Cardiovascular 3 Flashcards
Rh System…. (-) & (+) can receive which type of blood?
(-) cannot receive (+) blood
(+) can receive ANY blood
Homologous transfusion
receiving the same type of blood as your own
Autologous
donating blood to yourself
Why is whole blood given?
- to treat massive blood loss
- to increase blood volume — O2 carrying capacity of RBCs and volume expansion of plasma
Why are packed RBCs given?
- increase the O2 carrying capacity without volume expansion
- this must be ABO specific and Rh specific
- for symptomatic anemia, blood loss with symptoms
1 unit of blood is how many g/dl increase in hgb?
1 unit is approximately 1 g/dl increase in hgb
Platelet Pheresis
- to control or prevent bleeding caused by thrombocytopenia
- usually not given until counts are under 10,000 unless symptomatic
Fresh frozen plasma
- to increase clotting factors in pts w/ a deficiency (DIC, hemorrhage, liver disease, vit k deficiency, excess coumadin)
- contains coagulation factors in normal amounts
Cryoprecipitate
- cryo is removed from FFP and contains clotting factors
- all groups acceptable
Things to do before administration…
- confirm MD order
- check for type/cross match
- consent
- 2 NURSES confirm at the patients bedside
What is the only solution blood can be administered with?
Normal saline —no additive. (500 ml bag)
How long until the bag of blood must go back to the blood bank if not used?
30 minutes
Vital signs must be checked how often when administering blood?
check before and 15 minutes after bc usually transfusion rxns will happen within the first 15 mins of transfusion.
Blood transfusion must be completed within how many hours?
4 hours
What do you do when a transfusion rxn is suspected?
- STOP the transfusion
- hang new NS bag and run at KVO
- notify MD and blood bank and send whole thing back to blood bank
- obtain VS stat, document and assess
Acute Hemolytic Rxn
- usually from ABO incompatibilty
- low back pain, chills, pain at IV site, blood in urine
- prevent by verifying blood products, start slowly and check pt
Febrile Non-hemolytic rxn
- sensitive to leukocytes in blood
- chills, increase in temp over 2 dgrees
- prevent by premedicating with bendryl or antipyretic
Mild Allergic rxn
- sensitive to plasma proteins
- hives, pruritis, wheezing, hypotension
- prevent with pre-medicating with steroids or antihistamines
Anaphylactic Rxn
- rxn to pre-existing antibody in donor blood product
- respiratory distress and wheezing, severe hypotension/shock
- occurs with small amount of transfused blood
Circulatory overload rxn
- occurs with decreased cardiac function
- cough, chest and back pain, dyspnea, cyanosis
- prevent with pre-medicating with diuretics, transfuse slowly, monitor I&O
Bacterial sepsis Rxn
- bacterial contamination of blood product
- severe chills, high fever, N/V, hypotension
- prevent with checking blood product for bubbles, cloudiness, sediment prior to starting infusion
TRALI rxn
- transfusion related acute lung injury
- due to donor WBC antibodies
- severe chills, hypotension, hypoxemia, pulmonary edema without cardiac or pulmonary failure
Delayed Hemolytic rxn
- re-exposure to antigen in transfusion
- hgb drops
- fever, jaundice, and decreased hgb
3 main causes of anemia
- blood loss
- decreased production of erythrocytes
- increased destruction of erythrocytes
Anemia
- is not a specific disease, its a result of a disease
- classified by how big they are or by what causes it
- deficient number of erythrocytes, hgb, hct, and results in a decrease in oxygen transport and hypoxia
Mild Anemia
- may have no symptoms
- may have fatigue, dyspnea, palpitations
Moderate Anemia
- symptoms at rest or with activity
- ASK…if they are rested when they wake up
- dyspnea, fatigue, pallor, tachycardia/palpitations
Severe Anemia
- Involves many body symptoms
- many s/s
- eventually pulmonary congestion which could lead to HF (bc trying so hard to perfuse organs and can wear out)
General body responses to anemia
- sensitivity to cold
- wt loss
- fatigue
- pallor
- glossitis
- jaundice and pruritus
Cardiovascular response to anemia
- heart and lungs attempt to provide adequate oxygen to tissues
- maintain CO by increasing HR and SV
- MI and HF may happen
Anemia work up
CBC- (rbc, hgb, hct, reticulocytes) are all low
TIBC, ferritin, serum iron, and transferrin to see if iron is the cause
Treating Anemia
- correct cause of anemia
- O2 therapy
- volume replacement
- blood/blood products
- drug therapy (procrit)
When Hgb is below 8….
