AT Exam #2- Hemodynamic Monitoring, Sepsis, Shock, MODS (Chapters 65 & 66)

What is Neurogenic Shock?

-*Massive vasodilation without compensation* -Can occur as a result of spinal cord injury (may happen as fast as 30 minutes of the injury, and last for 6 weeks). -Vasodilation d/t loss of the SNS vasoconstrictor tone. -Blood pooling in vessels -Hypoperfusion to tissues There is massive vasodilation without compensation d/t loss the SNS vasoconstrictor tone. This loss of vasoconstricting tone causes a pooling of blood in the vessels which leads to hypoperfusion.

What is Cardiac Output (CO)?

-THe amount of blood pumped by the heart per minute -Expressed in L/min -Normal is 4-8 L/min - Determinants : CO= HR X SV -Heart Rate (HR) -Stroke Volume (SV) -Cardiac output is the volume of blood pumped by the heart in one minute. -Normally the ventricles pump the same volume -Normal is 4-8 L/Minutes -The cardiac output is measured by the heart rate and stroke volume. -SV- what is ejected with each beat -CO= HR x SV

Septic Shock: Specific Care Measures- What do we do for Septic Shock?

-Table 66-9, page 1600 -Fluid replacement with hemodynamic monitoring -Vasopressors with hemodynamic monitoring -Inotropic Agents -Antibiotics - broad-spectrum until blood cultures are resulted -Stress ulcer prophylaxis -DVT prophylaxis These pts require LARGE amts of fluid replacement. (Usually done with isotonic fluids and albumin - what are the isotonic fluids??? NS, LR. - These fluids work in the IV space, to increase IV volume! What does the albumin IV do??? It causes expansion of the volume in the IV space.... Review Table 66-7 for more on how fluid replacement works.) We do intensive monitoring of their hemodynamic status by measuring their CVP, CO, CI, SV, SCC, MAP (should cause an increased MAP, CVP, change in SVV)... If the pt stays hypotensive after fluid replacement, vasopressors may be added. 1st drug of choice: norepinephrine. Vasopressors may increase the BP but may also decrease the SV. So inotropes may also be added. (What's a common inotrope?? Dobutamine! Others include dopamine, epinephrine, etc. Table 66-8 has drug therapy detailed.) We titrate vasopressors based on their hemodynamic numbers per orders. (For example, we may titrate a norepi drip by increasing the rate based on the BP. If their CVP is still low, say 4 mm Hg, I could consult with the doc and maybe give more fluids b/c that CVP being low tells me that their blood volume is low. Point is, we titrate pressors and add/stop fluids based on the hemodynamics.) Abx - huge part of septic therapy. They should be started w/i the 1ST HOUR of septic shock! What do we do before we start an antibiotic??? Draw culutres!! (blood cultures!) The blood culture guides the therapy based on whatever type of bug is in their bloodstream! Blood cultures usually take about 3 days to result, so until we have the final results back, we administer broad-spectrum abx, and then the providers narrow down the abx therapy to more specific abx when the culture results are back. What's a common lab yall think may be elevated in septic shock? Blood glucose!! When the body is stressed, the glucose goes up! We need to keep glucose <180 mg/dL to avoid allowing extra stress on the body (b/c the body has to work to bring that glucose down.) -Last, stress ulcer prophylaxis with a PPI and DVT prophylaxis with a blood thinner like Lovenox is used for pts with high bleeding risk factors or DVT risk factors (which will basically be most pts with septic shock b/c their coagulation is affected in this syndrome, and their mobility is usually low d/t being in the bed). -Sepsis is very important to recognize so we can treat it quickly!!

What are the 4 Stages of Shock?

1.Initial stage (early shock) 2. Compensatory stage 3. Progressive stage 4. Refractory stage Stages of Shock is a progression on a continuum Earlier you can intervene the earlier you can make sure it doesnt' get to that worse stage where you can ultimately can recover Initial= (Early) Refractory= end organ stage

What are the 3 types of Distributive Shock?

1.Septic shock 2. Neurogenic shock 3. Anaphylactic shock

Treatment of Anaphylactic Shock?

1st - try to prevent exposure to known allergens! -Acute care: IM epinephrine (Epi-Pen) -Epinephrine: causes peripheral vasoconstriction, bronchodilation, and opposes the inflammatory effects of histamine. -Maintain airway!! May need intubation depending on the severity of laryngeal edema and any presence of resp distress. -They will also need histamine-blockers (like ranitiditine - Zantac, Benadryl) and maybe steroids to stop/slow the inflammatory histamine response. -We also will likely be giving bronchodilators to help open the airway.

Relationship Between Shock, SIRS and MODS?

**Refer to slide chart on ppt slide #119**

S&S of Neurogenic Shock?

**hypotension from the massive vasodilation and bradycardia from parasympathetic stimulation without the opposing SNS.** Other s/s: -Lack of body temp regulation (like in the Me Before You movie) -Initially, the skin is warm d/t the vasodilation, but as the heat disperses, the pt can become cool and be at risk for hypothermia - largely depends on the temp of the room/environment. -Bradycardia and HYPOTENSION - not fluid deficit because of vasodilation -Skin will feel warm and look flushed

What is the Compensatory Stage of Shock?

*Drop in BP* (classic sign of shock) SNS/neurohormonal system causes vasoconstriction, increased HR, increased heart contractility This maintains BP, CO Body shunts blood from lungs, kidneys, GI tract, and skin - resulting in cool, clammy skin, hypoactive bowel sounds, decreased urine output ↑ RR Perfusion of tissues is inadequate ↑ Blood glucose Confusion may occur Compensatory Stage=AKA Fighting stage, trying to compensate to fix itself (The Fighting Stage!) The receptors (baroreceptors and chemoreceptors) in arteries detect **a drop in BP** (detect low fluid volume in the vessels) d/t a ↓CO. The nervous system releases epi and norepi to increase the HR and contractility so that there will be ↑ CO. This increased HR and contractility cause systemic vasoconstriction (and coronary artery dilation d/t to the heart's ↑O2 demands). Blood is shunted away from most organs to preserve blood flow to the most vital organs (heart and brain). It is shunted away from the lungs, kidneys, GI tract, skin, and extremities. (Crazy how the body doesn't view the lungs as one of the most vital organs! But we have to have a pump and brain to tell it to pump!) Well, since the blood is shunted away from the lungs, the bronchial smooth muscles relax, which causes the RR to increase and the respiratory depth increases as the body tries to improve oxygenation. SO - remember how we talked about ventilation and perfusion mismatches in respiratory unit?? Do you think this shunting of blood away from the lungs will result in a V/Q mismatch?? Yes! What kind??? Perfusion cause! (Some areas of the lungs are not participating in gas exchange b/c they are not getting blood flow - only parts of the lung are getting perfused and do adequate gas exchange ---- so what are some signs you may see from this???? ↓PaO2! Will the CO2 be high or low in this stage??? LOW b/c if the RR is ↑, they are breathing OFF the CO2!!) SO, do you remember what we learned last week about CO2? It is a potent...... vasodilator! So if we're blowing off all of our CO2, what will that do the cerebral vessels??? Allow them to vasoconstrict.... Which may decrease blood flow to the brain! UH-OH! Other s/s you may see in this stage?? Impaired GI motility d/t low flow to the gut (so hypoactive bowel sounds)... Cool/clammy skin d/t low flow to the skin... ↓UO b/c of low flow to kidneys... And what happens when our kidneys don't have great blood flow?? The RAAS system is activated!! So what happens when this is activated?? ADH is released, aldosterone causes Na+ and H20 to be retained, AT II causes even more vasoconstriction (which hurts the body even worse at this point!) So will the BP be up or down at this point?? Up! How does this affect the heart?? This will cause there to be an increased return of venous blood flow to the heart! (B/c we're retaining fluid now, so there is more fluid in the body, the vessels are vasoconstricted, which raises the BP.... But this also makes the heart's workload higher - d/t increased BP). The blood sugar will also be higher in this stage b/c the body is under stress, and sugar levels go up when the body is physically stressed (which is good for the brain - b/c why?? It requires PLENTY of glucose to fxn!) AT this point, if the cause of shock can be corrected, the patient can likely recover (if he/she is healthy enough overall without other major stressors present). But if this stage is not corrected, the pt will go into the progressive stage of shock... -Decreased cardiac output -Increased pulse -Decreased blood pressure -Narrowed pulse pressure

Anatomy of the Heart

*Function: -Stores about 65% of total blood volume capacitance vessels -Help to redistribute blood to or from the heart to maintain optimum cardiac filling pressures *Low pressure - does not contribute to blood pressure or other hemodynamic parameters *Valves prevent retrograde blood flow *These capacitance vessels can accommodate changed in blood volume. These vessels have the ability to readily accommodate changes in blood volume. Generally considered to be veins. *Typically the body have more veins, the heart is a low pressure, doesn't contribute to BP or other hemodynamic parameters,

What is Anaphylactic Shock?

*Occurs d/t an hypersensitive allergic reaction. *Causes massive vasodilation, and capillary permeability. *Fluid leaks into interstitial space *Causes = laryngeal edema, bronchospasm *Treatment: -1st - try to prevent exposure to known allergens! -Acute care: IM epinephrine (Epi-Pen) -Occurs d/t an hypersensitive allergic reaction. -Causes massive vasodilation, and capillary permeability. LEAKY CAPILLARIES -So fluid leaks from the vascular space into the interstitial space. -Causes laryngeal edema in the airway and severe bronchospasm. -Causes swelling of lips/tongue and airway, wheezing, stridor. -Can cause circulatory failure d/t massive vasodilation if not corrected QUICKLY!

Nursing Responsibilities for PA Line Maintenance Care?

*Ongoing monitoring of pressures of heart *Maintain the system ("zero" the pressure transducer daily) *Obtain PAWPs as indicated/ordered *Make sure the catheter rests in the PA *Sterile dressing changes per facility policy (usually q4days) *Troubleshooting: -Inability to obtain a wedge reading - could be d/t a ruptured balloon - if unable to obtain, check centimeter markings of catheter to see if placement has changed, check CXR to determine why you're unable to get a reading. -Damped pressure tracing - try REzeroing the pressure waveform. -Over-wedging: stop, re-position, try again x1.

