UCF Exam 2 Physiology Lab

UCF Physiology Lab Exam 2

Location of the heart

Between 2nd and 5th intercostal spaces, thoracic cavity in the mediastinum

Pericarditis

Inflammation of the pericardium, can lead to adhesions causing visceral and parietal pericardia to stick together

Pericardium

Fluid-filled sac surrounding the heart

Layers of serous pericardium

Parietal layer and visceral layer

Layers of heart wall

Epicardium, myocardium, and endocardium

Myocardium

Composed mainly of cardiac muscle, forms the bulk of the heart

Arteries

Carry blood away from heart

Veins

Carry blood towards heart

Semilunar valves

Prevent backflow into the ventricles when ventricles relax

Pulmonary valve

Controls flow of deoxygenated blood from R. side of heart into pulmonary trunk

Aortic valve

Regulates the oxygenated blood flow from the L side of the heart into the aorta

Atrioventricular valves

Prevent backflow into the atria when ventricles contract

Tricuspid valve

Right side between R. atrium and ventricle

Bicuspid (mitral) valve

Left side between L atrium and ventricle

Pulmonary circuit

O2 poor blood pumped to the lungs to pick up O2 and dispel CO2

Systemic circuit

Receives oxygenated blood from lungs and pumps it throughout the rest of the body

S1 “lub“

First sound; produced by turbulent blood flow through AV valves

S2 “dub“

Second sound; produced by turbulent blood flow through semilunar valves

Areas of auscultation

Tricuspid, bicuspid, primary pulmonic, secondary pulmonic, aortic

Systole

Ventricular contraction, 0.3 seconds of cardiac cycle

Diastole

Ventricular relaxation, 0.5 seconds of cardiac cycle

Cardiac output

Amt of blood pumped out by each ventricle in one minute. Product of HR and stroke volume.

Stroke volume

Volume of blood ejected from ventricles with each beat (~70ml). SV = EDV - ESV

End systolic volume (ESV)

Total volume of blood left in ventricles at the end of systole (~50ml)

End diastolic volume (EDV)

Total volume of blood left in ventricles at the end of diastole (~120ml)

Systolic pressure

The maximal arterial pressure following L. ventricular ejection into aorta

Diastolic pressure

The minimal arterial pressure following L. ventricular relaxation

Sphygmomanometer

Used to measure aortic BP

Low BP

Below 90/60

Order of the conduction system

SA node > Internodal pathway > AV node > AV bundle (bundle of His) > Right/left bundle branch > Purkinje fibers

ECG cannot show the electrical activity of:

SA node, AV node, bundle of His, bundle branches, Purkinje network

Sinus bradycardia

Sinus rhythm rate less than 60bpm

Sinus tachycardia

Sinus rhythm rate greater than 100bpm

Supraventricular tachycardia (SVT)

P and T waves are together instead of separate - P waves essentially absent

Atrial flutter (A-flutter)

Consecutive atrial depolarization waves (“flutter” waves)

Atrial fibrillation (A-fib)

Caused by many ectopic atrial foci firing at rapid rates

Ventricular tachycardia (V-tach)

Characteristic wide QRS complexes

Ventricular fibrillation (V-fib)

A type of cardiac arrest, no effective pumping by the heart. Requires immediate CPR and defibrillation

First-degree AV block

PR interval prolonged - greater than 0.2 second or one large square

Second-degree AV block

Some atrial depolarization (P waves) can conduct to ventricles, but some are blocked - leaves lone P waves without an associated QRS complex

Third-degree AV block

Total block of conduction from atria to ventricle. No relationship between P and QRS waveforms

Hematopoiesis

Process by which WBCs are formed

Blood composition

55% plasma, 45% formed elements.