the patient is immediately put on 3L of O2
Anemia and Aging…
- anemia may go unrecognized and mistaken for normal aging
- common s/sx: pallor, fatigue, malabsorption, dietary insufficiency, renal insufficiency
Iron Deficient Anemia
-one of the most common hematological disorders
susceptible populations: pregnant and menstruating women, infants, children, adolescents. poor diets
Iron deficiency anemia causes
- inadequate dietary intake - 5-10% ingested absorbed
- malabsorption - absorbed in duodenum
- blood loss (2 ml whole blood contains 1 mg iron)
Signs and Symptoms of Iron deficient anemia
-pallor is the most common
-glossitis is the second most common
cheilitis-cracked inflamed lips
Tx of Iron deficient anemia
- treat underlying process (intake or absorption)
- diet increase in iron
- oral supplements
- parenteral supplements- IV or IM
- transfusion of packed RBCs
Megaloblastic Anemias
group of disorders characterized by large and abnormal RBCs
- due to impaired synthesis, defect RBC maturation, large fragile cell membrane
- MAJORITY due to vitamin deficiencies (B12 and folic acid)
Megaloblastic Anemia: Cobalamin (B12) deficiency
- Most common cause is pernicious anemia
- gastric mucosa is not able to secrete intrinsic factor (so B12 cannot be absorbed)
- can be due to gastric surgery or disorders
- long term use of antacids
Signs and symptoms of B12 deficiency
- glossitis, anorexia, NV, abd pain
- Neuromuscular manifestations - impaired production of myelin on nerves (muscle weakness, paraesthesias of hands and feet)
Diagnostic studies for B12 deficiency
- low CBC
- MCV elevated (big cells)
- Positive shillings test
- gastric biopsy bc risk for gastric CA
Best diagnostic study for B12 deficiency
positive SHILLINGS TEST
If not treated for B12 deficiency
-pt will die in 1-3 yrs
-neuromuscular damage can be permanent
-increasing oral intake does not help bc you’re not absorbing it
-lifetime maintenance will be needed of monthly B12 shots
evaluation for gastric CA needs to be monitored frequently
Folic Acid deficiency
- very common
- can be due to dietary insufficiency, chronic alcoholism, malabsorption, meds
- needed for DNA synthesis and erythropoiesis
Signs and Symptoms of folic acid deficiency
- slow and insidious onset
- people appear thing, emaciated and ill
- malnourished
- related to neural tube defects
- very similar to B12 deficiency but no neuromuscular defects
Diagnostic studies for folic acid deficiency
- low H/H
- MCV high (large and abnormally shaped)
- low serum folate
- Negative shillings test
Tx for folic acid deficiency
- folic acid po 1 mg/day
- multivitamin
- well balanced diet - potatoes, veggies and fruits, dairy
- AA for alcoholics
Normocytic Anemia
- underproduction of RBCs
- RBCs survive less than 120 days
- causes are chronic liver disease and malignant tumors
Treatment for normocytic anemia
- treat the underlying cause
- blood transfusion
- erythropoietin therapy (procrit, Aranesp)
Aplastic Anemia
- impaired production of RBCs
- bone marrow is severly hypocellular
- pancytopenia develops
- can be congenital or acquired
- can be fatal if bone marrow does not regenerate after offending agent is removed
Pancytopenia
low counts of RBCs, WBCs, and platelets
Cause of Aplastic Anemia
- onset insidious or rapid
- primary congenital
- secondary: chemicals, drugs, viral/bacteria; rxn
- all ages/sexes affected
Signs and symptoms of Aplastic anemia
- pt critically ill (bc no cells in the body)
- pallor, fatigue, dyspnea, palpitations
- susceptible to infection , fever due to low WBCs
- prone to bleeding/bruising due to low platelets/thrombocytes
Diagnosis of Aplastic anemia
- normal size just not enough
- neutropenia, thrombocytopenia
- low reticulocyte count
- bone marrow exam
Bone marrow exam for aplastic anemia
- hypocellular so….
