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277 Cards in this Set
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What is Shock?
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Inadequate blood flow, oxygen, and cellular perfusion to vital organs, cells, and tissues.
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Shock patients typically have decreases?
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Cardiac Output
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3 Reasons for Inadequate Perfusion
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1. Inadequate Blood Volume
2. Poor pump ( pump failure) 3. Loss of compensation mechanism of the Peripheral Blood Vessel ( they contstrict or dilate) |
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PAC
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Pulmonary Artery Catheter
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How is a PAC inserted?
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Inserted throught the right atrium, right ventricle, and pulmonary artery.
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What is another type of PAC?
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Swan Ganz Catheter
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Right Atrium reading reads Right Atrial Pressure called?
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CVP (central venous pressure)
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CVP normal value is?
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2-4 mm Hg
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CVP ( central venous pressure) is a reflection of?
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Right Sided Preload
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How do you measure Left Sided Pressure?
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By Wedgeing the balloon into the pulmonary artery. By inflating air into the balloon from out side of the end of the catheter. As balloon inflates the tip of the catheter gives you a left sided reading.
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Left Sided Pressure is called?
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Wedged Pressure or PAO
(Pulmonary Artery Obstruction) think balloon is obstructing right side of the heart to measure the left side of the heart. |
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PAO aka Wedged Pressure normal value is?
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6-12 mmHg
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Cardiac Output is?
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The amount of blood pumped by ventricle in 1 min.
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Normal Cardiac Output value is?
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4-6L per min
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Heart Rate X Stroke Volume=?
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Cardiac Output
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Stroke Volume is ?
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The amount of blood pumped with each heart beat.
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Stroke Volume Norm is ?
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60- 70 ml
example HR 80X ST 60= 480 which is 4.8L which is adequate cardiac output. |
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Cardiac Output is influenced by?
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Preload, Afterload, and Contractility.
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Preload is?
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AKA end diastolic pressure is the amount of stretch in ventricle at the end of diastole
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Right Sided Preload is known as?
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CVP ( central venous pressure)
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Left Sided Preload is known as?
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Wedged Pressure of PAO
(pulmonary artery obstruction) |
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Starlings Law-
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If you have a healthy ventricle and you have an adequate preload or stretch of the ventricle that during systole because is stretch will contract effectively. aka greater volume of blood entering during diastole greater blood volume ejected during systolic contraction (sv)
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Influencing factors of preload?
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Venous return, total blood volume, and compliance
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Afterload-
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Ventricular wall tension or stress during systole ejection ( how much resistance is the ventricle coming up against during systole which is when ventricle contracts.
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SVR (systemic vascular resistance) aka afterload influences?
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Left Ventricle
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If SVR is high casue of vasoconstriction it is going to increase?
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Left Ventricular Workload ( this with chronic HTN which is how we get left ventricle hypertrophy.
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PVR ( pulmonary artery resistance is a reflection of afterload on which side of the heart? and influences which ventricle?
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Right side of the heart
Influences Right Ventricle |
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What is Contractility?
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Hearts contractile force called Inotropic Property.
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Inotropic Property is the hearts _____ force?
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Contractile Force
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What is Positive Inotropes ?
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Anything causeing an increase in contractile force of the heart.
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What is Negative Inotropes ?
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Anything casuesing a decrease in contractility of the heart.
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What is an example of a Postitve Inotrope?
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Digoxin
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What is an example of a Negative Inotrope?
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pentobarbitol ( used to decrease intracranial pressure) but can also decrease heart contractility.
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Influencing factors of Contractility are?
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Oxygen Transport which is a reflection of cardiac output, Hemoglobin, O2 sat, 02 consumption and 02 extraction.
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Hemoglobin ( Hg ) normal values for male and female are?
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Male 14-18 mg/dl
Female 12-16 mg/dl |
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The majority of oxygen is attached to____ and transported by______.
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attached toHemoglobin
transported by Hemoglobin |
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02 Sat is measured by?
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Pulse Oxcimetry same as SP02 and blood gas.
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02 sat should be between what levels?
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> 95- 100%
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Oxygen Consumption-
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oxygen supply needs to meet oxygen demand ( fever, anxiety, pain, infection, agitation all increase oxygen consumption.
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Treatment for over consumption of oxygen would be to?
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To decrease oxygen consumption such as giving diprivan ( Propofol)
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Oxygen Extraction-
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Has to do with 02 being tightly bound vs. not tightly bound to Hg.
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If patient is metabolic or respiratory alkalosis this is going to casue a shift to the____ which means_____?
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Shift to the left which means that 02 will stay tightly bound to the Hg and it wont be able to let go of 02 to go to into the cells.
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Shock results from?
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sustainded, inadequate tissue perfussion leading to alterations in tissue metabolism and function at the cellular and organ level.
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Name the each classification of Shock.
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1. Hypovolemic
2. Cadiogenic 3. Obstructive 4. Distributive |
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Primary problem for Hypovolemic shock is?
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Blood Volume Problem
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Primary problem for Cardiogenic shock is?
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Pump Problem
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Primary problem for Obstructive shock is?
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Pump Problem
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Primary problem for Distributive shock is?
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Peripheral Vascular Problem because of Vasodilation.
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3 types of Distributive Shock?
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1. Septic
2. Neurogenic 3. Anaphylactic |
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Progress of Shock-
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Initial Stage (early shock)
Nonprogressive Stage aka(compensatory stage) Progressive Stage (intermideate stage) Refractory Stage (irreversible Stage) |
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Initial Stage (early stage)
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minimal s/s Early s/s include agitaions, and restlesness and as they progress decrease LOC
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Nonprogressive Stage aka
(Compensatory Stage) |
Initial decrease in cardiac output and tissue perfusion. Decrease in aerobic metabolism and increase in anaerobic metablolism casued lacted acid production. Compensatory mechanisms being and initially maintain cardiac output and tissue perfusion. No clinical manifestations are evident.
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Progressive Stage
(intermediate stage) |
very important and should be treated rapidly within 1 hour. Compensatory mechanisims fail to maintain cardiac output and BP to perfuse vital organs
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Refractory Stage
(irriversible stage) |
Final stage of shock. Body becomes refractory to all therapuetic measures. Multiple organ failure develops. Severe death is imminent.
