CCA/ PCA Final Study Guide revised 6/13BEHAVIORAL: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 medications3. 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 one’s behaviors and interpersonal relationships, 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, H’s and T’s 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 pt’s 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 What’s 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

Beta blockers (1st 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 MI’s 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 Pt’s with CHf may have a lower than normal BP and therefore, the hold

criteria for these medications may be lower than in pt’s 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 pacingwill 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)1st Letter 2nd letter 3rd letter 4th letter 5th letterChamer paced

Chamber sensed

Response to sensing

Programmability Antitachycardia fx

O= noneA= atriumV= ventricleD= dual

O= noneA= AtriumV= ventricleD= dual

O= none (fixed rate)I= inhibitedT= triggered (if PR interval is too long)D= Dual

R= rate modulation which means the HR will increase with the pt’s activity

O= function N/AP= antitachycardial pacing is enabledS= ability to shockD= 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 Bradyarrythimias- congenital or acquired 3rd drgree and 2nd 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 hypothermiaENDOCRINE: Risk factors for and symptoms of diabetic ketoacidosis

Polyuria, polydipsia, polyphagia N/V HA Dehydration Fatigue Increased BG blurred vision Hypotension and tachycardia Kussmaul’s 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 >5.5

Na <125

BUN/ Cr Elevated

Serum osmolality In proportion to glucose

pH <7.3

HCO3 < 15

Diagnostic indicator of efficacy of insulin administration HGBA1C

Hallmark of HNNS Serum glucose> 650 Serum osmolality> 350 Severe dehydration No ketones No kussmaul’s

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 1—15 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 ketoacidosisDiabetic 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 PRESENTATIONThe 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 kussmaul’s 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/LSodium < 125mEq/LBUN - elevatedCr - elevatedSerum Osmolality in proportion to serum glucosepH < 7.30serum bicarbonate < 15mEq/L DKA PATIENT MANAGEMENTThe 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/O’s 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 ½ NS @ 300-

400mL 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 Onset Peak Duration

Appearance

Fast-acting

Regular ½-1 hr. 2-4 hr. 6-8 hr. clear

Lyspro/ Aspart/ Glulisine

<15 min.

1-2 hr. 4-6 hr. clear

Intermediate-acting

NPH 1-2 hr. 6-10 hr. 12+ hr. cloudy

Long-acting

Detemir 1 hr. Flat, Max effect in 5 hrs.

12-24 hr. clear

Glargine 1.5 hr. Flat, Max effect in 5 hrs.

24 hr. clear

Know symptoms of diabetes insipidus Clinical presentation

Polyuria, urine output in excess of 300ml/hr, polydipsia, alteration in bowel habits, and signs of dehydration

LabsSerum Osmolality >300

Urine osmolality <300

Urine specific gravity <1.005

Serum Na >145

Vasopressin 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

Addison’s Results from inadequate adrenal function and cortisol secretion Primary Addison’s is due to an autoimmune or idiopathic process

that destroys the tissue of the adrenal cortex Secondary Addison’s 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 body’s 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 addison’s

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 bleedingHEMATOLOGY: 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. Pt’s 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 transfusionMULTISYSTEM: 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 heart’s failure to pump blood resulting inadequate 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 WBC’s 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 Co Heart rate > 90 BPMo RR >20 BPM or a PACO2 >32mmHGo 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 perfusiono Follow changes in PAOP, CO, and tissue perfusion

Fluid challengeo 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 15-18mmHg

Preload reducersa) 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 pt’s with renal insufficiencyd. 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 IVb) 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) Morphinea. 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 pt’s 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/c’d

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 pt’s with renal or liver dysfunction or with patients receiving greater than 2-3mcg/kg/min for linger than 72 hours

e) Milrinonea. Reduces preload and afterload and causes an increased in CI

and SVIManaging 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 PVRo 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 SVRo A high SVR (> 1200dysen/sec/cm5) 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

o A low SVR (<800 dysenc/sec/cm5) 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/mino 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 pt’s 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 contractilityo Negative inotropic effects can be seen with hypoxia, acidosis,

and hypercapniao 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 shockShock type CVP PAOP SVR COHypovolemic Down Down Up DownCardiogenic Up Up Up DownDistributiveAnaphalactic Down Down Down DownNeurogenic Down Down Down DownSeptic (hot or hyperdynamic)

