LEC notes Flashcards
What are 4 functions of blood?
Oxygenation
Hemostasis
Immune function
Transport
How does Oxygenation happen in blood?
Hemoglobin?
RBC transport oxygen from lungs to tissues and CO from tissues back to lungs for excretion.
Hemoglobin contains iron which allows it to pick up oxygen. “Heme” - iron, “globin” - oxygen transport protein
Hemostasis
Balance between clot formation and clot dissolution
*blood vessels will constrict to reduce bleeding, platelets form platelet plug and coagulation is initiated.
What is transportation function of blood
blood carries, oxygen, nutrients, hormones and waste products
Made possible by pumping of heart
Function of bone marrow?
Majority are produced in?
Spongy center of bones where RBC , platelets and WBC’s are made and stored
Majority are produced in vertebrae, ribs, sternum, skull, pelvis, long bones of legs
What is the function of the liver?
Manufacturer clotting factors, albumin, bile (critical in absorption in fat soluable vitamins K, A, E, D).
Cleans and removes dead RBC
Stores large quantities of blood and extra iron
Purpose of vitamin K
produces blood clotting factors.
What is the function of the spleen?
Removes old RBC from circulation,
Helps make RBC,
Filters bacteria,
Stores RBC and platelets
What is the purpose of clotting factors?
Form fiber matrix around wound to protect site while healing / scab
essential for preventing excessive bleeding and forming clots
What is Plasma
Carry RBC, platelets and clotting factors
Contains primary water, plamas protein and globuins, albumin
What are 3 types of blood cells?
Erythrocytes
Leukocytes
Thrombocytes
a single erythrocytes can carry how many hemoglobin modules?
1 can carry 300 hemoglobin modules
*hemoglobin gives blood its red color
What
Thrombocytosis
too many platelets
Body clots alot. RISK for stroke, heart attack, PE
What are neutropenic precautions?
Set of guidelines to prevent infection in people with low neutrophils
Diet, handwashing, PPE, room restrictions, avoid rectal procedures
Thrombocytopenia
Too few platelets in blood which can lead to excessive bleeding
BLOOD TRANSFUSION
5 important things
- Need to have a type and cross match
- Usually good for about 3 days
- Have consent and patient ID
- two nurses MUST verify
- Vitals before, during and after. Nurses stay 1st 15 mins after blood hits
What is the universal donor blood
O-
What is your universal recipent blood?
AB+
PRBCS
Packed reb blood cells
Transfuse over 2-4hours
4hr for pt who are worried about circulatory overload
Trauma - super fast even rapid transfusion
Hemolytic reaction to blood transfusion
Type of reaction
S/S
Time frame
Intervention
Antigen-antibody reaction
S/S: Fever, chills, nausea, dyspnea, chest pain, back pain
Happens shortly after starting
Stop transfusion and notify MD
Anaphylactic reaction to blood
Type of reaction
S/S
Time frame
Intervention
Hypersensitivity reaction
S/S urticaria, wheezing, dyspnea, hypotension
Within 30 mins of start
Stop transfusion, notify MD, prepare epi & steroids
Febrile reaction to blood
Type of reaction
S/S
Time frame
Intervention
Recipients antibodies react to donors leukocytes
S/S fever, chills
within 30-90 mins of starting
Stop transfusion, notify MD
Circulatory overload reaction to blood
Type of reaction
S/S -4
Time frame
Intervention - 4
CV system unable to manage fluid
S/S cough, frothy sputum, cyanosis, hypotension
Anytime during and several hours after
Stop transfusion, get help, prepare to admin O2 and lasix
Hemolytic and Febrile reactions to blood will both be shown with
Increase in temp
What is the 1st line of defense in immune system?
Sweat glands?
Sebacous glands?
Skin and GI tract?
Mammary glands, GI and resp?
Normal flora?
Silia, motility and slough?
Skin and mucous membranes
Sweat glands that secrete lysosomes
Sebacous glands that secrete sebum
acid secretions from skin and GI tract - inhibits pathogens from growting
Secretions from mammory glands and respiratory and GI - contain immunoglobin
Normal flora that helps to keep pathogens from entering
Silia in resp tract and motility in GI. Slough dead skin
What is the 2nd line of defense?
Inflammation and phagocytosis
-Help rid invading microoraganisms
What is 3rd line of defense?