Hypovolemic Shock Specific Care Measures- What should you do about Hypovolemic Shock?

*Stop fluid loss. Restore fluid volume/blood loss* Medical management Tx underlying cause Fluid, blood replacement Redistribution of fluid Pharmacologic therapy (vasoactive drugs, dilate or constrict) Nursing management -Establishing and maintain IV access for fluid replacement (might require 2 IV lines both Right and Left depending on volume loss, can take massive amounts of fluid!) (Will need at least 1 large-bore access - 14 - 16 gauge) -Administering blood, fluids safely -Monitor fluid status (by how?- do daily weights, I&Os, look at parameters of CVP and PAWP/wedge pressure, if CVP is low fluid is low if CVP going up then CVP getting better or is high) **How would we monitor fluid status?? Daily weights, I&O, CVP 15 mm Hg; PAWP 10-12 mm Hg.

What is Cardiac Index (CI)?

- CO divided by the individuals body surface area (BSA) -Normal CI= 2.5-4 L/min/m2 -CI= CO/BSA Cardiac index is the CO/BSA. It is more precise measurement for the efficiency of the pumping of the heart. You can see why as it is based on body surface area NOrmal is = 2.5 - 4 L/min/m2 CI= More specific because based on Body Surface Area (BSA)

Complications of fluid replacement include what?

- fluid overload, pulmonary edema (check/auscultate lung sounds!!) What are some complications from large fluid resuscitation?? Hypothermia and coagulopathy. (We're pushing large amounts of room-temp fluid into their veins! Coagulopathy - we could clog their vascular system which may make them clot in the smaller vasculature.)

What is Ejection Fraction (EF)?

- is a measurement, expressed as a percentage, of how much blood the left ventricle pumps out with each contraction. An ejection fraction of 60 percent means that 60 percent of the total amount of blood in the left ventricle is pushed out with each heartbeat. EF= parameter we receive when we do an echocardiogram, tells us how the heart is working and pumping and how it provides oxygen and nutrients that the body needs Want it to be around 60-65%, lower than that the heart is sick and not pumping properly We assess EF when we are examining heart function such as heart failure.

What is Hemodynamic monitoring ?

- measurement of the pressures, flow, and oxygenation within the CV system. -The results of hemodynamic monitoring assess heart fxn, fluid balance, and the effects of IV fluids and drugs on the CO. -These measures of monitoring include systemic and pulmonary arterial pressures (PAP), central venous pressure (CVP), pulmonary artery wedge pressure (PAWP), CO, CI, SV index, SVV (stroke volume variation), and mixed venous O2 saturation (SvO2).

What is Shock?

-**Decreased tissue perfusion** -**Widespread abnormal cellular metabolism** -Oxygenation and tissue needs are not met -"Whole-body" response; "syndrome" -Any problem impairing oxygen delivery to tissues and organs can start shock, lead to life-threatening emergency -The exchange of oxygen and nutrients at the cellular level is essential to life. -When a cell experiences a state of hypoperfusion, the demand for oxygen and nutrients exceeds the supply at the microcirculatory level.

What is Contractility?

-3rd component of Stroke Volume -Refers to heart's contractile force -Also called inotropy Positive = stronger contraction Negative = weaker contraction -Contractility can be increased by Starling Mechanism or SNS can have a positive inotrope (increase force of contraction) or negative inotrope (decrease force of contraction) Contractility describes the stretch of contraction. Contractility increases as preload is unchanged yet the heart contracts more forcefully. Can be greatly affected by pharmacological agents -No direct ways to measure it -PAWP and CO indirectly reflect contractility -Drugs that can increase it: epinephrine, norepinephrine, dopamine, dobutamine, digoxin (positive inotropes) + inotropes --> increased contractility d/t stimulation of B1 receptors in the myocardium Remember Increased contractility---> increased myocardial O2 demand Epinephrine, norepinephrine, (Levophed), isoproterenol (Isuprel, Dopamine, dobutamine, digitalis-like drugs, calcium and milrinone. Milrinone is a vasodilator that works by relaxing the muscles in your blood vessels to help them dilate (widen). This lowers blood pressure and allows blood to flow more easily through your veins and arteries. Milrinone is used as a short-term treatment for treat life-threatening heart failure. These drugs are positive inotropes -Contractility is decreased with negative inotropes such as calcium channel blockers, β-adrenergic blockers, and clinical conditions such as acidosis Increase in contractility increases SV and increases myocardial oxygen requirements. It is working harder -No direct measure but can measure PAWP and CO. Contractility is reduced in the failing harts.

What does a PA Catheter do?

-A PA catheter provides assessment of the right ventricular function, pulmonary vascular status, and indirectly the lefet ventricular function. -RA, RV, PA pressures as well as the PAWP can be measured -PA catheters with a thermistor have the capability of determining cardiac output. -Can measure CO with the catheter that has the syringe attached to it in pic -Youtube video shown in class= Swan Ganz Physiology -Standard catheter has multiple lumens used to measure PA pressures. -Properly positioned the distal lumen port or catheter tip is within the PA and is used to monitor -PA pressures and sample mixed venous blood to evaluate O2 saturation. -A balloon connected to the external valve surrounds the distal lumen port. -Inflation of the balloon has two purposed: to allow blood to float in the catheter forward and to allow the PAWP measurement. -The proximal lumens have exit ports in the right atrium or the right atrium and the right ventricle. -The right atrium port is used to measure CVP which we have already spoken about, injection of fluid for CO determination and withdrawal of blood specimens. -The second port if there is one is used for infusion of fluids and drugs or blood sampling. -A temperature sensor is located near the distal tip and is wired to an external connection. This is used to monitor core temperature and for thermodilution method of measuring CO. -Can also continuously monitor the patient SVO2 which is an indicator between oxygen delivery or supply and oxygen consumption or demand

Ventricular Systole - QRS

-Aortic & pulmonic valves open -Tricuspid & Mitral valves close -Stroke Volume = amount of blood ejected by LV with each beat usually more than ½ of total ventricular volume ejected. -Ejection Fraction = ratio of stroke volume ejected from the LV per beat to the volume of blood in the LV @ end of diastole (LVEDP). -Expressed in %. -Normal > 50% usually around 65% Remember we talked about this with the arrhythmias and identified this as the electrical activity that is seen with the QRS complexes

What are Factors Affecting Afterload?

-Arterial resistance *Vasoconstriction (increased SVR or systemic vascular resistance) -Aortic impedence *High diastolic aortic pressure, aortic stenosis -Blood viscosity -Septal hypertrophy *Obstructs outflow from ventricle SVR and arterial pressures are indices of left ventricular afterload -Similarly PVR and pulmonary arterial pressure are indices of right ventricular afterload. -Increase in afterload results in decreased CO and increased oxygen demand, CO can be restored and myocardial oxygen needs reduced by decreasing afterload Vasodilator drug therapy can reduce afterload -Resistance offered by the aortic valve -Arterial resistance= if arteries are very constricted -Aortic impedence= aortic valve might be dysfunctional or stenosed (on Left-side of heart so causes even more pressure that the aorta has to contract) -Septal Hypertrophy= ventricles too thick and wide which obstructs outflow from the ventricles

Nursing Responsibilities with Insertion of PA Catheter?

-Assemble equipment -Prepare patient -Place sterile dressing over secured line (should be sutured by provider after insertion) -Monitor rhythms during insertion -Record and print the rhythms for documentation -Ensure that a CXR is done to confirm placement -Do not use the line (administer fluids) until CXR has been performed and read by provider. -Document the centimeter/sonometer markings where it exits the skin, and continue to assess this placement routinely to check for catheter position change -Labs to look at: look at = PT, PTT, and INR for clotting, look at electrolytes (high or low potassium, magnesium off can create irritability and increase risk of arrhythmias)

What is the Irreversible/Refractory Stage of Shock?

-At this point, organ damage so severe that patient does not respond to treatment and cannot survive -BP remains low -Renal, liver function fail -Anaerobic metabolism worsens acidosis -Multiple organ dysfunction progresses to complete organ failure (MODS) -the body has profound hypotension and hypoxemia. -The organs have failed/are near-failing, so metabolic acidosis worsens and cell waste products (like lactate, urea, ammonia, and CO2) build-up. -Recovery is not likely at this stage. Why?? (The organs have failed, or are in failure, so the body's compensatory mechanism are overwhelmed.) -Although there is massive hypotension and the organs are not being perfused well at all, they will usually have some peripheral vasoconstriction (at the very ends of extremities - fingers and toes - so they may be dark and necrotic - see pic). -Too little oxygen reaches tissues; cell death and tissue damage result -Body cannot respond effectively to interventions; shock continues -Rapid loss of consciousness, nonpalpable pulse, cold, dusky extremities; slow, shallow respirations; unmeasurable oxygen saturation -Too little oxygen reaches tissues; cell death and tissue damage result

Arterial Line Care- How do we care for arterial lines?

-Before insertion, perform modified Allen test. *If pinkness returns <7 seconds: OK to use. *If it takes 7-15 seconds to pink up: delayed response. *If it takes >15 seconds to pink up: do NOT use! -System set-up (will need at least 20g angiocath; betadine; clear dressing; pressure bag with NS; IV pole; transducer holder; cable to connect readings to monitor). -Ensure consent on chart is signed. -Ongoing care: *Dressing changes and tubing changes as ordered/per policy (USE ASEPTIC TECHNIQUE!!!) *Do a daily zero and calibrate of readings -Before insertion, perform modified Allen test (where you obstruct the ulnar and radial artery and hand will then become pale/mottled looking and then release on radial side and will pink up then ulnar side and will pink up so we can know there is enough blood flow to the hand before arterial line is put in!) WHY?? To ensure that arterial circulation is good enough to provide blood flow to the hand if the artery being used for the art line were to be damaged.

What are the Parameters for Hemodynamic Monitoring?

-Cardiac Output- how much the heart is able ot pump and meet demands of body -Cardiac Index -CVP (Central Venous Pressure) -PAS/PAD -PAWP (PCWP)- wedge pressure -SVR & PVR- how constricted the system is -Preload -Afterload -Stroke Volume -Mean Arterial Pressure (MAP) -Venous Oxygen measurement

Clinical Assessment- SIRS/MODS: What do you see during assessment that would alert you to patient going into SIRS or MODS?

