance test should be performed and will be abnormal. In this stage, the patient is asymptomatic so it is important to protect the patient from further insult. STAGE 2: RENAL INSUFFICIENCY 75% of the nephrons are damaged. Mild increase in BUN Increase in creatinine, azotemia (high levels of nitrogen containing compounds), anemia, impaired urine concentrating ability Protect pt from infection, dehydration, cardiac failure, and nephrotoxic drugs. STAGE 3 : ESRD 90% of nephrons damaged. S&S N/V, diarrhea, edema, weight gain, pruritus, and neurologic changes Fatigue, peripheral neuropathy, stupor, difficulty concentration, coma Azotemia and uremia (wastes excreted in blood stream vs. urine) progress as ptsworsens. Pt will require dialysis soon CHRONIC KIDNEY DISEASE PATIENT MANAGEMENT

Restrict fluids/Sodium intake Dialysis/Transplant Acute kidney injury or failure is a potentially reversible clinical syndrome characterized by the sudden deterioration in renal function resulting in a decrease in the glomerular filtration rate (GFR). The decrease in the GFR causes an inability to filter waste products, as well as an imbalance in the electrolyte and acid-base systems. RIFLE Acute Dialysis Work Group classification system for acute kidney injury. The acronym stands for Risk, Injury, Failure, Loss of function, and End stage renal disease. This classification uses urine output and creatinine as separation criteria Risk Increased creatinine x 1.5 or GFR decrease > 25% UO < 0.5ml/kg/hr x 6hours Injury Increased creatinine x 2 or GFR decrease > 50% UO < 0.5ml/kg/hr x 12 hours Failure Increase creatinine x 3 or GFR decrease > 75% or creatinine > 4mg/dl acute rise of > 5mg/dl UO < 0.3ml/kg x 24 or Anuria x 12 hours Loss of Function Persistent ARF = complete loss of renal function > 4 weeks End Stage Renal Disease Function of Loop of Henle Dilution or concentration of the filtrate occurs in Henles loop, which is composed of the descending and ascending limbs. Reabsorption of water occurs primarily in the descending limb, whereas absorption of electrolytes occurs in the ascending limb. Functions at Distal convoluted tubule DISTAL TUBULE The hypo-osmotic filtrate moves through the distal convoluted tubule in the cortex of the kidney, where further refinements in water and electrolyte reabsorption take place. The first portion of the distal tubule contains the cells of the macula densa, which are specialized cells that are a component of the juxtaglomerular apparatus important in blood pressure control. The first section of the distal tubule is impermeable to water and transports solutes such as sodium, bicarbonate, calcium, and potassium. The later section of the distal tubule further regulates sodium, bicarbonate, potassium, and calcium according to hormonal influences and the acid-base and electrolyte balance needs of the body. The permeability of the late distal tubule is influenced by antidiuretic hormone (ADH). In the presence of ADH, the late distal tubule is impermeable to water but resorbs some solutes, and the filtrate remains hypo-osmotic. In the absence of ADH, the late distal tubule is more permeable to water and the filtrate may become isomotic. Roles of the kidneys Regulation of fluid and electrolyte balance, and elimination of waste are key functions of the kidney. Functional unit of the kidney and its primary role The nephron is the functional unit of the kidney. There are more than one million nephrons contained in each kidney.

