LEC notes Flashcards by Z Q

What are 4 functions of blood?

Oxygenation
Hemostasis
Immune function
Transport

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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

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Hemostasis

Balance between clot formation and clot dissolution

*blood vessels will constrict to reduce bleeding, platelets form platelet plug and coagulation is initiated.

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What is transportation function of blood

blood carries, oxygen, nutrients, hormones and waste products

Made possible by pumping of heart

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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

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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

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Purpose of vitamin K

produces blood clotting factors.

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What is the function of the spleen?

Removes old RBC from circulation,
Helps make RBC,
Filters bacteria,
Stores RBC and platelets

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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

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What is Plasma

Carry RBC, platelets and clotting factors

Contains primary water, plamas protein and globuins, albumin

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What are 3 types of blood cells?

Erythrocytes
Leukocytes
Thrombocytes

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a single erythrocytes can carry how many hemoglobin modules?

1 can carry 300 hemoglobin modules

*hemoglobin gives blood its red color

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What

Thrombocytosis

too many platelets

Body clots alot. RISK for stroke, heart attack, PE

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What are neutropenic precautions?

Set of guidelines to prevent infection in people with low neutrophils

Diet, handwashing, PPE, room restrictions, avoid rectal procedures

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Thrombocytopenia

Too few platelets in blood which can lead to excessive bleeding

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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

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What is the universal donor blood

O-

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What is your universal recipent blood?

AB+

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PRBCS

Packed reb blood cells
Transfuse over 2-4hours
4hr for pt who are worried about circulatory overload
Trauma - super fast even rapid transfusion

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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

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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

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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

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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

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Hemolytic and Febrile reactions to blood will both be shown with

Increase in temp

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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

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What is the 2nd line of defense?

Inflammation and phagocytosis

-Help rid invading microoraganisms

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What is 3rd line of defense?

Specific immune response and Natural killer cells

-Very specific to an organism. Have to have exposure first

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What are 5 types of WBC

Neutrophils
Macrophages
Monocytes
Basophils
Eosinophils

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Neutrophils

Largest portion of WBC
First line of defense
Fight bacteria, infection, inflammation
Short life - 12-18hrs

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Macrophages

From stem cells in bone marrow
Turn into matures monocytes
Surrounds and kills organisms, removes dead cells, stimulates action of other cells

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Monocytes

Can last months to years / largest WBC
Protect against invasion and tissue injury
Phagocytosis
repair injured tissues

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Basophils

Initiate inflammatory response release histamine

defense against allergens, parasites, and pathogens:

0.5-1% of WBC

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Eosinophils

Releases in allergic reactions
help the body fight infections, parasites, allergens, and other foreign organisms

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ANTIGENS

Any substances capable of stimulating a response from immune system (usually foregin)

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Antibodies

Aka immunoglobin
Proteins created in response to antigens so next time ready to fight

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Steps of phagocytosis

Exposure
Attract forgein
Adhere (stick to cell)
Recognition (realize its forgein)
Cellular ingestion (eat cell)
Phagosome formation
Degradation (break into pieces)

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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.

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IgG

in serum and tissues (interstitial fluid)
role in blood borne and tissue infections
Activates the complement system
phagocytosis
Crosses placenta

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IgE

in serum
allergic and hypersensitivity reactions
parasitic infections

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Natural Active immunity

Natural contact with antigen through infection
“Happens naturally, you just get sick”
Chicken pox, mumps, measles

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Natural passive immunity

Passed through placenta to unborn infant or through breast milk (igA)
“Happens naturally”

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Artifical Active immunity

Immunization with antigen
Given an immunization body has to look at antigen and CREATE antibodies aka ACTIVE

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Artifical passive immunity

Injection or infusion of human immune globulin
Body given antibody so no real work = passive

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Inflammatory process
Means?
Causes:
Physical
Chemical
Biological

Means “the fire within” / inflammed
Causes:
Physical - sunlight, xrays
Chemical - venom, other chemicals
Biological - bacterial, viruses

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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.

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Inflammation vs infection

Inflammation - nonspecific reaction to injury
Infection - specific cause to tissue injury, usually bacterial organism

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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

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Autoimmune disease
Treatment

Corticosteroids, NSAIDS, immunosupressive therapy

Adequate rest, hydration, nutrition, prevent infection

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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

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If you run a CBC on a pt with systemic lupus erythematosus what would you see?

Pancytopenia - decrease in all types of cells

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SLE - treatments

Immunosuppressants
Steroids - bad side effects (look them up)
Suppress tissue inflammation

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Acid

Substance that releases hydrogen iron when dissolved in water

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Base

Substance that binds with hydrogen when released in water

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Acidic
Neutral
Alkaline

Acidic 1-6.9
Neutral 7
Alkaline 7.1-14

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What is our bodies natural pH level?

7.35-7.45

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**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

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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

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MUST KNOW!!!!

NORMAL VALUES
pH
pCO2
HCO3
PaO2

pH - 7.35-7.45
pCO2 - 35-45mmHg
HCO3 22-26mEq/L
PaO2 - 80-100mmhg

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What do ABGs tell us

Acid base balance
Oxygenation status

usually from an artery, typically from wrist, usually done by respiratory therapist

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PaO2
Mild hypoxemia?
Moderate
Severe?

Normal - 80-100mmhg
Mild - less than 80
Moderate - less than 60
Severe - less than 40

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How to remember Alkalosis
Acidosis

Alkalosis - KICKING up the pH = greater than 7.4
Acidosis - Down = less than 7.4

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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

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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

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