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Most Common Type of Shock is?
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Hypovolemic Shock
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Hypovolemic Shock is casued by?
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(Most common type of shock) Casued by loss of whole bloood, plasma, fluid loss such as diarreha, vomiting, and DKA ( which casues dieresis)
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Hypovolemic Shock is?
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Is primarily a volume loss problem, cardiac output may increase to compensate but ultimately decrease if not treated. Tissues and organs will not be perfused and go through anaerobic metabolism resulting in lactic acidosis.
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Blood values to look at for Hypovolemic Shock?
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Lactid Acid Levels
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Acid- Base for Hypovolemic Shock will show?
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Respiratory and Metabolic Acidosis
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2 types of Hypovolemic Shock
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1. Absolute Hypovolemic Shock
2. Relative Hypovolemic Shock |
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Absolute Hypovolemic Shock is?
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External blood loss, hemorrhagin, truama, GI bleeding, and surgical patients, Is easiest to detect
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Relative Hypovolemic Shock is?
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Internal blood loss or fluid shift such as burn patient casue fluif shift.
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Classifications of Hemorrhagic Shock
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Class I, II, III, IV
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Class I Hemorrhagic Shock-
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Blood loss up to 750ml ( no major significant s/s but early symptoms of agitation and anxiety. Usually normal urine output
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Class II Hemorrhagic Shock-
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Blood loss 750-1500ml. 1500ml is considered 30 percent of our total volume. s/s: agitation, anxiety, mild tachycardia, 100-120 bpm, BP normal- low. Urine output may start to drop a little, 20-30ml per hour, might see some skin changes, cool, pale, delayed capillary refill.
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Class III Hemorrhagic Shock-
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(considered major) blood loss of 1500-2000ml which is same as 2L, HR 120>, BP will be low, urine output continues to drop, RR increases to compensate for acidosis. Blood gas will show metabolic acidosis with partial compensation.
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Class IV Hemorrhagic Shock-
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(severe profound) loss of blood 2L or more, decrease LOC, lethargic, unresponsive, very low BP, very high HR, thready, weak pulse, skin will be mottled and cold.
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Cardiogenic Shock casues-
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Is primarily a pump problem, and form of obstructive shock, number 1 casue is MI, especially anterior wall MI. Other reasons can be open heart surgery, cardiac arrest, valvular problems, dysrythmias brady or tachy dysrythmias end up with a pump problem and decrease cardiac output.
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Cardiogenic Shock leads to-
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Heart Failure right, left or right nad left heart failure.
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Clinical Manifestations of Uncompensated Cardiogenic Shock-
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Decreased sensorium, SBP <90 mm Hg, narrowed pulse pressure, mean atrial bp will drop as well, weak thready pulse, possible dysrythmias, summation gallop, oliguria <400 ml in 24 hours , with elevated BUN and creatinine levels, extra S3, and S4 close together causes what is call summation gallop, ABG resp alkalosis if increase in breathing eary on, as it persist then metabolic acidosis partially comp, but if continure to spiral down and lose comp you will have resp and meabolic acidosis.
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Obstructiive Shock is part of ____ shock.
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Part of cardiogenic shock
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Obstructive Shock-
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part of cardiogenic shock, Something obstructing the hearts ability to pump such as, cardiac tamponade, tension pneumothorax
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In Obstructive Shock, if patient has tension pneumothorax to the right what will happen?
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Everything will shift to left compressing the heart which will casue Obstructic cardiogenic shock.
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Treatment for Obstructive Shock will be?
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To treat underlying cause.
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Treatment for Tension Pneumothorax?
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Chest tube.
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Treatment for Cardiac Tamponade?
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Pericardialcentisis.
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Distributive Shock
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In general is the problem is blood vessels which are vasodilating. ( inadequate vascular tune which leads to massive vasodilation)
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Septic Shock-
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Multi system response to infection which unlike any other form of shock, the fall in bp and resultant insuficient perfusion of vital oragans does not respond to fluid administration.
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Most Fatal Shock is?
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Septic Shock ( higher mortality rate of 30-40%)
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Pathophysiology of Septic Shock
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Infection--> Bacteremia--> SIRS(systemic inflammatory response syndrom)--> sepsis-->Septic Shock-->-gram neg or posti can cause this but predominantly casued bacteria--> MODS ( multi-organ dysfuction syndrome) organ failure and death.
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4 Major Changes Occuring in Shock
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1. Massive Vasodilation (because of all the chemical releaseing)
2. Capillaries become more leaky or permeable so there will be fluid shift. 3. Myocardium becomes depressed ( decreased contractility) 4. Thrombus starts to form ( clot) |
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2 Stages of Speptic Shock
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1. Hyperdynamic
2. Hypodynamic |
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Hyperdynamic Septic Shock is
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CO is normal or increased initially. SVR ( systemic ventricular resistance( afterload) is decreased. CBP ( r atrial pressure) is decreased
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Hypodynamic Septic Shock-
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Can progress to this, contriction occurs, and SVR may increase. Contriction when we are acidotic, it can lead to constriciton
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Treatment for Speptic Shock-
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Increase SVR b/c of dilation and treat infection.
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Neruogenic Shock-
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Is a type of distributive shock, major cause is spinal cord injury, nerve blocks
(epidurals, etc) Loss of sympathetic tone--> neurogenic shoc. SNS vasoconstrics our blood vessels normally. Vasodilation-->blood return decreases--> CO decreases-->hypotentsive. Dont become tachycardic b/c the SNS is not working thus they are bradycardic. Their skin is warm and dry because they are not vasoconstricting. |
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Neruogenic Shock Clinical Manifestations-
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Hypotension, Bradycardia, warm and dry skin.
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Anaphylactic Shock-
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A hypersensitivity reaction. A reaction to an antigen. Causeing vasodilation and fluid shift.
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Anaphylactic Shock Ig-E mediated-
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Is when person had an exposure and created antibodies and then had a reaction to second exposure.
