exam 2 Flashcards
Normally oxygen delivery to cells meets the metabolic needs of the body
Stress –> oxygen requirements increase –> body compensates
-when body compensates, sympathetic NS kicks in and see S/S of SNS
Shock-clinical conditions that result in cellular hypo-perfusion
Shock
in shock cells get hypoperfused
Cardiac output-amount of blood ejected from the left ventricle each minute (measured in liters)
-HRxSV=CO
-Normal adult=4-8mL/min.
Stroke volume-volume of blood ejected per ventricular contraction (measured in liters/beat)
-Normal 60-100mL/beat
-3factors that effect SV: preload, afterload, and contractility
Preload-amount of stretch placed on cardiac muscle at the end of diastole
Preload is affected by the volume at the end of diastole (diastole = rest/filling)
-Left ventricular preload is represented by left ventricular end-diastolic pressure (LVEDP)
basic hemodynamics - cardiac output and stroke volume and preload
for preload: force of contraction decreases, chamber fills with blood r/t it not pumping well –> overfills with blood –> heart muscle stretches the contraction and gets weaker with each one
Inflammatory response is activated systemically
Manifested by 2 or more: T->100.1 or <96.8, RR > 20, HR > 90, WBC >12,000 or <4,000
Cause: Shock, Massive blood transfusions, Trauma, Brain injury, Surgery, Burns, Pancreatitis
Many times SIRS happens right before someone goes into septic shock
*Systemic response –> inflammatory response –> involvement of endothelial cells & generalized activation of inflammation & coagulation
Inflammatory response-release of cytokines which break apart the endothelial cells which causes the capillaries to become permeable and plasma leaks into the interstitial spaces
Platelet aggregation, coagulation cascade: Fibrin and WBC
-endothelial cells: lining of interior surface of blood vessels
–Function: vessel tone and hemostasis
–If damage, will weep/capillary permability
Result of SIRS: Inflammation!, Coagulation, Disruption of capillaries, Intravascular volume loss, Oxygen supply & demand imbalance
SIRS
Stage 1: initial, non progressive -Compensatory mechanisms work, misdiagnosed Stage 2: intermediate, progressive -Tissue perfusion begins to fail -Inflammatory response more pronounced -Signs of failure in 1 or more organs Stage 3: final and irreversible -Cellular & tissue injury -Cellular hypoxia & death -MODS -Fatal
stages of shock
A result of inadequate circulating volume
Caused by: Sudden blood loss and Severe dehydration
Decrease in intravascular volume –> decreased cardiac output –> cellular hypo perfusion & inability to meet cellular oxygen requirements for metabolism –> LACTIC ACIDOSIS
-Inadequate venous return –> decrease cardiac output
-Because tissue perfusion/hypoxia Lactic Acid will increase
-Lactic acid: <2; cleared from kidneys, liver and muscles
SNS tries to compensate
Increases workload of heart
Ischemic damage due to cellular hypo perfusion & decreased oxygen to heart
End organ failure
hypovolemic shock
Usually r/t extreme congestive heart failure
Loss of contractility
Cause: *MI (after heart muscle dies so watch), Heart muscle rupture, Ventricular septal rupture, Cardiomyopathy (enlarged heart so poor contractility), Myocarditis, Valve disease, Dysrhythmias
Decreased cardiac output
Compensatory mechanisms increase preload—retain sodium and water
Afterload increases due to vasoconstriction
Ventricle becomes distended and can’t eject blood, blood pools in pulmonary system, alveoli can’t exchange gas, cells die
cardiogenic shock
anything that alters contractility (like CHF) –> cardiogenic shock
Afterload-force or PRESSURE against which a cardiac chamber must eject blood during systole
-Vascular resistance in the systemic or pulmonic vessels is the biggest factor in determining afterload
-Example: if systemic vascular resistance increases due to constriction of arteries, it takes more force for the left ventricle to pump SV decreases
Inotropic capabilities and cardiac workload refers to contractility
-Increased inotropic action increases the oxygen consumption (increased workload and increased oxygen demand)
AN INCREASE IN HEART RATE INCREASES OXYGEN DEMAND
AN INCREASE IN STROKE VOLUME INCREASES WORKLOAD
basic hemodynamics - afterload and contractility