Specific immune response and Natural killer cells
-Very specific to an organism. Have to have exposure first
What are 5 types of WBC
Neutrophils
Macrophages
Monocytes
Basophils
Eosinophils
Neutrophils
Largest portion of WBC
First line of defense
Fight bacteria, infection, inflammation
Short life - 12-18hrs
Macrophages
From stem cells in bone marrow
Turn into matures monocytes
Surrounds and kills organisms, removes dead cells, stimulates action of other cells
Monocytes
Can last months to years / largest WBC
Protect against invasion and tissue injury
Phagocytosis
repair injured tissues
Basophils
Initiate inflammatory response release histamine
defense against allergens, parasites, and pathogens:
0.5-1% of WBC
Eosinophils
Releases in allergic reactions
help the body fight infections, parasites, allergens, and other foreign organisms
ANTIGENS
Any substances capable of stimulating a response from immune system (usually foregin)
Antibodies
Aka immunoglobin
Proteins created in response to antigens so next time ready to fight
Steps of phagocytosis
- Exposure
- Attract forgein
- Adhere (stick to cell)
- Recognition (realize its forgein)
- Cellular ingestion (eat cell)
- Phagosome formation
- Degradation (break into pieces)
Humoral immunity
-Antibody response-
Exposure to foregin invader - B cells lymphocytes turn into plasma cells which manufacture antibodies and release. Antigen antibody binding = agglutination & opsonization, promote release of histamine and other substances in inflamm response. . Get rid of antigen and remember.
IgG
in serum and tissues (interstitial fluid)
role in blood borne and tissue infections
Activates the complement system
phagocytosis
Crosses placenta
IgE
in serum
allergic and hypersensitivity reactions
parasitic infections
Natural Active immunity
Natural contact with antigen through infection
“Happens naturally, you just get sick”
Chicken pox, mumps, measles
Natural passive immunity
Passed through placenta to unborn infant or through breast milk (igA)
“Happens naturally”
Artifical Active immunity
Immunization with antigen
Given an immunization body has to look at antigen and CREATE antibodies aka ACTIVE
Artifical passive immunity
Injection or infusion of human immune globulin
Body given antibody so no real work = passive
Inflammatory process
Means?
Causes:
Physical
Chemical
Biological
Means “the fire within” / inflammed
Causes:
Physical - sunlight, xrays
Chemical - venom, other chemicals
Biological - bacterial, viruses
Signs of inflammation
(5)
Process of inflammation
Rubor - redness
Calor - heat
Tumor - swelling
Dolor - pain
Decrease function
Hemodynamic changes, dilation of cap bed = increase blood flow to area = cause warmth and redness. Increased permeability = things flow in and out of vessels. Chemical mediators cause leukocytes to line blood vessels walls near injured site. WBC inhibit area. Permeability cause fluid to flow into intersitial space = swelling. Prostaglandins, histamins and leukotrines, cytokins, kinin, complement system, - released.
Inflammation vs infection
Inflammation - nonspecific reaction to injury
Infection - specific cause to tissue injury, usually bacterial organism
Autoimmune disease
Immune system reacts against & destroys itself
Genetic factor: tends to be familial
Can involve tissue or organ system
Causes injury in 3 ways:
-Effect of antibodies on cell surfaces
-Deposit of antigen-antibody complexes
- Through action of senitized T cells
Autoimmune disease
Treatment
Corticosteroids, NSAIDS, immunosupressive therapy
Adequate rest, hydration, nutrition, prevent infection
Systemic Lupus Erythematosus
Symptoms
Tachypnea, cough, pleural inflam/effusion
Photosensitivty -rash to areas exposed to sun
Weight loss, fatique, fever, arthritis
Emotional liability,
Butterfly rash over cheeks
Raynauds phenomenon, pericarditis, vascular inflamm
Lupus nephritis - protein uria, hematuria
avoid harsh soaps and substances
*affect women more in childbearing years 20-40
If you run a CBC on a pt with systemic lupus erythematosus what would you see?
Pancytopenia - decrease in all types of cells
SLE - treatments
Immunosuppressants
Steroids - bad side effects (look them up)
Suppress tissue inflammation
Acid
Substance that releases hydrogen iron when dissolved in water
Base
Substance that binds with hydrogen when released in water
Acidic
Neutral
Alkaline
Acidic 1-6.9
Neutral 7
Alkaline 7.1-14
What is our bodies natural pH level?
