Cardiac Anatomy & Physiology

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Cardiac Anatomy & Physiology

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Cardiac Anatomy & Physiology. The Heart. Hollow, four chambered, muscular organ. The heart is found in the mediastinum between the right and left lungs. The four chambers are subdivided 2 atria (right & left) 2 ventricles (right & left). Atria. - PowerPoint PPT Presentation

Transcript of Cardiac Anatomy & Physiology

Cardiac Anatomy & Physiology

The Heart

Hollow, four chambered, muscular organ. The heart is found in the mediastinum

between the right and left lungs. The four chambers are subdivided

2 atria (right & left)2 ventricles (right & left)

Atria

Each atrium has thin-walls and is separated by the interatrial septum.

The atria act as collecting or holding chambers.

Ventricles

Each ventricle has thick muscular walls and is separated by the interventricular septum.

The ventricles act as pumps.The right ventricle pumps the unoxygenated blood

from your organs and tissues to the lungs.The left ventricle pumps the oxygenated blood

from your heart to your organs and tissues.

Circulation

The vasculature of your lungs is called pulmonary circulation.

The vasculature that supplies the heart with oxygen and nutrients is called coronary circulation.

The vasculature of all of your organs and tissues (everything besides your lungs and heart) is called systemic circulation.

Circulation

The right ventricle is responsible for pulmonary circulation.

The left ventricle is responsible for systemic & coronary circulation.

Valves of the Heart

You have four valves that separate the four chambers of the heart.Atrioventricular Valves (tricuspid and

bicuspid)

Semilunar Valves (pulmonic and aortic valves)

The Valves of the Heart

Atrioventricular Valves (tricuspid and bicuspid)

Semilunar Valves (pulmonic and aortic valves)

Valves

The first valve is between the right atrium & right ventricle. This valve is called the tricuspid valve. The valve is called tricuspid because the valve has three

flaps. The flaps are held in place by tendinous cords called

chordae tendinae. The chordae tendinae are secured to the walls of the

ventricle by the papillary muscles. When the ventricles contract the tricuspid valve closes. When the ventricles relax the tricuspid valve opens.

Valves

The second valve is between the right ventricle and the pulmonary trunk. This valve is called the pulmonary semilunar. The valve is called semilunar because of it’s new moon

shape. When the ventricles contract the pulmonary semilunar

valve opens. This allows the blood from the right side of the heart to be

pumped to the lungs. When the ventricles relax the pulmonary semilunar

valve closes.

Valves

The third valve is between the left atrium and the left ventricle. This valve is called the mitral or bicuspid valve. The valve is called bicuspid because the valve has two

flaps. The two flaps connect to the left ventricle by the same

principle as the tricuspid valve. When the ventricles contract the bicuspid valve closes. When the ventricles relax the bicuspid valve opens

Valves

The forth valve is between the left ventricle and the aortic trunk. This valve is called the aortic semilunar. The valve is called semilunar because of it’s new moon

shape. When the ventricles contract the aortic semilunar valve

opens. This allows the blood from the left side of the heart to be pumped

to the body.

When the ventricles relax the aortic semilunar valve closes.

Valves

Valves are suppose to be one-way however they can malfunction.Valve regurgitation = weak & leaky valveValve stenosis = constriction or narrowing of

passageway

Valves

Why do valves leak?Rheumatic feverAgingCongenital heart defects

Layers of the Heart

The heart is enclosed in a double walled sac called the pericardium. It consist of 2 layers

The outer layer is called the fibrous pericardium. The inner layer is called the serous pericardium.

The serous pericardium consist of 2 layers Parietal layer Visceral layer; also called epicardium.

Layers of the Heart

What is Pericarditis? It is inflammation of the double walled sac called the

pericardium. What causes pericarditis?

Trauma Infection Tumors

What are the symptoms? Chest pain Audible friction rub

Layers of the Heart

If worsening pericarditis or pericardial effusion can result in cardiac tamponade.

Cardiac tamponade = intrapericardial pressures increase to the point that it impairs the filling of the heart

Cardiac Tamponade is life threatening and is sometimes treated with pericardiocentesis.

Layers of the heart

The wall of the heart is made up of three layers.

Epicardium Corresponds to the visceral pericardium. Functions as an outer protective layer. Serous membrane that consists of connective tissue

covered by epithelium. Includes blood capillaries, lymph capillaries, and

nerve fibers.

Layers of the heart

The wall of the heart is made up of three layers.

Myocardium Relatively thick. Consists largely of cardiac muscle tissue responsible for

forcing blood out of the heart chambers. Muscle fibers are arranged in planes, separated by

connective tissues that are richly supplied with blood capillaries, and nerve fibers.

Layers of the heart

The wall of the heart is made up of three layers.

