nurs 420 quiz 2 (updated)

cardiac output

* CO = HR x SV
* SV = volume of blood ejected by the heart during each beat
* Normal adult SV = 60-70 mL
* Low SV
* Shock → septic, neurogenic and anaphylactic
* High SV
* Vasoconstriction → increase catecholamine


* Volume of blood pumped by heart in 1 minute → amount of blood that leaves the heart w/ each contraction
* Normal is 4-8L/min
* Figure out why this is low/high if abnormal → if this is a pump, volume or arterial issue
* Low output
* MI, HF, cardiogenic shock
* Hypovolemia, cardiac tamponade, late sepsis
* High output
* Early sepsis, fever
* Hyperthyroidism
* Exercise
* Measured by Swan Ganz Catheter
* Manual intermittent bolus thermodilution
* Continuous cardiac output monitoring (avg/3 min)

ejection fraction

* Percentage of blood in the ventricle at the end of the diastole that is ejected from the heart w/ each beat from the left ventricle
* **Determined by echocardiogram/TEE**
* Normal is 55% or higher
* If less than this → impeded
* Systolic HF → low EF, can give digoxin
* Diastolic HF → normal EF, cannot give digoxin

preload

* **Degree of stretch** of the cardiac muscles at the end of diastole
* Period when filling volume in the ventricles is the highest and degree of stretch on the muscle fibers is the greatest
* Greatly dictates stroke volume and CO
* Known as filling pressure, used to estimate fluid volume
* Think about this as venous return → more on the R side of the heart!!!


* Depends on:
* Amount of blood in the ventricles (venous return)
* Compliance/extensibility of the ventricle at the end of diastole
* Ability of the ventricles to stretch


* **If we put in an invasive line, we can measure preload!!!**
* **Can be done via central venous line → measured in central venous pressure (CVP)**
* **2-6 mmHG**
* **Low preload → heart can’t stretch or volume is missing**
* **Ex: dehydrated patient → increase fluids**
* High preload → heart is stretching too much, volume is not being pushed forward correctly
* Ex: heart failure patient → give pt diuretics or vasodilators
* Increased preload/volume
* Exercise → b/c of increased in HR causing an increase in preload
* Increased blood volume
* Fluid administration
* Decreased preload/volume
* Dehydration
* Blood loss
* Decreased venous tone (sepsis, neurogenic shock)
* Vasodilators

Starling’s law

* effects of preload
* The greater the stretch of the heart muscle at the end of diastole, the greater the force of the next contraction
* **Greater the stretch = greater the contraction**
* At some point, the volume will overpower and elasticity will be lost

afterload

* **Pressure or resistance that the ventricle must overcome to eject blood through the valves and into the peripheral blood vessels or pulmonary vasculature**
* Forces include:
* Systemic and pulmonary arterial pressures
* Systemic vascular resistance (SVR)
* This is why diabetics have high BP → b/c arteries become “tighter” and less flexible
* Severe aortic stenosis would affect this
* Resistance offered by the aortic and pulmonic valves
* Diameter of the blood vessels
* Mass and density of the blood to be moved
* Blood viscosity

purpose of hemodynamics

* Measurement of pressure, flow and oxygenation of blood within the cardiovascular system
* The patient is connected to a transducer via an invasive catheter (central IV line, arterial line) and pressure tubing (similar to IV tubing but smaller in diameter and less pliable)
* The transducer converts physiologic signals (reads pressures) to electrical energies (numbers and waveforms)
* Connects to monitor → shows if invasive line is working correctly
* Always want to zero this at the beginning of your shift\*\*\*
* Do this by turning the stop cock upwards and removing cap


* When to use hemodynamic lines
* Shock, AMI
* Heart failure
* Surgery
* Guide for therapy → fluid vs. diuretics
* Evaluate pharmacological treatments

phlebostatic axis

* In order for transducers to accurately report what they’re measuring, they must be level to the heart
* This means the transducer is level w/ the heart
* Level of right atrium 
* Lies at the 4th intercostal space at the mid-axillary line
* Patient is supine but accuracy has been determined to be 0-60 degrees

\
* Zeroed minimum of every 8 hours or position change → to keep level w/ heart
* Need to check institution policy

arterial lines

* Can sit in radial or femoral arteries → femoral is usually for emergent situations
* Only doctors, respiratory therapists and nurse anesthetist can place these
* **Can stay in for up to a week, sometimes longer**
* **Insertion site → bigger gauge (18 or 16)**
* **Stabilizer can be sutured in if needed**
* **Need consistent fluid bag to get readings!!! → we want to keep the line patent**
* **NORMAL SALINE ONLY**
* **This will continuously flush as a “drop”**


* Make sure to maintain the “**green line pressure**” to allow for a little drip of fluid and make sure this is working correctly


* Need to flush this line at the start of every shift/as needed

\
* Used for:
* ABGs → esp if recurrent b/c these are painful
* Frequent lab draws
* Continuous BP/MAP → gives 24/7 read
* MAP of at least 60 mmHg to perfuse vital organs
* Low MAP = low CVP, and vice versa- same treatment regimen
* **YOU DO NOT PUSH MEDICATIONS THROUGH AN A-LINE**
* **QUESTION THE ORDER IF THIS IS AN EXAM QUESTION!!**
* **major risks - ex. limb falling off**