-Complete assessment important to pick up cardinal signs early including: -LOC -Skin -Urine -V.S. - Lab -diagnostic tests -Continuous EKG monitoring, -Hemodynamic measurements

Pathophysiology SIRS/MODS

-Consequences of inflammatory response *Release of mediators *Direct damage to endothelium *Hypermetabolism *Increase in vascular permeability *Activation of coagulation cascade *Increase in vascular permeability allows mediators and protein to leak out of the endothelium and into the interstitial space. *White blood cells begin to digest the foreign debris, and the coagulation cascade is activated (see Chapter 29). -Organ and metabolic dysfunction *Hypotension *Decreased perfusion *Formation of microemboli *Redistribution or shunting of blood -Cardiovascular system - it FAILS! *Myocardial depression and massive vasodilation *Results in SVR and BP *Baroreceptors respond to enhance CO *Albumin and fluid move out of blood vessels *The baroreceptor reflex causes release of inotropic (increasing force of contraction) and chronotropic (increasing heart rate) factors that enhance CO. *To compensate for hypotension, CO increases with an increase in heart rate and stroke volume. *Increases in capillary permeability cause a shift of albumin and fluid out of the vascular space, further reducing venous return and thus preload. *Other signs include decreased capillary refill, skin mottling, increased CVP and PAWP, and dysrhythmias. -Neurologic system *Mental status changes due to hypoxemia, inflammatory mediators, or impaired perfusion *Often early sign of MODS -Renal system *Acute kidney injury (AKI) *Hypoperfusion *Release of mediators *Activation of renin-angiotensin-aldosterone system *Nephrotoxic drugs, especially antibiotics *Decreased perfusion to the kidneys activates the SNS and the renin-angiotensin system. *The stimulation of the renin-angiotensin system results in systemic vasoconstriction and aldosterone-mediated sodium and water reabsorption. *Careful monitoring of drug levels is essential to avoid the nephrotoxic effects. *BE VERY CAREFUL WITH NEPHROTOXIC DRUGS, make the kidneys sick, so these NEED TO BE USED WITH CAUTION!! CAN CAUSE A PERSON TO GO INTO SIRS/MODS -GI system *Motility decreased: abdominal distention and paralytic ileus *Decreased perfusion: risk for ulceration and GI bleeding *Potential for bacterial translocation *In the early stages of SIRS and MODS, blood is shunted away from the GI mucosa, making it highly vulnerable to ischemic injury. -Hypermetabolic state *Hyperglycemia or hypoglycemia *Insulin resistance *Catabolic state *Liver dysfunction *Lactic acidosis *Glycogen stores are rapidly converted to glucose (glycogenolysis). *Once glycogen is depleted, amino acids are converted to glucose (gluconeogenesis), reducing protein stores. *Fatty acids are mobilized for fuel. *Catecholamines and glucocorticoids are released, resulting in hyperglycemia and insulin resistance. *The net result is a catabolic state, and lean body mass (muscle) is lost. * The liver cannot make albumin, one of the key proteins that has an essential role in maintaining plasma oncotic pressure. -Consequently, plasma oncotic pressure is altered and fluid and protein leak from the vascular spaces to the interstitial space. -Administration of albumin does not normalize oncotic pressure in these patients at this point. *As the state of hypermetabolism persists, the patient cannot convert lactate to glucose, and lactate accumulates (lactic acidosis). Hematologic system *DIC= causes simultaneous microvascular clotting and bleeding caused by depletion of clotting factors and platelets, combined with excessive fibrinolysis. *Electrolyte imbalances=are common and result from the hormonal and metabolic changes and fluid shifts. These changes exacerbate mental status changes, neuromuscular dysfunction, and dysrhythmias *Metabolic acidosis= results from impaired tissue perfusion, hypoxia, and a shift to anaerobic metabolism with a resultant increase in lactate levels. =Metabolic acidosis results from impaired tissue perfusion, hypoxia, and a shift to anaerobic metabolism with a resultant increase in lactate levels. Progressive renal dysfunction also contributes to metabolic acidosis. *coagulopathy

Pathophysiology of Hypovolemic Shock

-Decreased Blood Volume -Decreased Venous Return -Decreased Stroke Volume -Decreased Cardiac Output -Decreased Tissue Perfusion With hypovolemic shock, there is essentially a low circulating blood volume which decreases the venous return to the heart.. So that decreases the heart's SV.. Which decreases CO.. Which impairs O2 delivery to tissues so cells can go into anaerobic metabolism, and then die. Commonly caused by hemorrhage (external or internal), dehydration (absolute hypovolemia forms). In relative hypovolemia, fluid volume moves from the vascular space into the extravascular space, which is called third-spacing. -**Decreased BV** -**Decreased Venous Return to the Heart** -**Decreased SV** -**Decreased CO** -**Decreased Tissue Perfusion**

Preload Manipulation w/ DECREASED PRELOAD- How do we manipulate or fix the problem?

-Decreased preload when there is decreased volume returning to the ventricles -Decreased CVP, PAWP -TX: Volume replacement therapy (ex. Crystalloid &/or colloids) -Decreased Preload= not enough fluid volume, DRY need to fill the tank -Would indicate CVP and PAWP low, so need to give volume replacement therapy/fluids, like crystalloids or colloids

What is Hemodynamic Monitoring?

-Direct measurement of blood -Measurement of the pressures in the heart and pulmonary artery -Performed through Central line in the inferior and superior vena cava -Threaded through the right heart into the pulmonary artery Hemodynamic monitoring is the measurement of pressure, flow and oxygenation within the cardiovascular system. The purpose is to assess heart function, fluid balance and the effects of fluids and drugs on CO We do both invasive monitoring and noninvasive monitoring to obtain hemodynamic parameters. Values we obtain include systemic and pulmonary arterial pressures, central venous pressure, pulmonary artery wedge pressure, , cardiac output and cardiac indx, stroke volume and stroke volume index, SVV,, oxygen saturation of the hemoglobin of arterial blood (SaO2), and mixed venous oxygen saturation (VvO2). When you combine these data you get a picture of the patient's hemodynamic status and the effect of therapy over time. You monitor trends. Not necessarily an isolated reading.

Dopamine

-Dose (mcg/kg/min) X weight (kg) X (60 min/hr) -Concentration mcg/mg -2 to 10 mcg/min -stimulates beta 1 and beta 2 receptors, increases CO and blood pressure. -10 mcg/kg/min and greater, increases systemic vascular resistance, afterload

Calculations for Vasoactive Drips?

-Drips ordered in mg/hr or units/hr (morphine, diazepam, heparin) -Drips ordered in mcg/min (nitroglycerine, norepinephrine, epinephrine) -Drips ordered in mcg/kg/min (dopamine, dobutamine, nitroprusside) -Keep MAP at 65 when giving these drips!!!

Complications w/ a PA Catheter?

-Dysrhythmias- important to check electrolytes! -Balloon Rupture- if not able to wedge, maybe no balloon on there -Emboli (air or blood/thrombus) -Kinking of catheter in the heart -Damage to cardiac structures- can potentially rupture a pulmonary artery! -Infection- with any invasive line worry about -Pneumothorax from insertion- reason to get CXR and check placement and might have sudden onset SOB with insertion so might want to stop the procedure immediately if seen -Pulmonary ischemia or infarction -Rupture of pulmonary artery

For all Types of Shock, What Should We Do?

-Early identification, timely treatment -Identify, treat underlying cause -Sequence of events for different types of shock will vary -Management, care of patient will vary

What are the Principles of Invasive Pressure Monitoring?

-Equipment must be referenced and zero balanced to environment and dynamic response characteristics optimized -Referencing: positioning transducer so zero reference point is at level of atria of heart or phlebostatic axis -Zeroing: confirms that when pressure within system is zero, monitor reads zero -Done by opening reference stopcock to room air With initial setup and periodically thereafter -Pressure monitoring equipment is referenced and zero balanced to the environment and dynamic response characteristics optimized for accuracy. Referencing means positioning the transducer so that the zero reference point is at the level of the atria of the heart. -The stopcock nearest the transducer is usually the zero reference for the transducer. -To place this level with the atria, you use an external landmark, the phlebostatic axis. -***You need to ZERO out the equipment, zero means it is at the level of the atria of the heart or AKA phlebostatic axis*** -Zeroing confirms that when pressure within the system is zero, the monitor reads zero. To do this, open the reference stopcock to room air (off to the patient) and observe the monitor for a reading of zero. This allows the monitor to use the atmospheric pressure as a reference for zero. -Zero the transducer during the initial setup, immediately after insertion of the arterial line when the transducer has been disconnected from the pressure cable or the pressure cable has been disconnected from the monitor, and when the accuracy of the measurements is questioned. Always follow the manufacturer's guidelines.

Risk Factors for SIRS/Sepsis?

-Extremes of age -Indwelling lines/catheters -Immunocompromised states -Malnutrition -Alcoholism -Malignancy -Diabetes -Cirrhosis -Male sex -Extremes of age= older adults that have more comorbidities that put them at risk -Immunocompromised sates= puts them at risk for infection and sepsis -More prominent in males

Indications for Hemodynamic Monitoring

-For diagnostic and monitoring purposes!! Diagnostic: -R/O Cardiogenic Shock -R/O RV MI -R/O Cardiac Tamponade -Other CV disorders Monitoring: -Early detection of hemodynamic stages -Optimization of therapy - is done for diagnostic purposes like to r/o cardiogenic shock, RV MI, cardiac tamponade, and other CV disorders. -Can give us an early indication of any hemodynamic changes and problems and optimizes therapy/tx regimens

Oxygenation and Ventilation for Shock

-Have to increase O2 delivery to tissues! -This is done by: *Optimizing the CO with fluids/medications *Increasing the hemoglobin through transfusion *Increasing the PaO2 with supplemental O2 and mechanical ventilation -We need to increase the O2 delivery in the tissues! Main point of oxygenation. 3 ways to get this done: -Optimizing the CO with fluid replacement or drug therapy. -Increasing the Hgb thru transfusion of whole blood or packed RBCs. -Increasing the arterial O2 saturation with supplemental O2 and mechanical ventilation.