S/S: MAP <70 (<65 indicates decreased organ perfusion), Weak pulse/ (r/t decrease contractility), Chest pain (r/t MI), Cool, pale, moist skin(r/t decrease perfusion), Decreased LOC (esp with weak pulse), Dyspnea, Tachypnea, Crackles, Oliguria
Labs: elevated cardiac bio markers (troponin (indicates mi), BNR (released by ventricles in response to body having too much fluid)), increase BNP
NM: Correct the cause, Reverse hypoxemia, Diuresis, Decrease workload of heart, Opioids and sedatives (low O2 demands and rest the heart), Mechanical ventilation, Increase cardiac output, Pacer/dysrhythmia care, Electrolyte balance, IABP (intra-aorta balloon pump rests the heart), LVAD (left ventricle assistive device - replaces LV and works in place of it)
Meds: dopamine (give inotropic to increase contractility), mirion
Want to maximize CO to decrease work on heart: want to increase contractility and CO to increase CO and perfusion
cardiogenic shock 2
S/S: Altered LOC, Tachypnea, labored breathing, Cool, clammy skin, Tachycardia, Hypotension, Decreased urine output (r/t kidney compensate by holding onto urine) (all S/S of decreased CO/organ perfusion)
Labs: lactate, ABG
NM: Isotonic solutions* (LR, NS), Blood products or Albumin, Large bore IV, Respiratory assessment (watch baseline so you can evaluate intervention), Cardiovascular assessment* (when EF is low can’t tolerate as much fluids), Monitor VS frequently* (hourly or more)
Monitor urine output
hypovolemic shock 2
Anaphylactic- due to anaphylaxis (immediate intervention or will die)
Neurogenic- loss of sympathetic tone
Septic- sepsis** (Most common)
*Decreased venous return and loss of blood vessel tone
distributive shock
decrease venous return/muscle return with all of these
Allergic reaction
Life threatening
Medications & insect stings are most common in adults
Death from circulatory collapse or bronchoconstriction
Must avoid the allergens!
S/S: Early: Redness, Itching, Anxiety, Restlessness, Progressive: Wheezing, Nausea, Bronchoconstriction/Stridor, Circulatory collapse: Hypotension, Hypoxia, Unresponsiveness
NM: Treatment depends on symptoms!, *Oxygen, Antihistamine (Diphenhydramine-Benadryl), **Epinephrine-more severe symptoms, Corticosteroids, Bronchodilators, Vasoconstrictors & inotropes if circulatory collapse, *Maintain airway, Monitor vitals closely, Comfort, Re-evaluate allergies, Educate!
Distributive - anaphylaxis
main concern: airway and circulatory collapse
Loss of sympathetic tone –> peripheral vasodilation decreased tissue perfusion
*Most common cause-spinal cord injury above T6
S/S: Hypotension (r/t loss of sympathetic), bradycardia, hypothermia, decreased cardiac output, bradycardia, warm skin (r/t vasodilation)
Parasympathetic tone takes over –> arterial vasodilation –> decreased cardiac output
NM: Fluid resuscitation, Vasopressors, Frequent vitals, Neuro assessment (r/t spinal cord injury), Respiratory assessment (r/t venous pooling and decrease CO), Cardiac assessment (HR = bradycardic)
Distributive neurogenic
Incidence is increasing: in age, antibiotic resistance, number of immunocompromised patients, More high risk surgeries, Increased recognition
From an infection
Could be: Pulmonary, Urinary (UTI), GI (perf bowel), Wounds (dressed properly), Invasive lines/devices (central line associated blood stream infection - CLABSI; catheter associated UTI - CAUTI)
patho: Proinflammatory cytokines are secreted –> increased capillary permeability
Imbalance between procoagulant & anticoagulant factors
In sepsis-procoagulant state –> further inflammation
Risk factors: Elderly, Malnutrition, Debilitated (immobile –> pneumonia, pressure ulcer), Drug/ETOH (not clean needles), Neutropenia (no WBC to protect them), Splenectomy, Organ failure
*Proinflammatory & procoagulant responses= loss of homeostasis of every organ
Distributive septic shock
Cardiovascular
-Vasodilation-decreased venous return to heart, decreased CO, decreased SVR
-Myocardial depression-decreased ventricular ejection fraction, dilation of the ventricles
Pulmonary
-Bronchoconstriction
-Interstitial edema
-Poor pulmonary perfusion
-Pulmonary hypertension
-Increased work of breathing
-Hypoxemia
-ARDS: frequently associated with septic shock
Hematological:
-Platelet abnormalities
-Over activation of the coagulation cascade*, clotting factors decrease and the potential for DIC exists
Metabolic
-Hypermetabolic state
-Insulin resistance: look for hyperglycemia (will need insulin drip)
-Proteins break down (hurts/fails liver - get increased protein urea nitrogen)