Down Down Down Up

Septic cold or hypodynamic

Up Up Down down

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 pt’s 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. UTI’s 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 patient’s 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 (doll’s 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 brain’s 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:AVM’s are imaged best by using MRI’s. 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 Wenicke’s 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 pt’s 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 strokeo 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 pt’s 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 patient’s 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 don’t 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. Cushing’s 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. Cushing’s reflex causes the symptoms of Cushing’s triad

Cervical spinal cord injury management Support ABC’s 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 patient’s 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 interpretationpH < 7.35 acidosis > 7.45 alkalosisPaCo2 >45 acidosis < 35 alkalosisHCO3 < 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 pressuresIntrapleaural 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 ARDSThe 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 ARDSExudative 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 vasculatureProliferative 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 PEDx is based on physical findingsThe 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, and fever. On auscultation, the pulmonic component of the 2nd 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 LE’s.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 tubesDrainage 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 patient’s 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 ventLow 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 triadThree predisposing factors (collectively called Virchow’s 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 edemaRespiratory 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 bronchospasmsIn 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 VAPPerform 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 functionCreatinine 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 failureThe 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 DYSFUNCTIONDefined by conditions with normal tubular and glomerular function; GFR is depressed by compromised renal perfusion.

INTRARENAL OR INTRINSIC RENAL FAILUREDisease of the glomerulus or tubule, which are associated with release of renal afferent vasoconstrictors.

POSTRENALPostrenal 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 FailureAcute 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 pt’s serum creatinine and UO.Monitor the pt’s creatinine, UO, I/O’s.Prerenal failure may be due to hypovolemia or to low cardiac outputHypovolemia S&SOliguriaHypotensionTachycardiaOrthostatic BP changesCVP less than 5mmHGDry Mucous MembranesFlat jugular veinsLethargy progressing to coma

LOW CARDIAC OUTPUT S&SHypotensionTachycardiaPeripheral and Systemic EdemaClammy SkinElevated 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 GFRThe 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/LFractional 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 MANAGEMENTCenters 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 kidney’s 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 FAILUREAcute 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 FAILURESTAGE 1: DIMINISHED RENAL RESERVE50% of the nephrons are damagedAlthough 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 INSUFFICIENCY75% of the nephrons are damaged.Mild increase in BUNIncrease in creatinine, azotemia (high levels of nitrogen containing compounds), anemia, impaired urine concentrating abilityProtect pt from infection, dehydration, cardiac failure, and nephrotoxic drugs.

STAGE 3 : ESRD90% of nephrons damaged.S&S N/V, diarrhea, edema, weight gain, pruritus, and neurologic changesFatigue, peripheral neuropathy, stupor, difficulty concentration, comaAzotemia and uremia (wastes excreted in blood stream vs. urine) progress as ptsworsens. Pt will require dialysis soonCHRONIC KIDNEY DISEASE PATIENT MANAGEMENTRestrict fluids/Sodium intakeDialysis/TransplantAcute 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.

RIFLEAcute 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 criteriaRiskIncreased creatinine x 1.5 or GFR decrease > 25%UO < 0.5ml/kg/hr x 6hoursInjuryIncreased creatinine x 2 or GFR decrease > 50%UO < 0.5ml/kg/hr x 12 hoursFailureIncrease creatinine x 3 or GFR decrease > 75% or creatinine > 4mg/dl acute rise of > 5mg/dlUO < 0.3ml/kg x 24 or Anuria x 12 hoursLoss of FunctionPersistent ARF = complete loss of renal function > 4 weeksEnd Stage Renal Disease

Function of Loop of HenleDilution or concentration of the filtrate occurs in Henle’s 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 kidneysRegulation of fluid and electrolyte balance, and elimination of waste are key functions of the kidney.