Nursing Diagnoses- for SHOCK

-Ineffective peripheral tissue perfusion -Risk for decreased cardiac tissue perfusion, ineffective cerebral tissue perfusion, ineffective renal perfusion, impaired liver function, ineffective GI perfusion RELATED TO low blood flow or maldistribution of blood flow -Anxiety related to severity of condition and hypoxemia

What are some Complications of Arterial Lines?

-Infection -Accidental blood loss -Impaired circulation -Site needs to me open and easy to monitor -Use aseptic technique with dressing changes and insertion -Use aseptic technique with blood draws Accidental blood loss (if gets accidentally pulled out or dislodge, pt can lose lots of blood!) , use leur locks, immobilize the extremity so that it is not dislodged or pulled out; set alarms, evaluate pressure system Impaired Circulation= Monitor!, monitor color sensation, temperature movement, cap refill, pulses if pt says hand is beginning to feel numb, etc- might be done as often as every hour, PRIORITY NURSING INTERVENTION!!

What are the Complications of CVP Catheter?

-Infection -Thrombosis -Air Embolism Infection= Can get infection with CVP catheter placement= Verify with blood cultures. Sometimes will remove catheter and culture the tip by cutting it off and sending to lab Thrombosis= can form of different sizes; smaller no consequences but larger may occlude circulation to the limb; may need thrombolytic agents. Will lose waveform or you may see changes in assessment Air Embolism= Air enters the tubing, through the vena cava to the to the right ventricle. Will see sudden hypotension as the first indicator. This can be lethal!!! You wills see lightheadedness, confusion, anxiety and may even unresponsiveness (altered mental status, may even become totally unresponsive!!!) What to do about air embolism? - You want to turn the patient to the LEFT side in Trendelenberg (head down!) to allow the air rise to the wall of the right ventricle to improve blood flow. 10-20 ml of ear to enter before symptomatic.

Vasoactive Drips

-Inotropes = Dobutamine, Milrinone, Dopamine,Epinephrine, Norepinephrine (Levophed) -Vasodilators = Nitropruside (Nipride) (arterial, vennous); Nitroglycerin (mostly venous), Ca++ Blockers (- "pines"); Milrinone (Primacor); Ace Inhibitors (-"prils"); ARBs (-sartans); Hydralazine (Apresoline) -Vasopressors =Norepinephrine (Levophed);Dopamine (high dose); Neosynephrine (Neo); Epinephrine; Vasopressin -Used to manipulate preload; afterload & contractility. -Negatively inotropic agents weaken the force of muscular contractions. Positively inotropic agents increase the strength of muscular contraction. -Vasodilators widens the blood vessels, which in turn decreases resistance to blood flow and lowers blood pressure. -Vasopressors vasopressor" causes vasoconstriction and an "inotrope" increases the force of cardiac contraction. Vasopressors and inotropes work via the Autonomic Nervous System. -GIVE THROUGH CENTRAL LINE b/c massive vasoconstriction might be pale

What are Circulatory Assist Devices (CADs)?

-Intraaortic Balloon Pump (IABP)- provides temporary circulatory assistance to a sick heart reducing afterload and augmenting the aortic diastolic pressure -Ventricular Assist Devices (VAD) - provides short and long term support for the failing heart to augment or preplace the action of the ventricle. Bridge to recovery or heart transplantation -Cardiogenic Shock -Might be used as a bridge to heart transplantation -Can be used in cardiogenic shock -Ventricular Assist Device, takes over the ventricular function

Arterial Line

-Invasive methods of hemodynamic monitoring will usually have pressure transducer system. -The catheter measures pressures inside the patient. Outside the patient, the catheter tubing connects to a pressure transducer, which is connected to a pressure bag of fluid and a monitor. Transmission of pressure signal from patient to transducer occurs through the fluid filled tubing. The transducer should be kept at the "phlebostatic axis" which is at the 4th ICS (axillary is your marker!). Important to keep at right level b/c: If transducer too low--> False high measurements If transducer too high--> False low Your "zeroing" reference confirms that when the pressure w/i the system is zero, the monitor reads zero. To do this, open the stopcock to air and off to the pt, and observe the monitor for a reading of "0". This allows the monitor to use the atmosphere pressure as a reference for zero. When to "zero": After insertion of line; if the transducer gets disconnected from the pressure cable/monitor, and when you're unsure if the readings are correct. You can do a "square wave test" q 8-12 hours to test the accuracy of readings - it is doing a fast flush of the fluid in the pressure bag. This is referenced and zero balanced to the environment Referencing means the transducer is at the level of the right atrium The stopcock nearest the transducer is f=sed for the zero reference This is the phlebostatic axis. Position the port of the stopcock nearest the transducer level at the phlebostatic axis ad tape in in place or mount it on a pole Zeroing confirms that w hen pressure within the system is zero the monitor reads zero. You do this by opening the stopcock to room air and observe the monitor for a reading of zero You zero during the initial set up, immediately after insertion, when the transducer has been disconnected from the pressure cable or the pressure cable has been disconnected from the monitor and when accuracy of the measurement is questionable. Be sure to check for correct placement after position changes!

PA Catheter Insertion

-Subclavian, jugular, or femoral vein approach. -Threaded to junction of vena cava all the way into the RA. -Balloon is then inflated. -Venous circulation carries the catheter tip through the RA and RV to a branch of the PA. -Balloon will wedge -Then the balloon is deflated, and the -Deflated balloon will drift into PA -During insertion, it is RN's job to monitor the waveforms (saying like in the pulmonic valve, etc) and print the cardiac rhythms throughout insertion - monitoring the rhythm allows us to know if we're in the right location of heart based on the different rhythms observed.

Triggers for SIRS- Things that Cause/Trigger SIRS??

-Mechanical tissue trauma: burns, crush injuries, surgical procedures -Abscess formation: intraabdominal, extremities -Ischemic or necrotic tissue: pancreatitis, vascular - disease, MI -Microbial invasion: bacteria, viruses, fungi -Endotoxin release: gram-negative bacteria -Global perfusion deficits: postcardiac resuscitation, shock states -Regional perfusion deficits: distal perfusion deficits

Care Measures for Cardiogenic Shock- What do we do for Cardiogenic Shock?

-Medical management -Hemodynamic monitoring -Correction of underlying causes -Goal: Restore blood flow to the myocardium by restoring balance b/t the O2 supply and demand (give Oxygen!!!) -Medication goals: Reduce the heart's workload -Invasive treatment: circulatory assist devices -Initiation of first-line treatment *Oxygenation *Pain control *Hemodynamic monitoring *Laboratory marker monitoring *Fluid therapy *Mechanical assistive devices *Other Pharmacologic Therapy *Dobutamine, Nitroglycerin, Dopamine, Other vasoactive medications & Antiarrhythmic medications -If ischemic cause, a cardiac cath is done asap. If valve cause, corrective valve surgery done asap. -Medication goals: Reduce the heart's workload -First oxygenate them, give them oxygen! -Medications can achieve this by: decreasing the preload (diuretics), afterload (vasodilators), HR (Beta-blockers). -Invasive treatment (circulatory assist devices): such as an intra-aortic balloon pump (IABP); ventricular assist device (VAD); heart transplant maybe. These invasive tx work to decrease the SC=VR and LV workload. -Common IV meds seen with this: *Dobutamine - positive inotrope/vasopressor which acts on Beta-1 receptors (where are these receptors located?? In the heart!) *Nitroglycerin - potent vasodilator *Dopamine - positive inotrope/vasopressor which acts on alpha and Beta-1 receptors (where are the alpha receptors located?? In the arteries!) *Other vasoactive medications *Antiarrhythmic medications -Monitor CK-MB specific to cardiac injury which is released 4-12 hours after injury. -Troponin is a protein in cardiac muscle. Released with injury as I, C, T. Released in 2-4 hours so is a more predictive than CK-MD -CRP is also a marker for inflammation and injury. Released by the liver

What is MODS (multiple organ dysfunction syndrome)?

-Multiple organ dysfunction syndrome (MODS) is failure of two or more organ systems *Homeostasis cannot be maintained without intervention *Results from SIRS -These two syndromes represent the ends of a continuum. -Transition from SIRS to MODS does not occur in a clear-cut manner.

Calculation of Afterload?

-Not directly measurable -Systemic Vascular Resistance = Afterload for Left ventricle SVR = (MAP-CVP) X 80 \ CO End result expressed in dynes/second/cm Normal = approx. 1000 dynes/sec/cm-5 Pulmonary Vascular Resistance (PVR) = Right ventricle Normal = ¼ of systemic value (< 250 dynes/sec/cm-5) SVR= afterload for Left Vent SVR= (MAP-CVP) X 80/CO PVR= afterload for Right vent

Nutritional Therapy for Shock

-Nutritional support needed to meet increased metabolic, energy requirements prevent further catabolism, due to depletion of glycogen -Support with parenteral or enteral nutrition -Start with trophic feedings -Daily weights! -They need protein and calories! They are trying to heal! -Enteral (in the gut) nutrition should be started w/in the first 24 hrs if possible!! If the gut works, use it! Dr. Barnes said Typically started within 24-48 hrs -Pt is started on a trophic feeding initially.... What is this?? A slow drip of small amounts of enteral nutrition (like 10-20 mL/hr). -These small feedings can help the GI tract stay better perfused. -Typically started slow, dieticians will be on board with this and monitor lab values for this -Weigh pt daily!! This can help us monitor the fluid status of patient! -DO DAILY WEIGHTS important for nurse to do!

What do we need to monitor in Arterial lines?

-Observe EKG and pressure tracings together Complications of arterial lines include: -hemorrhage -infection - thrombus formation -neurovascular impairment - loss of limb. -Keep alarms activated -Inspect insertion site for s/s infection, change tubing ad transducer based on facility policy (96 hours) -Circulatory impairment can occur as a result of formation of thrombus around the catheter, release of an embolus, spasm or occlusion of the circulation by the catheter. -Allen's test should be done prior to using the radial artery. Ulnar artery must be patent. -Activate the flush system every 1-4 hours to make sure pressure is at 300mmHg, fluid is in the bag, system is delivering a continuous flush (1mL/hr). Typically use normal saline due to possibility of HIT -You need to assess the neurovascular status distal to the arterial insertion site hourly checking for temperature, color, capillary refill, and symptoms of neurological impairment, pain, paresthesia paralysis. - Check for S/S of infection or neurovascular impairment, & contact HCP.