7.35-7.45
**Buffer system **
Lungs
RESPIRATORY BUFFER SYSTEM
Lungs - retain Carbonic acid in form ofCo2 or by rapid respirations excreting CO2
Can be quick to change respirations
Buffer system
Kidneys
METABOLIC BUFFER SYSTEM
-Retain or excreting NaHCO3
Excreting acidic or alkaline urine
Reabsorbing NaHCO3- or secreting free H+ ions
*Slower than lungs. Can take hours to days
MUST KNOW!!!!
NORMAL VALUES
pH
pCO2
HCO3
PaO2
pH - 7.35-7.45
pCO2 - 35-45mmHg
HCO3 22-26mEq/L
PaO2 - 80-100mmhg
What do ABGs tell us
Acid base balance
Oxygenation status
- usually from an artery, typically from wrist, usually done by respiratory therapist
PaO2
Mild hypoxemia?
Moderate
Severe?
Normal - 80-100mmhg
Mild - less than 80
Moderate - less than 60
Severe - less than 40
How to remember Alkalosis
Acidosis
Alkalosis - KICKING up the pH = greater than 7.4
Acidosis - Down = less than 7.4
Causes of acidosis?
**Respiratory causes ** -HYPOVENTILATION- Things that make them not breathe as well (drug OD, Pulmonary edema, chest trauma, COPD, airway obstruction, over sedation- narcotics)
**Metabolid causes ** - DKA, Salicylate oD, Shock, sepsis, severe diarrhea, renal failure
Causes of Alkalosis?
Respiratory causes: HYPERVENTILATION = Anxiety, high altitudes, pregnancy, fever, hypoixa, initial stages of pulmonary emboli
**Metabolic causes: **loss of gastric jucies, potassium wasting diuretics, overuse of antacids
SYMPTOMS of
RESPIRATORY ACIDOSIS
LUNGS CANNOT GET RID OF ACID (CO2)
Rapid shallow respirations
Decreased bp with vasodialtion
Dyspnea (SOB)
Headache
Hyperkalemia
Dysrhythmias
Drowiness, dizzy, disorientation
Muscle weakness
What is a late sign of hypoxia
What are earlier signs?
Cyanosis
Earlier - tachycardia/tachypnea
Nursing interventions for respiratory acidosis
Maintain patent airway - if OD narcan, intubate
Encourage fluids to decrease secretions
chest physiotherapy
Symptoms of RESPIRATORY ALKALOSIS
Seizures, deep rapid breathing, hyperventilation, tachycardia, decreased for normal bp
Hypokalemia
Numbness and tingling of extremities
Lethargy and confusion
Light headedness
Nausea/vomit
Symptoms of METABOLIC ACIDOSIS
Headache
Decreased BP
Hyperkalemia
Muscle twitching
Warm flushed skin
Nausea, vomit, diarrhea
Changes in LOC
Kussmaul respirations
METABOLIC ACIDOSIS
Treat the cause
DKA
Hypovolemia
Lactic acidosis
Renal
DKA - treat hyper/hypo glycemia
Hypovolemia - volume expanders, blood transfusions
lactic acidosis - oxygen and bicarb
Renal - treat renal failure
Metabolic alkalosis
symptoms
Restlessness followed by lethargy
Dysrhythmias
Compensatory hypoventilation
confusions
Nausea, vomitting, diarrhea
Tremors, muscle creamps, tingling of fingers and toes
hypokalemia
Metabolic alkalosis
Treatement
Check labs, admin potassium, observe for disrythmias, monitor I&O, monitor neurologic changes, treat cause
How do you know if you have an acid or base with normal value of 7.35-7.45 pH
Less than 7.4 = acid
Greater than 7.4 = base
How to know if acid or base of HCO3?
Less than 22 = acid
Greater than 26 = base
How to know if its an acid or base for pCO2
Less than 35 = base
Greater than 45 = Acid
Symptoms of Air Embolism
Chest pain, shortness of
breath
Symptoms of circulatory overload
Shortness of breath, crackles,
chest pain/hyper/hypotension
Symptoms of Sepsis
Malaise, fever, neutrophilia
Signs of hyperglycemia
Polyuria, blurred vision ,
headache
Signs of hypoglycemia from abrupt stopping of TPN
Tremors, abrupt
discontinuation from TPN
Pernicious amenia B!2
-How ppl get it
-How its treated
-Acute/chronic?
-Why need B12
Not absorbed from stomach. Lack of intrinsic factor needed for b12 to be absorbed. Weight loss surgery can take it away or ppl are born without it.