Allen’s test

Checks collateral circulation in the hand, done before A-line placement

arterial line waveforms

* __Normal__ → shows systolic (first peak) and diastolic (second peak)


* __Overdampened__ → NO systolic or diastolic
* **May have to replace or flush d/t kinks or clotting in tubing**


* __Underdampened__ → doesn’t look like a normal flowing wavelength
* **Flush this to see if this is a flow issue**

arterial monitoring

* Complications:
* Limb impairment
* Infection


* **Remove under sepsis protocol if necessary**


* thrombosis/arterial occlusion → from blood sitting in the area


* Nurses CAN take an A-line out
* **Give pressure for 5 minutes, then dress w/ pressure dressing**


* **Don’t tape whole circumference or else this will lead to compartment syndrome**


* When in doubt → correlate readings w/ BP cuff and compare readings
* **Nothing is better than a manual BP**
* When in doubt, always confirm!!

central venous line/pressure

* AKA right atrial pressure (RAP)
* Catheter sits in the right atria → measuring right atrial filling pressure/PRELOAD
* **Tip of the catheter should lie in the lower ⅓ of the SVC**
* **3 lumens**
* **Brown (distal) = transduce CVP**
* **Blue (medial)**
* **White (proximal) = drips?**
* Connect to transducer for CVP reading
* Will give you a constant, continual reading
* This is the ONLY measurement you can get → NO BP
* Normal CVP reading → 2-6 mmHg
* If low → hypovolemia or vasodilation
* If high → hypervolemia, vasoconstriction, HF, pulmonary hypertension, cardiac tamponade

nursing interventions - CVP

* Maintain dressing change → dry sterile occlusive dressing in place
* Central lined can stay up to 6-8 months
* Will require **weekly sterile dressing changes** b/c this sits directly in the heart


* Patient and healthcare personnel are **masked**


* Change of tegaderm, clean the site and then replace


* **Confirmation of initial placement w/ an x-ray before administering ANYTHING through the line**
* **Need order saying “clear for access” → do NOT take doctor’s word for this**
* **Make sure to document which doctor OKs use**
* Monitor CVP readings (look at trends)
* **Can give fluids, IV dye and medications through this**

CVP complications

\
* Infection
* Aseptic technique for insertion and set-up and dressing change w/ occlusive dressing
* Monitor for local and systemic s/s of infection
* Remove if infection is suspected
* Do NOT leave in place longer than necessary
* Pneumothorax
* Air embolism

pulmonary line/PAP

* Pulmonary artery pressure monitoring (PAP)
* Aka Swan Ganz Monitoring
* Balloon tipped, flow directed catheters that have distal and proximal lumens


* Can have 4 or 5 lumens


* Right atrial lumen (proximal)


* Pulmonary artery lumen (distal)


* Balloon lumen


* Thermistor lumen


* Subclavian location most often used


* Measures:
* R atrial pressure or CVP
* Pulmonary artery pressure
* PAOP = pulmonary artery occlusion pressure (wedge pressure)
* CO= cardiac output
* CI= cardiac index


* Indicated for patients who are:
* Hemodynamically unstable
* Assesses left ventricular function (CO)
* Diagnosing etiology of shock
* Need fluid management
* Continuous cardiopulmonary assessment
* Receiving multiple or frequently given cardioactive drugs
* Shock, trauma, cardiac disease, multi-organ system failure
* Pacing, oximetry, CO measurement

PAP insertion

\
* Performed at the bedside, cardiac cath lab or in the OR
* Can be inserted using fluoroscopy
* Large vein
* External jugular
* Subclavian
* Femoral
* Nursing considerations
* Patient needs to **consent**
* Want to have a good history b/c we are using fluoroscopy
* I.e. metformin use, kidney disease
* Continuous monitoring

PAP pressure measurements

\
* Pulmonary artery systolic pressure (peak pressure): 15-25 mmHg
* Pulmonary artery diastolic pressure: 8-15 mmHG
* Sensitive indicator of fluid volume status and cardiac function
* **Increased w/ fluid overload in HF**
* **Pulmonary capillary wedge pressure (PCWP or PAOP)**
* **Measured by inflating the balloon w/ max of 1.5 mL of air (wedge)**
* **Inflate for

nursing responsibilities - PAP

\
* Ensure system is set up properly **without air bubbles**
* **Check that the transducer is positioned at the level of the atria (phlebostatic axis) prior to measurements**
* Establish zero reference point in order to ensure the system is functioning properly