- “dry tap”…due to low counts of everything
- done on the posterior iliac crest
Tx for aplastic anemia
- stop offending agent
- blood transfusions
- immunosuppressive therapy
- hematopoietic stem cell transplant (young ppl)
- poor prognosis if untreated
- prevent the complications of pancytopenia (anemia, hemorrhage, infection)
Acute blood loss anemia
- result of sudden hemorrhage (hypovolemic shock, hypoxemia)
- signs and symptoms are more important than lab values
- major complication is shock
Acute blood loss treatment
- replace volume (IV NS or LR)
- ID and stop the bleeding source
- body needs 2-5 days to replace loss
- take iron supplements
- usually no long term therapy needed once fluid and blood volumes are replaced (once fixed then pt is fine)
Anemia of chronic blood loss
- chronic blood loss: ulcer, colon cancer, dysfunctional utero bleeding
- similar symptoms to iron deficient anemia
- iron stores depleted (may need supplement)
- manage by stopping the bleeding
Hemolytic Anemia
- destruction or hemolysis of RBCs at rate that exceeds production
- hereditary or acquired
- hemolysis occurs
- macropahges destroy old, defective RBCs
- bilirubin levels rise
Signs and symptoms of Hemolytic Anemia
- jaundice
- enlarged spleen and liver (all of the broken down RBCs are sitting in these organs)
- possible tubular necrosis ( kidneys fail bc broken down RBCs clog it up)
- low H/H
- increased reticulocyte count bc body is trying to make more RBCs
Tx of Hemolytic Anemia
- possible splenectomy
- blood transfusion
- corticosteroids (suppress spleen from recognizing and destroying RBCs)
- adequate IV fluids to flush kidneys
Hemochromatosis
- too much iron in the blood
- inherited disorder
- increased iron absorption and deposition into tissues
- liver enlarges and develops cirrhosis
- skin is bronzed
- elevated serum iron
- treat with phlebotomy (reverse transfusion -forever)
Polycythemia
Polycythemia Vera (primary: excessive bone marrow production of erythrocytes leukocytes, and platelets)—at risk for clot formation
Secondary: due to chronic hypoxia.(high altitude, COPD, CV disease)
-low O2 stimulates erythropoietin production in kidney
Signs and symptoms of Polycythemia
- HTN (dizzy, HA, tinnitus, visual disturbance)
- pruritus
- overfull blood vessels
- increased clotting/thrombus with complications
- enlarged liver and spleen
- elevated blood cell counts
Tx for polycythemia
- reduce blood volume and viscosity
- reduce bone marrow activity
- phlebotomy -300-500ml removed every other day
- hydration to thin out blood
- myelosuppressive agents
- low dose aspirin
Bone Marrow
- soft material in the core of the bone
- red marrow produces blood cells
- marrow is able to respond and meet the body’s demands
- produces hematopoietic stem cells that mature and differentiate to become rbc, wbc, and platelets
Hematopoiesis
- blood cell production
- occurs in red marrow of flat irregular bones (sternum femur, ribs, pelvis, etc)
arterial blood is…
bright red
venous blood is…
dark red
3 major functions of blood
- transportation: of oxygen, nutrients, hormones, waste products
- regulation: fluid, electrolytes, acid-base balance
- protection: clotting, combat infection
Plasma
- composed of water, proteins,electrolytes, gases, nutrients and wasre
- serum is plasma without clotting factors
Erythropoiesis/erythropoietin
- stimulated by oxygen requirements (hypoxia)
- erythropoietin is released by the kidney then stimulates bone marrow to increase RBC production
Essential nutrients needed to produce healthy RBCs
iron, B12, and folic acid
RBCs last for how many days?
120 days
Reticulocyte
immature RBC
- mature into erythrocyte w/in 48 hours of release
- reticulocyte count measures rate at which RBCs appear in circulation
Hemolysis
- erythrocyte destruction
- occurs in bone marrow, spleen, liver
- macrophages remove the abnormal/defective/damaged RBCs from circulation
- hemoglobin is destroyed and heme to bilirubin and iron is recycled
Leukocytes
2 classes: granulocytes (neutrophils, basophils, eosinophils) and agranulocytes (monocytes and lymphocytes)
First and second responders injury site
1) Neutrophils
2) monocytes
Bands
immature neutrophils
-shift to the left refers to increase in number of immature wbcs called to fight severe infection
Eosinophils
formed during allergic response to allergen
defense against parasitic infections
Basoohils
Allergic AND inflammatory reactions
-release heparin, serotonin and histamines
Lymphocytes
- responsible for immune response
- B and T cells
Monocytes
- potent phagocytic cells
- engulf bacteria, dead cells, tissue debris, defective RBCs
- second to arrive at injury
Thrombocytes
- aid in clotting
- must have enough and be functional
- activated at site of tissue or vessel damage
Lymph system
- works through diffusion
- carries fluid from interstitial space to blood, preventing edema (fluid is pale yellow)
- lymph capillaries carry fluid to lymphatic duct or thoracic duct
- lymphatic duct drains into subclavian veins
- lymph nodes filter bacteria and foreign particles
Lymphadenopathy
- disease of the lymph nodes
- also used to indicate enlarged lymph nodes
Lymphangiography
- radiologic visualization of the lymph system after injecting contrast medium
- lymph node angiography after injection of the blue dye in the webbing of your toes
Lymphadenitis
inflammation of one or more lymph nodes
Lymphangitis
inflammation of one or more lymphatic vessels
-can be caused by cats
Lymphedema
- tissue swelling from lymph accumulation due to obstruction
- develops when there is interference with the reabsorption of fluid or increase in lymph fluid
Spleen
- Located in LUQ of abdomen
- produces RBCs during fetal development
- removes old and defective RBCs from circulation
- returns iron from hgb to the bone marrow for reuse
Liver
RUQ
stores iron
produces anticoagulants (vit K) essential to hemostasis and blood coagulation
Affects of aging on blood production
- stem cells decrease with age and are replaced with fat cells
- usually anemic and difficulty fighting infection
- platelets unaffected- easy bruising related to changes in vascular integrity
MCHC
saturation of RBCs with Hgb (how well you’re carrying O2)
MCV
size of RBCs
What diagnostic study must be done to confirm any blood disorder?