The role of the nephron is to remove metabolic substances and waste products while retaining essential electrolytes and water through the formation of urine. What does release of Angiotensin II cause Stimulated by angiotensin II, the adrenal cortex secrets aldosterone, which works in the distal convoluted tubule of the nephron to pull additional sodium from the filtrate into the intravascular compartment. This causes water to be reabsorbed also again increasing extracellular fluid volume. Other factors affecting the release of aldosterone include hypovolemia, hyponatremia, hyperkalemia, and severe physical or emotional stress. ALDOSTERONE stimulates reabsorption of sodium. Different treatments of renal failure Different types of renal replacement therapy-indications for management of, complications of. Urinary output does not represent renal function The most common clinical indications for renal replacement therapy are: Fluid overload Severe hypertension Hyperkalemia Metabolic acidosis Uremia PERITONEAL DIALYSIS is used when hemodialysis is not available or cant be done/is contraindicated Poor uremia control, high risk of infection HEMOFILTRATION and DIAFILTRATION can aid in the removal of fluids and electrolytes. HEMODIALYSIS is used when removal of large amounts of fluids and electrolyte imbalances are needed quickly. COMMON INDICATIONS FOR INITIATING RRT OLIGURIA (UO <200ML/12HR) OR 16ML/HR ANURIA/EXTREME OLIGURIA (UO<50ML/12HR) OR 4ML/HR HYPERKALEMIA (K>6.5 mEq/L) SEVERE ACEDEMIA (Ph < 7.1) AZOTEMIA (UREA > 30mg/dL) CLINICALLY SIGNIFICANT ORAGAN EDEMA I.E. PULMONARY EDEMA UREMIC ENCEPHALOPATHY UREMIC PERICARDITIS UREMIC NEUROPATHY/MYOPATHY SEVERE DYSNATREMIA NA<115 OR NA > 160mEq/L HYPERTHERMIA RX OVERDOSE HEMODIALYSIS For pts that are hemodynamically stable. The dialysis machine is a pump which forces blood into a filter (semipermeable membrane) a dialysate (usually deionized water) which flows in and out, and then blood is returned to the patient. With this machines high flow and clearance rate, pts only require 3-4 hrs of dialysis 2-3 times a week. There are huge

swings in fluid between the intravascular and extravascular compartments, causing transient hypotension and disequilibrium during hemodialysis treatment. PERITONEAL DIALYSIS 2 TYPES CONTINUOUS AMBULATORY PERITONEAL DIALYSIS CAPD A fresh bag of dialysis soln is drained into the abdomen. After 4-6 hours of dwell time, the soln is drained out into the bag. This method consists of 3-4 exchanges during the day and one evening exchange with long overnight dwell time while the pt sleeps. CONTINUOUS CYCLER ASSISTED PERITONEAL DIALYSIS CCPD Automated cycler to perform 3-5 exchanges during the night while the pt sleeps. In the morning, there is once exchange with a dwell that lasts the entire day. CVVH is a continuous venovenous hemofiltration, a form of convective (heat) dialysis. The ultrafiltration rate is high, and replacement electrolyte soln is required to maintain hemodynamic stability. This mode is also very effective for clearing midsized molecules, such as inflammatory cytokines (proteins produced by wbcs regulate immunological aspects of cel growth and function during inflammation and immune response) which may play a role in improving outcome in sepsis. SCUF SLOW CONTINUOUS ULTRAFILTRATION is used for volume control in fluid overload patients. SCUF does not require the use of replacement fluid and fluid removal is 300-500ml/hr CVVHD is CONTINUOUS VENOVENOUS HEMODIALYSIS, wish is continuous diffusive dialysis. The dialysate is driven in a direction countercurrent to the blood. This provides reasonably effective solute clearance, although mostly small molecules are removed. CVVHDF CONTINUOUS VENOVENOUS HEMODIAFILTRATION is the most popular method of dialysis. It combines convective and diffusive dialysis. Both small and middle molecules are cleared, and both dialysate and replacement fluids are required. SLED SLED is SUSTAINED LOW EFFICIENCY DIALYSIS, a hybrid modality that involves the application of a conventional hemodialysis machine with reduced dialysate and blood flow rates for 12 hr nocturnal treatments. PERITONEAL DIALYSIS Peritoneal dialysis uses osmosis, diffusion, and active transport that the kidneys use to regulate the bodys fluid and remove unwanted substances. As in hemodialysis, the dialysate composition is such at it encourages the movement of substances and fluid from the blood. THREE FACTORS AFFECT THE REMOVAL OF WASTE AND FLUID DURING PERITONEAL DIALYSIS

