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Final Exam 221
Terms in this set (90)
What is Hypovolemia?
- Most common type
- A decrease in intravascular volume which results in multiple organ failure due to inadequate perfusion
- 10-15% fluid loss is too much!
- Best outcome is if we intervene early
Hypovolemic Shock is a _____________ problem
- Decrease in Intravascular Volume
- Decrease venous return (Preload)
- Decrease in SV
- Decrease in CO
- Decrease in tissue perfusion
- Cell Death
In the initial stages of Hypovolemic shock, what S + S will you see?
Increase HR (Compensatory Mechanism)
Changes in LOC
If patient is taking _________ medication, it can mask the effect of HR on a Hypovolemic patient
What three types of situations can create a Hypovolemic State?
2. Burns (Third Spacing)
In what areas of the body can life threatening hemorrhage occur
2. Thigh (2 L)
3. Abdomen/Pelvis (3L)
4. Outside of Body (All of it)
What is the goal of treatment for Hypovolemia?
Increase supply and decrease demand (Control further blood loss and give oxygen which helps to decrease demand)
How do we treat the problem of decrease volume (Preload)?
FLUID RESUSCITATION! Two large bore catheters and can use isotonic, colloids or blood (If blood, X match or O+/-)
What is the main difference between crystalloids and colloids?
colloids have STARCH (volume expanders). Use NS (LRS can further increase lactate in Hypovolemic pts)
Which patients are good to receive Isotonic Solutions?
BURN patients. Watch for hypervolemia
Which type of fluid is NOT good for people with little volume?
HYPERTONIC (3% NACL, D10W, D50). Watch for overload and pulmonary edema
What are key points to remember about colloids?
- Large molecule
- Remain in intravascular space
- EXPAND plasma (oncotic pressure)
- Less volume required than crystalloids
- Hetastarch, Pentaspan, Albumin, FFP
- Watch for fluid overload
Two key points to remember about blood products include?
RBC: FFP ratio should be 2:1
Early admin = Better outcome
What is our main concern with Hypovolemia ?
PRELOAD FIRST! CO is biggest concern and getting rid of underlying factors.
Then increase Afterload (Vasopressors to ^ BP), treat contractility, high flow O2. Don't treat HR as it is Comp. mech.
How will you know if interventions are working?
NOT SO EASILY MEASURED:
Central venous pressure - Taken from a central line and monitors preload on the right side of the heart. Reflects how much stretch is occurring in the right atria
Arterial pressure: Radial artery and you get second by second BP and MAP
ONLY IN ICU:
Pulmonary Capillary Wedge Pressure (PCWP) - Large bore into IJ and monitors pulmonary pressure (Left Ventricular Preload)
Systemic Vascular Resistance (SVR) -
Cardiac Output / Cardiac Index
What is Cardiogenic Shock?
A "pump problem".Failure of the heart to pump blood forward which leads to decrease perfusion and end organ perfusion.
What is the most common cause of Cardiogenic Shock?
LEFT Ventricular MI > 40% loss of functional myocardium
What three things with the heart can ultimately lead to Cardiogenic Shock?
1. Primary Ventricular Ischemia --> Ineffective flow
2. Structural Problems -> Cardiomyopathy
3. Dysrhythmias --> Atrial fibrillation.
How do you treat Cardiogenic Shock
Treat underlying cause then balance O2 supply and demand. ALWAYS treat PRELOAD first. With CS, it is too high because blood not going gwd. Treat with: Vasodilator (Nitro). Can also give diuretic, morphine or dialysis
Dopamine, Dobutamine (vasopressors) increase HR and contactility
In Cardiogenic Shock, when is the only time that you should give a BB?
If patient is having an active MI then treat HR
What drugs can only be given if a patient has a patent central line?
Any drug that causes vasoconstriction!! If not can cause tissue necrosis
What is an Intraaortic Balloon Pump?
Potential for ruptured aorta. CATHETER THROUGH femoral into aorta and sits in front of aortic valve to help decrease workload and perfusion of the heart. Can be inserted for a few days. Balloon inflates during diastole which traps blood, increasing perfusion to myocardium. Before systole, vacuum is created to suck blood out of left ventricle and making it easier for broken pump to pump! NEED TO HAVE CARDIAC MONITORING DEVICES!!!