Endocardium Consists of epithelial and connective tissue that contains

many elastic and collagenous fibers. Connective tissue also contains blood vessels and some

specialized cardiacmuscle fibers called Purkinje fibers. Lines all of the heart chambers and covers heart valves. Is continuous with the inner lining of blood vessels--

endothelium.

Wall of the Heart

What is endocarditis? It is an infection and inflammation of the heart's inner lining

(endocardium). It is most common in people with damaged, diseased, or artificial heart valves.

What causes it? It is caused by bacteria that enter the bloodstream and settle on the heart

valves. What are the symptoms?

Chills & Fever Fatigue Weight loss Painful joints Persistent cough and SOB

How is it treated? IV Antibiotics

Blood supply to the Heart

The two main arteries that feed the heart:Left coronary artery

Circumflex branch Anterior interventricular branch

Right coronary artery Marginal branch Posterior interventricular branch

Blood supply to the Heart

The main veins that drain “used” blood from the heart: Great cardiac veins

drains the anterior side of the heart Middle cardiac vein

Drains the posterior side of the heart

The great cardiac and middle veins merge together into a cavity called the coronary sinus.

The thebesian vein then carries the “used” blood into the left and right atria.

Disorders

Atherosclerosis = hardening of the arteries which promotes clots and/or occlusions.

Thrombosis = a clot /coagulation of blood Embolism = thrombosis that has traveled from

location it was formed. Myocardial Ischemia = decreased oxygen availability

to the heart because of decreased blood flow or decreased oxygen in blood.

Myocardial Infarction = tissue death due to a loss of blood & glucose to the heart muscle.

Disorders

Congestive Heart Failure (CHF) = condition where the left side of the heart is damaged.

Cor Pulmonale = condition where the right side of the heart has decreased function.

Angina Pectoris = a severe pain or pressure in the chest caused by inadequate blood flow and oxygen content to the heart muscle.

Treatment for Disorders

Coronary Angioplasty = treats blockages of vasculature with a catheter or balloon.

Coronary Artery Bypass Graft (CABG) = artery graft from the leg or arm is inserted into coronary vasculature to bypass blocked arteries.

Blood flow through the Heart

Inferior Vena Cava/ Superior Vena Cava Right Atrium Tricuspid Valve Right Ventricle Pulmonary Semilunar Valve Pulmonary artery trunk Pulmonary artery Left/Right pulmonary artery Lungs

Blood flow through the Heart

Left/Right pulmonary vein Left Atrium Bicuspid/Mitral Valve Left Ventricle Aortic Semilunar Valve Aortic artery trunk Ascending Aorta

Brachiocephalic artery Left common carotid artery Left Subclavian artery

Descending Aorta xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx

Show cardiac cycle video

Cardiac Cycle

Cardiac cycle is the term referring to all or any of the events related to the flow of blood that occur from the beginning of one heartbeat to the beginning of the next

The frequency of the cardiac cycle is the heart rate

Every single 'beat' of the heart involves three major stages: atrial systole ventricular systole complete cardiac diastole The term diastole is synonymous with relaxation of a

muscle.It is the period of time when the heart relaxes after contraction in preparation for refilling with circulating blood.

The term systole is synonymous with contraction (movement or stretching) of a muscle. Think squeeze

The term diastole is synonymous with relaxation of a muscle. Think dilate.

It is the period of time when the heart relaxes after contraction in preparation for refilling with circulating blood.

Heart Rate

Heart rate is a term used to describe the frequency of the cardiac cycle.

It is considered one of the four vital signs Usually it is calculated as the number of

contractions (heart beats) of the heart in one minute and expressed as "beats per minute" (bpm).

Normal Heart rate in adults 60-100 bpm

Stroke Volume

Stroke volume is the amount of blood pumped by the left ventricle of the heart in one contraction

The heart does not pump all the blood out of the ventricle. Normally, only about two-thirds of the blood in the ventricle is put out with each beat Normal range

60 -120mL

Cardiac Output (Qt)

Cardiac output is the volume of blood being pumped by the heart, in particular a ventricle in a minute.

Cardiac Output (CO) = SV × HR Normal range is 4-6 lpm

Electrophysiology of the Heart

Contraction of the heart is initiated by an electrical stimulus

These contractions are a function of action potentials (electrical currents)

Action potentials consist of 5 phases0 = depolarization1-4 represent polarization

Electrical System of the Heart

Depolarization = electrical activity that triggers contraction of the heart muscle. Depolarization typically results from the influx of

positively charged sodium ions into the cell.

Repolarization = The restoration of a polarized state across a membrane, as in a muscle fiber following contraction. Repolarization results from the movement of

positively charged potassium ions out of the cell.