complications - PAP

\
* Pneumothorax
* Infection and sepsis
* **thrombus/embolus formation** 
* **Continuously flushed w/ slow infusion of heparinized saline**
* Bleeding, hematoma
* **Pulmonary infarction and pulmonary rupture**
* **Fragments of ruptured balloon**
* **Never infiltrate w/ more than 1.5 mL of air for more than 4 breaths**
* **Pressure tracing will appear wedged if the PA catheter remains or advances into the wedged position**
* **Call MD to have this repositioned**
* **Air embolism**
* **Causes → air in tubing, balloon rupture**
* **Keep tubing free of air**
* **Inject only 1.5 mL of air while inflating**
* **Use and tighten luer-lock connections on all pressure line connections**
* Pulmonary thromboembolism
* Ventricular dysrhythmias
* During insertion or removal
* Migration of the tip to the RV

heart failure

\
* The inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen and nutrients
* Pump problem → the heart cannot pump the volume needed to manage the body’s needs, leading to end organ damage
* Any condition that impairs the ability of the ventricles to fill or eject blood can cause HF
* Causes
* post-MI
* Infection
* Cardiomyopathy
* **Uncontrolled hypertension → 75% of patients!!!**

left-sided heart failure

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* Disturbance of left ventricle → results in low CO state → leads to vasoconstriction that raises SVR (high afterload)
* Patient findings
* Decreased peripheral perfusion (pulses, capillary refill, color)
* Pulmonary edema (lung sounds- “wet sounds”, crackles, pink frothy sputum)
* Dyspnea and hypoxemia
* Eventually right sided failure as well
* see attachment for clinical manifestations

right-sided heart failure

\
* Think fluid overload
* **JVD**
* **High CVP**
* Edema
* Hepatomegaly
* GI symptoms → feeling of fullness, decreased PO intake
* see attachment for clinical manifestations

systolic heart failure

* HF w/ reduced ejection fraction
* **Decreased contractility** of the L ventricle
* L ventricle loses its ability to contract b/c it becomes loose
* Heart can’t fill properly w/ blood during resting period between each beat
* **Thin heart walls are a sign of systolic HF**
* Ejection fraction → 45-50%
* **Ejection fraction

diastolic heart failure

\
* aka HF w/ normal ejection fraction
* **Impaired relaxation and filling of the heart**
* **stiff/thick heart muscle**
* **Thick heart walls are a sign of diastolic HF**
* Patient characteristics → older, women, obesity, hypertensive
* Treatment
* More dependent on the underlying disease
* Calcium channel blockers → decrease afterload/workload the heart has to pump against
* ACE inhibitors → decrease afterload, and prevent ventricular remodeling 
* Beta blockers → slow HR conduction and contraction
* Diuretics can be added
* **DIGOXIN IS CONTRAINDICATED**

pulmonary edema

* Clinical findings
* Extreme breathlessness/anxiety
* **Feeling of suffocation**
* **Pink frothy sputum**
* Thrashing, feeling of drowning
* Tachypnea, accessory muscle use, nasal flaring
* Diaphoresis, cool skin, cyanosis
* Lung sounds, loud inspiratory and expiratory gurgling/wheezing
* Can occur b/c of L-sided HF or from non-cardiac causes
* Non-cardiac can be an inflammatory response
* To distinguish which this is → **look at BNP**
* NP is released from cardiac ventricles in response to increased wall tension
* This measures ventricular stretch


* HR causes increased wall tension b/c of excess preload in the ventricles leading to increased wall stretch
* If this is elevated → cardiac issue, degree of HF increases w/ BNP

medical management of acute HF patients

\
* Control symptoms → fluid overload, enhance cardiac performance
* **Diuretics**
* Morphine
* vasodilators/nitrates
* inotropes/inodilators 
* Medical management
* ACE inhibitors/ARBs
* Beta blockers if tolerated
* Digoxin **for systolic HF ONLY**
* CRT/biventricular pacing/ICD
* Underlying cause → cath or echo
* **Palliative care**

nursing management - acute HF

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* Assessment → want to catch any complications before this becomes a code issue
* Optimize oxygen delivery
* Dysrhythmia monitoring
* Monitor labs → electrolytes, BNP, renal function, drug toxicity, ABGs
* Aggressive pharmacological interventions
* **Urine output**
* Body weight
* Activity, positioning
* Nutrition → decreased sodium/fluid restriction
* Patient education
* **Palliative care if appropriate**

cardiomyopathy

* Can contribute to heart failure
* __Hypertrophic__ → genetic
* Stiffening of the left ventricle
* Known correlation to sudden cardiac death
* __Dilated__ → both ventricles are dilated
* Ischemic vs familial vs acquired
* Restrictive → myocardial fibrosis w/ ventricular wall rigidity

vascular heart disease

\
* Structural and/or functional abnormalities
* Stenosis vs regurgitation

cardiac pacing

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* an electric device used to pace the heart when the normal conduction pathway is damaged or disrupted
* Consists of a power source (battery-operated pulse generator), conducting lead, to the myocardium
* Battery is placed on the non-dominant side of the patient
* Methods/types
* Transcutaneous pacing (TCP)
* Endocardial (transvenous)
* Epicardial (transthoracic)
* Permanent

indications for pacing

\
* Temporary
* Prophylaxis after open heart surgery
* AMI
* Bradycardia, bradydysrhythmias
* Permanent
* 2nd or 3rd degree heart block
* Afib with slow ventricular response
* Cardiomyopathy
* SA node dysfunction
* Tachydysrhythmias

complications of pacers

\
* Local infection at the entry site
* Pneumothorax
* Bleeding, hematoma
* Dislocation of lead
* Cardiac perforation

single chamber vs. dual chamber - pacers

* Single → just needs to be paced in one site, usually in the ventricle


* Dual → both an SA node and a heart block issue
* The end sits in each chamber of the heart

failure to pace

* AKA failure to *work →* ***these patients will be symptomatic w/ bradycardia***
* Failure of pacer to deliver the stimulus set → **need to get to OR to replace batteries**
* Usually d/t pulse generator or battery problem, broken wire, loose connection “mechanical problem”


