bio 251

arteries

carry mostly O2 rich blood away from heart

veins

carry mostly O2 poor blood back to heart

capillaries

\-thin exchange vessels

\-bridge arterial + venous structures

\-form beds/networks within tissues

\-permit exchange between blood + interstitial fluid

\-tunica interna

mediastinum

just behind sternum between pleural cavitities

pericardial cavity

open space

pericardium

serous membrane lining cavity

epicardium

visceral pericardium, covers heart

parietal pericardium

lines cavity

pericardial fluid

lubricates between layers

left side

oxygenated

right side

deoyxgenated

atria

chambers that receive blood at top of heart

coronary sulcusles

\-laterally

\-separates atria from ventricles

ventricles

inferior chambers of heart

interventricular sulcus

\-runs vertically

\-separates left + right ventricles

epicardium

visceral pericardium= outer surface/covering

myocardium

middle layer w concentric layers of cardiac muscle tissue + produce squeezing contraction

endocardium

internal layer that lines chambers + valves

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simple squamous epithelium

cardiac muscle cell characteristics

\-smaller than skeletal muscle

\-1 nuclei, striated, organized into sarcomeres

\-high amount of mitochondria

\-intercalated discs

\-involuntary

\-wider t-tubules w simpler SR

intercalated discs

synchronizes contraction (contracts as one)

interatrial septum

separates atria

interventricular septum

separates ventricles

atrioventricular valves (AV valves)

valves that separate atria from ventricles

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folds of fibrous tissue prevent backflow

biscupid valve

left AV valve

tricuspid valve

right AV valve

right atrium receives blood from

inferior + superior vena cava + coronary sinus

chordae tendineae

CT fibers that pull on valves

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\-support cardiac muscle fibers

\-distribute force of contraction evenly

\-add strength/prevent overexpansion of heart

\-provide elasticity

papillary muscle

muscular ridges that pull of fibers

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pulmonary semi-lunar valves

prevent backflow to ventricles (3 cusps)

coronary circulation

blood to heart

coronary arteries

arise from aortic sinus + rn transverse w/ sulci

cardiac veins

drain to coronary sinus

coronary artery disease

\-blockage of coronary circulation decreasing O2 flow

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\-leads to reduction of cardiac performance

atherosclerotic plaque

fatty deposit or clot that reduces blood flow due to vessel narrowing

myocardial infarction

heart attack, death of cardiac muscle cells

conducting system

autorhythmic fibers that initiate + distribute contractile stimulus- “specialized cardiac cells”

pacemaker cells

cells that set normal heart rate

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nodal cells (cluster of cells)

conducting cells

cells that interconnect 2 nodes + distribute contractile stimulus to myocardium

autorhythmicity

conducting cells control heartbeat w out neural/hormonal control

contractile cells

receive signals + contract

\-make up 99% of heart cells

sinoatrial node (SA node)

wall of right atrium contain pacemaker cells that establish heart rate

atrioventricular node (AV node)

floor of atrium receives impulse from SA node via internodal pathway

internodal pathway

links SA node to AV + triggers contraction of pectinate muscles

threshold

minimal voltage reached on membrane near intercalated disc

rapid depolarization

fast voltage gated sodium\` OPEN, sodium RUSHES in

plateau (+ 30 mV)

sodium channels close

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slow voltage gated calcium channels OPENS + RUSHES into cell

repolarization

calcium channels close

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slow potassium channels OPENS + RUSHES OUT

ECG or EKG or electrocardiogram

detects electrical events of cardiac muscle

p wave

atrial depolarization or contraction

qrs complex

ventricles depolarize (contraction shortly after)

t wave

ventricles repolarize (relaxation)

arrhythmias

abnormal patterns of cardiac electrical activity

atrial fibrillation (Afib)

no p-wave, normal QRS complex, irregular timing

ventricular fibrillation

no QRS complex, no rhythmic contraction of myocardium

systole

volume shrinkage → pressure increase

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BLOOD EJECTED

diastole

pressure is low, volume increases, blood passively fills chamber

atrial systole

contraction of atria the results in inc pressure + ejection of blood to ventricle

atrial diastole

relaxation of atria resulting in decreased pressure; max blood in ventricle = EDV; AV valves close to keep blood in ventricle

ventricular systole

contraction of ventricle

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first phase builds pressure (isovolumetric contraction)