DEPOLARIZATION  

  REPOLARIZATION  

  RESTORATION OF IONIC BALANCE

Cardiac Cell Types

Contractile Muscle Fibers Bulk of myocardium responsible for the pumping

activity of the heart

Autorhythmic cells Pacemaker cells 1% of tissue, mostly located in the SA node Unique ability to spontaneously initiate an action

potential which in turn cause muscle fibers to contract

Cardiac Cells Four Properties

Automaticity Generates an action potential without stimulation

Excitability Irritability; lower stimulus needed to activate cell

Conductivity Transmits electrical current effectively; intercalated

disksContractility

Shortening and contraction in response to stimulus

Electrical Conduction System of the Heart

There are four structures embedded in the walls of the heart muscles that generate strong impulses and conduct them rapidly through the heart wall.

Electrical System of the Heart

Sino-atrial NodeSA node

Pacemaker 60 -100 bpm

Atrioventricular NodeAV node 40- 60 bpm

Bundle of HisAV bundle 20 – 40 bpmRight and Left bundle branches

Purkinje Fibers

Electrical System of the Heart

EKG

Electrocardiogram = graphic representation of the electrical activity of the heart’s conductive system over time. “electrical NOT mechanical” EMD/PEA

Leads are placed on the patient to evaluate the electrical system of the heart. 3 lead (monitoring) 12 lead (diagnostic)

standard limb lead configurations

A typical ECG tracing of a normal heartbeat (or cardiac cycle) consists of

a P wave, a QRS complex a T wave.

A small U wave is normally visible in 50 to 75% of ECGs.

The baseline voltage of the electrocardiogram is known as the isoelectric line.

Typically the isoelectric line is measured as the portion of the tracing following the T wave and preceeding the next P wave.

EKG

EKG

EKG

Des Jardins Pg. 416-417 Normal durations

P wave = 0.08 – 0.11 secP-R interval = 0.12 – 0.20 secQRS complex = < 0.10 secS-T segment = < 0.12 secT wave = < 0.20Q-T interval = < 0.38

EKG BASICS

EKGs are printed on standardized graph paper

The Y axis represents VOLTAGE The X axis represents TIME The Y axis is generally set at 5 or 10

mm/mV The X axis units are seconds

There are two sized boxes. 5 small boxes make up one large box Each small box equals 40 msec. Each large box equals 200 msec 5 large boxes equals 1 second

ECG paper is designed to move through the ECG machine at 25 mm per second.

Each of the smallest boxes are l mm square making the darker lined boxes 5 mm square.

Thus, at the usual rate of 25 mm/second flow of the paper through the machine, 5 large boxes pass through the machine per second or (5 x 60 seconds) 300 boxes

per minute.

Large boxes are used to estimate heart rate. Measure from QRS to QRS. Rates are approximate:

1 large box = 300 bpm.2 large boxes = 150 bpm.3 large boxes = 100 bpm.4 large boxes = 75 bpm.5 large boxes = 60 bpm.

Basic ECG Interpretation

NORMAL SINUS RHYTHM

Impulses originate at S-A node at normal rate. All complexes normal and evenly spaced.Rate 60 - 100/min

SINUS BRADYCARDIA

Impulses originate at S-A node at slow rate. All complexes normal and evenly spaced.Rate < 60/min

CAUSES OF SINUS BRADYCARDIA Coronary artery disease Increased intracranial pressure Hypothyroidism Hypoxemia Vagal stimulation

Gagging Coughing Suctioning

SINUS TACHYCARDIA

Impulses originate at S-A node at rapid rate. All complexes normal and evenly spaced.Rate 100-160/min

CAUSES OF SINUS TACHYCARDIA Fever Sepsis Hypoxemia CHF Shock Fear Exercise

ATRIAL FLUTTER

Impulses travel in circular course in atria. Rapid flutter waves and ventricular response can be irregular.

ATRIAL FIBRILLATION

Impulses have chaotic, random pathways in atria. Baseline irregular; ventricular response irregular.

PREMATURE VENTRICULAR CONTRACTION (PVC) A single impulse originates in the right ventricle. Time

interval between normal R peaks is a multiple of R-R intervals.

VENTRICULAR TACHYCARDIA

Impulse originates at ventricular pacemaker. Wide ventricular complexes. Rate here is> 120/min

VENTRICULAR FIBRILLATION

Chaotic ventricular depolarization. Rapid, wide, irregular ventricular complexes.

ASYSTOLE

Rate: none P wave: may be seen, but there is no ventricular response QRS: none Conduction: none Rhythm: none

Neural Control of the Heart

Many things play a role in controlling heart rate.Autonomic nervous systemBaroreceptorsAnxietyBody temperature

Baroreceptors

Arterioles are controlled by sympathetic impulses.