What is SvO2 (Venous O2 Saturation)?

-Obtained from fiberoptic sensor in PA catheter -Measures amount of O2 remaining in the venous blood after it has passed through the capillaries. -Normal SvO2: 60-80% -Reflective of SaO2/PaO2/CO/Hgb -↓SvO2 with suctioning, respiratory or cardiac dysfunction, anemia, or increased tissue demands. -↑SvO2 with decreased tissue utilization of O2 (sepsis) and with increased Hgb to hang on to O2. **Page 1565, Table 65-4 - REVIEW!!** -Good indicator of oxygen use by the body SUPPLY AND DEMAND ISSUES -Measures amount of O2 remaining in the venous blood after it has passed through the capillaries. So, it measures O2 supply and demand, along with the utilization of O2 by the tissues. -Obtained from fiberoptic sensor in PA catheter Normal SvO2: 60-80% Reflective of SaO2/PaO2/CO/Hgb Decreased SvO2: suctioning, resp or cardiac dysfunction, anemia, decreased arterial O2 level, low CO, or increased O2 consumption or extraction form the tissues.... If it is low, check for s/s of decreased O2 perfusion ---- AMS, UO, pulses, cap refill, skin color and warmth. Increased SvO2: may indicate an improvement in status, OR a problem (like sepsis) (in sepsis, O2 is not extracted properly at the tissues, which can result in an increased SvO2). SvO2 is a good indicator of O2 use in critically-ill patients.

What is a Square Wave Test Configuration?

-Optimizing dynamic response characteristics involves checking that the equipment reproduces, without distortion, a signal that changes rapidly. -Perform a dynamic response test (square wave test) every 8 to 12 hours and when the system is opened to air or the accuracy of the measurements is questioned. It involves activating the fast flush and checking that the equipment reproduces a distortion-free signal. -a small, downward deflection observed on the downstroke of an arterial pressure waveform. It represents closure of the aortic or pulmonic valve at the onset of ventricular diastole. Dicrotic notch.

What is Pulmonary Artery Pressure (PAP)?

-PA pressures give an estimate of the venous pressure within the lungs and the mean filling pressure of the left atrium and ventricle *Information that is fundamental in detecting pulmonary congestion and determining cardiac output -Also reflect LV dysfunction, since in absence of pulmonary stenosis PA pressures increase with LV failure -Pressure read from the distal port of the Swan-Ganz catheter (or pulmonary artery catheter) Fluid therapy based on PA pressures can restore fluid balance while limiting the problems of over or under correction. Monitoring these pressures gives a means for precise therapeutic manipulation of preload allowing CO to be maintained without placing the patient at risk for pulmonary edema. PAP= on the left side of the heart so higher pressure system, gives an estimate of the venous pressure of the lungs and also mean filling pressure of the LA and LV PAP= good indicator of LV dysfunction! If have a high PAP, then have high pressure in lungs

Nursing Diagnoses for Hemodynamic Monitoring ?

-PC: Thromboembolism -Infection r/t invasive line -Knowledge deficit: Patient/family r/t equipment, procedures -Anxiety r/t unfamiliar surroundings and unknown outcome

Afterload Manipulation- How to Manipulate Afterload?

-Peripheral vasoconstriction = increased afterload -May manipulate with drugs or volume replacement depending on cause Vasodilators- ie. Nitroprusside, NTG -Peripheral vasodilation = decreased afterload -May manipulate with drugs Vasopressors- ie. Levophed, Neosynephrine (Neo), Epi - to decrease afterload give meds like vasodilators (nitroprusside or NTG), or to increase afterload by give vasopressors such as Levophed, Neosynephrine, Epi

Arterial Lines cont'd.....

-Pressure lines inserted into radial or femoral artery -Utilizes same pressure tubing -Reading not read through the Swan Ganz catheter -Use an arterial line for continuous arterial BP monitoring, It is invasive monitoring- indicated for hypertension, hypotension, respiratory failure, shock, neurologic injury, coronary interventional procedures, continuous infusion of vasoactive drugs and frequent blood sampling. ABGs. -Typically done in the radial or femoral artery. Site depends on the size of the size of the artery, accessibility and blood flow distal to the insertion Inserted and sutured in place Immobilize the site to prevent dislodging or kinking Used for systolic, diastolic and MAP -Arterial lines are inserted into the radial usually but can be inserted into femoral -Radial arteries are very assessible and easy to monitor, prefer radial -Used if having a BP that is very labile and hard to control might need a continuous monitoring Might also need it for frequent blood monitoring or if giving vasoactive meds, need continuous monitoring of BP to make sure no negative effects Want to immobilize the site for arterial line -Pressure bag, usually/typically use saline- don't typically use heparin in pressure bags anymore b/c can cause issues, so will use NS

What is Mean Arterial Pressure (MAP)?

-Pressure lines inserted into radial or femoral artery -Utilizes same pressure tubing/transducer system -Reading is read thru an "art (arterial) line" -Provides continuous measurement/monitoring of arterial BP - more accurate than a BP cuff. -Used frequently when vasopressors are needed or when frequent ABGs will be needed. -Provides the BP with MAP readings. -Line up at the 4th ICS (phlebostatic axis). -This is used to evaluate perfusion of vital body organs -Normal is 70 - 100 mm Hg

What is Central Venous Pressure (CVP)?

-Subclavian vein to Vena Cava from the proximal port -Reflects the Right atrial pressure or RV preload or RVEDP -Normal (2-6mmHg) 4-10cmH2O with water manometer -Low value can indicate: *Low vascular blood volume *Decreased venous return - is a measurement of right ventricular preload and reflects fluid volume status -Most often measured with a PA catheter using the proximal port placed in the internal jugular or subclavian veins -CVP is measured as a pressure at the end of expiration Normal CVP= 2-6, so if CVP of 11 is high (too much volume) Low value= indicates low volume, dry If CVP is high= LISTEN TO LUNGS!! First priority for nurse

Preload- PA Monitoring

-Pulmonary Artery Wedge Pressure (PAWP): measures pulmonary capillary pressure, and reflects LV-end diastolic pressure -Periodic measurement of PAWP/PAOP "wedge" pressure -Normal PAWP = 6-12 mm Hg -Sensitive indicator of heart function and fluid volume status. -Measures pressure in the pulmonary artery (PA). -PA-diastolic and PAWP pressures increase in HF and volume overload. -PA-diastolic and PAWP pressures decrease with volume depletion. This measurement uses a balloon-tipped thermodilution catheter (called a Swan-Ganz catheter). It allows continuous monitoring of pressures in the RA, RV, and pulmonary artery (PA). We can do periodic measurement of the PA occlusive pressure (PAOP) or "wedge" pressure (PAWP). This PAWP pressure reflects estimated LV-end diastolic pressure. Normal PAWP = 6-12 mm Hg. Balloon on the catheter allows it to be "floated" by blood higher into the PA to measure PAWP (to estimate LV end-diastolic pressure) If LV function is poor, the PAWP will be elevated. Sensitive indicator of heart function and fluid volume status. Measures pressure in the PA. PA-diastolic and PAWP pressures increase in HF and volume overload. PA-diastolic and PAWP pressures decrease with volume depletion. The PA catheter is called a Swan-Ganz catheter, and it has multiple lumens, which can be used to infuse meds, draw blood, measure sample mixed venous blood (to evaluate O2 saturation), or measure pressures in different parts of the heart through which it runs (which could be in the RA, RV, & PA). The RA port is used for measurement of CVP, drawing blood for blood samples. The second proximal port is used for IV fluids/meds or blood sampling. The thermistor (temperature sensor) is used to monitor core temp and for measuring CO.

Key Nursing Roles in Shock Care?

-RECOGNIZE s/s of shock!! -CAB assessments -Assessment of tissue perfusion -Monitoring of fluid balance -Monitor for s/s of infection and treat appropriately -Monitoring of cardiac rhythms and ABGs -Manage any hypo- or hyperthermia. -Skin hygiene RECOGNIZE s/s of shock!! *Recent source of infection? *Recent MI? *Spinal injury/trauma? *Reason for dehydration? *Exposure to allergen? S/S of shock?? Increased HR, decreased BP are key!! Fever - think sepsis! CAB Assessments. Tissue perfusion assessments: cap refill, pulses, skin temp/color/turgor, UO, mental status, neuro status. As tissue perfusion decreases, the pt will have decreased UO, decreased neuro status, skin becomes cooler and mottled, diminished peripheral pulses. So, in this case, what about our O2 sat monitor?? Place it on an ear, nose, or forehead to get a more accurate reading! Monitor neuro status at least every hour. Why?? It's the best indicator of cerebral blood flow. Most therapy for shock is based on the pt's cardiovascular status - that's why it's so important that we do good head-to-toe exams and accurate hemodynamic monitoring (including daily weights). If they are septic, they will likely have a fever - we need to treat the fever with acetaminophen (if appropriate). If this doesn't get it down, we should do other measures to bring the fever down (fans, ice packs, maybe cooling blanket). Let's talk about the skin - the skin may not be getting good blood flow in shock, so it's important that we take extra care of the skin to prevent it from breaking down! But we have to be gentle and careful with the skin, b/c if it's getting hypo-perfused, it may tear/break down easily with us manipulating it! So, do gentle bathing/cleaning of the skin. Also, when we bathe them, it requires more O2 from their body, which stresses the body! Turn the pt q2hours to prevent pressure sores. You will have to prioritize care needs to limit the demands for increased O2! Cardiac rhythm and ABG monitoring - very important! Shock frequently can cause dysrhythmias and acid-base imbalances. Only time you wouldn't turn a patient is if they are hemodynamically unstable!!** Need to document it though if they became hemodynamically unstable like became hypotensive or had an increase RR or HR, etc.

What is Afterload (SVR)?

-Resistance that the left ventricle has to overcome to eject the blood from the heart -BP - one of the easiest ways to estimate afterload! -Afterload= End-Diastolic Wall Stress or RESISTANCE!! -refers to the forces opposing the ventricular ejection -Afterload= resistance, NOT volume -BP= easiest way to estimate afterload, good indicator of afterload!

What is Pulmonary Vascular Resistance (PVR)?

