hemodynamic notes

8/2/2019 Hemodynamic Notes

1/14

Chapters 41 & 42Hematologic Problems

Anemia

Reduction in either the number of red blood cells, the amount of hemoglobin, or the hematocrit Clinical sign (not a specific disease); a manifestation of several abnormal conditions

Average number of RBCsper cubic millimeteris 4,400,000 to 5,200,000 Each RBC contains nearly 300 million hemoglobin molecules. Each can carry 4 O2

molecules

When, for any reason, the hemoglobin content in the bloodstream dips below theminimum for body needs, the result is anemia, meaning (although not literally) "no

blood." Anemia is a reduction in the number or volume of RBCs. This reduction in RBCs

results, obviously, in a reduction in the amount of hemoglobin and, therefore, in a

reduction in the body's oxygen-carrying capacity. Another cause of anemia could be a

diet deficient in iron-rich foods.

Explain Hematocrit method to include Buffy Coat Layer. Spin 3000rpm, 3 min(Hemoglobin is generally the Hematocrit divided by 3)

Hct (%)= (0.0485 x ctHb (mmol/L) + 0.0083 x 100Cardiovascular Effects of Anemia

Desaturation, Dyspnea, Fatigue, Hypotension, Headache, Pallor & Tachycardia.

(Dizzy, Devious Fat Harold Had Peaches & Tomatoes.)


2/14

Anatomy and Physiology Review

Bone marrow Red blood cells (erythrocytes) White blood cells Platelets

Accessory Organs of Blood Formation

RBCs are terminally differentiated; that is, they can never divide. RBCs live about 120 days and then are ingested by phagocytic cells in the liver and spleen. Most of the iron in their hemoglobin is reclaimed for reuse. The remainder of the heme portion of the molecule is degraded into bile pigments and excreted

by the liver.

Some 3 million RBCs die and are scavenged by the liver each second. Erythropoietin (EPO), produced by the kidneys, enhances the production ofred blood cells

(RBCs).

Blood Cell Differentiation


3/14

Review of RBC Growth Cycle

Hemostasis/Blood Clotting

o Platelet aggregationo Blood clotting cascadeo Intrinsic factorso Extrinsic factorso Fibrin clot formation

Review of Platlet Growth Cycle


4/14

Platelets and Blood Clotting

Hageman (Intrinsic Pathway)(12)-- D-Dimer (Extrinsic Pathway)

VonWillebrand (Platelet Adherence to wall) (8)

Heterodimer (Tf)

Alterations to Clotting Cascade


5/14

Intrinsic Factors = Within the blood

Extrinsic Factors = Outside the blood (trauma, shape & smoothness of capillary

HemophiliaFactor IX

Coumadin works on Factor X

HeparinFactor Xa---> Factor V

Anticlotting Forces


6/14

Assessment Critical Foci

Patient history Functional Patterns

Activity Intolerance Nutrition-Metabolic Pattern

Types of food Medications (see Table 41-3)

Respiratory & Cardiac AssessmentDrugs

Anticoagulantsinterfere with steps in blood clotting; limit or prevent extension of clots andprevent new clots

Fibrinolyticsselectively degrade fibrin threads in the formed blood clot Platelet Inhibitorsprevent platelets from becoming active or activated platelets from clumping

together

Aspirin & PlavixPhysical Assessment

Skin Head and neck Respiratory Cardiovascular Renal and urinarybleeding, ESRD & EPO Musculoskeletal AbdominalSpleen size, GI Bleed Central nervous systemRestlessness, Headache PsychosocialCoping, Support Nutritional status Family history and genetic risk Current health problems

Co-Morbidities Anemia as a Sign & Symptom of a Disease


7/14


8/14

Story of Sickle Cell Crisis at High Altitude Bolivia or anesthesia

Sickle Cell Disease: Pathophysiology

Normally, Sickled cells return to normal shape when low O2 condition is reversed

Main problem of the disorder is formation of abnormal hemoglobin chains Response to local or systemic hypoxia

RBCs sickle, decrease o2 carrying capacity & clog capillaries Sickle cell crisis

Symptomatic after enough capillaries shut down Incidence/prevalence

In the Unites States, around 72,000 people are symptomatic with the disease The disease occurs in about 1 in every 500 African-American births and 1 in every 1000

to 1400 Hispanic-American births 2 million Americans, or 1 in 12 African Americans, carry the sickle cell trait.

Sickle Cell Disease: Clinical Manifestations

Cardiovascular changes Heart Failure SOB & Fatigue


9/14

Skin changes Cool, Pallor or Cyanosis, Clubbing

Abdominal changes Pain, firm large lumpy liver & spleen

Renal and urinary changes Priapism Chronic Kidney Disease

Musculoskeletal changes Pain & Ulcers

CNS changes Fever, Infarcts, Seizures & Gait Disturbances

Sickle Cell Disease: Assessment

Besides assessing for the system changes common to SCD Assess Level, Location, Character and Duration of Pain Assess mental status changes O2 Saturation Levels Family and Patient Coping Mechanism and Support Systems

SCD: Laboratory Assessment

Hemoglobin S (HbS) < 1% for those without SCD 5% - 50% for those with SCD Trait May exceed 90% for those with SCD

Number of RBCs with permanent sickling Hematocrit

Low Reticulocyte count Elevatedanemia of long duration Total bilirubin

ElevatedRelease from damaged RBCs Total white blood cells

Elevated Imaging assessment

Crew-cut skullSickle Cell Disease: Interventions

Pain is the most common problem: Drug therapy48 hours of IV analgesics


10/14

O2 Therapy Hypotonic IV & Oral hydration Complementary and alternative therapies (Warm & Calm) TransfusionsAvoided Fe Overload