There are sympathetic fibers located in the vessels.

The medulla receives information from the baroreceptors located in the carotid & the aorta.

The medulla (vasomotor center) then feeds the impulses to the vessels based on the information.

Baroreceptors

The vessels either dilate or constrict based on the area of the body. In the heart, brain, and skeletal muscles:

↑ sympathetic impulses = vasodilatation ↓ sympathetic impulses = vasoconstriction

In the rest of the body: ↑ sympathetic impulses = vasoconstriction ↓ sympathetic impulses = vasodilatation

Baroreceptors

Normally there is a continuous stream of impulses which cause the vessels of the body to always be slightly constricted.This is called vasomotor tone.

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BLOOD

Blood is a highly specialized circulating tissue consisting of several types of cells suspended in a fluid medium known as plasma.

Responsible for transportation and protection The cellular constituents are:

red blood cells (erythrocytes), white blood cells (leukocytes), platelets (thrombocytes –cell fragments),

Blood Volumes

Blood volumesWhole blood

4 to 6 L average 7 to 9% of total body weight

Normal volumes of blood fractions Plasma = 2.6 L Formed elements = 2.4 L

Blood Plasma Liquid fraction of whole blood minus formed

elements. 55% of total blood volume Composition

90% water 10% dissolved substances

Foods & Salts About 3% O2 carried in plasma About 5% CO2 carried in plasma Most abundant solutes dissolved in plasma are plasma

proteins: Albumins Globulins Fibrinogen Prothrombin

Blood Plasma

Plasma minus clotting factors, proteins, is called serum.

Serum is liquid remaining after whole blood clots. Serum contains antibodies.

Formed Elements

Red Blood Cells (erythrocytes) White BloodCells (leukocytes)

Granular leukocytes Neutrophils Eosinophils Basophils

Nongranular leukocytes Lymphocytes Monocytes

Platelets (thrombocytes)

Erythrocytes (RBCs)

Characteristics:

Biconcave disk shape (thin center and thicker edges) results in large cellular surface area.

Tough and flexible plasma membrane deforms easily allowing RBCs to pass through small diameter capillaries.

Absence of nucleus and cytoplasmic organelles limits life span to about 120 days but provides more cellular space for iron containing hemoglobin.

Erythrocytes (RBCs)

Named according to size: normocytes (normal size about 7-9 μm in diameter) microcytic (small size) macrocytic (large size)

Named according to hemoglobin content of cell:

normochromic (normal Hb content) hypochromic (low Hb content) hyperchromic (high Hb content)

Erythrocytes

Erythrocytes (RBCs)

Hematocrit Percentage of RBCs in relation to total blood volume

Normal Men 45% Women 42%

Hemoglobin the iron-containing oxygen-transport metalloprotein in the red blood cells

of the blood Measured as weight per 100 ml

Men 14-18 gm/dl women: 12-16 gm/dl

Content Men 5,000,000 mm3 Women 4,000,000 mm3

Erythrocytes (RBCs)

General functions:Transportation of O2 and CO2

Combined with hemoglobin Oxyhemoglobin (Hb + O2) Carbaminohemoglobin (Hb + CO2)

Important role in homeostasis & acid base balance.

Leukocytes or WBCs

General function is protection of body from microorganisms by phagocytosis or antibody formation.

WBC normal range is 5,000 to 10,000/mm3 of blood. Leukopenia—total numbers below 5,000/mm3 of blood.

Infrequent but may occur with malfunction of blood forming tissues or diseases affecting immune system, such as AIDS.

Leukocytosis—total numbers over 10,000/mm3 of blood. Frequent finding in bacterial infections Classic sign in blood cancers (leukemia)

Differential WBC count is a component test in CBC; measures proportions of each type of WBC in blood sample.

Leukocytes

Leukocytes or WBCs

Leukocyte types and functions: Granulocytes

Neutrophils Eosinophils Basophils

Agranulocytes Monocytes in peripheral blood (macrophages in tissues) Lymphocytes

B lymphocytes (Plasma cells) T lymphocytes

Leukocytes or WBCs Functions of WBCs

Neutrophils Most numerous type of phagocyte Numbers increase in bacterial infections

Monocytes Largest leukocyte Aggressive phagocyte—capable of engulfing larger

bacteria and cancer cells Develop into much larger cells called macrophages after

leaving blood & entering tissue spaces

Leukocytes or WBCs

Eosinophils Weak phagocyte Active against parasites and

parasitic worms Involved in allergic reactions

Basophils Related to mast cells in tissue

spaces Both mast cells and basophils

secrete histamine (causes inflammation)

Basophils also secrete heparin (an anticoagulant)