Functional unit of the kidney and it’s primary roleThe 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 failureDifferent types of renal replacement therapy-indications for management of, complications of. Urinary output does not represent renal functionThe most common clinical indications for renal replacement therapy are:Fluid overloadSevere hypertensionHyperkalemiaMetabolic acidosisUremia

PERITONEAL DIALYSIS is used when hemodialysis is not available or can’t be done/is contraindicatedPoor uremia control, high risk of infectionHEMOFILTRATION 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 RRTOLIGURIA (UO <200ML/12HR) OR 16ML/HRANURIA/EXTREME OLIGURIA (UO<50ML/12HR) OR 4ML/HRHYPERKALEMIA (K>6.5 mEq/L)SEVERE ACEDEMIA (Ph < 7.1)AZOTEMIA (UREA > 30mg/dL)CLINICALLY SIGNIFICANT ORAGAN EDEMA I.E. PULMONARY EDEMAUREMIC ENCEPHALOPATHYUREMIC PERICARDITISUREMIC NEUROPATHY/MYOPATHYSEVERE DYSNATREMIA NA<115 OR NA > 160mEq/LHYPERTHERMIARX OVERDOSE

HEMODIALYSISFor 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 machine’s 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 TYPESCONTINUOUS AMBULATORY PERITONEAL DIALYSIS – CAPDA 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 – CCPDAutomated 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 wbc’s – 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 DIALYSISPeritoneal dialysis uses osmosis, diffusion, and active transport that the kidneys use to regulate the body’s 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 DIALYSISUREMIAFLUID OVERLOADELECTROLYTE IMBALANCEREMOVAL OF HIGH MOLECULAR WEIGHT TOXINS

CONTRAINDICATIONS FOR PERITONEAL DIALYSISPERITONITISRECENT ABD SURGERYABDOMINAL ADHESIONSPREGNANCYNOT TO BE USED WHEN RAPID REMOVAL OF FLUID/WASTE IS NECESSARY

COMPLICATIONS OF PERITONEAL DIALYSISPERITONITISATELECTASISPNAPERFORATION OF BOWEL OR BLADDERRESPIRATORY DISTRESSMAINTAIN STERILITYMONITOR ELECTROLYTES/FLUID BALANCE

HEMODIALYSISAlthough 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 hrsWhen 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 pt’s 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 patient’s circulation through the use of an electronic pump.

INDICATIONS FOR HEMODIALYSISHYPERKALEMIAFLUID OVERLOADMETABOLIC ACIDOSISSYMPTOMS OF UREMIA : PERICARDITIS, GI BLEEDING, MENTAL CHANGESBUN > 100mg/dLCREATININE > 10mg/dLETOH, RX OVERDOSE, POISONSIN PATIENTS WHEN MEDS AND DIET NO LONGER MAINTAIN ADEQUATE CONTROL OVER EXCRETION OF WASTE PRODUCTS

CONTRAINDICATIONSUNSTABLE HEMODYNAMIC PROFILE (cardiac arrest/death)UNABLE TO COAGULATEUNOBTAINABLE 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:THROMBOSISINFECTIONVASCULAR 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 SHUNTSTHROMBOSISINFECTIONSKIN BREAKDOWN AT INSERTION SITE

CRRT CONTINUOUS RENAL REPLACEMENT THERAPYUsed 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 pt’s 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 CRRTSLOW CONTINUOUS ULTRAFILTRATIONCONTINUOUS ARTERIOVENOUS HEMOFILTRATIONCONTINUOUS ARTERIOVENOUS HEMODIALYSISCONTINUOUS 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 pt’s 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 pt’s 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 HEMODIALYSISAdding 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 CRRT’s 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 output30-50ml/hr. of course measuring the creatinine clearance is a better way of measuring renal function.

Enteral feedings in acute renal failureNUTRITIONHigh 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 TBRenal 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 attorneyMedical - 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)