Bone marrow study/biopsy
what must happen after bone marrow biopsy
- pressure dressing,
- 5-15 min pressure to site
- frequent VS
- must be hand delivered to lab
Thrombocytopenia
reduction of platelets below normal level needed for clotting
- disorders can be inherited, most acquired
- decreased production— viral, drugs/etoh, radiation, aplastic anemia, food herb ingestion, bone marrow suppression or failure (chemo)
Signs and Symptoms of thrombocytopenia
- epistaxis -petechiae - ecchymosis - purpura
- most asymptomatic
- most common symptom is bleeding. major complication is hemorrhage (weakness, fainting, dizziness, tachycardia, abd pain, hypotension)
Systemic vascular resistance
the force opposing the movement of blood
–specifically the diameter/radius of blood vessels
If SVR increases and CO increases or stays the same then what will happen to BP
it will increase
Sympathetic Nervous System
(fight or flight)
a decrease in BP activates the SNS w/in seconds/minutes
—-increasing HR, contractility. stimulates vasoconstriction and promotes release of renin from kidneys
SNS: Baroreceptors
when BP rises baroreceptors (stretch receptors) are stimulated. inhibitory impulse sent to the sympathetic vasomotor of the brainstemm.
dilates arterioles, decreases HR, contractility. CO lowers and BP lowers….when BP SNS activated again.
Renal System and BP
Kidneys help with B by regulating Na and fluid volume. drop in BP causes Na/water to be retained (aldosterone). results in increase in extracellular volume. so there is an increase in venous return, SV, CO & BP
RAAS
decrease in blood flow through kidneys-> renin secreted by kidneys and converts angiotensinogen to angiotensin 1. ACE converts angoiotensin 1 to angiotensin 2 (vasocontrictor). Angiotensin 2 stimulates the adrenal cortex to secrete aldosterone which tells the body to hold onto Na/fluid
Endocrine system and BP
SNS-> epi/norepi
increase in HR and contractility and CO
vasocontricts
stimulates adrenal cortex to release aldosterone
ADH released from pituitary gland to increase fluid amount
When to treat high BP with meds….
> 60 150/90
<60 140/90
MEDSS GIVEN REGARDLESS OF LIFESTYLE CHANGE
Systolic HTN
SBP >140. DBP fine
more common in older adults
loss of elasticity in arteries
Pseudo-HTN
- seen in atherosclerotic vessels.
- sclerotic arteries don’t collapse when cuff inflated so BP is artificially elevated
- suspect when are rigid or other cardiac signs found
- only way to measure is intra-arterial catheter
Primary HTN
elevated BP without identified cause
—most cases are primary
Secondary HTN
HTN identified and correctable cause (pregnancy, illegal drug use)
can lead to HTN crisis
tx: eliminate the underlying cause
Age-related changes and HTN
- loss of tissue elasticity
- increase in vessel collagen (dont dilate as well)
- Increased SVR and PVR
- baroreceptors less sensitive to stimulus
- decrease in renal function (hold onto fluid)
- decrease renin response and sodium/water depletion
- altered absorption/metabolism of HTN meds
Signs and symptoms of HTN
Most common…NOTHING. until end organ disease
Secondary: fatigue, dizzy, palpitations, angina. dyspnea
3 characteristics that tell you you’re in a HTN CRISIS
- early am HA
- blurred vision
- epistaxis
HTN complications on organs
- left ventricular hypertrophy
- more risk for stroke
- renal failure
- vision
HTN tx
1 MEDS!
- lifestyle changes
- wt reduction
- sodium restriction
- moderate alcohol
- avoid smoking
- DASH diet
Drug therapy for HTN in non-blacks
Begin HCTZ (diuretic)
CCB
ACE inhibitor
ARB
Drug therapy for HTN in blacks (including diabetics)
HCTZ
CCB
-ace inhibitor not as effective/ greater risk for CVA risk than CCB
CKD- add ace inhibitor or ARB