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Anaphylactic Shock Non Ig-E mediated-
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Reaction to the 1st exposure
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Treatment for Anaphylactic Shock-
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Stop histamine production, give antihistamine, EPI, bronchodilators (albuterol), May be used with steroids after to prevent delayed reaction.
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Initial Stage of Shock
(revised) |
Base line mean arterial pressure ( MAP) decreased by <10 mm Hg, heart and respiratory rate increased from the baseline or a slight increase in diastolic BP, adaptive responses of vascular constriction and increase HR
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Nonprogressive Stage
(revisedl) |
MAP decreases by 10-15 mm Hg, kidney and hormonal adaptive mechanisms activated, tissue hypoxia in nonvital organs, Acidosis, and hyperkalemia. AKA as Compensatory stage--> full compensation is in action, Renin-agiotensin-sldosterone system is working to conserve H20 and vasoconstrict, ADH--> helps us hold on to volume/fluid. Acidotic- increased free H+ ions--> H+ moves into cell to try and fix it and then K+ moves out into intravascular space--> hyperkalemia ( weakness, fatigue, peaked T wave, can lead to V dysrythmias)
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Treatment for Nonprogressive Stage-
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Give regular insulin and D50 or glucouse, can give bicarb or calcium. If nonemergent, give kayexilate
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Progressive Stage of Shock
(revised) |
Treatm emergently. Sustained decrease in MAP of more than 20 mm Hg for baseline, Vital organs develop hypoxia, life threatening emergency, immediate interventions are needed, conditions causeing shock need to be corrected within 1 hour of the onset of progressive stage.
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Refractory Stage of Shock
(revised) |
Irriversible, patient goes into organ failure, too much cell death and tissue damage result from too little oxygen reaching the tissues, body can no longer respond effectively to interventions and shock continues.
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Managment of Shock
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Assesment: get a history-->MVA ( assess for cardiogenic , hypovolemic, neurogenic shocks) ; 2 days post op from abdominal surgery ( assess for hypovolemic, septic shock); MI ( cardiogenic shock). Physical findings--> agitation/restlessness initially. then VS changes, skin changes, decreased urine output ( eventually many be come anuric), weak and thready pulse, decrease cap refill, O2 sat is low, and continues to fall. Assess I & O. Look for s/s of dehydration ( dry mucus membranes, poor skin tugar)
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Lab finding for Shock managment
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Look at Lactid Acid Levels, BUN and Creatinine, H&H, clotting studies, electroytes, WBW, and C&S
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Managment of Shock Contined ABG orderq
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Give oxygen and ventilation support, may need ET tube,
Positioning: Elevate legs, Have HOB flat with legs elevated or if needed HOB 30 degrees for airway problems.Keep in a MODIFIED Trensdelenberg which is HOB flat with legs elevated |
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When not to elevate legs?
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In Cardiogenic Shock ( dont want to increase workload)
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What do Beta 1 medications promote?
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Increased HR and increased Contractility
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What do beta 2 medicaitons promote?
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Bronodilate the lungs with ( Albuteral) May also vasodilate the arteries
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Alpha medications promote?
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Vasocontriction of blood vessels.
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Medications that Affect Preload.
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1. Epinephrine: alpha and beta agonist (increase HR and vasocontriction) improve preload, increase HR and O2 demand.
2.Norepinephrine- very potent. Primarily alpha agonist, Vasoconstricts. Use for Distributive shocks. Patients onf Levophed "leave them dead". Such a potent vasoconstrictor that it can decrease perfusion. Thus you must do CMS checks and watch extremities ( can get necrotic) 3. Nitroprusside- vasodilator. this decreases preload. This is used for Cardiogenic shock. |
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Medications that Affect Afterload.
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Dopamine: has different properties at different does ranges.
1. 2-5mcg/kg/min: low does: improves renal perfusion 2. 5-10mch/kg/min: mild rage:predominantly a Beta agonist. Thus its a positive inotrope( increases hear contractility) 3. Greater then 10mcg/kg/min: high does; predominantly Alpha agonist. This vasoconstricts therefore increasing afterload. ( good for distributive shock) NorEPI: Levophed. Vasoconstricts (increases afterload) Phenylephrine: Neosynephrine. Vasoconstrict (increases afterload) Nitroprusside: Vasodilate. (decrease afterload à cardiogenic shock) Nitroglycerin: Vasodilate (decrease afterload à cardiogenic shock) |
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Positive Inotropic Contractility Meds
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1)Dopamine (mid range DA)à beta effect. Improves HR and increases contractility.
2)Dobutamine (Dobutrex): primarily Beta. Improves contractility (cardiogenic shock) 3)NorEPI 4)Amrinone-Inocor: for heart failure Monitor their effectiveness à look at BP (assess why we’re giving it) PT is getting DA at 6mcg/kg/min. Doc says to DC it. Must taper the patient off of these drugs Vasoactive: have some action on the blood vessel. MUST taper these drugs and monitor BP and HR. Atropine: positive chronotropic(rate). Used for symptomatic bradycardia. Used in neurogenic shock or in some forms of cardiogenic shock (when brady dysrhythmias cause the shock) |
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Positive Chronotropics:
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Atropine
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Sepsis Management:
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Sepsis: there is an infection. Do a C&S and start antibiotics within 1st 3 hrs of admission. use tight glycemic control. Keep blood sugar in the normal range…prolly gets insulin.
•Recombinant Protein G (Xigris): there are lots of clots that form and this drug is used to prevent the clots. Risk for bleeding. (like an anticoagulant) •often will use steroids too •Antibiotics •Tight glycemic control •Recombinant Protein C |
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Remeron
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mirtazapine
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tetracyclic antidepressant
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Why is Epinepherine used for the heart?
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It is used to improve preload by increaseing heart rate which increases oxygen demand and increasing vasoconstriction. It is a alpha and beta agonist.
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Noriepinephrine
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It is a very potent drug, primarily alpha agonist. It vasoconstricts. Used for Distributed shocks. Can decrease profusion.
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What are some side effects from Noriepinephine?
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Can cause decreased profusion. So you should do CMS checks and watch the patients exremities ( can get necrotic)
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Nitroprusside
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Is a vasodilator, this decreases afterload, and is used for Cardiogenic Shock.