What is a common cause of Cardiogenic Shock?
a large portion of the myocardium is damaged
MI - BIGGEST CAUSE - KNOW FOR NCLUX!!!!!
When does shock follow an MI?
When a large portion of the myocardium is damaged.
What is Distributive Shock?
"Pipe Failure". BV's dilate, there is increased vessel capacity and not enough fluid in the tank
-Most common form of Distributive Shock
What are the biggest signs and symptoms?
- Flushed Skin
- May not look sick until the very end
What is the BIGGEST difference in S + S for Septic Shock that is different from Hypovolemia?
FEVER and FLUSHED FACE
Who is most at risk for Septic Shock?
- IV drug users
- Immunocomp. patients
Why is Septic Shock so BAD?
Can lead to Respiratory Failure and Death. 40% mortality with severe sepsis and 60% if go to ICU
When you have an inflammatory response that is no longer contained, it is known as_________________?
SIRS (Systemic Inflammatory Response Syndrome)
What is the SIRS criteria?
Two or more of the following:
- Temp >38 OR <36
- HR >90
- RR >20 or PaCO2 <32mmHg
- WBC's > 12,000 or <4000 or >10% bands
- Altered LOC
To be labelled as Sepsis, patient must have ______ + ________?
SIRS criteria plus an Infection
What does severe sepsis include?
Sepsis + organ dysfunction (Renal, Liver, Troponin for heart, ABG's, Coagulation)
What does Septic Shock incorporate?
SIRS criteria, organ dysfunction , severe sepsis and Hypotension despite fluid resuscitation!!! KNOW THIS
What is the clinical definition of sepsis?
A systemic inflammatory response and documented or suspected infection.
What is the clinical definition of Septic Shock?
Acute circulatory failure even after crystalloid fluid challange
What is Acute Circulatory Failure?
Persistent Arterial Hypotension (SBP <90 and MAP <60) or a reduction in SBP >40 from baseline despite adequate volume resuscitation
In Septic Shock, patients are in a Hyperdynamic State. What does this mean?
They have an increased CO and a decreased SVR
What are signs and symptoms of Septic Shock?
- Temp. Dysregulation (Initially warm and pink then cold and cyanotic)
- Decrease U/O
- Neuro changes
- GI dysfunction
- ARDS = Acute respiratory distress syndrome because of vasodilation and leaky capillaries! Lungs become non-compliant and hard
DIC: Disseminated Intravascular Coagulation. Clotting and bleeding at the same time!
What are the two MOST critical vitals to detect Septic Shock early???
Pulse and RR
What diagnostic test is KEY for Sepsis
What are other diagnostic tests for Sepsis
1. Blood and other cultures (Sputum,stool, urine and wounds)
2. CBC with diff
3. Coagulation Profile
5. C-Reactive Protein = marker of vascular inflammation
Explain the correlation of Lactate and Sepsis...
- Sepsis (a hypermetabolic state; massive inflammatory reaction) is accompanied by increased glycolysis and hyperlactatemia
- In sepsis, hyperlactatemia should not be interpreted as tissue hypoxia but rather related to the hyperkinetic state
- In sepsis, high lactate levels may lack precision as a measure of tissue metabolic status, but do support aggressive resuscitation
Once septic patients develop macrovascular shock (refractory hypotension) or microvascular shock (elevated lactate), they are on the steep part of the mortality curve and immediate identification and intervention is critical to avert rapid deterioration and death
What is the treatment process for Sepsis?
1. **ATB's - Treat Cause after you have obtained sample for C +S
+ enteral feeding and tylenol to decrease fever
3. IV access
4. If patient has SIRS criteria, low blood volume - GIVE FLUIDS (BOLUS) 2L NS OVER 10 MINUTES! (TREATS PRELOAD). 1 L of fluid = 1kg. Even if fluid is third spacing, still give lots of fluids (up to 10 L)
5. Treat Afterload: Patient must have a Central Line!!! Need to monitor Central Venous Pressure
6. Sepsis Vasopressor = Nor - Epi (Alpha)or Vasopressin both of which cause vasoconstriction
7. Treat contractility = Dobutamine! (Beta 1 effects)
8. Intubation and Ventilation mainly because of third spacing
9. Is HgB optimized??
What are other treatments for Septic Shock?