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second phase ejection of stroke volume out of heart

ventricular diastole

relaxation of ventricles + passive blood flow

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early phase= isovolumetric relaxation (all valves closed) -blood fills atria

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late phase- AV valves open, blood passively fills ventricles

heart murmur

caused by regurgitation thru valves

cardiodynamics

movements + forces generated by cardiac contractions

edv

MAX VENTRICULAR VOLUME before systole

esv

blood after contraction

stroke volume

blood ejected from heart after one stroke

cardiac output

volume of blood pumped per 1 minute

CO=

SV x HR

cardiac output indicator

of perfusion

fibers increase

sympathetic neuron via cardioaccelerator centers

fibers decrease

parasympathetic neurons via cardioinhibitory centers

hormonal adjustments

E, NE, + thyroid hormone increase HR

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acetylcholine decreases HR

agglutinogens

surface proteins that allow body to recognize “self”

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blood type based off antigens

type a

has antigen A, produces B antibody

antibody

circulating protein that recognizes foreign substances causes agglutination

antigens

A, B, AB, Rh

O

no antigens BUT both antibodies

rhesus +

antigens but no antibodies

rhesus -

no antigens, produces antibodies after initial exposure

4 main blood types

A, B, AB, and O

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AND rhesus factor

O neg

no antigens on surface, antibodies can’t detect them

cross-reactions

antibodies interact causing agglutination

leukocytes

\-WBCs in immune response

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\-lack hemoglobin; have nucleus + organelles

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\-defend body against infectious agents + remove toxins + wastes

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\-connective tissue proper + lymphatic system organs

granulocytes

contain secretory granules in cytoplasm

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neutrophil, basophil, eosinophils

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small

agranulocytes

lack secretory granules

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monocytes + lymphocytes

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1-10 day life span

WBC characteristics

\-migrate outside bloodstream by diapedesis movement thru capillaries into tissue

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\-attracted to specific chemical stimuli = chemotaxis= guides them to pathogens

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\-responds to 1 specific threats/pathogens/antigen

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lymphocytes= specific (adaptive) immune response

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neutrophils, eosinophils, basophils, monocytes= response to any threat = nonspecific immune response

neutrophils

\-most common

\-first to arrive at injury

\-attack bacteria

eosinophil

\-rare

\-PARASITES

\-allergic reaction

basophil

\-least numerous

\-SECRETE HEPARIN + HISTAMINE

monocyte

\-low #

\-migrate to tissues becoming macrophages

\-phagocytize large particles/pathogens

lymphocytes

\-large #s in CT + lymphatics

\-specific defense

3 classes of lymphocytes

T cells, B cells, natural killer cells

T cells

cell-mediated immunity

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attack foreign cells directly

B cells

humoral immunity

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differentiate into plasma cells (found in plasma) that secrete antibodies

natural killer cells

detect + destroy abnormal tissue cells (cancers) + have general attack on most cells

platelets

cell fragments for clotting system

platelet roles

1. reduce size of vessel injury by vascular spasm (smooth muscle contraction)
2. temporary “patch” vessel via platelet plug (cluster of platelets)


1. release clotting factors for coagulation by series of chemical reactions

hemostasis

stopping of bleeding by ceasing blood flow through damaged vessels

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(vascular + platelet phase)

vascular phase

constrict blood vessel

platelet phase

forms plug, releases chemicals; positive feedbaclk loop

coagulation

Factor X stimulates PROTHROMBIN ACTIVATOR

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converts prothrombin to THROMBIN

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converts soluble fibrinogen to FIBRIN (THREADS THAT WORK W PLATELETS TO COLT BLOOD)

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CLOT RETRACTION: CLUSTER OF PLATELETS + FIBRIN RESTRACT PULLING VESSEL WALLS CLOSER