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Dopamine given at 2-5mcg/kg/min ( low dose) helps improve?
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Renal perfusion
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Dopamine at 5-10mcg/kg/min ( mid range) predominantly?
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A Beta agonist and increases contractitly making it a positive inotrope.
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Dopamine greater than 10mcg/kg/min ( high dose) is predominantly?
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A Alpha agonist, this vasoconstricts therefore increasing afterload ( good for distributive shock.
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Levophed ( Norep)
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Vasoconstricts and increases afterload.
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Phenylephrine (Neosynephrine)
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Vasocontricts and increases afterload.
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Nitroglycherin
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Vasodilates and dcreases afterload
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What is the primary cause of Hyperparathyroidism?
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Hyperparathyroidism is primarily causes by a Tumor in the Parathyroid gland. Making it Primary Hypoparathyroidism. ( when problem is with the glands themselves)
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What is another cause of Hyperparathyroidism and why?
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Chronic Renal Failure ( there is low calcium level) so CRF causes a secondary form of parathyroidsim.
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What is Hyperparathyroidism and what does it do?
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Is an over secretion of PTH. Elevated levels of PTH cause elevated calcium serum. leading to hypercalcemia and decreased levels of Phosphate ( hypophosphotemia)
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Hyperparathyroidism clinical manifestations.
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High levels of calcium can cause anorexia, Nausa/Vomiting, bone fragility, cardiac abnormalities, increases risk of fractures, could also lead to renal calculi, and decreased Deep Tendon Reflexes.Phosphate levels will be low. ( when CA is high Phosphate is low vise versa) GI disterbances and neuromuscular impairment
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Diagnostic Test for Hyperparathyroidism.
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Serum Calcium, Phosphate and Parathyroid levels.
24 hr calcium excretion Bone mineral density scan- shows decreased done mineral densitymass, and check for presense of renal calculi |
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In Hyperparathyroidism flank pain is significant of?
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Renal Calculi
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Managment for Hyperparathyroidism goal.
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Decrease serum calcium levels.
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Managment for Hyperparathyroidism.
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Give lots of fluids to prevent renal calculi (N/S) monitor I&Os, strain urine
Diuretics: Loops/Lasix ( Dont give Thiazides becasue they are not going to decrease calcium. Monitor activity cautiously, replace phosphates, Moderate calcium intake to moderate. |
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Srugical treatment for Hyperparthyroidism.
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Parathyoridectomy for removal of mass or tumor, Post-op: airway percaution since it involves neck, Have trach kit by bed side in case Dr may need to do emergency trach.
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Possible problems after Parathyroidectomy.
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Hypocalcemia ( check for positive Chvostek's and Trousseau's Signs, Tetani, corcumoral, larengyalspasms, TX for this would be calcium.
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Hypoparathyroidism causes:
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Surgery of thyroid or parathyroid glands, radiation to the neck.
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Hyoparathyroidism is-
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Hyposecretion of PTH, so serum calcium is low, phosphate levels are high.
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What two imbalances potentiate digoxin toxicity?
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Hypercalcimia and Hypokalemia
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Diagnostic Test for Hypoparathyroidism.
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Serum Calcium, Phosphate and PTH levels
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Clinical Manifestation for Hypoparathyroidism.
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GI symptoms, anorexia, n/v
Respiratory symptoms: laryngospasm and cardiac issues. |
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Managment for Hypoparathyroidism.
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Calcium supplementation
Vitamin D supplament- Calcitriol Fluids Eye exam yearly: increased risk for cataract development monitor for hypercalcemia associated with treatment, wear med alert bracelet, May give foslow to decrease GI absorbtion of phosperous or aluminum hydroxide. |
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Where are Adrenal Glands located?
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On top of the kidneys.
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What is the adrenal cortex and what is it in charge of?
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It is the ourter portion of the adrenal glands responsible for secreting aldosterone which increases sodium water retension.
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What is the Middle Layer of the adrenal gland and what is it in charge of?
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Secretes cortisol- antinflammitory process and is highest in the mornings.
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What is the Adrenal Medulla and what does it do?
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Inner layer that secrets androgen responsible for our secondary sex characteristics, also secrets epinephrine and noriepinephrine ( catacholamines)
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Cushings Syndrome
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Problem related to middle layer of the cortex causes over secretion of serum cortisol. Most commonly caused by tumor in the pituitary gland you can also have the tumor in the adrenal gland ( hyperplasia)
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Tumors from outside the endocrine system that can cause Cushings Syndrome would be called an ____ tumor.
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Ectopic tumor- for example lung cancer causes ACTH which can causes Cushing syndrom.
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Long Term use of steroids can cause?
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Cushings Syndrome, steroids lead to elevated cortisol levels.
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Clinical Manifestations for Cushings Syndrome.
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Catabolic metabolism: Protein loss; replaces with fat causeing a buffalo hump, abnormal fat metabolism, emotional, NA and Water retention, hypertension, increased androgen.
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Cushings Syndrome clinical manifestations repeated.
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increased adepoise tissue, decreased protein, high blood sugar, increased cholesterol, mood swings ( liable mood) , may have sodium and water retention, HTN. ( due to mineralcorticoids properties in cortisol, can also increase androgen secretion ina woman leading to hirtuism ( facial hair) immune response is repressed so person will be at risk for infection.
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Managment goal for Cushings Syndrome.
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Decrease Cotrisal levels.
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Medications for treatment of Cushings Syndrome.
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Ketokonozole ( antifungal) s/e suppression of adrenal gland.
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Primary Treatment for Cushings Syndrome.
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Treat the cause. If tumor remove it.
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Transphemoidal Surgical Approach to remove tumor causing Cushings Syndrome.
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Incision in he gum line and go through the sinus to remove the tumor.
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Post-op care for Transphemoidal Surgery for Cushings Syndrome.
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Precaution for nasal obstruction due to nasal packing, cant use straw, no flossing, dont cough, blow nose, sneeze with mouth open or not at all.
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Complications with removal of the Pituitarty Gland.
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You will have no ADH, causing development of Diabetes insipitus, lots of urination etc.