Leukocytes or WBCs

Lymphocytes B lymphocytes involved in

immunity against disease by secretion of antibodies

Mature B lymphocytes are called plasma cells

T lymphocytes involved in direct attack on bacteria or cancer cells (not antibody production)

Platelets and Blood Clotting

Platelets Play essential role in blood clotting

Normal platelet count 150,000—340,000/mm3

Blood vessel damage causes platelets to become sticky and form a “platelet plug”

Accumulated platelets release additional clotting factors that enter into the clotting mechanism

Platelets ultimately become a part of the clot itself

Platelets

Platelets and Blood Clotting

Clotting in a nutshell Damaged tissue cells along with platelets release

prothrombin activator. Prothrombin activator, along with calcium converts

prothrombin the thrombin Thrombin combines with fibrinogen to form fibrin Fibrin creates a “net” that begins to form the “plug”.

Altering the blood clotting mechanism

Application of gauze (rough surface) to wound causes platelet aggregation and release of clotting factors

Administration of Vitamin K will increase synthesis of prothrombin

Coumadin will delay clotting by inhibiting prothrombin synthesis

Heparin delays clotting by inhibiting conversion of prothrombin to thrombin

A drug called tissue plasminogen activator (TPA) is used to dissolve clots that have already formed

Red Blood Cell Disorders

Most often related to either: overproduction of RBCs, called polycythemia low oxygen carrying capacity of blood,called

anemia

Polycythemia

Cause is generally cancerous transformation of red bone marrow Dramatic increase in RBC numbers—often in excess of 10

million/mm3 of blood—hematocrit may reach 60% Signs and symptoms include:

Increased blood viscosity or thickness Slow blood flow and coagulation problems Frequent hemorrhages Distension of blood vessels and hypertension

Treatment may include: Blood removal Irradiation and chemotherapy to suppress RBC production

Polycythemia

Anemia

Caused by either: low numbers or abnormal RBCs low levels or defective types of Hb

Normal Hb levels 12-14 g/100 ml of blood Low Hb level (below 9 g/100 ml of blood) classified as

anemia Majority of clinical signs of anemia related to low

tissue oxygen levels Fatigue; skin pallor Weakness; faintness; headache Compensation by increasing heart and respiratory rates

Types of Anemia

TypesHemorrhagic anemiaAplastic anemiaDeficiency anemiaHemolytic anemia

Hemorrhagic anemia

AcuteBlood loss is either:

immediate surgery or trauma

chroniculcers or cancer

Aplastic anemia

Characterized by low RBC numbers and destruction of bone marrow

Often caused by: toxic chemicals irradiation certain drugs

Aplastic anemia

Deficiency anemia

Caused by inadequate supply of some substance needed for RBC or hemoglobin production.

Types: Pernicious anemia Iron deficiency anemia Folate deficiency anemia

Iron deficiency anemia

Caused by deficiency or inability to absorb iron needed for Hb synthesis (dietary iron deficiency is common worldwide)

RBCs are microcytic and hypochromicHematocrit is decreasedTreatment is oral administration of iron

compounds

Iron deficiency anemia

Pernicious anemia

Caused by Vitamin B12 deficiency Genetic related autoimmune disease Decreased RBC, WBC, and platelet

numbers RBCs are macrocytic Classic symptoms of anemia coupled with

CNS impairment Treatment is repeated Vitamin B12 injections

Folate deficiency anemia

Folate, also called folic acid, is necessary for red blood cell formation and growth.

RBCs are macrocytic. Some medications, such as Dilantin (phenytoin),

interfere with the absorption of this vitamin. Because folate is not stored in the body in large amounts, a continual dietary supply of this vitamin is needed.

Vitamin B12 and folate deficiency anemia.

Hemolytic anemia Caused by either:

decreased RBC life span increased RBC rate of destruction

Symptoms are related to retention of RBC breakdown products: Jaundice Swelling of spleen Gallstone formation Tissue iron deposits

Types: Sickle Cell Anemia Thalassemia Erythroblastosis fetalis

Hemolytic anemia

Sickle Cell Anemia

Genetic disease resulting in formation of abnormal hemoglobin (HbS) primarily in the African American race

RBCs become fragile and assume sickled shape when blood oxygen levels decrease

Sickle cell trait is mild (one defective gene) Sickle cell disease more serious (two defective

genes); causes blood stasis, clotting and “crises” that may be fatal

Affects 1 in every 600 African American newborns

Sickle cell anemia

White Blood Cell Disorders

Two major types of WBC cancers or neoplasmsLymphoid (lymphatic cells) neoplasms—result

from B and T lymphocyte precursor cells or their descendent cell types

Myeloid (bone marrow cells) neoplasms—result from the malignant transformation of precursor cells of granulocytic WBCs, monocytes, RBCs, and platelets