IM injection of Vit 12 (cyanocobalamin) for rest of life
Acute or chronic - body compensates - increase respiratory or circulatory rate to try and circulate more RBCs, tries to increase erythproesis to increase more RBC.
Need b12 to move folicate acid into cell for DNA synthesis and RBC production.
Difference between antiplatelets and anticoagulants?
Antiplatelets - Prevent platelets from clumping together
Anticoagulants - Slow down bodys process of making clots but interfereing with proteins involved in process of making clots
What are antiplatelet drugs?
Ticlopidine HCL / Ticlid
Clopidogrel bisulfate / Plavix
Aspirin
prevent formation of platelet plugs - plavis ticlid / used for heart disease
What are anticoagulant drugs:?
Coumodin / warfarin
Enoxaparin sodium / levonox
Heparin
do not dissolve clots / inhibit new clot formation in venous system and inhibit further growth of existing clots / used in heart disease and stroke prevention
Metabolic acidosis
Low pH due to increased H+ and low bicarb
-gain of H+ or loss of bicarb
In what ways can body lose Bicarb?
Diarrhea, Lower intestinal fistula, diuretics, renal insuff, excessive chlorid, TPN w/o bicarb
In what ways does body excessively accumulate acids?
Lactic acidosis, salicylate poisioning, renal failure, DKA, starvation
Bodys 3 main means of defense?
Phagocytoic immune response
Humoral / antibody response
Cellular response
Stages of a response to an invasion
Recognition stage - lymph nodes or lymphocytes
Proliferation - T and B enlarge and proliferate (T=cytotoxic, B=antibodies)
Response - Function in either humoral or cellular response
Effector - Antibody of humoral response or cytotoxic of cellular response connects with anitgen
Role of antibodies
Agglutionation - Clumping together
Opsionization - removal of offending organisms
Also release of vasoactive substances - histamine, and slow reacting substances
Types of T lymphocytes
Effector T - Helper T (stim rest of immune) & cytotoxic (lysis)
Suppressor T - decrease B cell productions
Memory T- recognize antigen from previous exposure
What cells are apart of humoral?
B lymphocyte - produces antibodies
What cells are apart of cellular immunity
T lymphocytes
Helper T
Supressor T
Memory T
Cytoxic T
Thermal burns
most common type
Causes by flame, flash, scould or contact with hot objects
Severity depends on temp and duration of contact time
**Too hot water, stove / often with children
Chemical burns
Result of a contact with acids, alkalids and organic compounds
Acids can be found in many household cleaners
*dont add water could make worse!! / quickly remove chemical and clothing. Can have tissue destruction up to 72 hours
Electrical burns
Necrosis caused by intense heat generated by electric current
Damage to nerve, vessels, tissue anoxia and death
Enters, goes through body and comes out somewhere else
What tissues offer the most resistances against burns?
Fat and Bone
Nerve and muscles offer least resistance
Electrical injury puts pt at risk for
dysrythmia, cardiac arrest, severe metabolic acidosis, myglobulinuria which can lead to kidney prob
*watch for dysrythmias!! can be delayed up to 24 hours
Smoke inhalation S/S
Soot stinged sputum
Singed nasal hairs
Facial burns blisters
Redness of airway and edema
- can cause damage to rr tract. Major predictor of morality
Metabolic asphyxiation
Carbon monoxide poisioning
Causes hypoxemia and death
How to treat carbon monoxide inhalation?
