Acid-Base And Shock Objectives

Front 1

Describe the relationship between free hydrogen ion level and pH

Back 1

as free H increases ph decreases (becomes more acidic) as free H decreases the pH increases (becomes more basic

Front 2

Explain the role of bicarbonate in the blood

Back 2

Bicarb(HCO3-) binds with (or releases) free H to bring blood pH into range of 7.35 - 7.45 Known as a buffer

Front 3

explain the concept of compensation

Back 3

the body uses 3 methods to compensate for pH shifts. Blood(Bicarb),Respirations(blow off or retain CO2), kidneys(reabsorb Bicarb and excrete free H ions as ammonium)

Front 4

Compare the role of a buffer in conditions of acidosis and alkalosis

Back 4

HCO3- grabs free H ions in acidosis and releases them in alkalosis

Front 5

Compare the roles of the respiratory system and the renal system in maintaining acid-base

Back 5

Respiratory is fast to act. You breath off CO2 to increase pH or breath shallow to save CO2 and decrease pH

Front 6

Identify clients at risk for acidosis

Back 6

any impaired gas exchange or blood flow. i.e. pneumonia, COPD, MI, trauma, Shock. Diarrhea

Front 7

Prioritize nursing care for the client with alkalosis

Back 7

ABC's, start an IV, treat the underlying cause, give supportive care

Front 8

Describe the clinical manifestations associated with the compensatory mechanisms for shock

Back 8

(all of these are to increase blood flow and O2 concentration) Increase HR, increase or stablize BP, restlessness, increase in respirations, decrease urinary output, decrease in blood flow to skin (clammy and cold skin)

Front 9

Identify clients at risk for hypovolemic shock

Back 9

blood loss(post surgery,trauma) fluid loss (dehydration, insensible loss) just being a pt. in an acute care setting increases the risk of shock

Front 10

explain the basis for intravenous therapy for shock

Back 10

increase fluid volume, buffer the blood, replace lost electrolytes

Front 11

Describe the mechanisms of action, side effects, and nursing implications for pharmacologic management of shock

Back 11

vasoconstrictors-constric veins(dopamine,NE) -increase BP so we monitor BP.
Increase Myocardial contractility-make the heart beat harder and faster(atropine)-monitor for s/s of an MI
Increase Myocardial perfusion-increase blood flow to hear(nitropress)-monitor HR
ALL DRUGS GIVEN IN MCG DOSAGE EXCEPT ATROPIN AND EPI

Front 12

Prioritize nursing care for the client experiencing the nonprogressive stage of hypovolemic shock

Back 12

monito ABC's and LOC. Start an IV, give O2, monitor I and O's, draw labs, treat underlying cause.

Front 13

Compare the pathophysiology and clinical manifestations of the hyperdynamic and hypodynamic phases of septic shock

Back 13

Hyperdynamic is unique to septic shock.
Hyperdynamic(Hot shock)-increase HR, Increased systolic BP, increased Temp and increased respirations.
Hypodynamic shock(cold shock)-Widening pulse pressure, decreas in diastolic BP, cold and clammy skin, decrease in temp and respirations

Front 14

Why do we get shock? (let's say we have an infection in our toe that gets into our blood stream)

Back 14

as the waste products from the infection seep into our body, we mount an inflammatory response. Like all other inflammatory responses, we get increases in VS to try to fight off the infection. The endotoxins and inflammation response trigger the formation of thousands of little clots that clog up the blood vessels. At this point, the blood vessels have dilated from the inflammation and the clots are causing blood to back up. The blood has nowhere to go, except into the periphery(third space). Our cardiac output drops, pulse drops, BP drops and we have just entered the cold phase.

Front 15

Prioritize nursing care for the client experiencing the hyperdynamic stage of septic shock.

Back 15

ABC's and LOC, start an IV, start antibiotics, give drugs to increase CO, give Heparin in this phase to combat clots(DO NOT GIVE IN THE COLD PHASE). Give O2.

Front 16

Prioritize nursing care for the client experiencing the hypodynamic stage of septic shock

Back 16

Hypovolemic-causes=volume loss.S/S=restlessness, increased HR, Decrease systolic BP, decreased Urinary output (even when intake is adequate BIG INDICATOR) narrowing pulse pressure
Cardiogenic-causes=heart damage or dysrhythmia. incresed HR, decreased systolic BP, ahrrythmias or dysrhythmias, decrease Co2, narrowing pulse pressure
Distributive-causes-sepsis, anaphylaxis, capillary leak, increased HR, Decreased diastolic BP, widening pulse pressure

Front 17

1st stage of Shock
Initial stage of shock

Back 17

MAP decrease 5-10mmhg, increased sympathetic stemulation; mild vasoconstriction from epi/NE, increased HR, decreasing CO.

Front 18

2nd stage of shock
Non-progressive

Back 18

restlessness begins, compensation is in full swing and working, MAP down by 5-10mmHg, increased HR, decreased pulse pressure, decreased Urinary output, increased thirst, mild acidosis, mild hyperkalemia

Front 19

3rd stage of shock
Progressive stage

Back 19

cold and clammy, diaphoretic,mottled,oliguria(<30cc hr.)MAP down by >20mmHg, moderate acidosis and hypokalemia. Possible failure to save. Cold phase of septic shock. anoxia of nonvital organs, hypoxia of vital organs, tissue ischemia(capillary refill 73 seconds)

Front 20

4th stage of shock
Refractory stage

Back 20

Irreversible stage. severe tissue hypoxemia with ischemia and necrosis, release of myocardial depressant factor from the ishemic pancreas. Build up of toxic metabolites results in multiorgan dysfunction syndrome. (failure to save, anoxia of vital organs, Stupor, coma, death)