-Liver starts to fail-amino acids build up
-All of this leads to cell death
distributive Septic shock types
Cardiovascular
Pulmonary
Hematological
metabolic
All r/t coagulation cascade
DIC = disseminated intravascular coagulation: clotting in small blood vessels, normal clotting becomes disturbed
-Clotting and bleeding concern
S/S: Altered LOC (r/t lack of O2 and not good perfusion - ex: confusion, anxious, ALOC), Tachypnea-due to metabolic acidosis - kusmal breathing r/t lung compensation, fever r/t septic shock, hypothermia, Edema, Intravascularly dry r/t fluid shift, Bleeding r/t DIC coagulation cascade and platelet aggregation, Decreased perfusion
Labs: cultures (central line tip, wound/stool/blood/urine/sputum/spinal fluid culture), CBC, chemistry panel (see hyperglycemia), ABG, CT scan, CXR, Lactate (high lactate = decrease perfusion)
NM: Start early!, Maximize oxygen delivery, Stop inflammatory process, Fluid resuscitation, Sedation, Electrolytes, glucose control, Cultures-identify cause, Prevent new infection
DVT prophylaxis, Stress ulcer prophylaxis
Distributive septic shock 2
Cardiovascular
Pulmonary
Hematological
metabolic
See pp. 1228-1229
Progressive physiological failure of several organs in acutely ill patients in which homeostasis cannot be maintained without intervention
Loss of integrity in mucosal barrier cause bacterial toxins from the gut to circulate-damaging multiple organs
Tissue hypoxia –> organ failure
Failure of one organ makes another organ failure more likely
Lungs, heart, kidneys 1st to go
Liver is usually later r/t better compensation
To prevent MODS
-Must increase perfusion & oxygenation (if 1 fails, must increase perfusion to other organs)
-Decrease the inflammatory response
Lungs are usually 1st due to increased capillaries-decrease gas exchange
Cardio-decreased CO 2nd to dysrhythmias, myocardial depression
Heme-thrombocytopenia
Neuro-altered LOC
Renal-poor perfusion
Hepatic-affects many other body systems
S/S/Labs: Vital signs (signs of SIRS - tachycardia, tachypnea, high temp/WBC, low BP), Coags (PTT, PT, INR, platelets, fibrinogen r/t prevent coag cascade –> DIC), increase WBC, Lactate (in shock check lactate 1st - >2 = sign of shock), Renal function
MODS
Liver effects clotting, drugs, metabolism - big deal r/t effects so many things
Preload- volume within the ventricle at the end of diastole
-Measurements:CVP-central venous pressure:* RIGHT ventricular preload*
Afterload-pressure
-Measurements:
–SVR-systemic vascular resistance-resistance in the vascular system. This reflects afterload
—The resistance against which the left ventricle must pump to eject volume
—Increased SVR = increase BP = decreased cardiac output (secondary to increased workload of the heart)
Contractility: Squeeze - Strength of the contraction
-The heart has to be able to contract to pump effectively-directly affects cardiac output
-Measurements: No direct way to measure
-Meds: digoxin*, dopamine (+inotropic to increase contractility) (digoxin: hold if <60, if toxic (S/S: Nausea, pt sees green/yellow halos)
Perfusion-delivery of oxygen rich blood to organs or tissues
-Inadequate tissue perfusion= tissue/cell death: change in cellular function and energy production ultimately leading to organ dysfunction and FAILURE.
-The use of hemodynamic monitoring guides treatment and drug therapy: helps us to know how to treat pt. (CPV tells if FVE FVD)
preload, afterload, contractility, perfusion
low blood volume = poor perfusion
not enough preload = not enough circulation blood
A way to evaluate cardiac function and intravascular volume, pressures, and cardiac function Why do we use hemodynamic monitoring? 1.Diagnosis 2.Decide treatment 3.Evaluate response to treatment Who needs hemodynamic monitoring? -Critically ill patients - ICU -Shock r/t intravascular dry -MODS -ARDS -Cardiac surgery Types: -Arterial lines: can't infuse meds -Central venous pressure: must have central line to read CVP (sits in superior vena cava artery) -Swan-Ganz catheters
hemodynamic monitoring
Provides diagnostic info to rapidly determine hemodynamic pressures, CO, and blood sampling for mixed venous oxygen saturation
-Sits in pulmonary artery
-Measures pulmonary artery wedge pressure - left ventricular
–Normal wedge pressure: 8-12
-Can only get pulmonary artery pressure from swan-ganz*
Measures: CVP, PAP, C.O.