* **Batteries last approximately 10 years but we replace this way earlier (i.e. 8 years) to make sure this continues working**

failure to capture

Loss of capture → pacer fires, but fails to initiate a myocardial depolarization, **charge from battery isn’t enough**

failure to sense

Fails to recognize spontaneous atrial or ventricular activity and fires inappropriately

nursing management - pacing

* Airport management
* Will set off security
* Medical alert bracelet
* Doctor’s note
* Lifting precaution
* Important in immediate phase
* Can’t move arm above shoulder height for 6-8 weeks
* Wear arm sling even during night time
* Can’t hold > 5 lbs on affected side (a gallon of milk)
* Generator is placed on non-dominant side


* Infection
* Make sure to dry off affected side armpit to prevent bacteria migration
* Log of HRs
* CXR
* Incision care
* Can’t submerge for 4 days
* **Can’t go into MRI w/ pacemaker**

other methods for countershock

* Internal paddles
* Aka “spoons” 
* Cardiac surgery
* Open-chest CPR
* Lower joules used
* AICD → automatic implantable cardioverter device
* Recognizes ectopy
* Delivers counter shocks
* Prevents episodes of sudden death
* This should NOT be just going off, this only shocks during lethal dysrhythmias
* The patient typically will pass out during these shocks
* Teach the patient not to go in a body of water by themselves due to risk of passing out and drowning

shock

* Life threatening response d/t impaired tissue perfusion
* Imbalance of cellular oxygen supply and demand ⇒ not enough cardiac output from heart that won’t be able to perfuse the rest of the body
* **At least one of the four** circulatory components become compromised
* Blood volume → hypovolemic shock, losing circulating volume
* Myocardial contractility → blunt-force trauma that causes acute heart failure, no contractility, no cardiac output
* Blood flow
* Vascular resistance → massive vasodilation causes lack of blood to get back to the heart
* Cells begin to convert from aerobic to anaerobic metabolism
* End result is organ dysfunction due to decreased blood flow through the capillaries


* Can lead to MODS and death

stages of shock

1\.) initiation

2\.) compensatory

3\.) progressive

4\.) refractory

initiation stage - shock

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* Decreased cardiac output
* Can be extremely quick → if hypovolemic you will lose blood at a rapid rate
* Vital signs aren’t changed yet

compensatory stage - shock

* Symptoms become more apparent
* Vital signs begin to change
* Increase in HR is one of the first signs/symptoms (as well as change in mental status)
* BP will start to drop


* Shock may still be able to be reversed
* Neural compensatory
* Neural compensation
* Increased HR, contractility, vasoconstriction
* Shunting of blood to the vital organs


* Endocrine compensation
* Glucocorticoid production (causes increase in blood glucose levels)
* Body is trying to make more energy = increased glucose levels
* RAAS initiated
* Produces angiotensin II → vasoconstriction, promotion of aldosterone (increasing sodium and water retention)
* Kidneys recognize they aren’t getting enough perfusion → causes fluid retention to perfuse the kidneys longer
* ADH released → released to keep fluid from leaving for better kidney perfusion


* Chemical compensation
* Rate and depth of respirations increase

progressive stage - shock

* this is HARD to treat, want to prevent at all costs
* Failed compensatory mechanisms


* Cells begin anaerobic metabolism to produce energy


* Lactic acid is produced as a by-product (lactic acidosis)
* 4 millimoles is a very high lactic level → once it’s this high it’s hard to come back from


* Increased vascular permeability-intravascular hypovolemia, tissue edema


* Cellular death → inability to utilize oxygen

refractory stage - shock

* Irreversible or unresponsive to therapy → no turning back, will have to talk about palliative care/withdrawing care
* These patients will be in the ICU w/ 1-2 invasive lines
* When people reach this stage of shock, you can bolus the “heck out of them” and the CVP won’t improve b/c the vascular permeability doesn’t allow fluid to sit into the vascular space


* MODS → 2 or more systems failed
* ARDS (acute respiratory distress system)
* b/c the fluid leaks out of the vascular space, it gets into the lungs
* This causes issues w/ gas exchange → patient most likely will need to be placed on a ventilator 


* Death due to ineffective tissue perfusion

hypovolemic shock

* Inadequate fluid volume in the intravascular space
* This leads to decreased tissue perfusion and initiation of shock states
* Identified by stage (severity) → do NOT need to know the differences between stages


* Relative vs absolute hypovolemia
* Relative → may be hypovolemic, not so sure, can’t directly see what’s causing it (ex. burn victims)
* Absolute → definitely hypovolemic


