Blood and Heart

Six general functions of blood?

Transport, Immune component, clotting, temperature regulation, pH (Proteins, RBCs), and osmotic fluid distribution

3 determinants of blood plasma osmolarity

sodium concentration, RBC, and plasma protein (albumin created by the liver)

polycythemia

elevated RBC

Average blood volume

5 Liters

Three main proteins in the blood

albumin, globulins, fibrinogen

Components of blood

Plasma: protein(7%), water (91%), other solutes (2% i.e. waste, nutrients ions, etc.); Cells: Platelets, White blood cells, RBCs

Function of the 5 main white blood cells (WBCs) found in blood?

protect the body from infections

granulocyte vs agranulocyte

Granulocytes contain visible granules that can be used to attack foreign cells or alert other immune system cells

Agranulocytes do not contain visible granules, serving to either eat pathogens through phagocytosis or alert other cells about the infection.

Hematopoiesis

Blood cell production

Cytokines

Chemicals released by the immune system communicate

Erythropoiesis: Location and stimulator

red bone marrow and EPO from kidneys/liver

Typical life span of RBC

~120 days (no nucleus)

Hematocrit def. and gender percentatges

% of blood samples that are RBCs; Men: 42-52%, Women:37-48%

How does respiratory illnesses like emphysema or chronic bronchitis impact hematocrit levels?

Decreased oxygen from the respiratory system results in increased EPO production leading to a increased hematocrit

Effects of polycythemia versus anemia

Polycythemia: increased RBC, viscosity, Blood volume, and decreased heart rate (HR);

Anemia: decreased RBC, viscosity, blood volume, and increased HR

Causes of Hypoxia

decreased RBC count, Decreased hemoglobin, Decreased Oxygen availability

Effect of emphysema on RBC count

decreased oxygen access->increased EPO synthesis->increased RBC count->polycythemia

Components of Hemoglobin complex

Heme(4 and contains iron that oxygen binds with) and globin (2 alpha and 2 beta)

Shape of red blood cell

biconcaved disc

Sickle cell

HbS results from one amino acid difference in beta chain; result is aggultination (clumping), poor oxygen capacity, and hemolysis

Other components needed for erythropoiesis

EPO, Iron, B12, folic Acid, Vitamin C, Copper

Iron Deficiency Anemia

anemia resulting when there is not enough iron to build hemoglobin for red blood cells

Where RBCs go to die

RBCs cannot die in circulation because Hb will clog kidneys ; thus, consumed and broken down by macrophages in spleen and liver.

disposal proticol for broken down RBCs

Old red blood cells in spleen/broken down. Amino Acids/Iron return to red bone marrow while bilirubin is transported to liver to be excreted as bile. If liver cannot break down bilirubin, the chemical build ups in blood→result in jaundice.

jaundice

accumulation of yellow pigmented bilirubin in the blood that results in the skin and eyes developing a yellow pigment

Hemostasis

balancing clotting when injured and not clotting when no damage is present

Steps in forming a clot

vascular spasm->platelet plug->coagulation->clot retraction->thrombolysis

Vascular spasm

smooth muscles contract and platelets release serotonin that stimulate vasoconstriction

platelet plug formation

Damaged tissues release vWF to alert platelets. Recruited platelets release cytokines to alert more platelets to and the process continues until the damage site is covered in a soft plug of platelets loosely held together.

Coagulation

Fibrinogen is converted to fibrin by Thrombin and forms a hard blood clot

Two primary types of Coagulation amplification cascades that leads to blood clot

Extrinsic pathway(damage through the wall of a blood vessel or surrounding tissue) and Intrinsic pathway (damage within the vessel itself)

Important steps in the Coagulation amplification cascade

extrinsic and intrinsic factors and calcium->activate Prothrombin activator-> convert prothrombin to thrombin-> convert fibrinogen to fibrin

3 main steps in thrombolysis

healed tissue releases tPA which activates plasminogen converting it to Plasmin that then breaks down fibrin

chemicals that inhibit clot formation

antithrombin(liver) and heparin(mast cells and basophils)

emolus

traveling clot

deep vein thrombosis

formation of a blood clot in a vein deep in the body, most commonly the leg

stroke

Damage to the brain from interruption of its blood supply, often due to a blood clot.

cause of heart attack

clot blockage of coronary arteries

heart is housed inside

pericardial cavity made up of visceral pericardium(epicardium) and parietal pericardium

Systole/diastole

contraction and empties/relaxation and filling

How does cardiac muscle differ from skeletal muscle?

cardiac muscle contains intercalated discs creating a network or branching cells to enable electrical signal transmission.