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Adrenalectomy is
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removal of the adrenal gland tumor, make sure patient gets life time support of hormonal drugs to avoid adrenal crisis. Hormone given is cortisol IV after surgery. Then PO cortisone acetate.
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Cortisone Acetate administration considerations-
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Higher dose in the mornings and lower dose given at night. Cant miss dose teach patient imprtance of life time use of this drug.
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Another med used for after Adenalectomy is Aldosterone called?
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Florinef
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Diagnostic Test for Cushings Syndrome.
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24 hours urine free cortisol
Serum ATCH Dexamethasone (Decadron) suppression test: give a steroid and it should supress the adrenal gland activity of cortisol- asses blood levels of cortisol ( should be lower, if not, further research should be done) CRH stimulation test |
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Nursing Care for Cushings Syndrome.
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Monitor for elevated NA and decreaed K+, monitor glucou, monitor risk for infection. Diet: low sodium, low fat, low cholesteral, may need meds for High BS, address body issues, provide rest periods, monitor electrolytes, glucouse, WBC, prmote wound healing, medic alert, reduce stress.
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Primary Aldosteronism casues and pathopsysiology.
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Elevated secretion of aldosteron from the cortex. Primarily from the Adrenal Gland.
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Primary Aldosteronism Clinical Manifestations.
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Increased aldosteron levels causesing HTN, high BP, Hypernatremia, and Hypokalemia
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Other couses of Primary Aldosteronism.
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Heart Failure and Renal Failure this is b/c anything that causes hypoperfusion to kidneys can trigger release of aldosteron b/c volume is low.
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Diagnostic Testing for Primary Aldosteronism.
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Elevated plasma aldosteron levels and decreased plasma renin activity levels- CT/MRI
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Managment for Primary Aldosteronism.
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Treatment lower aldosteron levels, treat cause, medications for HTN such as Spinolactone (a K+ spairing diuretic) promote K+ intake, restrict sodium from diet, avoid ETOH, weight control- activity ( b/c fluid overload)
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Addison's Disease is
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An autoimmune disorder where not enough Aldosteron is being secreted. Also happens with removal of adrenal gland.
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Addisons Disease
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An autoimmune diease. Hyposecretion of adrenal cortex hormones ( glucocorticoids and mineralcorticoids)
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Addisons Disease clinical manifestations
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Low blood sugar, low sodium, high potassium, low blood pressure. Could lead to circulatory collapse.
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Diagnostic examinations for Addisons disease.
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Urine 17KS this is related to aldosterone levels. You would expect levels to be low for this condition.
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Signs and Symptoms related to Addisons Disease
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Hyperpigmentation of the skin (bronze color), most evident with someone who has primary adrenal insufficiency, emotional changes.
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Treatment for Addisons Disease
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Hydrocortisone replacing cortisol, Florinef replacing aldosteron ( mineralcorticoid) Hydrocortisone ( is cortisol) frist drug of choice given IV
Minimize stress |
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Phechromocytoma
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Hypersecretion of the adrenal medulla- related to a tumor on the adrenal gland secreting catecholamines, primarily Norepinephrine whic his primarily Alpha which vasoconstrics.
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Clinical Manifestations of Phechromocytoma
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HTN related to secretion of Norepinephrine and the 5ps
1. Pressure ( HTN ) 2. Palpitations 3. Pale Pallor cause of vasoconstriction 4. Perspiration 5. Pain ( chest pain) |
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Diagnostic Testing for Phechromocytoma and percaustions before adrenalectomy
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24 hr urine test will show metanephrins (high levels) , CT and MRI will show tumor. Before surgery its important to give Catecholamine Blockage - alpha adrenergic blocker flowed by beta blocker.
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Acute Renal Failure
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Rapid loss of kidney function from renal cell damage which occurs abruptly, can be reiversible, near normal or normal kidney function may resume gradually
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Acute Renal Failure signs and symtoms
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Primarily caused by the retension of waste, rentention of fluids and kidneys inability to regulate electrolytes. Leads to cell hyperfusion, cell death, and decompensation of renal function.
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Three different causes:
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1. Prerenal
2. Intrarenal 3. Postrenal |
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Prerenal-
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Outside the kidney; caused by intravascular volue depletion, dehydration, decreased cardiac output, decreased peripheral vascular reistance, decreased renovascular blood flow, and prerenal infection or obstruction.
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Intrarenal-
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Withing the parechyma of the kidney;caused by tubular necrosis, rplonged prerenal ischemia, intrarenal infection or obsruction, and nephrotoxicity.
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Postrenal-
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Between the kidney and urethral meatus, such as bladder neck obstruction, bladder cancer, calculi, and postrenal infection
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Acute Renal Failure Phases
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Onset
Oligurgic Diuretic Recovery |
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Onset Phase (ARF)
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The onset is the initial phase of injury to the kidney. Reversal or prevention of kidney dysfunction is possible at this stagen by early intervention. Physiologic effect: hypotension, ischemia, hypovolemia, S/S: Subtle, Duration: Hours -days
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Oliguric Stage (ARF)
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INability to regulate electrolytes: hyperkalemia, hyponatremia, acidosis, hypocalcemia, hyperphosphatemia. Inability to extrete fluid loads: fluid overload, hypervolemia. Hematologic dysfunction: anemia, platelet dysfunction, lekopenia, May still require dialysis. (Mckay) 8-15 days; longer the duration the less chance of recovery, sudden decrease in urine less than 400ml/day or less than 30 ml/day. S/S: n/v, cardiac dysrythmias, electrocardiogram changes, kussmauls resp, drowsiness, confusion, coma, HF, PE, nech vein distention, HTN, fatigue, bleeding, infection
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Diuretic Phase (ARF)
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Urinary output > 1000 than 1000ml/day increased production of urine, High BUN initially, slowly increasing excretion of metabolic wastes, hypovolemia, loss of sodium, loss of potassium, gradually returns to baseline. S/S: Urinary output of up to 4-5L/day, postural hypotension, tachycardia, improving mental alertness and activity, weight loss, thirst, dry mucous membranes, decreased skin turgor. Duration: 2-6 wks after onset of oliguric; druation varies
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Recovery Phase (ARF)
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Kidneys returning to normal functioning, some residual renal insufficiency, 30% of the patients do not attain full recovery of GFR. S/S decreased energy levels Duration: 3-12 months
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Lab Values in Prerenal Stage of ( ARF)
BUN Creatine BUN/Creatinine ration |
BUN:increased
Creatinine: normal BUN:Creatinine ration: 20:1 or greater |
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Lab Values in Intrarenal Stage of ( ARF)
BUN Creatine BUN/Creatinine ration |
BUN:increased
Creatine:increased BUN/creatinine ration: increased |
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Lab Values in Intrarenal Stage of ( ARF)
BUN Creatine BUN/Creatinine ration |
BUN:increased
Creatine:increased BUN/creatinine ration: normal to slightly increased |
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3 electrolyte imbalances are
|
Hyperkalemia
sodium imbalace Metabolic Acidosis Low Calcium and High Phosporous |
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Which assesment parameter will the nurse monitor ina client with CRD to determin fluide and sodium retention status?