* Internal vs external
* Internal loss
* GI bleeds → melena, coffee-ground stools, upset stomach
* Trauma → penetrating, blunt-force
* ALWAYS WORK UP FOR INTERNAL DAMAGE
* Surgery
* Ruptured organs
* External loss
* Loss of blood, plasma, body fluids
* Can occur from trauma, surgery, birth, coagulation issues, DIC, burn injuries, GI loss, DI

clinical signs of hypovolemic shock

* Mild (less than 20% blood volume loss):
* Cool extremities
* Increased capillary refill time
* Diaphoresis
* Anxiety


* Moderate (20-40% blood volume loss) same as mild, plus:
* Tachycardia
* Tachypnea
* Oliguria → b/c blood is being shunted from the kidneys to other organs
* Orthostatic changes


* Severe (over 40% blood volume lost) same as moderate, plus:
* Hemodynamic instability
* Marked tachycardia
* Hypotension
* Mental status deterioration

diagnostic criteria - hypovolemic shock

* **Hypernatremia (Na > 145)**
* **Elevated serum lactate (lactate > 4)**
* Hemodynamic findings
* Low CVP/RAP (can be less than 2 or lower end of the 2-6 range)
* Low wedge pressure/PAWP

management of hypovolemic shock

* **Early identification!!!**
* Correct underlying cause
* Restore tissue perfusion
* Aggressive fluid therapy, expand intravascular volume
* 3 for 1 rule
* For every 1 mL that is lost, replace w/ 3 mLs
* Normal saline
* LR won’t usually be choice b/c this has lactate in it and this will already be elevated


* Hemodynamic monitoring
* Want MAP to be at least 60-65 to ensure good organ perfusion


* Blood products


* Evaluating treatment of hypovolemic shock
* Increasing CVP 
* MAP (at least 60)
* Adequate urine output (at least 30 mL/hour)
* Shows the kidneys are responding to fluid therapy
* Watch respiratory status for pulmonary congestion
* Crackles!!!

cardiogenic shock

* Failure of the heart to pump adequately
* Caused by decrease in myocardial contractility
* Usually results from left ventricle MI
* Can be a byproduct of something happening to the body
* Blunt force trauma to the chest

symptoms of cardiogenic shock

* SBP

hemodynamics of cardiogenic shock

* Low cardiac output
* High PAWP → b/c of ineffective contraction and volume build-up
* High CVP/RAP
* High SVR → shunts more blood back into heart
* Compensatory mechanism that ISN’T helping, this happens b/c the body recognizes there is a CO issue but doesn’t know it’s a cardiogenic issue
* Give ace inhibitors to help this

treatment of cardiogenic shock

* Identify problem
* Medications 
* Inotropic agents → increase contractility
* Dig, dopamine
* Vasopressors → to maintain BP when hypotension is severe
* Not the norm, last-ditch effort
* Diuretics → decrease preload
* Antidysrhythmic agents → suppress dysrhythmias that affect CO


* Intubation and mechanical ventilation to optimize oxygenation
* **Intra Aortic balloon pump** used if drugs are not working to fix shock state
* Temporary measure to decrease myocardial workload by improving myocardial supply and decreasing myocardial demand
* Improves coronary artery perfusion and reduces left ventricular afterload


* **ECMO** → extra corporeal life support w/ membrane oxygenator to support the patient
* These devices sustain effective organ perfusion, allowing time for the ventricle to heal or transplant to take place


* **VAD → ventricular-assist device**
* **When conventional therapies fail**
* **Helps the left ventricle contract**

distributive shock

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* Vessel or diameter issue
* Arteries and veins in the body lose all tone
* i.e., anaphylactic shock, septic shock, neurogenic shock

anaphylactic shock

* Immediate hypersensitivity reaction
* Substances known as antigens
* Can be introduced by injection of ingestion through skin or respiratory contact


* Allergies to be aware of → food, drugs, bites/stings, chemicals
* As you age, you become more sensitive and can have a response to things you have not previously

clinical presentation - anaphylaxis

* Symptoms usually in minutes/may take up to 1 hour


* Cutaneous effects may be seen first → rash


* Respiratory effects → laryngeal edema, stridor, wheezing


* Cardiovascular effects → decreased BP, increased HR


* GI effects → N/V/D


* Neurologic effects → anxiety, decreased LOC

hemodynamics - anaphylaxis

* hypotension secondary to anaphylactic shock


* Low CO/CI


* Low CVP/RAP


* Low PAWP


* Low SVR

treatment of anaphylaxis

* Remove the antigen and promote tissue perfusion


* Reverse effects of biochemical mediator


* ABCs


* If the reaction is a response to blood, dye, or infusion, STOP IMMEDIATELY


* Drug management
* Epinephrine (can be repeated every 20-30 minutes)
* To treat histamine response
* Benadryl
* Given IV
* Will knock the patient out
* Corticosteroid (solu-medrol, dexamethasone)
* Laryngeal swelling will reduce w/ this
* Fluid replacement
* Positive inotropes
* Vasopressors