Goals of Treatment--- Chart 42-3 Pg. 898

Management of vaso-occlusive crisis Management of chronic pain syndromes Management of chronic hemolytic anemia Prevention and treatment of infections Management of the complications and the various organ damage syndromes associated

with the disease

Prevention of stroke Detection and treatment of pulmonary hypertension

Sickle Cell Interventions: Potential for Sepsis

Interventions include: Prevention and early detection strategies spleen often non-functional

Excellent Infection control practices (Handwashing) for all family & care-givers Drug therapy

Prophylactic BID PCN Acute chest syndrome. Similar to pneumonia, this life-threatening complication is caused by

infection or trapped sickled cells in the lung. It is characterized by chest pain, fever, and an

abnormal chest X ray.

Sickle Cell Disease Interventions: Potential for Multiple Organ

Dysfunction

Interventions include: Hydration (200ml/hr) Oxygen therapy (Monitor ABGs) Transfusion therapy (Cautiously)

Goal to dilute the HbS levels Monitor patients FE levels closely Desfereral drug of choice

Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency Anemia


11/14

Most common type of inherited hemolytic anemia G6PD necessary for the RBC to produce energy to survive normal life expectancy Effect of exposure to some drugs, benzene and other toxins Screening for this deficiency necessary before donating blood, because cells deficient in G6PD

can be hazardous

Hydration Osmotic diuretics Transfusions ------RBCs break

RBC Indices

MCV Mean Corpuscular Volume MCH Mean Corpuscular Hemoglobin MCHC Mean Corpuscular Hemoglobin Concentration RDW Relative Distribution Width

Iron Deficiency Anemia (Microcytic)

This common type of anemia can result from blood loss, poor intestinal absorption, orinadequate diet.

If mildsymptoms of weakness and pallor. Evaluate adult patients for abnormal bleeding, especially from the GI tract. Treatmentincreasing oral intake of iron from food sources, oral iron supplements, or IM iron

solutions.---Z-track

Factors Influencing Fe Absorption

Calcium competes with iron for absorption Substances that diminish the absorption of ferrous and ferric iron include phytates, oxalates,

phosphates, carbonates, and tannates

Starch and clay eating produce malabsorption of iron and iron deficiency anemia (Pica) Low gastric acid conditions whether naturally occurring (Celiac Disease), surgically or medication

induced.

Extensive surgical removal of the proximal small bowel or chronic diseases (eg,untreated sprue or celiac syndrome) can diminish iron absorption

Vitamin B12 Deficiency Anemia (Macrocytic)

Lack of vitamin B12 causes improper DNA synthesis of RBCs. Poor intake of foods containing vitamin B12, small bowel resection, tapeworm, overgrowth of

intestinal bacteria.

Glossitis smooth beefy tongue


12/14

Fatigue & wt loss Paresthesias hands & feet, poor balance Weight loss surgery

Pernicious Anemia

Same as pervious slide except due to specific cause Anemia resulting from failure to absorb vitamin B12 Caused by a deficiency of intrinsic factor

Folic Acid Deficiency Anemia

Manifestations similar to those of vitamin B12 deficiency, but nervous system functions remainnormal

Common causespoor nutrition, malabsorption (Crohns), alcoholism and drugs Green Leafy, Liver, Beans & Nuts

Aplastic Anemia Deficiency of circulating RBCs because of failure of the bone marrow to produce these cells Injury to the pluripotent stem cell Pancytopenia common Treatment:

Blood transfusions Immunosuppressive therapy Splenectomy

Polycythemia VeraCancer of the RBCs

Disease with a sustained increase in blood hemoglobin or hematocrit Massive production of red blood cells Excessive leukocyte production Excessive production of platelets Treatment:

Phlebotomy Hydration Anticoagulants

Myelodysplastic Syndromes


13/14

Group of disorders caused by the formation of abnormal cells in the bone marrow Blood and platelet transfusions Erythropoietin Chelation therapy Drugs for iron overloaddeferasirox and deferoxamine mesylate

Transfusion Therapy

Pretransfusion responsibilities to prevent adverse transfusion reactions: Verify prescription. Test donors and recipients blood for compatibility. Examine blood bag for identification. Check expiration date. Inspect blood for discoloration, gas bubbles, or cloudiness.

Transfusion Responsibilities

Provide patient education. Assess vital signs. Begin transfusion slowly, and stay with patient first 15 to 30 minutes. Ask patient to report unusual sensations such as chills, shortness of breath, hives, or itching. Administer blood product per protocol. Assess for hyperkalemia.

Blood Typing

llele from

Parent 1

Allele from

Parent 2

Genotype of

offspring

Blood types of

offspring

A A AA A

A B AB* AB

A O AO A

B A AB* AB

B B BB B

B O BO B


14/14

O O OO O

Human blood type is determined by co-dominant alleles This makes six different genotypes. Rh Pos or Neg makes 12 different blood types

Types of Transfusions

Red blood cell Platelet Plasmafresh frozen plasma Cryoprecipitate Granulocyte (white cell)

Transfusion Reactions Febrile transfusion reactions Hemolytic transfusion reactions Allergic transfusion reactions Bacterial transfusion reactions Circulatory overload Transfusion-associated graft-versus-host disease

Autologous Blood Transfusion

Collection and infusion of patients own blood Eliminates compatibility problems; reduces risk for transmission of bloodborne disease Types:

Preoperative Acute normovolemic hemodilution Intraoperative autologous transfusion Postoperative blood salvage

hemodynamic notes

Documents