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Weight and Blood Pressure
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Treatment for Hypovolemia r/t ARF?
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Hypotonic solutions,PRBCs for blood and or plasma losses, loop diuretics
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TX for Hypovolemia r/t (ARF)
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Hypotonic solutions, PRBC's, for blood and or plasma losses, loop diuretics
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TX for Nephrotoxicity and Ischemia r/t (ARF)
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Mannitol, loop diuretics, dopamine
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TX for Inflammation r/t to (ARF)
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Glocorticosteroids
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TX for Progressive Azotemia, Hyperkalemia, Metabolic Acidosis
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Dialysis
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Treatment for Acute Renal failure
|
Give fluids if hypovolemic. Stop the offending agent if its nephrotoxicity ( give loops to helpget through the oliguric state w/ caution, DA low dose fro renal perfusion improvement
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Diet for Acute Renal Failure
|
restrict fluids, low potassium, moderate/restrict protein, avoid fatty foods and give small frequent meals if n/v. Avoid mag
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CRRT (continuous renal replacement therapy)
|
Removes fluids and toxins. This is used more than dialysis b/c the patient is unstable, this occurs in 24 hrs ( unlike dialysis which happens in 2-4 hours, pulls out a lot of fluid in a short time. CRRT uses convection ( hydrostatic pressure) and diffusion ( from hight to low concentration using a hemofilter) Must have a vascular access.
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Continous Venovenous Hemofiltration
|
Favored by teh clinicians; does not require arterial access
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Continous Arteriovenous Hemofiltration
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Relies on patient blood pressure for flow rates; removes large amounts of plasma, water and solutes.
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Continuous Venovenous Hemodialysis
|
Most recent development does not require arterial access
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Continous Arteriovenous Hemodialysisok for s
|
Can be used as primary dialysis in various types of critical patients.
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Slow continuous ultrafiltraion:
|
Effective in patients with CHF unreponsive to diuretics; unstable in ARF with azotemia, or electrolyte imbalances
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Gerontolic Considerations in ARF
|
Mortality highest in this group, kidney may already be taxed by chronic illness, polypharmacy, signs may be vague; treatment not initiated early, may not tolerate ARF treatements, increased risk for complications
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Nursing Care for ARF
|
Maintain fluid and electrolyt balance, maintian nutrition, prevent injury: skin breakdown, bleeding, seizure activity, prevent infection , facilitate coping, do daily weights, I&Os, BP, monitor electrolytes, look for signs of fluid overload in oliguric phase, ( CVP would be high) and signs of fluid deficit in diuretic stage ( low CVP)
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Primary Prevention of ARF
|
Primary prevention measures: Control of nephrotoxic drugs, chemicals, labeling requirments, and dispensing by prescription; home use and storage precaustions
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Secondary Prevention of ARF
|
Detection and treatment of risk factors
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Chronic Renal Failure
|
Damage to the kidneys is irriversible and kidneys can no longer maintain an internal evironment consistant with life.
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|
When does CRF usually occur?
|
Over years
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S/S of CRF result from
|
fluid and electrolyte imbalances, alterations in regulatory functions such as erythropoietin production, and retension of solutes.
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With Chronic Renal Failure you are either ____ or ____
|
Oliguric or Anuric
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|
DM and HTC can cause Chronic
|
Renal Failure
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|
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Decreased Kidney Reserve
|
Patient is asymptomatic
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|
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Kidney insufficiency
|
BUN?Creatinine start to rise,
Mild anemia, nocturia, polyuria ( difficutly concentrating urine) |
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Kidney Failure
|
Elevated BUN/Creatinine, anemia, acotemiam, metobolic acidosis
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|
|
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End Stage Reanl Disease
|
High levels BUN/Creatinie, symptoms as above ( Kidney Failure) but oliguria
|
|
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Complications with Endstage Chronic Renal Failurparin in dialysisn
|
Fluid and electrolyte imbalance, spepsis, anemia, pulmonary edema, secondary to fluid overload, peptic ulcer disease, altered platelent function, increased risk for bleeding b/c use b/c heparin in dialysis, Electrolytes, high, K, MG, phosporous.CA is low; NA is low b/c of overloaded, metabolic acidosis, tend to have decreased saliva flow--> anorexia, n/v
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Multisystem Changes with Chronic Renal Failure
|
Electrolyte imbalances
Metabolism GI tract Medication metabolism Musculoskeletal system Neuro: Seizure activity risk Uremic Frost: White color to skin, related to uremic toxins that the kidneys are not excreting. Causes Puritis |
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Chronic Renal Failure Testing
|
Diagnostic: Serum Creatine
12 or 24 hour urinary creatine clearance Electrolytes, CBC |
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Chronic Renal Failure Managment
|
Medications: HTN control, diuretics, sodium bicarbonate, Kayexalate, phosphate binding agents, calcium supplements, vitamin D, Epogen ( monitor hematocrit to see if this is working) , folate, vitamin B12 injections
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|
Kayexalate is given for CRF when
|
Potassium is elevated
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|
|
Peritoneal Dialisis permits patients to ____ themselfs at home.
|
Treat
|
|
|
|
The access choice for the hemodialysis patient is
|
Aterovenous Fistula ( AVF)
Peripheral access is created by anastomosing the patients native vessels to allow arterial blood to be diverted into the vein. |
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|
|
Dialysis
|
Based on difusion; driven by dialysit fluid. Osmosis and hydrostatic pressure.
