Systems Phys Exam 2 Study guide

What are the functions of blood? Transport, Regulation, Protection

Transport

• O2 and nutrients to body cells

• Metabolic wastes to lungs and kidneys

Regulation

• Maintaining body temperature by absorbing and distributing heat

• Maintaining normal pH

• Maintaining adequate fluid volume in circulatory system

Protection

• Preventing blood loss - Platelets initiate clot formation

• Preventing infection

  • Antibodies

  • white blood cells

What is the composition of Blood?

45% RBC, 55% Plasma

What are the 3 types of blood
(formed elements)

Erythrocytes (RBCs), leukocytes (WBCs), thrombocytes (platelets)

Plasma contains

90% water, Nutrient, gases, hormones, wastes, proteins, dissolved solutes

Erythrocytes contain the protein____ to which O2 and CO2 reversibly combine

Hemoglobin

Types of Blood Vessels

arteries, arterioles, capillaries, venules, and veins

Arteries carry____ away from heart

Oxygenated blood

Veins carry___ to the heart

Deoxygenated blood

2 types of circulation

Pulmonary & systemic

Pulmonary circulation

carries oxygen poor blood and then returns oxygen rich blood

(think of lungs and its output)

System circulation

Caries oxygen rich blood and then returns oxygen poor blood

(Thing of blood flood after leaving heart)

Pressure in blood flow

force exerted by the blood; measured in mmHg

blood flows from higher to lower pressure

Flow in blood

Volume of blood moved per unit time; mL/min

Resistance in blood

difficulty for blood to flow between two points

measure of friction that impedes flow

Resistance Factors

Blood viscosity

Blood vessel length

Blood vessel radius

Blood Viscosity

Friction between molecules of a flowing fluid; affected by water volume and the number of erythrocytes

Blood Vessel radius’ effects

Dilated vessels decrease resistance, while constricted vessels increase resistance

Radii of blood vessels do not stay constant

Most important determinant of changes in resistance

Hematopoiesis

formation of all blood cells; in Red Bone Marrow

too few rbcs lead to hypoxia

Hematopoietic stem cells

(HematoCytoblasts)

Stem cell that gives rise to all formed elements

Erythropoietin (EPO)

Stimulates formation of RBCs; Released by kidneys in response to hypoxia

Hypoxia causes

• Decreased RBC numbers
  (due to hemorrhage or destruction)

• Insufficient hemoglobin per RBC (ex: iron deficiency)

• Reduced O2 availability
  (eg. altitudes, pneumonia,
  lung problem)

RBC Composition

Heme, iron, globin

RBC component information

Iron bind to ferritin or hemosiderin; stored for reuse

Heme, degraded to yellow pigment bilirubin

Globin metabolized into amino acid, released into circulation

Bilirubin

Liver secretes Bilirubin into intestines; degraded to urobilinogen

Anemia

Low oxygen

O2 carrying capacity too low to support normal metabolism

not disease

Symptoms: fatigue, pallor, dyspnea, and chills

Polycythemia

Excess RBCS

increased blood viscosity

• Polycythemia vera: Bone marrow cancer

Secondary polycythemia

• low oxygen or increased EPO production

Leukocytes/WBCs

<1% total blood volume

defend against disease

Originate from hemocytoblast stem cells

Leukocytosis

WBC count higher than usual, → response to infection

Leukocytes grouped into two categories

Granulocytes

Agranulocytes

Granulocytes

Contain cytoplasmic granules

• Neutrophils, eosinophils, Basophiles

Agranulocytes

No cytoplasmic granules

• Lymphocytes

• monocytes

Lymphoid stem cells

produce lymphocytes

Leukopenia

Low WBC count

Leukemias

Bad WBCs

Cancerous condition involving overproduction of immature, nonfunctional, & abnormal WBC

• Cancer cells fill red bone marrow, leading to anemia & bleeding

Treatments: irradiation, antileukemic drugs; stem cell transplants

Thrombocytopenia

Deficient number of circulating platelets

treatment: transfusion of concentrated platelets

Thrombocytopenia: Impaired liver function

Inability to synthesize clotting factors

caused by: vitamin K deficiency, hepatitis

What is a thrombus

Clot

May block circulation, leading to tissue death

Embolus

ex: pulmonary or cerebral emboli

risk factors: atherosclerosis, slowly flowing blood or blood stasis from immobility.

Plaque in blood stream

Pathway of blood

Vena Cava → Right A → Tricuspid → Right V → Pulmonary Valve → Pulmonary trunk → R/L Pulmonary artery → Lungs → R/L Pulmonary veins → Left A → Bicuspid valve → Left V → Aorta → Body

Types of Cardiac Muscle cells

Contractile & Pacemaker cells

Contractile cells

responsible for contraction

Pacemaker cells

noncontractile cells that depolarize; Do not need nervous system stimulation

All cardiomyocytes contract as unit, or none contract

contraction of all cardiac myocytes ensures effective pumping action

Coordinated heartbeat is a function of

the presence of gap junctions

Intrinsic cardiac conduction system

Network of noncontractile (autorhythmic) cells

• initiate &distribute impulses to coordinate depolarization and contraction of heart

Sequence of Excitation

Cardiac pacemaker cells pass impulses, in order

SA node → AV node → AV bundle → R & L bundle branches → Purkinje fibers

SA node (Pacemaker)

Generates impulses about 75x / min (Sinus Rhythm)

Av node

If defective, may cause a heart block: Too slow to maintain adequate circulation

Treatment: Artificial pacemaker (recouples atria and ventricles)