1. Preload is #1 - Improve CO (fluids!)
2. Next comes Afterload and contractility. Can treat with vasopressors and oxygen
3. BG should be <8.33
4. Give ulcer prophylaxis with H2 receptor blocker (Ranitidine)
5. DVT prophylaxis (Meds or TEDS)
What is MODS and what are some S + S?
Multiple Organ Dysfunction!
- Altered LOC/Confusion
- Jaundice ( ^Liver enzymes with v in Alb)
- Metabolic acidosis with increase Lactate
- Tachycardia with Hypotension
- Oliguria, anuria
- Increase PT/INR/D -Dimer and decrease platelets and protein c
What is the onset of Anaphylactic Shock?
Immediate and life threatening
What is occurring in Anaphylactic Shock?
There is an Antigen-Antibody reaction that releases chemical mediators (Histamine). This causes vasodilation and leaky capillaries, decreasing CO
What causes Anaphylactic reactions?
Skin Contact = Pollen, Latex, etc
- Injection = Bee Sting
- Ingestion = Nuts or Meds
- Inhalation = Pollen or Dust
How does Anaphylaxis work (Patho)?
Patient has response (IgE) which activates mast cells which play an important part in anaphylactic shock. Most are found in airway and lungs (mast cells) and this is why we are concerned when patient have anaphylactic reaction because they are responsible for swelling around the airway. Bronchoconstriction and edema decreases O2 supply!!
What are some S + S of Anaphylactic Shock?
- SOB, ^ WOB, stridor, wheezing, ^ RR
- Hives with flushed, warm skin
- Tingling (changes in sensation)
- Anxiety/ Impending doom
- Decrease LOC
What are the treatments for Anaphylactic Shock?
REMOVE THE CAUSE
- O2 supply (Preload, Afterload and contractility) and O2 demand
What is the #1 treatment for Anaphylaxis?
Stop Vasodilation: Epinephrine IM or SQ!!! (1:1000 EPI; 0.2-0.5ML and can repeat dose up to 3x every 10-15 minutes). Alpha properties to cause vasoconstriction and Beta properties to cause Bronchodilation to open airways. Side effect: Beta 1: Sense of panic because of high increase in HR
**Do NOT give Epi IV unless patient is dead
Stop Bronchoconstriction: Epinephrine & Salbutamol (Ventolin) causing Bronchodilation and open airways
Antihistamines: H1(Benadryl IV/IM (25-50mg) /H2 Blockers (Found more in GI = Ranitidine or Zantac (IV 50MG). Cannot be given IM! They stabilize aggravated cells. Can give every 4-6 hours
- PUT FLUID IN THE TANK!! IV access before giving meds
A 15-year-old male who is allergic to peanuts eats a peanut butter cup. He then goes into anaphylactic shock and develops what??
Bronchoconstriction with hives, edema and hypotension
Why does Anaphylactic Shock cause severe Hypoxia so quickly?
The bronchoconstriction and edema reduce airflow
What is the Biphasic Response?
1 - 72 hours after successful treatment and resolution of the initial response, the patient can get another anaphylactic reaction
What type of medications can suppress the inflammatory response and prevent the Biphasic response?
What is Neurogenic Shock?
The loss or suppression of sympathetic tone (Relation to SC injury). It is rare
What is the cardinal sign of neurogenic shock?
What are others signs and symptoms of Neurogenic Shock?
- Temp dysregulation (Initially warm then heat dissipates and patient can become Hypothermic. More at risk of Coagulopathies)
- Poikilothermic (environment temp)
How do we treat Neurogenic Shock?
- Maintain HR (Atropine)
- Treat Preload (Fluids; NS)
- Afterload: Vasopressors like Dopamine
-Contractility (Dopamine or Dobutamine)
- Decrease Demand (O2, control temp)
- **Maintain BP > 90 and MAP > 60.
- **Maintain Normothermia!!
What is Shock?