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|
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|
Non canidates for AVF
|
can have placement of an arteriovenous graft, which uses a synthetic tubular material as a bridge between an artery and vein.
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Arterivenous Fistula (AVF)
|
Takes time to mature cant use it for at least 6 weeks. Once i can be used it is accessed 1 does to dialysate machine and the other goes to the fistula
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|
Assessment after AVF placement
|
Assess for a palpable thrill and hear a bruit ( with the bell) means turbulent blood flow. Avoid BP, IV and blood draws in AVF
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Arteriovenous Graft
|
Takes less time to mature, can be used in about 2 weeks, can cause infections or clots, same care: feel for thrill. listen fro bruit
|
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|
|
Dialysis Access Areas
|
Catheters can be placed in the Femoral, Internal Jugular, or Subclavian Vein to provide short and long term dialysis access.
|
|
|
|
Vascular Access Device
|
to be created for use when starting dialysis. If it is going to be long term use.
|
|
|
|
Careing For Renal Failure Patinet Undergoing Dialysis
|
Monitor fluid and electrolyte status, identify changes from baseline( start of treatment)
Prevent Injury and Infection Monitor Compliance with medical regimen and assessing need for ongoing patient/familu teaching Provide Support Provide Comfort Monitor BUN and electrolytes, Vital signs, * Especially BP, pre and post weight, monitor for bleeding, monitor dietary measures, fluid restriction, hold meds before dialysis, give after hold BP med unless super high. |
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|
Dialysis Complications
|
Technical problems: machines clotting
Hypotension Cardia Dysrhythmias b/c pulling electrolyts of quickly Air Embolus: from air bubble in the system Hemorrhage and gastric ulcers Restless legs syndrome nad muscle cramps: r/t electrolyte imbalance, pyrogenic reactions: infectious process ( invasive procedure) Dialysis Disequilibrium Syndrome: Secondary to rapid change in the fluid status. Can cause a shift in fluids, especially neruo. S/S neruologic, changes in LOC |
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|
Peritonial Dialysis
|
similar to hemodialysis but you use the patients peritoneum as the semipermeanle membrane, you can do it at home but increased risk of infection
|
|
|
|
Dialysate usually has a higher level of
|
Glucouse which increases risk for infection
|
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|
|
Phases of Peritonial Dialysis
|
Installation Phase: Put the fluid in the peritoneum
Dwell Time: Time we leave the fluid inside the preitonal cavity ( infectious period) Drainage Time: amount of time we drain it |
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|
|
Longest time for Peritonia Dialysis
|
Is the Dwell time
|
|
|
|
Peritonitits complications caused by Peritonal Dialysis
|
Infection casues peritonitis: rigid abdomen, rebound tenderness, elevated WBC, boardline abdomen. Respiratory Depression: most likely to occur during dwell phase. If this happens drain it. ( fluid is presing against diaphrgm)
Cathetor related clots or dislodgment Can also pull off too much fluid |
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|
|
Effluent:
|
The fluid that comes out of the patient in peritoneal dialysis. Measure this to keep accurate I&Os.
|
|
|
|
Renal Tranplantation
|
Most common and oldest kind of transplant
|
|
|
|
Sources for Renal Transplantation
|
can get a kidney from a living donor, a non heart beating donor ( dead from MI) or a deceased donor ( brain dead but heart is still beating)
Living donation is usually a family member |
|
|
|
Reanl Transplant Complications
|
UTIs, gradt rejection, cardippulonary complications, HTN, infection, malignancies,
|
|
|
|
Postoperative Care for Renal Transplantation
|
Careful monitoring of fluid balance
Maintain electrolyte balance Medications: Immunosuppressive therapy Dietary measures Care of donor provide education and couseling avoid raw fruits, vegis, and sushi avoid peoiple who are sick, use good hand hygine Donor needs to avoid nephrotoxic drugs and maybe psychosocial help after giving it up |
|
|
|
Complications of Rejections: 3 Phases
|
Hyperacute Phase: withing 48 hours after surgery,related to cross matching problem. Rare but can happne
2. Acute rejection: 1 week to 3 months following surgery( TX: high dose steroids) s/s of rejection- sudden weight gain, edema, increased BUN and Creatinine, decreased creatinine clearance, fever, flank pain. 3. Chronic Rejection:3 months or longer after surgery: prognisis is not good. Doesnt respond to high does steroids. |
|
|
|
Effluent:
|
The fluid that comes out of the patient in peritoneal dialysis. Measure this to keep accurate I&Os.
|
|
|
|
Renal Tranplantation
|
Most common and oldest kind of transplant
|
|
|
|
Sources for Renal Transplantation
|
can get a kidney from a living donor, a non heart beating donor ( dead from MI) or a deceased donor ( brain dead but heart is still beating)
Living donation is usually a family member |
|
|
|
Reanl Transplant Complications
|
UTIs, gradt rejection, cardippulonary complications, HTN, infection, malignancies,
|
|
|
|
Postoperative Care for Renal Transplantation
|
Careful monitoring of fluid balance
Maintain electrolyte balance Medications: Immunosuppressive therapy Dietary measures Care of donor provide education and couseling avoid raw fruits, vegis, and sushi avoid peoiple who are sick, use good hand hygine Donor needs to avoid nephrotoxic drugs and maybe psychosocial help after giving it up |
|
|
|
Complications of Rejections: 3 Phases
|
Hyperacute Phase: withing 48 hours after surgery,related to cross matching problem. Rare but can happne
2. Acute rejection: 1 week to 3 months following surgery( TX: high dose steroids) s/s of rejection- sudden weight gain, edema, increased BUN and Creatinine, decreased creatinine clearance, fever, flank pain. 3. Chronic Rejection:3 months or longer after surgery: prognisis is not good. Doesnt respond to high does steroids. |
|
|
|
Coronary Artery Disease (CAD)
|
is the narrowing or obstruction of one or more coronary arteries as a result of atherosclerosis which is an acumulation of lipid containing plaque in the arteris.