-Resistance that the right ventricle has to overcome to eject the blood from the heart -is the resistance of the pulmonary vascular bed. - This is a reflection of afterload -Right ventricular afterload =Very few drug selective to decrease PVR without decreasing SVR -Right ventricle sensitive to increased LV afterload --> right ventricular failure r/t pulmonary hypertension

Normal PA Pressures

-Right Atrium (CVP): Mean pressure: 2-6 mm Hg CVP normal= 2-6 Right Ventricle: Systolic Pressure 15-25 mm Hg Diastolic Pressure 0-8 mm Hg What does this waveform look like?? V-tach? B/c it's in the ventricle! Pulmonary Artery: Systolic Pressure: 15-25 mm Hg Diastolic Pressure: 8-15 mm Hg Mean Pressure: <15 mm Hg -The diastolic pressure is larger in the PA than it is in the RV b/c the PA is a smaller space than the RV! -The PA waveform has a dicrotic notch! Key identifier of this waveform compared to the Pulmonary Artery Wedge Pressure (PAWP): Mean pressure: 6-12 mm Hg PAWP Normal= 6-12

SIRS and MODS- what are they?

-SIRS (Systemic Inflammatory Response Syndrome): Inflammatory response to a variety of insults (including sepsis, ischemia, infarction (MI), injury). -MODS (Multiple Organ Dysfunction Syndrome): the failure of >=2 organ systems in acutely ill client so that homeostasis cannot be maintained without intervention. MODS results from SIRS. -Sepsis is seen in the SIRS stage. -Septic shock is seen in the MODS stage. -Goes from SIRS then to MODS SIRS--->MODS

What is Septic Shock?

-Sepsis: syndrome that is a response to infection characterized by new organ dysfunction -Septic shock: (Shock due to sepsis); subset of sepsis with profound circulatory, cellular, and metabolic abnormalities. -Septic shock is characterized by persistent hypotension despite adequate fluid resuscitation requiring vasopressors, along with inadequate tissue perfusion resulting in tissue hypoxia. -The main organisms that cause sepsis are gram-negative and gram-positive bacteria. -It is VERY common.. Stats from the CDC. Sooooo we need to know how to take care of it. -SEPSIS= INFECTION! -Septic shock- shock d/t sepsis, characterized by HYPOTENSION DESPITE ADEQUATE FLUID RESUSCITATION (requires vasopressors) along with inadequate tissue perfusion resulting in tissue hypoxia -EARLY RECOGNITION IMPORTANT!!!

What is the Frank Starling Law?

-The more muscles are stretched, the greater the force of contraction -Slightly stretched muscle contracts better than over or under stretched muscle -Preload is governed by Starling's Law: When cardiac muscles are stretched before contraction d/t an increased EDV (filling pressure), the resulting contraction will be of greater force. This explains the effects of preload. The more myocardial fibers are stretched during filling, the more is shortens during systole and the greater the force of the contraction. As preload increases, the force generated in the subsequent contraction increase, thus SV and CO increase. This also increases the oxygen requirements of the myocardium. Remember it is working harder. Diuresis and vasodilation decreases preload Fluid Administration increases preload. Frank starling law- the more the muscles stretch the greater the force of contraction Like a rubber band stretching it and then letting it release The more the stretch the more forceful contraction Don't want it to be stretched too little or too much, want it just right **What might decrease volume in heart?- diuresis, dilatation in circulation** ***How would we increase volume?- GIVE FLUID!!!*** Want to increase preload Preload is governed by Starling's Law Example = More air in a balloon more stretch. Let it go and it travels farther than with little air.

What is SIRS?

-The systemic inflammatory response syndrome is systemic level of acute inflammation, that may or may not be due to infection, and is generally manifested as a combination of vital sign abnormalities including fever or hypothermia, tachycardia, and tachypnea. -Systemic (body-wide) inflammatory response to a variety of severe clinical insults (pancreatitis, ischemia or reperfusion, multiple trauma and tissue injury, hemorrhagic shock and immune-mediated organ injury in the absence of infection. -"Sepsis" describes a progressive process that starts with a systemic inflammatory response syndrome (SIRS) triggered by an infectious or noninfectious cause. -The most common causes of sepsis are pneumonia, urinary tract infection, cellulitis, and postoperative infections. (Noninfectious triggers include traumatic injury, surgery, and blood product transfusion.)

Identification of the Phlebostatic Axis- How do you Identify the Phlebostatic Axis?

-To identify the phlebostatic axis, draw two imaginary lines with the patient supine. Draw a horizontal line down from the axilla, midway between the anterior and posterior chest walls. -Draw a vertical line laterally through the fourth intercostal space along the chest wall. The phlebostatic axis is the intersection of the two imaginary lines. -Mark this location on the patient's chest with a permanent marker. Position the port of the stopcock nearest the transducer level at the phlebostatic axis. Tape the transducer to the patient's chest at the phlebostatic axis or mount it on a bedside pole. -Found At the 4th ICS at the side of the atria

Dopamine (Intropin)

-Used in shock states to increase cardiac output, blood pressure, and blood flow to organs -Dose: 1 to 20 mcg/ kg / minute -Central Line Strength 400 mg in 250 cc D5W - 400mg/250 ml Concentration Mix = 1600mcg/ml -Don't have to know drip dose -Titrate drips based on response

Why do we do Hemodynamic Monitoring on pts?

-Used to evaluate function of the heart -Used to evaluate fluid status -Helps determine treatment effect -tells us how the heart is functioning, tells us how sick the patient is, evaluates fluid status (if not enough CVP tell us we don't have enough circulating blood volume or fluid- need more fluid or blood), and helps determine best treatment effect

Vasoactive Drugs for Shock

-Used when fluid therapy alone does not maintain MAP -Support hemodynamic status; stimulate SNS -Check vital signs frequently; continuous monitoring of vital signs every 15 minutes or more often -Give through central line if possible -Extravasation may cause extensive tissue damage Dosages usually titrated to patient response and hemodynamic monitoring -Maintain the MAP >65 mm Hg. -Most vasopressors are sympathomimetics (meaning they stimulate or mimic the sympathetic nervous system's effects). -This happens by binding to alpha or Beta- adrenergic receptors on cells. -They are used when fluid therapy alone does not maintain MAP. -Should be given thru central venous line b/c if the medication were to extravasate a vein, they can really damage the tissues (so that's a lot less likely to happen if given thru a main central line). -These drugs can cause SEVERE peripheral vasoconstriction and an increase in SVR... So the vasoconstriction is great for the general vasodilation we see with shock, but shock also causes peripheral vasoconstriction to the hands and feet, so if we further increase the vasoconstriction to the extremities... that's when we can definitely see some fingers and toes getting dark! Why?? B/c we have altered the perfusion! -So, we need to closely monitor their s/s of circulation- what would these be?? (cap refill, pulses, skin color/warmth/turgor, BP, MAP, UO, neuro checks, etc...... AND the serum lactate level to ensure that tissue perfusion is adequate!) Why monitor lactate? B/c when perfusion is impaired, the cells go into anaerobic metabolism and lactate builds-up! -We also should closely monitor the hemodynamic values b/c dosages/flow rates usually titrated to patient response and hemodynamic monitoring. -Our goal with vasoactive meds: Maintain the MAP >65 mm Hg.

What is the Initial Stage of Shock?

-Usually no apparent s/s of shock, BUT, cellular changes begin now. -The cells shift from aerobic metabolism (burning O2 to perform cell fxns) to anaerobic metabolism - what is anaerobic metabolism?? -Anaerobic metabolism: less cellular energy in the form of ATP (adenosine triphosphate) is produced, and lactic acid (a waste product of anaerobic metabolism) is produced which causes tissue acidosis and impairs cellular metabolism. -Anaerobic metabolism is the creation of energy through the combustion of carbohydrates in the absence of oxygen. This occurs when your lungs cannot put enough oxygen into the bloodstream to keep up with the demands of your muscles for energy. -AKA early shock

Conditions That Alter Afterload?

-Vasodilation= (sepsis, spinal or epidural anesthesia, anaphylaxis, arterial dilating drugs such as Nitroprusside, ACEI, ARBs, Milrinone) -Vasoconstiction =(HTN, compensatory vasoconstriction, and drugs such as neosynephrine, levophed, high dose dopamine, epinephrine, vasopressin)

What is Stroke Volume (SV)?

-Volume of blood ejected with each heartbeat -Difference between the volume of the left ventricle at end diastole (end of filling period to be ejected) and the volume remaining in the ventricle at end systole (end of ejection). -60-150mL./beat= normal SV -SV = CO/HR

What is the Progressive Stage of Shock?

-↓ CO, BP, systemic perfusion, capillary blood flow, which causes cellular hypoxia -Metabolic acidosis -↓ capillary blood flow -Capillary permeability -Interstitial edema -Blood clots -Decreased venous return to heart -Myocardial depressant factor (MDF) released -More hypoperfusion -Alevolar edema -Liver failure -DIC This stage begins as the compensatory mechanisms begin to fail... **Changes in mental status are important findings in this stage** (as they are in any stage!). -Prolonged vasoconstriction from comp. stage -> leads to ↓ CO, BP, systemic perfusion, capillary blood flow, which causes cellular hypoxia. -Anaerobic metabolism worsens, causing more lactic acid buildup, causing metabolic acidosis. -Remember: Anaerobic metabolism -> ↓ ATP production -> cellular swelling and death. -Since there is ↓ capillary blood flow, the capillaries dilate in an attempt to allow more blood flow into them. But d/t the cell changes in the capillaries, blood accumulates in the capillaries, which ↑s capillary pressure, pushing fluid out of capillaries (capillary permeability) and into the interstitial spaces (causing interstitial edema). Proteins are then lost thru enlarged capillary pores. -As IV blood volume decreases, blood flow is slowed and gets clogged, forming clots... Which causes a decreased venous return to the heart. -So, coronary artery perfusion is decreased and myocardial depressant factor (MDF) is released, which causes a decreased contractility. Soooo, what are some s/s we will see at this point?? Weakened pulses d/t hypoperfusion, edema from interstitial edema, ischemia of distal extremities eventually (discolored fingers/toes, mottled skin maybe)... MDF is released by the ischemic pancreas, which causes a decrease in myocardial contractility... so we'll see decreased CO, maybe some dysrhythmias, possibly an MI since the blood flow to the heart is going down. D/t more decreasing blood flow to lungs, the pulmonary arterioles constrict, causing an increased pulmonary artery (PA) pressure - which worsens the lung perfusion and V/Q mismatch. The capillary permeability that is present allows fluid to get into the alveoli. -So what resp s/s would we see now?? Tachypnea, crackles, increased WOB. GI system becomes ischemic, may allow the gut to develop ulcers and bleeding. For the kidneys, the lack of adequate blood flow can cause renal tubular ischemia. (Would this be a pre-renal, intra-, or post-renal AKI?? PRE!!- It happens b/c of lack of blood flow!) If we're giving them antibx (if this shock develops d/t infection), whew! Watch out! They may go into complete renal failure! -What type of renal s/s would we see now?? -Metabolic acidosis, increased creatinine and BUN (the kidneys can't reabsorb bicarb or excrete acids - esp lactic acid, when they are not hydrated and working well!) -I mentioned earlier that perfusion to the gut is really lacking now. Well, that's also the case with the rest of the GI tract. Loss of effective flow to the liver causes liver failure.... (jaundice, elevated liver enzymes like ALT, AST, bilirubin, and lactate). When the liver fails, it cannot metabolize drugs - and LOTS of meds are processed through the liver! Also, the liver is heavily involved in the formation of RBCs and clotting cells. So if the liver is going into failure, this puts the pt at high risk for something called DIC (disseminated intravascular coagulation). DIC = A condition in which there are microemboli (tiny clots) developed in multiple areas of the body.. So the body sends out fibrin-busters (cells that perform fibrinolysis) to rid the body of the clots, but this actually causes bleeding throughout the body that worsens with time. So you may see this patient start to bleed at IV sites, in the gums, urine, etc.