Formed elements of blood

Erythrocytes, buffy coat (<1%, leukocytes and platelets)

Plasma

90% water, remaining 10%: proteins (7-9%), electrolytes, gases, hormones, waste

Albumin (plasma protein)

Maintains osmotic pressure, helps keep water from diffusing out of the bloodstream into the extracellular matrix of tissues

Alpha and Beta Globulin (plasma proteins)

Transport lipids and fat-soluble vitamins

Gamma globulin (plasma proteins)

Antibodies produced by lymphocytes

Fibrinogen

Forms fibrin threads essential in blood hemostasis

Lifespan of RBCs

100-120 days, can be altered by “shear effect”

Hematocrit

Percent of blood that consists of red blood cells

Healthy hematocrit levels

Men: 46% ± 5%
Women: 42% ± 5%

Erythropoietin (EPO)

Maintains the balance between production and destruction of RBCs

Neutrophils

First responders to infection, phagocytose

Eosinophils

Acts against parasitic infection, phagocytic, kill cancer cells, assist basophils in allergies

Basophils

Releases histamine, responding to allergens

Monocytes

Become macrophages, phagocytose bacteria, cell debris

Lymphocytes

Part of adaptive immunity, produce antibodies, cytotoxic, and helper T-cells, natural killer cells for cancer cells

4 blood groups in the ABO system

Group A, Group B, Group AB, Group O

Universal donor

Type O

Universal recipient

Type AB

Rh factor

“D-antigen,” either present (+) or absent (-)

Rh blood transfusion compatibility rules

Only Rh negative blood is given to Rh negative patients, but Rh positive OR Rh negative blood can be given to Rh positive patients

Ways anemia can develop

Insufficient amount of erythrocytes; inability of the erythrocytes to bind to the normal amount of oxygen.

Cause of pernicious anemia

Body cannot absorb enough vitamin B12

Cause of iron-deficiency anemia

Body lacks enough iron to produce normal levels of hemoglobin (blood loss, impaired absorption, increased iron demand, inadequate iron intake)

Anemia

Results from the inability of the erythrocytes to deliver the needed amount of oxygen to the cells

Cause of aplastic anemia

Bone marrow doesn’t make enough new RBCs, WBCs, and platelets because blood cell-producing stem cells are damaged or destroyed.

Cause of sickle cell anemia

Genetic mutation of the HBB gene located on chromosome 11

Causes of hemorrhagic anemia

Rapid or gradual loss of red blood cells faster than bone marrow can replace them (anemia due to excessive bleeding)

Polycythemia

Abnormal excess of erythrocytes in blood, blood doping

Rh incompatibility

After their first exposure to Rh+ blood, Rh- people can develop antibodies coding for the Rh+ genes. Therefore, during the second exposure to Rh+ blood, the antibodies of the Rh- individual will attack the Rh+ blood.

Clinical blood test (CBC)

Basic assessment of overall health, can detect a wide range of disorders

CBC with Differential (CBC with Diff)

In-depth preliminary assessment of overall health

% and concentration of each class of leukocyte

Determining type of infection a patient may have

Healthy distribution of neutrophils

50-70%

Healthy distribution of lymphocytes

25-33%

Healthy distribution of monocytes

3-9%

Healthy distribution of eosinophils

1-4%

Healthy distribution of basophils

0.5-1%

Comprehensive metabolic panel (CMP)

State of metabolism, can also monitor known conditions like hypertension, and check for kidney or liver-related side effects of medicines

Full lipid panel

Part of a cardiac risk assessment to determine an individual’s risk of disease

Includes: total cholesterol, HDL, LDL, and triglycerides

Total cholesterol equation

Total cholesterol = HDL + LDL + 1/5 triglycerides

If clumping reaction occurs in a blood well (dotted structure):

You have that antigen – (ex: if reaction in anti-A well, you have type A blood)

Reasons for a pulse deficit

Pre-existing heart condition that weakens blood flow to the wrist, human error

Systolic blood pressure patterns during exercise

Before: baseline

During: increased

After: decreasing to baseline

Diastolic blood pressure patterns during exercise

Should remain roughly at baseline before, during, and after

PQ interval measures

AV conduction time

QRS complex measures

Ventricular depolarization