|
|
|
|
Microvasular Angina
|
results from poor function of the smaller blood vessels that supply the heart.
|
|
|
|
The most common cause of CAD is?
|
Atherosclerosis
|
|
|
|
Risk Factors for CAD classiffied as?
|
Nonmodifiable and Modifiable
|
|
|
|
Nonmodifiable risk factors include:
|
1. Age
2. Gender 3. Race 4. Family History 5. Genetics |
|
|
|
Modifiable risk factors include:
|
1. Diabetes
2. HTN 3. Tabacoo 4. Sedentary lifestyle 5. Obesity 6. Stress |
|
|
|
Stable Angina
|
Chest pain that last less than 5 mins relieved by rest or Nitroglycerin. Also called exertional angina, ocurs with activities that involve extertion or emotional stress, relived with rest or nitroglycerin, usually has a stable pattern of onset, duration, severity, and relieving factors.
|
|
|
|
Unstable Angina
|
Also called preinfarction angina occurs w an unpredictable degree of exertion or emotion and increases in occurrence , duration, and severity over time. Pain may not be relived by nitroglycerin
|
|
|
|
Variant Angina
|
Also call prinzmetals or vasospastic angina. Results from coronary artery spasm, may occur at rest, attacks may be associated with ST segment elevation noted on the electrocardiogram (ECG)
|
|
|
|
Intractable Angina
|
is a chronic incapcitating angina unresponsive to interventions,
|
|
|
|
Preinfarction Angina
|
associated with acute coronary insufficiency, last longer than 15 mins symptoms worsening cardiac ischemia, occurs after an MI, when residual ischemia may cause episodes of angina
|
|
|
|
Angina signs and symptoms
|
Pain can develop slow or quickely, pain usually is decribed as squeezing pain may occur, pain may radiate to the shoulders, arms, jaw, neck, and back, pain intensity is unaffected by inspiration and expiration, usually last less than 5 mins hoever it can last up to 10-20 min, dyspnea, pallor, sweating, palpitations and tachycardia, dizziness, and faintness, hypertension, digestive disturbances.
|
|
|
|
Diagnostic Studies for Angina
|
Electorcardiography: Readings are normal during rest w ST depression and or T wave inversion during pain.
Stress Testing: Chest pain or changes in the clectrocardiogram or vital signs during testing may indicate ischemia Cardiac Catheterization: Catheterization provides a definative diagnosis by providing information about hte patency of the coronary arteries. |
|
|
|
Interventions for Angina
|
Assess Pain
Provide Bed Rest Administer oxygen at 3L/min by nasal canula as prescribed Administer nitroglycerin as precribed to dilate the coronary arteries, reduce the oxygen requirements of the myocardium and relive chest pain. Obtain a 12 lead ECG Provide continuous cardiac monitoring |
|
|
|
If patient has chest pain/myocardiac ischemia greater than 20 mins this
|
is causeing tissue death and patinet will have an acute MI
|
|
|
|
During MI the SNS trys to help but increases O2 demand making it
|
worse so beta blockers are needed to blunt the SNS response
|
|
|
|
MI can lead to
|
Cardiogenic Shock
|
|
|
|
Transmural MI
|
is when an MI goes through all three layers of the heart. Epicardium, Myocardium, Endocardium.
|
|
|
|
For a Transmural MI and EKG will show
|
a Q wave called Q wave infraction.
|
|
|
|
Left anterior descending LAD
|
supplies ventricle. So an LAD MI (anterior wall MI – worse) includes bundle branch and left sided heart failure
|
|
|
|
If have right coronary artery – so supplies
|
the right side – for 10% of the population it supplies SA node for 90% it supplies AV node. So MI here (inferior wall MI) would result in right sided heart failure, and blocks – bradydysrythmias are common.
|
|
|
|
Myocardial Infraction
|
MI occurs when myocardial tissue is abruptly and severly deprived of oxygen. Ischemia leads to necrosis of the myocardial tissue if blood flow is not restored. Infraction does not occur instantly but over several ours. Physical Changes in the heart occur in 6 hours where the infracted area apears blue and swollen, after 48 hours it turns gray, with yellow streaks developing as neutrophils invade the tissue, By 8-10th days after infraction, granulation tissue forms. After 2-3 months necrotic area develops into scar tissue permanetly changes the size and shape of the enitre left ventricle.
|
|
|
|
Classical Symptoms of an MI
|
Chest pain
|
|
|
|
Non classical symptoms for Women
|
may experince atypical discomfort shortness of breath, or fatigue and trouble sleeping.
|
|
|
|
An older client with an MI may experience
|
SOB, pulmonary edema, dizziness, altered mental status, or a dysrhythmia.
|
|
|
|
Location of MI
|
1. Obstruction of Left Anterior
Descending Artery 2. Obstruction of Circumflex Artery 3. Right Coronary Artery |
|
|
|
Obstruction of Left Anterior Descending Artery
|
Results in anterior wall or septal MI, or both
|
|
|
|
Obstruction of the Circumflex
|
Results in posterior wall MI or lateral wall MI.
|
|
|
|
Obstruction of the Right Cornonary Artery
|
Results in inferior wall MI
|
|
|
|
Diagnostic Studies for MI
|
Tropnon Level
Total Creatin Kinase Level CK-MB isoenzyme Myoglobine LDL WBC ECG Excersice Tolerance Test Thallium Scan Multigated Cardiac Catheterization |
|
|
|
Pain characteristics:
|
Crushing, stabbing, generally on the left, may be in epigastric area, may radiate to jaw or neck or shoulders or back, many ppl think its just gas/indigestion – teaching imp esp in high risk population
|
|
|
|
S3
|
is often associated with heart failure - shows overload – heard after S2 – in young person is normal – with someone with cardiac hx signifies heart failure
|
|
|
|
S4
|
assoc with non-compliant ventricle – ventricular issues such as long term hypertension – heard right before S1 – both heard during diastole – S4 is late diastole S3 is early diastole
|
|