General Management of All Types of Shock Includes what?

1. Fluid replacement to restore intravascular volume 2. Vasoactive medications to restore vasomotor tone, improve cardiac function 3. Oxygenation & Ventilation 4. Nutritional support to address metabolic requirements 5. Further care varies on type of shock... -Abx for septic shock -HF therapies (meds/devices) for cardiogenic shock -Epinephrine for anaphylactic shock -Temp regulation for neurogenic shock ***100% O2, nutritional support, ABX for septic shock, HF therapies for cardiogenic, Epi for anaphylaxis, temp regulation for neurogenic shock***

What are the 5 Types/Classifications of Shock?

1. Hypovolemic: shock state resulting from decreased intravascular volume due to fluid loss 2. Cardiogenic: shock state resulting from impairment or failure of myocardium 3. Septic: form of distributive shock resulting from overwhelming infection causing hypovolemia 4. Neurogenic: shock state resulting from loss of sympathetic tone causing massive vasodilation 5. Anaphylactic: circulatory shock state resulting from severe allergic reaction producing overwhelming systemic vasodilation, relative hypovolemia Types of Shock= Hypovolemic, Cardiogenic, Distributive ( Types of Distributive= Septic, Neurogenic, and Anaphylactic!) -Hypovolemic= tank is empty from blood loss, severe dehydration, might be having exacerbation of CHF -Cardiogenic= typically seen after an MI or from HF -Septic= think about infection or microorganism cause this -Neurogenic= seen after Spinal Cord Injury or Spinal Anesthesia (can last for several weeks even) -Anaphylaxis= reaction to something

Dobutamine

=Sympathomimetic Agent, catecholamine -Used to treat low cardiac output states due to myocardial infarction, congestive heart failure, post cardiac surgery, shock, cardiogenic shock, CHF -Dosage: 2 to 20 mcg /kg/minute -Drip: 500 mg /250 ml Concentration of Mix 2000mcg/ml -Dose (mcg/kg min) X weight (kg) X ( 60 min/hr) -Concentration mcg/ml

A patient with a history of alcoholism is admitted to the ICU with hemorrhage from esophageal varices. Admission VS are BP 84/58 mm Hg, HR 105, and RR 32 breaths/min. The nurse recognizes the onset of systemic inflammatory response syndrome (SIRS) upon finding what? A.pulmonary edema. B. cardiac dysrhythmias. C. absent bowel sounds. D. decreasing blood pressure.

ANSWER --> A.pulmonary edema. Rationale: The respiratory system is often the first system to show signs of dysfunction in systemic inflammatory response syndrome. Increases in capillary permeability facilitate movement of fluid from the pulmonary vasculature into pulmonary interstitial spaces. The fluid then moves to the alveoli, causing alveolar edema and pulmonary edema.

A patient admitted to the hospital from a long-term care facility appears to be in the late stage of shock with systemic inflammatory response syndrome (SIRS). Which order implemented by the nurse has the highest priority? A. Insert an indwelling urinary catheter. B. Insert two large-bore intravenous catheters. C. Administer 0.9% normal saline at 100 mL/hr. D. Administer 100% oxygen by non-rebreather mask.

ANSWER--- > D. Administer 100% oxygen by non-rebreather mask. Rationale: A patient in the irreversible stage of shock (late stage) will demonstrate profound hypotension and hypoxemia. If the condition progresses to systemic inflammatory response syndrome, the patient may experience profound hypoxemia. Oxygenation is a priority and should be initiated first with a 100% oxygen delivery method such as a non-rebreather mask.

What is Preload?

Amount of blood loaded into the ventricles at the end of diastole that is ready to be ejected during systole -Preload= End Diastolic Volume (EDV) -End diastolic volume (EDV) Is the amount of blood within the ventricle at the end of diastole. When it relaxes and fills. -Direct measurements of the volume in the chambers are difficult so various pressures are used to estimate the volume. -Left ventricular end-diastolic pressure is called left ventricular preload -Pulmonary artery wedge pressure (PAWP) is a measurement of pulmonary capillary pressure and reflects the left ventricular end diastolic pressure under normal conditions. .Mitral valve dysfunction, intracardiac defect, dysrhythmia -Central venous pressure (CVP) measured in the right atrium or in the vena cava is the right ventricular preload or right ventricular end diastolic pressure when there is no defects like tricuspid valve dysfunction, intracardiac defect or dysrhythmia. -Preload= end diastolic volume, filling before it contracts

Afterload cont'd.....

Any factors that oppose ejection of blood from the ventricles ---> increased afterload Conditions that decrease afterload_--> -hypotension -Sepsis - vasodilitation Simply stated: Opposed ejection= afterload, anything that makes it harder for the ventricle to contract Anything that makes it easier for vents to contract= anything that would decrease afterload such as hypotension (decrease BP) or sepsis such as vasodilatation/dilation

Pulmonary Artery Waveform

Anytime a PA catheter is inserted, or anytime you as the RN measure the wedge pressure, you MUST print this strip and place in chart to document that you did not leave the PA catheter wedged (ballooned) in the PA b/c that will obstruct blood flow from going to the lungs!!

Afterload Manipulation- How do you manipulate or fix the problem??

Balancing Act! -Maintain preload as afterload is decreased --> optimal improvement in contractility and SV -Decreased preload frequently accomplishes decreased afterload secondary to arterial/venous dilation -Vasopressors alone usually inadequate management of hypotension associated with decreased CVP & PAW unless volume needs are considered

Review blood flow through heart

Blood flows through the SVC to the RA into the RV, from the RV goes up into the pulmonic valve into the pulmonary artery and then comes back by way of pulmonary veins, to the LA into the LV then out through the aorta to the body. R side- less pressure, L side= more work, more pressure "the work horse"

Factors that Effect Preload?

Fiber length: -Muscle fibers can reach a point of stretch beyond contraction no longer being enhanced stroke volume decrease heart failure Compliance: -Stiffness or increased thickness of the muscle wall- ex. Ventricular hypertrophy, heart not able to contract as easily Volume: -Venous return -Total blood volume -Atrial kick- amount of blood ejected at the end of systole in the atria Active atrial contraction forces additional volumes of blood into the ventricles (often referred to as "atrial kick"). The atrial kick contributes a significant volume of blood toward ventricular preload (approximately 20%).

Determinants of Cardiac Output (CO)?

CO- HR X SV SV= Preload, Afterload, and Contractility -Preload, afterload and contractibility determine SV, thus CO and BP - it is the volume of blood ejected with each heartbeat Preload- volume in vents after diastole Afterload- resistance that the vents have to overcome in order to pump that blood out where it needs to go Contractility= how strong the vens are contracting out

What are the Hemodynamic Indicators of Preload?

CVP - Central Venous Pressure - Right Ventricular EDP or preload PAWP - Pulmonary Artery Wedge Pressure - Left Ventricular EDP or preload -PAD - Pulmonary Artery Diastolic Pressure (measure of pulmonary hypertension!) -LVEDP - Left Ventricular End Diastolic Pressure -LVEDV - Left Ventricular End Diastolic Volume (volume left in the ventricle at the end of diastole)

Conditions that Alter Contractility?

Conditions that INCREASE Contractility: Pheochromocytoma= Benign tumor of the adrenal glands that increases hormones that causes elevated BP and heart rate which increases contractility Hyperthyroidism - increases body's metabolism, increasing heart rate (causes tachycardia) and -Positive inotropic drugs= Dobutamine, Dopamine, Levophed, Milrinone, Digoxin Conditions that DECREASE Contractility: -Cardiomyopathy - causes the heart muscle to become enlarged, thick or rigid. In rare instances, diseased heart muscle tissue is replaced with scar tissue. -Ischemia or ischaemia is a restriction in blood supply to tissues, causing a shortage of oxygen that is needed for cellular metabolism (to keep tissue alive). Ischemia is generally caused by problems with blood vessels, with resultant damage to or dysfunction of tissue. -Hypoxia tissues do not have enough oxygen -Acidosis -negative inotropic drugs (BBs, CCBs, antiarrthymics, many others)

SIGNS OF SHOCK

Decreased blood pressure; rapid, weak pulse; mottled to gray skin color; changes in mental status

Fluid Replacement for Shock

Fluid replacement: Table 66-7, page 1597 Crystalloids: Isotonics: 0.9% normal saline, lactated Ringer's solution Hypertonic solutions (3% hypertonic saline) Colloids (blood volume expanders): Albumin Dextran (dextran may interfere with platelet aggregation) Blood components for hypovolemic shock Packed RBCs, plasma, platelets 1st: Fluids are the cornerstone of therapy for septic, hypovolemic, and anaphylactic shock to gain volume expansion. To be able to do this, we need good IV access.. This can be done with 2 large-bore IVs (14 or 16-gauge) or a central venous line. You COULD do an IO (intraosseuous - in the bone) line IF there is zero good IV access or in quick emergency - but these bring a LARGE risk of infection and have to removed w/i 24 hrs. (I wouldn't recommend using them unless there is NO other option!) We have to closely assess their response to fluid administration. How could we do this???? (Hemodynamic monitoring - SVV, CO; vital signs; MAP; UO; cap refill; skin temp; UO; mental status checks.)