A SYNDROME characterized by DECREASED TISSUE PERFUSION and impaired cellular metabolism that results in an imbalance between the supply and demand for oxygen and nutrients. With decreased tissue perfusion, you get a build up of waste products (lactic acid) which is detrimental to our cells
What is a Syndrome?
A collection of signs and symptoms (shock is a process)
Explain Shock Imbalance...
There is an imbalance between how much oxygen is available versus how much oxygen is needed. The ultimate result is = Inadequate tissue perfusion and impaired cellular metabolism!
Imbalance with CO (Normal is 5000mls/min):
1. Contractility (The Pump)
2. Preload (Volume and HgB)
3. Afterload (The Pipes)
Failure of one of these can cause shock
What are the three components of oxygen supply?
3. Cardiac Output
What is Preload?
The amount of blood returning to the heart into the ventricles (volume and pressure in the ventricles during diastole). To maintain preload, we need venous return and time for the ventricles to relax and fill!!!
What is Afterload?
The force that the heart has to overcome to get blood out. Think Vessel diameter (dilated or constricted esp in aorta), valves (tight/non-compliant increases afterload), viscosity (thick vs thin blood).
What is Contractility?
The ability of the heart to contract which depends on PRELOAD!
Overstretch of the ventricle will ultimately decrease CO
What are the THREE stages of Shock?
1. Compensated Shock:
i. Little or no signs or symptoms = HELP STAGE
2. Uncompensated (Progressive) Shock:
i. Signs and symptoms are obvious = YIKES
3. Irreversible (Refractory) Shock:
i. It is over ......
What are key features of Compensatory Shock?
-Also called "Non-Shock"
- Compensation Mechanisms are still effective
- There is still adequate Cardiac Output
- There is something in the body affecting the pump, the pipes or the volume. The body is not getting enough O2.
**This is the most important stage of shock because we have the biggest chance of reversing problems.
What are the Compensatory Mechanisms activated?
a) Neural --> SNS activation --> Fight or Flight (Automatic Response). Activated when: Baroreceptors (Pressure) - Carotid bodies and aortic arch release EPI and Nor-epi (catecholamine's) help to maintain CO. Epi works on Beta receptors which increases HR and contractility, vasoconstriction to periphery and bronchodilation. Nor-Epi works more on alpha receptors in blood vessels so we see vasoconstriction. Also inhibits insulin release from pancreas and glucagon from liver; important if you have increased workload (fight or flight). Both cause diaphoresis and Pupil constriction
b) Biochemical --> Activated by H+, O2, CO2 concentrations Found in Chemoreceptors in carotid, aorta and medulla = very sensitive receptors that notice minute changes in O2, CO2. See increase in rate and depth of breathing as well as increase HR (INCREASE TV, RR, AND HR) = Respiratory Alkalosis
c) Hormonal -->RAAS ADH Renin-Angiotensin-Aldosterone System
•Angiotensin II = ↑Afterload & BP
•Aldosterone = ↑ preload
•ADH (Anti-diuretic hormone) aka Vasopressin = ↑ Afterload & BP
- Kidneys sense a decrease in blood flow and release Renin
-Angiotensin is a VERY POWERFUL VASOCONSTRICTOR which increases afterload and maintains CO
- Angiotensin 2 also stimulates aldosterone and ADH release (increase BP and CO)
What are the early signs and symptoms of Compensated Shock?
Skin normal or slightly pale, cool periphery
Increase respiratory rate; normal WOB and normal SpO2
Slightly restless; possibly mild confusion, decreased concentration
Mild tachycardia, strong pulses centrally, possibly slightly weaker peripherally, normal BP. First sign is: HYPOTENSION but there are others.
Decreased urine output and urine concentration; RAA conserves water and sodium
A patient was in a MVA and is now in Hypovolemic Shock. Why is it important for the nurse to check V/S frequently during the compensatory period?
Arteriole vasoconstriction can occur
What are the key components of Progression Shock?
-Compensatory mechanisms begin to fail
- Decreased CO
- Decreased End Organ Perfusion - Renin and SNS system start to get overwhelmed and cannot keep up with demand
- MODS = Multiple Organ Dysfunction
-Na+ is generally extracellular and K+ is intracellular = When the pump begins to fail and more sodium is inside, the cell starts to swell and patient gets EDEMA!