COMPOSITION The composition of the dialysate will determine how much is removed in terms of electrolytes and waste by regulating the concentration gradients TIME The length of time the dialysate remains in the abdominal cavity, or the dwell time. Longer dwell times up to a point translate into increased waste removal. BLOOD FLOW In capillary blood flow to the peritoneum may have a small effect on removal of wastes. INDICATIONS FOR PERITONEAL DIALYSIS UREMIA FLUID OVERLOAD ELECTROLYTE IMBALANCE REMOVAL OF HIGH MOLECULAR WEIGHT TOXINS CONTRAINDICATIONS FOR PERITONEAL DIALYSIS PERITONITIS RECENT ABD SURGERY ABDOMINAL ADHESIONS PREGNANCY NOT TO BE USED WHEN RAPID REMOVAL OF FLUID/WASTE IS NECESSARY COMPLICATIONS OF PERITONEAL DIALYSIS PERITONITIS ATELECTASIS PNA PERFORATION OF BOWEL OR BLADDER RESPIRATORY DISTRESS MAINTAIN STERILITY MONITOR ELECTROLYTES/FLUID BALANCE HEMODIALYSIS Although quite proficient at removing excess electrolytes, waste products, and fluid from the blood, the dialysis machine cannot remove all metabolites from the blood as efficiently as the kidneys organic processes. The process of hemodialysis incorporates the same principles of osmosis, diffusion and ultrafiltration in ridding the body of wastes. Tx 3-4 hrs When used in acute phase of renal failure, tx up to once a day or 3 times a week. Blood is removed through a vascular access and transported via tubing to a filter or dialyzer. An anticoagulant is added to the system as the blood enters the dialyzer to prevent clotting mechanisms. The dialyzer contains specially formulated fluid or dialysate and semipermeable membranes. As the pts blood passes on one side of the membrane and the dialysate flows in the opposite direction on the other side, excess electrolytes and toxins are removed by diffusion.

Because of the composition of the dialysate, a NEGATIVE HYDROSTATIC PRESSURE is created, which encourages excess fluid to be removed from the blood and collected for disposal. This process is called ultrafiltration. The removal of fluid using ultrafiltration also pulls along some of the excess electrolytes and toxins in a process known as SOLUTE DRAG WHEN EXCESS ELECTROLYTES AND TOXINS ARE REMOVED DURING HEMODIALYSIS IT IS CALLED SOLUTE DRAG. When the blood exits the dialyzer, it is returned to the patients circulation through the use of an electronic pump. INDICATIONS FOR HEMODIALYSIS HYPERKALEMIA FLUID OVERLOAD METABOLIC ACIDOSIS SYMPTOMS OF UREMIA : PERICARDITIS, GI BLEEDING, MENTAL CHANGES BUN > 100mg/dL CREATININE > 10mg/dL ETOH, RX OVERDOSE, POISONS IN PATIENTS WHEN MEDS AND DIET NO LONGER MAINTAIN ADEQUATE CONTROL OVER EXCRETION OF WASTE PRODUCTS CONTRAINDICATIONS UNSTABLE HEMODYNAMIC PROFILE (cardiac arrest/death) UNABLE TO COAGULATE UNOBTAINABLE VASCULAR ACCESS Rapid IJ, subclavian, femoral access used for 911 short term use AV FISTULAS FOR LONG TERN HEMODIALYSIS AV FISTULAS ARE THE PREFERRED TYPE Creating by connecting a native vein and artery through a surgery. B/c the pressure in the artery is greater than that in the vein, the vein itself swells and a pseudoaneurysm forms. This aneurysm is the site in which the large-bore dialysis needle can be inserted to withdraw blood from the circulatory system. A separate vein distal to the fistula is used to return blood to the pt after passing through the dialyzer. Fistulas are preferred access type in chronic dialysis patients because the native vessels are more durable and longer lasting than synthetic devices. The development of pseudoaneurysm may take several weeks; therefore, this type of access is not appropriate if dialysis is required immediately. COMPLICATIONS OF AV FISTULAS: THROMBOSIS INFECTION VASCULAR STEAL SYNDROME arterial insufficiency of the involved limb occurs resulting in pale, cool skin, pain, potential loss of the limb.

AV GRAFT Commonly used access in chronic renal failure patients requiring dialysis. Using a surgical technique, a piece of artificial tubing is inserted and sutured between an artery and vein, creating a connection. The artificial tubing, or graft is the insertion site for the large needles that remove and return blood during the dialysis procedure. AV SHUNT Used less frequently. An artificial device is inserted via a cutdown into a vein and an artery, creating the necessary connection between the two circulatory systems. When dialysis is performed, the external connector of the shut is separated into the outflow and inflow portions. When not in use, the shunt ends are reconnected btw the involved vein and artery. COMPLICATIONS OF AV SHUNTS THROMBOSIS INFECTION SKIN BREAKDOWN AT INSERTION SITE