neurogenic shock

* Loss or suppression of sympathetic tone (sympathetic nervous system)
* Causes the walls of the blood vessels to relax, and vasodilation follows
* Spinal cord injury patients
* Can be caused w/ certain medications as well → specifically spinal anesthesia

symptoms of neurogenic shock

* Hypotension


* Bradycardia


* Hypothermia

complications of neurogenic shock

* DVT, PE


* Lack of venous tone leads to stagnant tone


* These patients are already somewhat immobilized d/t spinal cord injury

treatment of neurogenic shock

* Remove cause


* Volume replacement (for SPB

septic shock

* Sepsis w/ hypotension despite adequate fluid resuscitation, along w/ perfusion abnormalities
* Bacteria introduced in the blood throughout the body
* Immune system vasodilates all over in response, causing a systemic inflammatory response (SIR)
* This is NOT the same as sepsis → worse
* BUT will treat sepsis the same as septic shock b/c we don’t want sepsis to worsen to shock levels
* Organs can die from this due to small clots
* Close to the refractory period
* Vascular permeability is increased so an increase in fluids doesn’t help w/ hypotension

symptoms of septic shock

* infection
* fever
* tachycardia
* hypotension
* full bounding pulses
* crackles
* tachypnea

hemodynamics of septic shock

* low SVR
* low CVP/RAP

diagnostic criteria - septic shock

* Leukocytosis w/ a shift to the left (bandemia- infant/immature WBCs)
* Means that new WBCs became active after new onset of infection


* Blood cultures
* Draw these before initiating antibiotics
* Takes 72 hours for results
* Can treat before this w/ broad spectrum antibiotics


* CRP elevation
* Byproduct of the liver that shows inflammation


* Coagulation abnormalities


* Increased lactate
* b/c of organs starting to die and supply/demand issues

treatment of septic shock

* Trend lactate levels


* Blood cultures x2, urine/pan culture


* Give antibiotics within 1 hour of sepsis diagnosis


* Fluids


* Vasopressors 


* Maintain CO


* Maintain blood glucose

obstructive shock

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* Fluid volume is generally normal, but an obstruction to flow results in impeded venous return to the heart or problems with cardiac filling and emptying
* Increased pressure on the heart and great vessels from tension pneumothorax
* Inability to pump effectively owing to excess blood in the pericardial sac from cardiac tamponade


* Obstructive shock has much in common with cardiogenic shock, and the two are frequently grouped together
* What causes obstructive shock?
* Blunt force trauma to the chest, head, neck
* Recent long bone fracture
* Pulmonary embolus, sickle cell disease, central venous catheters, coagulation disorders, use of birth control

systemic inflammatory response syndrome (SIRS)

* As shock progresses an inflammatory response happens
* SIRS may be caused by any type of shock or insults like trauma, brain injury, burns , pancreatitis, typically preceded by septic shock

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* **What happens**…
* Release of cytokines from macrophages
* Cytokine-small protein that at “cell signaling” they are not hormones
* Types of cytokines=tumor necrosis factor & interleukin 1
* Normally tight junctions between endothelial cells that line blood vessels
* Cytokines break these tight junctions and make capillary blood vessels “leaky”
* Plasma then leaks into the interstitial space
* Coagulation processes are stimulated, platelets attracted with WBC’s & clump & form fibrin clots that obstruct blood flow
* Then WBC’s, platelets, & activated endothelial cells release vasodilating substances such as nitric oxide (NO), histamine, and bradykinin. These substances also produce further capillary leak.
* Result =overwhelming unregulated inflammation and uncontrolled coagulation, disruption of the capillaries and major capillary leak.
* So there is no intravascular volume because it all leaks into the tissues and low to NO blood pressure, NO clotting mechanism (DIC=disseminated intravascular coagulation),  oxygen supply and demand IMBALANCED
* Tissue & organs die. MODS=DEATH

disseminated intravascular coagulation (DIC)

**AKA “Consumptive Coagulopathy”**

1)Abnormal disorder of bleeding & clotting

2)Uses up all clotting factors, platelets, & RBC’s

3)Results in the inability to form clots so bleeding (hemorrhage) occurs

4) Generates intravascular thrombin and fibrin, resulting in the thrombosis of small- to medium-sized vessels and ultimately organ dysfunction and severe bleeding

diagnosis - DIC

\-Prothrombin (PT)-prolonged

\-Activated partial thromboplastin time (aPTT)-prolonged

\-Platelet count (PLT)-decreased

\-D-Dimer-prolonged

\-Fibrinogen-decreased

\-Fibrin degradation (split) products (FDP): increased

DIC- nursing assessment

\-Petechiae, purpura, hematomas

\-Oozing from IV sites, drains, gums, & wounds

\-Gastrointestinal & GU bleeding

\-Hemoptysis

\-Mental status change

\-Hypotension, tachycardia

\-Pain

DIC- treatment

\-Minimize needle sticks, minimize BP measurements with cuff

\-Administer IV heparin during the first phase to inhibit

  platelet coagulation (for slowly evolving DIC)

