Biol 224 Exam 1 Wone Flashcards
Parietal Pericardium
Double walled outer sac
Tough
Pericardial Cavity
Filled with pericardial fluid
Lubricates the heart to reduce friction
Visceral Pericardium
= to epicardium
Epicardium
Outermost wall of the heart
Endocardium
Lines the heart chambers
Covers valve surfaces
Myocardium
Lies between the epicardium and endocardium
Performs the work of the heart
Blood flow in the heart
Vena cava -> R. Atrium -> Tri. Valve -> R. Ventricle -> pulmonary valve -> pulmonary trunk -> pulmonary artery -> lungs -> pulmonary veins-> L. Atrium -> Bi. Valve -> L. Ventricle -> aortic valve -> aorta -> body -> heart
What is the cause of angina?
Obstruction of coronary blood flow
Cause of MI
Sudden death of heart tissue from long-term obstruction of a coronary artery
Cause of congestive heart failure
Failure of either ventricle to eject blood properly
Tricuspid valve
Located between right atrium and right ventricle
Bicuspid valve
Located between left atrium and left ventricle
Pulmonary valve
Located between right ventricle and pulmonary trunk
Aortic valve
Located between left ventricle and aorta
Pacemaker potential
The gradual depolarization of polarized tissue
Cause: slow inflow of Na without compensating outflow of K
Calcium-induced calcium release
Bringing calcium into a cell to release the calcium in the SR
Electrical excitation of the SA node
SA node -> atrial myocardium -> AV node -> AV bundle -> purkinje fibers -> ventricular myocardium
P-wave
Atrial depolarization
QRS-wave
Atrial repolarization
Ventricular depolarization
T-wave
Ventricular repolarization
Arrhythmia
Abnormal cardiac rhythm
Tachycardia
Heart beats too fast
> 100 BPM
Bradycardia
Heart beats too slow
<60 BPM
Ectopic Focci
Spontaneous firing somewhere other than the SA node
“Lub” sound
Tri upside and bicuspid valve closing at the same time
“Dub” sound
Aortic and pulmonary valves closing
Ventricular filling
Ventricles expand and fill with blood
Atria polarize
Contraction
Ventricles depolarize
Atria depolarize
Contraction begins
Ventricular Ejection
Ejection of blood
Ventricles begin repolarization
Relaxation
Full ventricular repolarization
Relaxation of heart muscles
Cardiac Output (CO)
Amount of blood ejected by ventricle in one minute
Starlings law
The more heart muscle stretches, the stronger the contraction
Pre-load
Depends on amount of blood in the ventricles
Higher amount of blood = higher pre-load
After load
BP in aorta and pulmonary trunk immediately distal to semilunar valves
(Basically amount of blood left in heart after contraction)
Stroke Volume ( SV)
Increased: increase preload or contractility
Decreased: increased after load
Heart Rate
Increased: exercise, SNS
Decreased: rest, PNS
Tunica Interna
Lines inside of blood vessels
Exposed to blood
Tunica Media
Middle layer of blood vessel
Thickest layer usually
Produces vasomotion
Tunics Externa
Outermost layer of blood vessel
Anchors the blood vessel
Conducting arteries
Biggest
Aorta, common carotid, subclavian
VASOMOTION
Resistance Arteries
Smallest
No names, too small and numerable
Metarterioles
Connect Arterioles to capillaries
Distributing arteries
Deliver blood to specific organs
Brachial, femoral, renal, and splenic
Postcapillary venues
Smallest veins
More porous than capillaries
Muscular venues
Receives blood from postcapillary venules
Medium veins
Most veins with individual names
Radial,ulnar, etc.
Venous sinuses
NO VASOMOTION
veins with especially thin walls
Continuous capillaries
Occur in most tissues
Tight junctions and intercellular clefts
Fenestrated capillaries
Occur in kidneys and small intestine
In organs that require rapid absorption and filtration
VASOMOTION
Sinusoids
VERY LEAKY
liver, bone marrow
Allow things to enter circulation (new RBC’s)
Simple circulatory route
Heart to arteries to capillaries to veins to heart
Portal System
Blood flows through two cones consecutive capillary networks before returning to the heart
Cardiac shock
Cardiac abnormalities decrease ability of heart to pump blood
Hypovolemic shock
Diminished blood volume
Vascular shock
Decreased vascular tone / widespread vasodilation
Obstructed venous return shock
Obstructed blood flow
Septic shock
Bacterial toxins trigger vasodilation
Anaphylactic shock
Severe immune reaction
Hypertension
High resting BP
Hypotension
Low resting BP
Edema
Accumulation of excess fluid in tissue
Varicose veins
Pooling of blood in the legs from standing for long periods of time causes veins to become hyperextended.
Erythrocytes
Red blood cells
Pick up oxygen from lungs and co2 from the body
Platelets
Promotes clotting
Stick together to begin clot
Secrete vasoconstrictors to stop bleeding
Leukocytes
Protect us against disease
Neutrophils
Most abundant WBC
destroy bacteria
Eosinophils
Hard to find
Weaken/destroy large parasites
Ex: hookworm
Basophils
Rarest WBC
Secrete: histamine (vasodilator) and heparin (anticoagulant)
Lymphocyte
Second most abundant WBC
Monocyte
Largest
Premature macrophage
Hemopoiesis
Synthesis of blood cells
Leukopoiesis
Synthesis of leukocytes
Vascular spasm
Prompt contraction of a broken blood vessel
Platelet Plug Formation
Collagen fibers break platelets, causing them to rupture and stick together to for the beginnings of a clot
Stays active until broken vessel is sealed
Blood clotting
Last and most effective against bleeding
Fibrinolysis
Dissolution of a clot
Deoxygenated blood vessels of the heart
Vena Cava
Pulmonary Artery
Oxygenated blood vessels of the heart
Aorta
Pulmonary Veins
What vessels supply the heart itself with blood
Anterior and posterior interventricular branches
Circumflex branch
Right marginal branch