CRRT CONTINUOUS RENAL REPLACEMENT THERAPY Used in the treatment of acute and chronic renal failure. Provides ultrafiltration of extracellular fluid and clearance of uremic toxins in a slower, more controlled manner. This therapy tends to be used in critically ill patients when a large fluid shifts need to be carefully monitored. CRRT includes hemofiltration and hemodialysis. As in other forms of dialysis, vascular access and filter or dialyzer are necessary to accomplish removal of electrolytes, wastes, and fluid. The pts MAP is the driving force used to move blood from the pt through the dialyzing device. Once again, diffusion and osmosis are employed to accomplish this task. CRRT indicated when the need for rapid fluid volume removal is necessary but the patient is hemodynamically unstable and unable to tolerate hemodialysis. Other indications include hypervolemic or edematous pts who are unresponsive to diuretics or cannot tolerate anticoagulation. CRRT CONTRAINDICATIONS lack of vascular access and anemia FOUR TYPES OF CRRT SLOW CONTINUOUS ULTRAFILTRATION CONTINUOUS ARTERIOVENOUS HEMOFILTRATION CONTINUOUS ARTERIOVENOUS HEMODIALYSIS CONTINUOUS VENOVENOUS HEMODIALYSIS SCUF SLOW CONTINUOUS ULTRAFILTRATION is a treatment of choice for ARF & poor renal perfusion who have not responded well to the administration of diuretics. SCUF provides slow continuous removal of fluid (100-300ml/hr). The SCUF system requires access to a cannulated artery. The system is anticoagulated using heparin infusion to prevent clotting. The pts own blood pressure supplies the force by which blood is pumped though the tubing to the filter. While in the filter, excess fluid and waste are removed and flow down a tubing to the collection bag. The filtered blood then exits the filter returning to the

pt via a cannulated vein. No dialysate is employed and b/c fluid removal is done gradually and in lower volumes, replacement fluid is not required. CAVH - CONTINUOUS ARTERIOVENOUS HEMOFILTRATION is indicated in pts in whom rapid removal of large amounts of fluid are warranted. CAVH can remove between 300-1200ml of fluid per hour. The setup for CAVH is similar to SCUF. Removal of excess electrolytes and waste is accomplished by increasing the rate of flow through the filter by infusion of replacement fluid at a point prior to the filter. As with one CRRT systems, anticoagulation of this system is accomplished by infusing heparin into the tubing prior to the filter. CAVHD CONTINUOUS ARTERIOVENOUS HEMODIALYSIS Adding a dialysate infusion to the system filter will further increase the removal of excess electrolytes and waste. Continuous ArterioVenous Hemodialysis is the MOST EFFICIENT FORM OF CRRT and is most effective when used over days rather than hours. It is indicated for use in patients with severe uremia or acid base imbalances. CVVHD - CONTINUOUS VENOVENOUS HEMOFILTRATION differs from the three previous forms of CRRT because arterial access is not required in this system. CVVHD relies on an external pump to move blood through the filter the other CRRTs utilize the pts blood for this purpose. Therefore, CVVHD is ideal for pts with lower blood pressures who cannot support SCUF, CAVH, or CAVHD. Indications for CVVHD are similar to those for the other therapies to remove excess fluid, electrolytes, and waste products. Normal urine output 30-50ml/hr. of course measuring the creatinine clearance is a better way of measuring renal function. Enteral feedings in acute renal failure NUTRITION High risk for malnutrition r/t hypermetabolic or catabolic state. Hypermetabolic state occurs when the body switches to a destructive phase of metabolism. The goal for the patient becomes to reduce the intake of protein (which breaks down into nitrogen) and to prevent catabolism by encouraging or administering carbohydrates. The body then uses these carbs as an energy source rather than breaking down protein stores. Encourage the pt to restrict fluid intake and maintain a diet low in protein sodium, and potassium. Treatment of renal failure pt with TB Renal insufficiency complicates the management of TB disease because some anti-TB drugs are cleared by the kidneys. Alteration in dosing of anti-TB drugs is commonly necessary in patients with renal insufficiency and ESRD requiring hemodialysis. The dosage of anti-TB drugs should not be decreased because the peak serum concentrations may be low and smaller doses may decrease drug efficacy. Instead, the dosing interval of anti-TB drugs should be increased. Based on creatinine clearance, most anti-TB drugs can be given three times a week immediately after hemodialysis. What is health care power of attorney

Medical - Allows the patient to choose someone to make any and all health care decisions on their behalf. Allows the person to select medical: treatments, facilities, and even to end life support. Examples of Spiritual care being present (physically, psychologically, or spiritually) active listening, prayer, reading religious texts, reminiscence, touch, creative arts, religious support, meditation. (I googled this lol)