- See VASODILATION and LEAKY CAPILLARIES and start to get EDEMA
- Lactic Acid Buildup = switch from aerobic to anaerobic because of lack of oxygen, which in turn leads to Lactic Acid build up which affects your RBC's and O2 is less likely to bind to them, and interferes with Epi and Nor-Epi. Comp. mechanisms do not work well in presence of ACIDOSIS. Acidosis also affects contractility of the heart and the body's ability to clot (platelets are less sticky) and patient is at higher risk for bleeding. Buildup of C02 = Potent vasodilator on blood vessels!
What are signs and symptoms of progressive shock?
- Changes in LOC BECASE OF DECREASE PERFUSION AND WASTE PRODUCTS BUILDING UP
- Sensitive to small changes in O2 and Glucose
- MAP of at least 60 to maintain brain perfusion!
- Decrease BP
- Weak Pulses
- Potential for MI, dysrhythmias
- Modeling of skin peripherally, cyanosis, diaphoretic, cold, widespread edema
- Profound tachycardia
- Palpitations and Chest Pain
- Increase rate
- Accessory muscle use
- Increase RR
- Decrease perfusion (ileus or ulcerations leading to GI bleed)
- Nausea and Vomiting
- Decrease/No urine output
- 30mls/hr is what we want. Anything less, concern
- Increase in waste products (Urine and Creatinine)
- Unable to balance electrolytes (potassium, sodium, H+). Kidneys help to get rid of extra acid so if not working properly, acidosis
What are important lab values to monitor?
- Urea, Crea, GFR (v)
- Liver Enzymes (^)
- ABG's (Lungs) = CO2
- Coagulation (PTT, INR) = Both will be increased
During the progressive stage of shock, anaerobic metabolism occurs. The nurse expects that initially the anaerobic metabolism causes...?
Metabolic Acidosis - Progressive Shock
What are the key features of Irreversible (Refractory) Shock?
- Loss of compensatory mechanisms
- Profound cell destruction --> when cells die they spill out cytotoxic contents, which kills other cells
- Organ Failure and Death
What are some signs and symptoms of Irreversible Shock?
- Severe and profound Hypotension (cant get BP reading)
- Decrease central pulses
- CARDIAC ARREST!
- Widespread Edema
- ARDS (Acute Respiratory Distress Syndrome); look for crackles or consolidated and decreased resp sounds)
- FAST RR then starts to get slower and slower
- Less area on alveoli for gas exchange, and decrease O2 needed
- Respiratory and Metabolic Acidosis!
- Ischemic GUT
- HIGH levels of Ammonia and Lactate
- NO URINE OUTPUT!
What is DIC?
Simultaneously clotting and bleeding at the same time! End up with pooling and small emboli all over the body. All the platelets and clotting factors are used to deal with micro-clots and patients just bleed! WIDESPREAD HEMORRHAGING!!!! Minimal chance of survival. Common in burns, sepsis, cancers, maternity or trauma patients.USING UP ALL CLOTTING FACTORS AND BLEEDING!
A client is in profound (late) hypovolemic shock. The nurse assesses the client's laboratory values. Clients that are in late shock develop:
What can we do with patients in Irreversible Shock?
- **EARLY RECOGNITION
- Not everyone in shock looks sick
- **EARLY INTERVENTION
What are some principles for treating shock?
•Treat the underlying cause
•Optimize O2: Put them on O2, positioning, optiflow, intubation and ventilation
•Optimize Hgb: Give red packed cells
How would you treat a patient with a decreased preload?
IV fluids or blood
How would you treat a patient with an increased preload?
- Diuretics (Lasix) Helps to reduce preload
- Dialysis = Removes extra fluids and meds such as morphine, nitro that temporarily cause vasodilation
How would you treat a patient with a low Afterload?
Give medications that cause vasoconstriction (Nor-Epi)
How would you treat a patient with a high Afterload?
How would you treat a patient with a low contractility?
Medications such as Dobutamine that works specifically with increasing contractility in the heart (Lots of Beta 1 properties)
If a patient is in shock and has an increased HR, do we want to treat that and why?
No, because the patient is compensating. Need to find the underlying problem
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