White Blood Cell Disorders

Multiple myeloma Cancer of B lymphocytes (plasma cells) Most “deadly” blood cancer in people over age 65 Causes bone marrow disfunction and production of

defective antibodies Characterized by:

Recurrent infections and anemia Destruction and fracture of bones

Treatment includes chemotherapy, drug antibody therapy, and marrow and stem cell transplantation

White Blood Cell Disorders

Leukemias—WBC related blood cancersCharacterized by marked leukocytosis Identified as:

Acute = rapid development of symptoms Chronic = slow development of symptoms Lymphoid = lymphatic cells Myeloid = bone marrow cells

Chronic Lymphocytic Leukemia (CLL)

Average age of onset is 65; rare under age 30 More frequent in men than women Often diagnosed unexpectedly in routine physical

exams with discovery of marked B lymphocytic leukocytosis

Generally mild symptoms include anemia, fatigue, and enlarged often painless lymph nodes

Most patients live many years following diagnosis Treatment of severe cases involves chemotherapy

and radiation

CLL

Acute Lymphocytic Leukemia (ALL)

Primarily a disease of children between 3 and 7 years of age; 80% of children who develop leukemia have this form of the disease

Highly curable in children but less so in adults Onset is sudden—marked by fever, leukocytosis,

bone pain and increased infections Lymph node, spleen and liver enlargement is

common Treatment includes chemotherapy, radiation, and

bone marrow or stem cell transplants

ALL

Chronic Myeloid Leukemia (CML) Accounts for about 20% of all cases of leukemia Occurs most frequently in adults between 25 and 60

years of age Caused by cancerous transformation of granulocytic

precursor cells in the bone marrow Onset and progression of disease is slow with

symptoms of fatigue, weight loss and weakness Diagnosis often made by discovery of marked

granulocytic leukocytosis and extreme spleen enlargement

Treatment by new “designer drug” Gleevec or bone marrow transplants is curative in over 70% of cases

CML

Acute myeloid leukemia (AML)

Accounts for 80% of all cases of acute leukemia in adults and 20% of acute leukemia in children

Characterized by sudden onset and rapid progression Symptoms include leukocytosis, fatigue, bone and

joint pain, spongy bleeding gums, anemia and recurrent infections

Prognosis is poor with only about 50% of children and 30% of adults achieving long term survival

Bone marrow and stem cell transplantations have increased cure rates in selected patients

AML

White Blood Cell Disorders

Infectious mononucleosis Noncancerous WBC disorder Highest incidence between 15 and 25 years of age Caused by virus in saliva Leukocytosis of atypical lymphocytes with abundant

cytoplasm and large nuclei Symptoms include fever, severe fatigue, sore throat,

rash, and enlargement of lymph nodes and spleen Generally self-limited and resolves without

complications in about 4 to 6 weeks

“mono”

Leukocytes or WBCs

Lymphocytes B lymphocytes involved in

immunity against disease by secretion of antibodies

Mature B lymphocytes are called plasma cells

T lymphocytes involved in direct attack on bacteria or cancer cells (not antibody production)

Clotting disorders

Hemophilia A X-linked inherited disorder results from inability to produce

Factor VIII (a plasma protein) responsible for blood clotting In severely affected individuals frequent and extensive

episodes of bleeding can be life threatening Characterized by easy bruising, deep muscle hemorrhage,

blood in urine, and repeated episodes of bleeding into joints causing pain and deformity

Treatment includes administration of Factor VIII, injury prevention, and avoiding drugs like aspirin that alter the clotting mechanism

hemophilia

Hemophilia and inheritance

Clotting disorders

Thrombocytopenia—caused by reduced platelet counts Characterized by bleeding from small blood vessels,

most visibly in the skin and mucous membranes Platelet count below 20,000/mm3 may cause

catastrophic bleeding (Normal platelet count 150,000—340,000/mm3)

Most common cause is bone marrow destruction by drugs, chemicals, radiation, and diseases such as cancer, lupus, and HIV/AIDS

Treatment may involve transfusion of platelets, corticosteroid type drugs, or removal of the spleen.