What would you do for an increased CVP?

Give diuretic, give vasodilators, first listen to lung sounds b/c have too much fluid! Tx/ Need to give Diuretic therapy & Peripheral venous vasodilators Diuretic therapy--> decreased pulmonary congestion and decreased myocardial O2 demands and decrease excessive volume by increasing urine output and increasing venous pooling d/t venous vasodilation Venous Vasodilators --> -decrease PAWP d/t venous pooling -Effectiveness evaluated by return of PAW to normal and increase CO Use drugs cautiously in shock states --> worsen hypotensive state Decreased CO & BP --> tachycardia

What are some Conditions That Alter Preload?

Hypovolemia: -Hemorrhage -Dehydration -Burns= get a lot of leaky capillaries which goes into the intersitial space -Overdiuresis -Third Spacing= occurs when too much fluid moves from the intravascular space (blood vessels) into the interstitial or "third" space-the nonfunctional area between cells. This can cause potentially serious problems such as edema, reduced cardiac output, and hypotension. Seen with burns and trauma Hypervolemia (if someone is overhydrated such as in heart failure or renal disease): -Overhydration -CHF -Renal Disease Altered Size of Vascular Spaces: -Sepsis -Spinal or epidural anesthesia -Anaphylaxis (get vasodilatation and vasoconstriction which can alter preload) -Venous dilating drugs: NTG, ACE Is, ARBs, Neseritide, & Others (Vasoactive Meds!)

How to INCREASE Cardiac Output (CO)?

Increase Stroke Volume (SV) or Increase HR or Increase BOTH -Cardiac output and the opposing forces blood flow determine BP -SVR is the opposition from the left ventricle -Pulmonary vascular resistance is the opposition from the right ventricle -Can increase CO with meds, fluid, blood, etc. Blood flow= what determines BP People with HTN have atherosclerosis or hyperlipidemia or might be diabetic (vessels undergone structural changes) will usually have higher BP so the opposing force is what determines the BP So if have more opposing force, the BP will be higher or be increased

Preload Manipulation w/ INCREASED PRELOAD- How do we manipulate or fix the problem??

Increased preload --> increased volume returning to the ventricles Increased CVP, PAWP --> indicates excessive circulating volume -Diuretic therapy -Peripheral venous vasodilators -to increase preload we gotta increase their volume (fill their tank to meet the needs of the body) -So we would see an increased CVP, PAWP would indicate an excessive circulating volume (more volume than needed) so need to give diuretic/diuresis, or give vasodilator meds ***Auscultate lung sounds if fluid overload, listen to lungs!!***

Pathophysiology of Cardiogenic Shock

Insufficient cardiac output to meet metbolic demands of tissues Cardiogenic shock occurs when there is a dysfxn in the heart's pumping action (could be a systolic or diastolic problem). It causes a decreased CO. Decreased filling of the heart causes a decreased stroke volume. Commonly caused by an MI, CMP, pulmonary HTN, ventricular hypertrophy. Looks very similar to acute decompensated heart failure. Patho usually as follows: Due to some reason that affects the heart's pumping ability, there is a decrease in SV, which leads to a decrease in CO. When there is decreased CO and perfusion, this affect's the cells in tissues, and causes them to go into anaerobic metabolism instead of aerobic metabolism, which causes the development of lactic acidosis Focus of Cardiogenic Shock= want to reduce the heart's workload

SIRS/SEPSIS Cascade- How does it progress??

Local Infection--> Systemic Infection (early sepsis)--->SIRS--->Organ Failure (severe sepsis)--->MODS (septic shock) ---->DEATH

Septic Shock cont'd....

Microorganism enters the body The body has exaggerated response to the offending infection WBCs and clotting factors are released Microthrombi formed Vessel damage results Vasodilation ↑HR Maldistribution of blood flow Myocardial depression So what's the diff b/t sepsis and septic shock?? Sepsis - infection enters the bloodstream. Septic shock - infection in the bloodstream causes hypotension and "shock" effects (affects the perfusion of other other organs). VERY IMPORTANT TO DETECT AND GET TREATMENT GOING!! (Lots of different definitions out there, but this is the main difference in simplest terms.) -It begins with contracting an infection. A microorganism enters the body. (So there is usually a fever, may be very mild tho.) The body's immune and inflammatory responses are triggered... but have a hyper exaggerated response (this could be d/t the duration of infection or extent of infection). Both inflammatory and anti-inflammatory responses are initiated, coagulation increases, and fibrinolysis decreases. Microthrombi are formed so the microvasculature can become obstructed. The combined effects of all of these changes cause damage to the endothelium of vessels, vasodilation, increased capillary permeability, neutrophil (what is a neutrophil??? WBC) and platelets become clogged and adhere to the endothelium. So there are lots of changes happening in septic shock..... But what will see in the patient as a result of all of these changes?? ***Vasodilation, increased HR, maldistribution of blood flow, and myocardial depression.** This causes changes in the cells' metabolisms (aerobic to anaerobic, build-up of lactate), altered tissue perfusion, and multiple organ damage. So the patient may have a normal fluid volume on board, but b/c of the vasodilation, their BP will drop. With the maldistribution of blood flow, blood flow to the microcirculation (think fingers, toes, skin) will decrease, which causes poor O2 delivery to the tissues. B/c of a decreased BP, there is a decreased venous return to the heart which leads to a decreased EF. Resp failure is common in septic shock... initially the lungs breathe faster to compensate - so what ABG imbalance would we see?? Resp alkalosis! -But as the progression of sepsis worsens, the lungs are not able to continue compensating. It's at that point when acidosis develops- if it's primarily from resp failure, it would be resp acidosis.. But if the kidneys are affected, it could be metabolic acidosis.

Central Venous Pressure- A High Value can Indicate what?

RV failure Volume overload LV failure Pulmonary HTN CVP indicates right ventricular failure or volume overload, left ventricular failure or pulmonary hypertension A low CVP indicates hypovolemia CVP pressure= HIGH value, think Right SIDE LISTEN TO THE LUNGS means RV failure, volume overload, LV failure, and Pulmonary HTN HIGH VOLUME OR AFTERLOAD!! LISTEN TO LUNG SOUNDS if have HIGH CVP means high volume or afterload!!

What are the Components of Stroke Volume?

Preload Afterload Contractility Remember this is the amount of volume of blood ejected with each heartbeat. Preload is related to a number of variables Fiber length Stretch (compliance - ability of the LV to stretch) Volume (presented to the LV)

Increased/High CVP can indicate what?

RV failure Volume overload LV failure Pulmonary HTN

Most important to do for a patient in SHOCK???

Recognize early and treat rapidly!!!

Criteria for SIRS?

Requires 2 of the following 4 features to be present: -Temp >38°(100.4) or <36.0°(96.8) -Respiratory - Tachypnea (RR>20) or PaC02 below 32 mm Hg -CV - Tachycardia (HR>90, in the absence of intrinsic heart disease) -Lab Tests - WBC > 12,000/mm3 or <4,000/mm3 or >10% band forms on differential Bands: immature neutrophils (immature WBCs) Criteria for SIRS requires 2 of the following= Temp >100.4 or <96.8, RR >20 or PaCO2 <32 mmHg, Tachycardia (HR >90) in the absence of intrinsic heart disease, WBCs >12,000 or <4,000, and >10% band forms on a differential (CBC w/ diff)

The Sepsis Continuum- How does Sepsis progress from Sepsis to Septic Shock?

SIRS--> Sepsis-->Severe Sepsis---> Septic Shock

Relationship between SIRS and Sepsis

Same clinical response can be seen in the absence of infection such as multiple trauma, shock, pancreatits.

Care Measures for Neurogenic Shock?

Spinal precautions: C-Collar and patients with spinal precautions are turned very carefully to prevent flexion or movement of the vertebrae. *Vasopressors and Fluids* -Treat the massive vasodilation without compensation. -Bradycardia may treated with atropine. -Fluids infused cautiously b/c the cause of hypotension is not fluid loss. -Monitor for hypothermia (caused by hypothalamic dysfxn). Spinal precautions: C-Collar and patients with spinal precautions are turned very carefully to prevent flexion or movement of the vertebrae. People with neurogenic shock require very careful handling... want to LOG ROLL THEM when repositioning,etc. *Vasopressors and Fluids* -Gotta treat that massive vasodilation without compensation. -Bradycardia may treated with atropine. -Fluids infused cautiously b/c the cause of hypotension is not fluid loss. -Monitor for hypothermia (caused by hypothalamic dysfxn). BP down and HR down

What is the Allen's Test?

Test for patency of ulnar artery prior to placing a radial arterial line or performing an ABG; examiner occludes both ulnar and radial arteries w/ fingers as patient makes fist; patient opens fist while examiner releases ulnar artery occlusion to assess blood flow to hand Allen's test must be performed and adequate ulnar artery blood flow established before the radial artery is used.

Arterial Waveform

arterial line is a little delayed (compared to the central lines)

Increased CVP or PAWP can indicate what?

indicates excessive circulating volume

What is Anerobic Metabolism?

is the creation of energy through the combustion of carbohydrates in the absence of oxygen. This occurs when your lungs cannot put enough oxygen into the bloodstream to keep up with the demands of your muscles for energy.

What would be thigns that clue you in to a patient having S/S of Shock?

↑HR ↓BP ↑RR Maybe fever Recent cause for fluid loss, infection source, spinal injury, HF exacerbation. -You need to know how to pick up shock anywhere you work (icu, er, floor, clinic, home health, women's health, anywhere! B/c ANY of our pts - no matter HOW healthy they are - can go into shock!) -Young healthy ppl who die from flu... usually die from septic shock. So you gotta be able to pick up on it!