Location that electrical signal transfers from cardiac cell to adjacent cells

gap junctions

autorhythmic

heart beat without central nervous system control

Effects of ANS modulation

SNS=increase HR while PSNS (vagus)=decreased HR. PSNS is more in control at rest and sets our base rate at about 72 beats per min.

Which electrical signal=mechanical events?

Depolarization=systole; Repolarization=diastole

Flow of electrical depolarization across the heart.

SA node generate action potential->depolarizes both atriums->collects at atrioventricular node->travels down septum through the AV bundle to AV bundle branches->traverses apex to base through Purkinje fibers along the external wall of each ventricle

Times for electrical conduction in heart

Depolarization of atria (50msec); Pause (100msec) ventricles fill; ventricle myocardium depolarize (200msec)

arrhythmia

any irregular rhythm

The cause of slow steady depolarization of cardiac pacemaker cells

sodium slowly flows in the cell eventually reaching threshold

Parts of a cardiac contractile cells electrophysiology graph

0-1. Depolarization

2. Plateau

3. Repolarization

4. Resting Membrane potential

purpose of plateau phase

lengthens cardiac action potential (slightly slows heart rate to allows heart to fill with blood)

Ejection Fraction (EF)

Stroke volume/end diastolic volume

pressure in the left ventricle/right ventricle and pressure needed to over come to move through a valve

LV=120mmHg overcome 80mmHg in Aorta

RV=25mmHg overcome 10mmHg in the pulmonary trunk

cardiac output

volume of blood pumped per minute; CO=HR X Stroke Volume

Variables influencing heart rate

ANS: SNS (EPI and NE) increases HR while PSNS(Ach) decreases HR; fitness level, presence of ions and their concentrations

An effect that increases HR is...

positive chronotropic effect

An effect that decreases HR is...

negative chronotropic effect

An effect that decreases heart contractility is...

negative ionotropic effect

An effect that increases heart contractility is...

positive ionotropic effect

General limit to heart rate

230 bpm because of the refractory period of SA node

Variables that influence stroke volume

Preload: amount of stretch on wall of ventricle; Contractility: hearts ability to contract with force; Afterload: force against which a heart has to pump to eject blood

How preload influences stroke volume

increase in Blood volume and/or EDV->increases stroke volume

How contractility influences stroke volume

increased contractility->increased stroke volume

How afterload influences stroke volume

increased afterload->decreased stroke volume

Determinants for EDV

Length of diastole and venous return

How does ventricular stretch impact stroke volume

the more blood the ventricle receives the more it will stretch and the more blood that it will push as it rebounds through contraction.

universal blood donor

O- because it does not have surface antigens A, B, or Rh

universal blood recipient

AB+ because it does not have antibodies for A, B, or Rh

where doe the thumping sounds come from when you listen to your chest

The first sound is the AV closing and the second is the SL valves closing

4 primary stages of the cardiac cycle

Ventricular filling, isovolumetric contraction, ventricular ejection, and isovolumetric relaxation.

what is occurring during ventricular filling

Atrial pressure is greater than ventricle pressure so blood is forced through opening the tricuspid and bicuspid into the ventricles

what is occurring during isovolumetric contraction

Ventricle pressure is greater than atrial pressure so the tricuspid and bicuspid close (first heart sound) and blood flow from the atria is halted.

Blood is not ejected from the ventricles at this point because ventricle pressure is not greater than the pulmonary trunk and aorta pressure; their semilunar valves remain closed.

what is occurring during ventricular ejection

ventricle pressure is greater than the pulmonary trunk and aorta pressures; their semilunar valves open to let blood flow to the lungs and body.

Atria are repolarizing and accepting blood again. Tricuspid and bicuspid are closed.

what is occurring during isovolumetric relaxation

Pressure in the ventricles decreases as it progresses through diastole and repolarizes. Decrease pressure causes the semilunar valves of the pulmonary trunk and aorta to shut (second heart sound).

Atria continue through diastole filling with blood until the SA node triggers another action potential. Tricuspid and bicuspid are closed.

Parts of an electrocardiogram

P wave, QRS complex, T wave

The P wave of an ECG represents

atrial depolarization

The QRS wave of an ECG represents

ventricular depolarization (atria repolarization is masked/hidden)

The T wave of an ECG represents

ventricular repolarization

Identify the primary waves of an ECG

P, QRS, and T waves

Tachycardia vs. Bradycardia

tachycardia= rapid pulse over 100 bpm

bradycardia= slowed pulse under 60 bpm