Blood Types

ABO system Type A blood—type A antigens in RBCs; anti-B type

antibodies in plasma Type B blood—type B antigens in RBCs; anti-A type

antibodies in plasma Type AB blood—type A and type B antigens in RBCs;

no anti-A or anti-B antibodies in plasma universal recipient blood

Type O blood—no type A or type B antigens in RBCs; both anti-A and anti-B antibodies in plasma

universal donor blood

Blood Types

Rh systemRh-positive blood

Rh factor antigen present in RBCsRh-negative blood

No Rh factor present in RBCs No anti-Rh antibodies present naturally in plasma Anti-Rh antibodies, however, appear in the plasma

of Rh-negative persons if Rh-positive RBCs have been introduced into their bodies (pregnancy)

Erythroblastosis Fetalis

Hemolytic disease of newborn Caused by blood ABO or Rh factor incompatibility during

pregnancy between developing baby and mother The maternal antibodies fighting against “foreign” fetal

RBCs or Rh factor can cross placenta, enter the fetal circulation, and destroy the unborn baby’s RBCs

Symptoms in developing fetus related to decline in RBC numbers and Hb levels; jaundice, intravascular coagulation, and heart and lung damage are common

Treatment may include utero blood transfusions and early delivery of the baby

Prevention of Rh factor incompatibility now possible by administration of RhoGAM to Rh negative mothers

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Rh factor

Rh factor

Erythroblastosis fetalis

Erythroblastosis fetalis

Blood Pressure

“pressure generated by the blood” Highest in the arteries Lowest in the veins

Blood pressure gradient = difference between two blood pressures The difference between the beginning pressure and

the ending pressure within a circuit. What two pressures would we look at to compute the

systemic blood pressure gradient?

Blood Pressure

The maximum pressure generated during ventricular contraction is called the systolic pressure.

The lowest pressure that remains prior to the next ventricular contraction is called the diastolic pressure.

Blood Pressure

Hypertension = increased arterial pressureCan lead to ruptured vessels & stroke

Hypotension = decreased arterial pressureCan lead to the loss of circulation & life will

cease.Commonly seen with massive hemorrhage.

Blood Pressure

Factors that affect blood pressure Blood volume

Directly related to BP Force of heart contractions

Affects cardiac output directly, unless there is a noted decrease in blood volume i.e. hemorrhage

Heart rate Affects cardiac output directly. This is only true if the stroke

volume does not decrease sharply when the heart rate increases, due to less fill time.

Blood viscosity Directly related to BP

Pulse and Pulse points

Temporal Facial Carotid Brachial Radial Femoral Popliteal Posterior tibial Dorsal pedal

Circulatory Shock

Failure of the circulatory system to deliver oxygen to the tissues adequately, resulting in cell impairment.

Types Cardiogenic Shock Hypovolemic Shock Neurogenic Shock Anaphylactic Shock Septic Shock

Neural Control of Vascular System

Vasomotor center (medulla) coordinates vasodilatation & vasoconstriction by controlling the # of sympathetic impulses.

Systemic = increased impulses will vasoconstrict Systemic = decreased impulses will vasodilate

HOWEVER… Heart, brain, & skeletal muscle = increased

impulses will vasodilate Heart, brain, & skeletal muscle = decreased

impulses will vasoconstrict

Baroreceptor Reflex

Baroreceptors regulate the arterial BP by initiating reflex adjustments.

“stretch receptors” Found in:

Walls of the aortic arch Impulses travel along the vagus nerve

Walls of the carotid artery Impulses travel along the glossopharyngeal nerve

Effects of cardiac cycle on BP

BP rises & falls in a pattern like the phases of cardiac cycle.

When ventricles contract blood is forced into pulmonary trunk & aorta. At this point the pressure in the arteries increases sharply.

Pulmonary Blood Flow

Distribution of pulmonary blood flowProgressively decreases from the base to the

apex. Factors affecting distribution:

GravityCardiac outputPulmonary vascular resistance

Pulmonary Blood Flow

Blood is gravity dependant because it is relatively heavy.

Average lung is 30cm from the base to the apex. If blood was to fill the lung form the base to the apex it

would need 30cmH2O of pressure (22mmHg) to over come the gravitational force.

The pulmonary artery enters in the middle (hilum) so the blood that reaches the apex needs at least 11mmHg to over come the gravitational force.

Pulmonary Blood Flow

The vessels @ the base have greater pressure than those @ the apex.

The increased pressure in the vessels of the bases cause the vessels to widen, which decreases pulmonary vascular resistance.

These factors change based on lung position.

Zones of Pulmonary Circulation*These factors due change based on lung position

Zone 1 Least gravity dependant Worst perfusion Best aeration

Zone 2 Good perfusion Good aeration

Zone 3 Most gravity dependant Best perfusion Worst aeration

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Lung zones

Hemodynamics

The study of the forces that influence the circulation of blood.Consist of measurements and calculations.

A pulmonary artery catheter (Swan-ganz catheter) is used to collect hemodynamic measurements in critically ill patients.

Hemodynamics

Units used in hemodynamics:mmHgDyne

A unit of force which accelerates a mass of 1 gram @ a rate of 1cm/sec.