\-Administration of platelets and fresh frozen plasma (FFP) in

 DIC patients with active bleeding to replace the clotting factors

\-***Key- Identify the trigger of DIC & reverse it (if possible)***

   - *Sepsis (20% Gram – bacteria causes it) –Tx=give antibiotics*

   *- Other triggers: Endotoxins, metabolic acidosis & hypoperfusion, ischemia (shock), major trauma, solid cancers, hematological malignancies, obstetric emergencies (abruption), aneurysms, and liver diseases*

2 types of ventilation

* volume controlled
* pressure controlled
* both are pre-set

types of ventilators

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* Negative pressure
* Applied externally, not used in the ICU
* Positive pressure
* Helps to push volume during inhalation to assist volume entering the lungs

controls/settings - ventilation

* **Settings read as: breaths/tidal volume/fio2/peep**
* Tidal volume (VT)
* The amount of air volume used to cause inspiration/going into the lungs


* NOT oxygen concentration, this is FiO2!!!


* Measured in mLs → normal is around 500 mLs


* Rate
* Ventilator will have a set amount of respiratory rate/minute
* FiO2
* The amount of oxygen concentration within the full tidal volume of air being administered
* PIP- Peak Inspiratory Pressure
* Is the highest level of pressure applied to the lungs during inhalation
* PEEP
* Keeps the alveoli open for a longer duration during inspiration
* Allows for more gas exchange
* Uses
* Pulmonary edema
* Provides a counter pressure opposing fluid extravasation
* Lungs with diffuse disease unresponsive to FiO2 > 50%
* Loss of compliance or stiffness in the lung
* ARDS
* Severe hypoxemia

issues with PEEP

* contraindications/caution
* Highly compliant lungs (COPD)
* hypovolemia/low CO
* In order for PEEP to work, the lungs will be expanded longer and this will cause some compression on the heart which is the last thing you want when you are already low in volume or CO


* Side effects
* Decreased cardiac output
* Decreased blood pressure
* Reduces return of blood to the heart

pressure support vs. PEEP

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* PS reduces the workload of inspiration (overcomes resistance)
* PEEP restores the functional residual capacity (FRC) (holds airways open)
* Both helpful with sick and injured lungs

ventilation modes

* assist control (AC)
* synchronised intermittent mandatory ventilation (SIMV)
* pressure support
* CPAP
* Airway Pressure Release Ventilation
* high frequency oscillatory ventilation

assist control (AC) ventilation

* aka Continuous Mandatory Volume (CMV)
* Ventilator is set to deliver a preset amount of tidal volume for each breath
* If patient fails to take a breath during a set time, will get one delivered
* A patient can always go OVER the set number if they breathe on their own, but can never go under or else breaths will be induced


* **This is considered the most invasive b/c it sets a baseline respiratory rate**
* **Allows the patient to try to take their own breath but takes over breathing completely once initiated**
* **The breaths the patient take on their own are added to the mandatory RR set**

synchronized intermittent mandatory ventilation (SIMV)

* Preset TV and RR on ventilator
* Patient may take own breaths at their own rate and volume
* Ventilator breaths are synchronized to the patient's respiratory effort
* It is whatever the patient brings in on their own
* Will have a prescribed minimum RR setting, but the patient will also breathe on their own
* The vent breaths will get more tidal volume on the screen
* Want to use this to ensure patient is able to use their own muscles to compensate RR
* Will not work for people without this muscle capacity

pressure support

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* Typically a weaning mode (when used alone)
* Every breath is patient-initiated but the pressure support helps the lungs to expand for increased gas exchange
* PEEP is used to keep alveoli open to allow for this

CPAP

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* Spontaneous breathing mode that gives minimal support to increase functional residual capacity and improve oxygenation by keeping the airway (alveoli) open at the end of expiration
* Corrects for Dead Space in the ventilator circuit
* Can be used as a weaning mode on the ventilator
* Usually a trial of CPAP only is done prior to extubation
* CPAP may be combined with pressure support
* Pt must be doing all the breathing on their own at this time
* \*PS supports the inspiratory breath; CPAP supports the expiration (holding the alveoli open) 
* Used for patients with sleep apnea

airway pressure release ventilation (APRV)

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* Pressure control mode of mechanical ventilation using two different levels of CPAP (inspiratory & expiratory)
* It is timed. Applied for set periods of time to allow spontaneous breathing at both levels
* Utilizes an inverse ratio ventilation strategy
* It improves oxygenation and eliminates CO2
* An effective safe alternative for difficult to oxygenate patients with acute lung injury/acute respiratory distress syndrome
* Unlike spontaneous breathing or conventional ventilation, the time spent at maximal inflation is typically much longer than time deflated
* Used to maintain alveolar recruitment and minimize collapse of alveoli and reduces barotrauma

high frequency oscillatory ventilation

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* Delivers small volume of gas at a rapid rate
* Does not require breaths therefore prevents stretch injury
* HFV used when conventional ventilation compromises hemodynamic stability
* Requires sedation and often neuromuscular blockade

high frequency ventilation - types

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* HFV delivers small volume of gas at a rapid rate
* High frequency positive pressure ventilation (HFPPV); delivers 60-100 breaths/min
* High frequency jet ventilation (HFJV); delivers 100-600 cycles/min
* High frequency oscillatory ventilation (HFO); delivers 900-3000 cycles/min
* Volumetric diffuse respirator(VDR) delivers frequency of 500-900 cycles/min

ventilation alarms

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* High pressure alarm
* If pre-set pressure limit is exceeded
* Ex: coughing (may need to place patient on sedatives), secretions (may need to suction), tubing issue (check for kinks)
* Low pressure alarm
* Patient does not receive preset tidal volume (VT)
* Ex: circuit disconnection (can be from intense coughing, patient removing, etc.)