100% humidified oxygen
Superficial partial thickness
1st degree
Causes
Layer affects
S/S
Appearance
Sunburn, blanching,
Epidermis
S/S - Tingling, pain, peeling, itching
Red, blanches w/ pressure, dry, minimal edema, possible blisters
Partial thickness 2nd degree burn
Causes
Layer affects
S/S
Appearance
From flames, flash and scoulds
Epidermis and portion of dermis
S/S pain, hyperesthesia, sensitive to air
Blistered, mottled, red, weeping surface, edema
Full thickness - 3rd degree
Causes
Layer affected
S/S
Appearance
Flame, prolonged exposure, electric current, chemical, contact
Epidermis, dermis and sometimes subq; may involve connective tissue and muscle
S/S Shock, myoglobinuria (red pigment in urine), and hemolysis, possible entrance and exit wounds
Dry, pale, white, red, brown ,leathery, edema
Full thickness - 4th degree
Causes
Layer affected
S/S
Appearance
Prolonged exposure or high voltage electrical injury
Deep tissue, muscle and bone
S/S shock, myoglobinuria and hemolysis
Charred appearance
Burns phases
Immediate
Emergent
Acute
Rehab
Immediate - at scene
Emergent - 1st 36-48hrs until capillaries heal & fluid resuscitation is complete
Acute - 48-72 hours / diuresis occurs
Rehab- Grafting, PT, OT
Capillary leak syndrome
capillaries become more permeable and fluids leak out
Greatest fluid leak occurs in 24-36hr after injury
BURNS labs
K+
HCT
BUN/CR
ABG
K+ - elevated bc of hemoconcentration and fluid shifts. Possible to see low but typically elevated
HCT -increased due to hemoconcentration
BUN/CR -Elevated
ABG - imbalances
Rule of 9’s
Whole head is 9 - front and back = 4.5%
Torso = 18% each side
Arms = each arm is 9, each side 4.5%
Each leg is 18, 9 for each side
Genitals 1%
The parkland formula
Used for 1st 24 hour after burn injury / fluid replacment
Use Kg X % of TBSA X (2-4ml/per doc) = TOTAL. GIve 1/2 in first 8 hours give the rest in the next 16 hours
Escharotomies
Cut with scalpal bc skin gets so tight
Burn shock
if a burn injury over 20% = a lot of cap permeability
Fluids shift into intersitital = edema and decreased blood volume
Hematocrit increases and blood viscous = peripheral resistanace
Hypovolemic shock / happen rapidly
Shock - define
failure of what 4 things?
Inadequate tissue perfusion
Cardiovascular system failure: circulating blood volume, myocardial contractility, blood flow, vascular resistance
Without perfusion, oxygenattion is compromised and what takes place?
Anaerobic metabolim = lactic acid = metabolic acidosis
Hypovolemic
Define
Causes
Low blood flow - inadequate circulating blood volume which leads to decreased 02 to tissues
Hemmorage, severe diarrhea/vomit, excessive perisperation, intake fluid inadequate
Hypovolemic shock
Absolute
Relative
-Causes of relative
Absolute - circulating blood volume = lost volume
Relative - circulating volume = vessels dilated so not effectively getting around body
Causes = burns, peritonitis, intestional obstruction causes plasma shifting into body tissues = relative
Cardiogenic shock
Define
Causes
Low blood flow due to pump failure
Decreased C/O and Decreased tissue perfusion
Ex. Heart attack, dysrhythmias, valvular disease, myocarditis, cardiomyopathy, structural disorders
**Obstructive Shock **
Define
Causes
Mechanical obstruction to blood flow reducing cardiac output
Tension pneumothorax, cardiac tamponade, pulmonary embolism, things that cause a blockage
**Vasogenic (distributive) shock **
Define
3 types
Vessels, how vessels are reacting
Anaphylaic
Septic
Neurogenic
Symptoms of hypovolemic shock
Diagnosis made when
Increased systemic vascular resistance, poor skin tugor, thirst, oliguria, low systemic and pulmonary preloads, rapid heart rates
Diagnosis made after a loss of 15% intravascular volume
**Vasogenic shock - Anaphylactic shock **
Process
In reaction to something! Chemical mediators dilate blood vessels & increase capillary permeability
Fluid leaks out of caps into tissues
Decreased venous return & c/o
Bronchi constrict/airway obstruction
**Sudden and dramatic **
Vasogenic Shock - Septic shock
Define
Process
Systemic inflammatory reaction to infection
Pathogens release toxins = dilate blood vessels, decrease vascular resistance, increase cap permeability = inadequate tissue perfusion & oxygenation
Results in circulatory collapse
Septic shock treatment
Give fluids first, vasopressors
Septic shock symptoms
Metabolic acidosis
Oliguria
acute enchepalophy
coag disorders
Vasogenic shock - Neurologic shock
Sever brain damage results in collapse of body functions
Usually from brain stem, increase in ICP, cerebral herniation
Causes decrease in venous return and C/O
Bradycardia
Causes of neurogenic shock