Hemodynamics

Hemodynamics are either measured or calculated.Measured = an instrument is used to collect

information.Calculated = measurements are used in

formulas to compute additional information Because hemodynamic parameters will vary with

the size of the patient, some hemodynamic values are “indexed” by body surface area (BSA)

Hemodynamics

Calculation for BSA (m2)Centimeters & Kilograms

(Height (cm) X Weight (kg) /3600) .5

Inches & Pounds (Height (in) X Weight (lb) /3131) .5

For example… Me! I weigh about 100 kg, and my height is

about 188 cm (1in = 2.54 cm). So, my BSA is (188X100)/3600, then take

the square root of this… Answer is approximately 2.3m squared

Swan-ganz catheter

Swan-ganz catheter

Inserted into the internal jugular or the subclavian vein

Very invasive procedure; only used in critically ill patients under constant observation.

Complications include: Pneumothorax / Hemothorax Air emboli Infection Pulmonary artery rupture

Hemodynamics

Directly measured:Central Venous Pressure CVPRight Atrial Pressure RAPMean Pulmonary Artery Pressure PAPulmonary Capillary Wedge Pressure PCWPCardiac Output CO

Hemodynamics

Computed:Stroke Volume SVStroke Volume Index SVICardiac Index CIPulmonary Vascular Resistance PVRSystemic Vascular Resistance SVR

p.459 Des Jardins

Central Venous Pressure & Right Atrial Pressure (measured) RAP is very close to CVP CVP is a measure of atrial preload. Atrial preload is determined;

distribution of blood within the body total blood volume presence and force of atrial contraction

Mean Pulmonary Artery Pressure & Pulmonary Capillary Artery Wedge Pressure (measured)

PCWP

End-diastole represents the moment in the cardiac cycle when the ventricle contains the greatest volume of blood, just before it contracts and ejects its volume.

The wedged pulmonary artery catheter reflects LVEDP because at end-diastole, the mitral valve is open and this creates communication between the left atria, left ventricle, and pulmonary vascular bed. In other words, “the doors are all open” from the LV to the pulmonary capillary.

The “window into the left heart”

Cardiac Output

A bolus of sterile solution that is colder than the patients blood is injected into the proximal port of a pulmonary artery catheter located in the right atrium.

In the atrium, the solution mixes with the blood and passes through the tricuspid valve into the right ventricle.

A thermistor within the catheter senses the change in blood temperature as the blood passes the catheter tip located in the pulmonary artery.

The change in temperature over time is calculated by a computer and converted into a measurement of cardiac output.

Cardiac Output (measured)

Stroke Volume (computed)

Volume of blood ejected by ventricle with each contraction. Normal 40-80 mL

Stroke volume is derived by dividing the cardiac output by the heart rate

Determinants of stroke volume: Preload Afterload Myocardial contractility

Determinants of stroke volume

Preload = how much blood is returning to the heart, and how well can the heart muscle accommodate it

“rubber band” Afterload = the forces “past the heart” which the

ventricles must fight against Viscosity & volume = Pulling/pushing ketchup vs. water

through a straw Vascular cross-sectional surface area = Long straw vs. short

straw Vascular resistance = Coffee straw vs. Slurpee straw

Myocardial contractility Contractility = inotropism

Stroke Volume Index (computed)

A patient has a stroke volume of 40mL This patient is 6’5” 280lb Is this a good value for this patient? NO! How do we know if a stroke volume is

appropriate? Stroke Volume Index

Stroke Volume Index (computed)

SVI = SV/BSANormal = 30 – 65 Ml/beat/m2

Cardiac Index (computed)

Normalizes Cardiac Output (measured) to body surface area.

CI = CO/BSA

Normal 2.5-4.2 L/min/m2

Vascular resistance

Pulmonary system low resistance system “short straw”

Systemic system high resistance “long straw”

Vascular resistance (computed)

Blood pressure is directly related to vascular resistance.When vascular resistance increases this will

cause BP to increase. When the straw diameter gets smaller, you have to

pull/push harder!

Vascular resistance

Vascular resistance = blood pressure

cardiac output

You are looking at what pressure it takes to

eject a liter of blood.

Pulmonary vascular resistance

The PVR reflects the afterload of the right ventricle.

When looking at PVR, you must have your pressures represent the “beginning to the end” of the pulmonary circuit.

What is the beginning of the pulmonary circuit? What is the end of the circuit?

Pulmonary vascular resistance

PVR = (PA – PCWP/CO) X 80

The constant 80 is a conversion factor for adjusting to the unit of dyne/sec/cm-5

Systemic Vascular Resistance

The SVR reflects the afterload of the left ventricle.

When looking at SVR, you must have your pressures represent the “beginning to the end” of the systemic circuit.

What is the beginning of the systemic circuit? What is the end of the circuit?

Systemic Vascular Resistance

SVR = (MAP – CVP/CO) X 80

The constant 80 is a conversion factor for adjusting to the unit of dyne/sec/cm-5