care of artificial airway management

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* HOB minimum 30 degrees if tolerated to allow for better lung expansion
* Unless contraindicated (ex. head injury)
* **Mouth care → #1 complication of ventilators is pneumonia**
* **More at risk w/ intubation**
* **Every 2 hours → use mouth swabs connected to suction**
* **Endotracheal tube → rotate site every shift (left, middle, right)**
* **Check residuals to prevent pneumonia and ensure tolerating tube feedings**

weaning - ventilation

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* Done in *sprints*
* **Nurse must stay at bedside to make sure tolerating well during initial weaning period**
* Steps
* First → has the patient recovered from the illness that caused them to be intubated?
* Second → decrease sedation to see if patient is capable of “breathing on their own”
* Third → are they awake? Initiating breaths on their own?
* Fourth → does the patient have gag and cough reflexes? Can they protect their airway?
* Fifth → does the patient “have a leak”?
* Sixth → if there is no leak, does the patient need steroids?

nursing role in ventilation weaning

* Remain with the patient!!!
* Suction as needed
* Allow respiratory muscles to rest between trial “springs” → these are physically exhausting
* Ventilate overnight
* **Reassess sedation → neuro assessment EVERY HOUR**
* **May need to wake patient up for this if on propofol drip**


* DVT prophylaxis
* Chest PO
* Tube feedings

complications of ventilation

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* Ventilator-induced lung injury
* Barotrauma → too much pressure
* Keeping things open for longer than they need to
* Can cause damage to alveoli
* Volutrauma → too much volume
* Inducing volume in places it shouldn’t be
* Ex. pneumothorax
* CV compromise
* GI disturbances → paralytic ileus 
* Patient-ventilator dyssynchrony
* VAP (ventricular associated pneumonia)

pulmonary management

* **Physical Assessment**
* **Inspect**
* **Palpate** 
* **Percuss**
* **Auscultate**


* **Oxygen Therapy Principles/Delivery**
* **Oxygen is a drug**
* **Ordered in liter pr min (L/min) flow**
* **Primary indication is hypoxemia**
* **General Goal of therapy:**
* **PaO2 > 60 mm Hg**
* **SaO2 > 90%**


* **Nursing Management**
* **Nursing priorities for the patient receiving oxygen focus on:**
* **Ensuring the oxygen is being administered as ordered**
* **Assessing Status**
* **Observing for complications of the therapy**
* **Oxygen toxicity**
* **Carbon dioxide retention**
* **Absorption atelectasis**

oxygen delivery systems

* low flow systems
* reservoir systems
* simple face mask
* partial rebreathing mask
* non-rebreathing mask
* high-flow systems
* air entrainment mask
* high flow cannula systems

low flow nasal cannula/prongs

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* 1 L/min = 24% (room air = 24%)
* 2 L/min = 28%
* 3 L/min = 32%
* 4 L/min = 36%
* 5 L/min = 40%
* 6 L/min = 44%

low flow simple mask

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* Used for **short-term** O2 therapy
* **Contraindicated for those with CO2 retention**
* Difficult to **eat** or **talk** with mask in place
* Low-flow: **6-10 L/min = 35-60%**
* Need a **minimum of 5 L flow** to flush out the carbon dioxide
* **CANNOT wean to lower than 5 L**

Low-flow partial rebreather mask

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* Contains reservoir bag allowing patient to rebreathe some of their own exhaled air mixed with 100% O2
* Low-flow: 6-10 L/min = 40-70%

Low-flow non-rebreather mask (not common)

* Provides the highest concentration of O2 with a mask to a spontaneously breathing patient. **Has 2 one-way valves preventing rebreathing of exhaled air**.
* Low-flow: 6-15 L/min = 60-80%

Low-flow venturi mask

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* Delivers the most precise concentrations of O2 via a large tube with an oxygen inlet
* Delivers an exact % of O2 regardless of the patients TV (tidal volume)
* Low-flow: 4-10 L/min = 24-55%
* Ideal for patients with mod hypercarbia, hypoxemia, COPD’rs→ no need to humidify

Hi-flow Airflow Entrainment Mask

High humidity mask or face tent provides excellent humidification and oxygen from 28% to 100%- if kept in place…

hi-flow optiflow

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* Hi flow device
* Special N/C prongs
* Delivers 5-60 LPM of oxygen
* 21-80% oxygen

Bipap

last ditch before intubation

IPAP- inspiratory & expiratory airway pressure