Spinal cord injury above T5
Spinal anesthesia
Vasomotor center depression - severe pain, drugs, hypoglycemia
Shock effects on body systems
Respiratory
Acid-base balance
Respiratory - tissue hypoxia and anoxia, resp failure, ARDS
Acid-base - Metabolic acidosis
**Shock effects on body systems **
Immune
GI
Renal
Immune - depressed immune system
GI - decreased peristalisis, ischemia or intestinal submucosa, impaired liver function
Renal - decreased GFR, inadequate perfusion, tubular necrosis
Shock affects on body systems
CV
Neurondocrine
CV - myocardial depression, DIC
Neuro - release of catecholamines, mineralcorticoids, glucocorticodis, ADH
Decreased LOC when cerebral blood flow falls
Stages of shock
Initial
Compensatory
Progressive
Refractory
Initial stage of shock
Pt may not have clinical manifestations of decreased tissue perfusion
Lack of O2 occuring at cellular level
May have a decreas in MAP 5-10mmhh
HR will increase
Compensatory stage of shock
Decreased CO2 triggers neural, endocrine & chemical compensatory responses to overcome anerobic metabolism & maintain blood flow to vital organs
Increase in sympathetic nervous system = increase hr, constriction of peripheral vessels, decreased flow to kidneys, lungs, skin, muscles and GI tract, increased water and sodium retention, decrease blood pH and increase arterial Co2 = **resp increase resp rate and depth. **
Compensatory stage symptoms
Anxiety, restlessness, BP can remain normal, may decrease, pulse increases, tachycardia (unless in neuro). increase rr, decreased urine, skin cool and pale (warm and dry with septic) decrease bowel sounds, blood glucose increase, thirst
Progressive stage of shock
Compensatory mech function independently instead of cooperatively
Sluggish blood flow, clumping of cells, deprived of O2, increase in lactic acid and metabolic acidosis
**
Progressive shock symptoms
Listless confusion
BP drop (indication from compensated to decomp)
Pulse - weak, thready, tachycardia, dysrhythmias
Resp - increased, deep, crackles
Temp - subnormal
Irreversible (refractory) stage
Tissue perfusion deteriorates
Coronary artery perfusion reduced
Ischemia and dysrhythmias
Cerebral ischemia
Shock treatment basics
Airway
Breathing
Circulation
Airway basics
Intubation / ariway protection
Watch LOC, loss of gag reflex, severe bronchospasm
Breathing basics
Adequate 02
Mechanical vent
Watch for hypoventilation, hypoxia, pulm edema
Circulation basics
Main issue poor perfusion
Hypovolemia - IV fluids that increase vascular spaces
Vasopressers will not work without IV fluids
Watch for Arrythmias
Generally, in cardiogenic or neurogenic may not give fluids
What do Colloids do
Crystalloids?
Colloids - remain in vascular system and draw fluid INTO blood stream
Crystalloids - replace fluid and electrolytes
Pharamcologic agents used to increase BP
Dopamine
Dobutamine
Norepinephrine
Epinerphrine
Vasopressin
Meds used to decrease BP during shock
Nitroglycerin
Nitroprusside
Interventions - pt in shock with decrease C/O
Hemodynamic monitoring - vitals
Inotropic and antidysrhythmic agents
Reduce 02 consumption - gentle handling and coordinating care
Maintain adequate body heat; prevent shivering
Central venous pressure
The pressure created by volume in the right atrium
Preload
Define
Measured as
Increased in:
The amount of blood in ventricles at end of diastole
Measured as a / volume indicator
increased in: hypervolemia, regurgitation of cardiac valves, heart failure
Afterload
Define
Increased in
Resistance left ventricle must overcome to circulate blood
Increased in: hypertension, vasoconstriction
Increased AFTERLOAD = increased CARDIAC WORKLOAD
How can we influence afterload?
Dilating vessels
Constriction of vessels
What does it mean when afterload is high?
low?
Resistance is high and the heart works harder to pump
Resistance is low and heart is not working heard to eject blood
In septic shock, its all about vessles so we can use things like ____to increase afterload and bp?
vasopressors
Why would you want to increase afterload?
Septic shock
Stroke volume
Amount of blood ejected by ventricles with each systole
Cardiac output
Define
Normal
Amount of blood in liters / minutes pumped by ventriles
Normal - 4-8 L /min
Mean Arterial Pressure
Define
Formula
Goal
The average pressure in a pt arteries during one cardiac cycle
*Considered better indicator of perfusion to vital organs than BP
MAP = SBP + 2 (DBP) /
3
*usually 65
Pulmonary Capillary Wedge Pressure
Indirect measure of volume in left ventricle
Contractility
Define
Drug to increase?
Hearts ability to produce force during contraction
May use dobutamine to increase contractility