Benefit of longer AP and contraction

Sustained contraction ensures efficient ejection of blood

Contractile muscle fibers

make up bulk of heart muscle and are responsible for pumping action

Steps in AP of contractile cardiac muscle cells

Depolarization: Na+ influx, opens Na+ channels

Plateau phase: Ca2+ influx, K+ channels closed

Repolarization: Ca2+ inactivate, K+ channels opening

Waves of EKG

P wave

QRS Complex wave

T Wave

P-R interval of EKG

Beginning of atrial excitation to beginning of ventricular excitation

S-T Segment of EKG

Entire ventricular myocardium depolarized

Q-T interval of EKG

Beginning of ventricular depolarization through ventricular repolarization

EKG of heart

remember both, this bottom one is related to top one

Electrocardiogram(ECG or EKG)

Composite of all action potentials at given time

EKG detects

• Enlarged R waves - indicate enlarged ventricles

• Elevated or depressed S-T segment - indicates cardiac ischemia

• Prolonged Q-T interval reveals - repolarization abnormality that increases risk of ventricular arrhythmias

Systole

Period of heart contraction

Diastole

Period of heart relaxation

Cardiac cycle

Blood flow through heart during one complete heartbeat

Atrial systole & diastole; followed by ventricular systole & diastole

Ventricular Ejection Fraction

Ejection Fraction = (Stroke volume / End-Diastolic Volume) x 100%

ventricular contraction

when blood is forced out of ventricles

Isovolumetric contraction Steps

1. Atria relax; ventricles contract

2. Rising ventricular pressure; AV valves close

3. Split second period: Ventricles close, volume remains constant, ventricles continue contracting

4. Valves open when ventricular pressure exceeds large artery pressure

Isovolumetric Ventricular Relaxation Early Diastole

1. Ventricular repolarization (T wave); Ventricles relax

End-Systolic Volume

Ventricular pressure drops causing backflow of blood

Ventricles completely closed

Isovolumetric Ventricular Relaxation Mid

Ventricles relax, no blood is entering or leaving ventricles

AV Valves are closed, no change in volume

Ventricular Filling

AV valves open, blood flows from atria into ventricles

Atria contracts at end of diastole; 80% of filling occurs passively before atrial contraction

Heart Sounds

Lub-Dup: closing of heart valves

Lub (1st sound): Closing of AV valves at beginning of ventricular systole

Dup (2nd sound): Closing of SL valves at beginning of ventricular disatole

Extra Heart sounds

Heart murmurs

S3 (volume problem

S4 (pressure problem)

Cardiac Output

Amount of blood pumped out by each ventricle in 1 minutes (Liters/min)

Cardiac output equation

CO = Heart Rate x Stroke Volume

What is Stroke Volume

The amount of blood ejected by each ventricle during a single heartbeat.

SV = EDV (120mL) - ESV (50 mL) = 70 mL/beat

3 Main factors affecting Stroke Volume

• Preload

  • Changes in the EDV

• Contractility

  • changes in the magnitude of sympathetic nervous system input to the ventricles

• Afterload

  • Changes in afterload, the arterial pressures against which the ventricles pump

Venous Return

rate of blood flow back to the heart’s right atrium

Contractility

Increased contractility lowers ESV which is caused by

Epinephrine release stimulates increased Ca2+ influx, leading to more cross bridge formations

Afterload

Back pressure from arterial blood pushing on SL valves

• Aortic pressure is ~80 mmHg

• Pulmonary trunk pressure ~10 mmHg

Hypertension increases afterload, resulting in increased ESV and reduced SV

Hypertension ______ afterload, resulting in increased ESV and reduced SV

increases

Tachycardia

HR >100 beats/min

Bradycardia

HR slower than 60 beats/min

Congestive heart failure (CHF)

CO is so low that blood circulation is inadequate to meet tissue needs

Coronary atherosclerosis

Heart becomes hypoxic, contracts inefficiently

Persistent high BP

Causes myocardium to exert more force (weakens myocardium)

• Chronic increased ESV causes myocardium hypertrophy and weakness

Dilated cardiomyopathy

Ventricles stretch, become flabby, myocardium deteriorates

Cardiac Output Imbalance of Heart

• Left side failure = Pulmonary congestion

• Right side failure = Peripheral congestion

  • Known as Edema

Failure of either side weakens the other side

Treatment: removal of fluid, drugs to reduce afterload and increase contractility

Pulmonary congestion

Blood backs up into lungs

Only left side heart failure

Peripheral congestion

Blood pools in body organs

Called edema, only on right side of heart

Arteries

Oxygenated blood away from heart except when it comes to the pulmonary artery, which carries deoxygenated blood

Veins

Deoxygenated blood to heart except for the pulmonary veins

Capillaries

Exchange of gases, nutrients, wastes, hormones, etc

Flow of blood

Arteries → Arterioles → Capillaries → Venules → Veins

Blood Pressure from aorta to vena cava

Blood pressure decreases from Aorta to Vena Cava

Diastolic and Systolic pressure come together at the arterioles

Mean arterial pressure

Pressure that propels blood to tissues

MAP calculated by DP + PP

Diastolic + Pulse pressure

Pulse Pressure formula

PP = SP - DP

Systolic pressure - Diastolic pressure

Tunica Intima

Intimate contact with blood

Tunica Media

Of smooth muscle and elastin

Sympathetic vasomotor nerve fibers innervate this layer, controlling

Vasoconstriction

Vasodilation

Bulkiest layer responsible for maintaining blood flow and blood pressure

Tunica externa

Outermost layer of wall

Loose collagen fibers that protect and reinforce wall and anchor it to surround structures

Compliance

Volume/Pressure

Higher compliance means it is easily stretched