Indications
-Post MI
-Cardiac surgery major surgery
-Resuscitation
- Shock
-Pulmonary Edema
-Oxygen transport: ventilation and perfusion
swan=ganz cath pressure monitoring
Must zero and level these lines
- At least once/shift
- With each major movement
- When change is noticed (map changes 70 –> 30)
Zero and level to Phlebostatic axis
- 4th intercostal space and midpoint of the anterior-posterior chest
- Level of the right atrium
Zeroing:
- If the transducer is higher than your phlebostatic axis, your readings will be low
-If the transducer is lower than your phlebostatic axis, your readings will be high
Zero your lines:
-Once/shift
-If your patient is repositioned
-If you have a questionable reading
zero and leveling lines
if not zero/levels = inaccurate read
*always document whenever you do anything
Can be femoral or arterial - if comes out, will bleed out
Used for:
-*Continuous blood pressure monitoring
-Blood draws-especially ABGs
Indications:
-Vasoactive medications: must need arterial BP (its accurate)
-Cardiovascular instability: need good/accurate/continuous BP
-Unstable blood pressures
*Can not infuse medications into an arterial line
Who puts in an art line?
-Surgeon
-Anesthesiologist
-Respiratory therapist
Sterile procedure
Allen test to ensure both arteries have good blood flow
Complications: infection (always sterile), blood loss-set alarms, impaired circulation-assess CSM and
NM: maintain system, document data continuously (2-4X/hour), monitor trends (can’t treat/intervene with just 1 reading, check with cuff pressure
arterial lines
Catheter placed in the jugular or subclavian vein
Superior vena cava near right atrium
Reflects intravascular fluid volume and ventricular function
Normal=2-8 mmHg*
<2 means fluid volume deficient: s/s of dehydration - give fluids and blood
>8 means fluid volume excess: s/s edema, crackles, high BP, dyspnea
hx heart failure: FVE - have central line, hook up to CVP = 22 (pt is FVE), Dr orders diuretics, CVP =15 now, Dr. stops diuresis r/t kidneys might fail
-CVP range: can be 10-12, not just 12
Who needs CVP monitoring?
-fluid/electrolyte imbalances, heart failure, FVE, septic pt, ARDS, respiratory failure
Distal port (brown)
Must zero every shift or when a change is seen.
Complications: Infection-CLABSI, Thrombosis: blood clots in central lines, can use TPA to open PRN, Air Embolism
-How do you know if your patient has an air embolism?
–Air in system –> goes through vena cava into ventricle: S/S=dyspnea, pain, hypotension, anxiety, confusion
-What should you do if you suspect your patient has an air embolism?
–1st check connections, 2. tighten everything, 3. Trendelenburg to trap air in apex of heart and prevent it from traveling systemically
NM: Maintain system, Document, Monitor trends
Always, always, always compare with your patient’s manifestations. ASSESS.
central venous pressure (CVP)
Arterial line
- Must apply pressure
- Catheter intact
- Monitor for bleeding
Central line: patient must be supine or Trendelenburg
removal of hemodynamic lines
Cardiac output:
-Volume of blood ejected from the heart per minute (L/min)
-effected by heart rate, preload, afterload, contractility
-Normal= 4-8 L/min
Cardiac Index:
-Relates cardiac output to body size
-Normal= 2.5-4 L/min
Cardiac output is affected by changes in heart rate, preload, afterload & contractility
decreases cardiac output: tachycardia, preload, afterload, contractility, hypotension, hypertension, bradycardia
cardiac output and index
must know with hemodynamic line
MAP needs to be greater than 65 to perfuse organs and tissues
SVO2-mixed venous oxygen saturation
-Measures how much oxygen is extracted by the tissues
(tissues fill with fluid –> decreased perfusion –> cell death so no oxygen extracted from cells tissues)
Decreased SVO2 may be R/T
-Decreased cardiac output
-Decreased hemoglobin (if o2 demand is increased, more o2 will be extracted from hgb. If the patient is anemic, less RBC to carry oxyhemoglobin….so less O2 is delivered!
Increased SVO2 may be R/T
-*SEPSIS
mean arterial pressure and SVO2
Inflammation of the pericardium (surrounds heart, protects heart from infection)
Can happen alone or due to a MI
Etiology:
-Idiopathic (95% of cases)- viral?
-Infection
-Autoimmune
-Drugs
-Neoplasm
-Post ICD placement
-MI
-Renal failure
S/S: **Chest pain made worse by breathing deep or laying supine, pericardial friction rub usually, S/S of infection esp if infection was cause
Diagnostic studies: *EKG-ST elevation, Labs-CBC, cardiac enzymes, blood cultures
Treatment: Relief of symptoms, Eliminate infection if present, *NSAIDS, Possibly steroids
- if change position and pain goes away, no heart cath is needed
Pericarditis
