Cardiovascular
Membranes/Linings of the heart - Fibrous CT (anchors, protects), Parietal Pericardium, Visceral Pericardium (aka epicardium)
Heart Wall Layers - Epicardium, myocardium (autorrhythmic), endocardium (smooth mm to prevent clots)
Pulmonary Artery- carries deoxygenated blood from heart (right ventricle) to the lungs
Pulmonary Vein - carries oxygenated blood from lungs to heart (left atrium)
Auricles- appendages that increase atrial volume, right’s posterior wall is smooth, anterior is ridged
Pulmonary circuit - Right side of heart
Systematic circuit - Left side of heart
Left side of heart anatomy - higher BP because pushing to more extremities, walls thicker to have stronger contractions
Blood supply of Myocardium - coronary circulation
Coronary vessels deliver blood to the myocardium when - heart relaxed
Extra pre-existing pathways for blood - anastomoses
Extra created pathways for blood - angiogenesis
Sinoatrial node - natural pacemaker for heart w/out extrinsic factors,
Atrioventricular node - special cardiac mm that slows conduction to allow complete atrial atria
Bundle of HIS/AV Bundle- receives and transmits impulses to bundle branches.
Purkinje fibers- transmit impulses to ventricular myocardium
Atria and ventricle is NOT connected by- gap junctions
P wave - depolarization of atria
QRS complex - depolarization of ventricles + depolarization of atria
T wave - depolarization of ventricles
systole - contraction
diastole - relaxation
atrial diastole - blood flows into atria
atrial systole - blood moves PASSIVELY into ventricles
ventricular systole - blood moves ACTIVELY into semilunar valves
Lubb- long slow 1st sound, contraction of ventricles/closing of AV valves
dubb- short sharp 2nd sound, closing of semilunar valves
What Is the slight pause in a heartbeat called? - quiescent period
Cardiac output formula- (stroke volume x heart rate)/1000
Cardiac output- amount of blood going through body in 1 minute
Stroke Volume- amount of blood pumped by ventricle in 1 beat (60-80 ml)
Starling’s law of the heart- the more stretched the heart mm @ start of contraction, the stronger contraction is
untrained exercise effects on heart - CO increases due to HR/SV increasing, SV plateau’s but HR increases
trained exercise effects on heart- athlete’s develop greater SV due to mm efficiency. CO increases and HR decreases
Heart rate responds to input from - aortic arch and carotid sinuses
raises heart rate - anger, anxiety, fear, exercise, hormones, warm blood
lowers heart rate - grief, pain, cold blood
tunica intima- smooth to prevent clotting, innermost
tunica media- smooth mm and elastic CT, changes vessel’s diameter, maintains normal BP, regulated by SNS
tunica externa- fibrous ct w/nerve fibers. lymph vessels, some elastin, holds vessel open/prevents ruptures
elastic (conducting) arteries- thick walled arteries near heart, contain more elastin, expand as blood ejected, pressure smoothing effect
muscular (distributing) arteries- thickest tunica media. more active in vasoconstriction, less stretchy
arterioles- lose tunica externa as they get smaller, mainly tunica media, determine blood flow into capillary beds
anastomosis- pre-existing alternate pathways for blood, not adequate supply
angiogenesis- new alternate pathways for blood
continuous capillaries- least permeable, most common, abundant in skin/mm
fenestrated capillaries- some have pores, found wherever active absorption/filtration occurs (ex. kidney, small intestine)
sinusoids of sinusoidal capillaries- leaky, in liver as macrophages, spleen as phagocytes, destroy/remove pathogens
places with poor capillary supply- tendons, ligaments, cartilage, cornea, lens
simple diffusion- O2 Co2
intercellular clefts/fenestrations- small water soluble solutes (amino acids, sugars)
pinocytotic vesicles/caveole- larger molecules (proteins)
Metabolic controls of blood flow- decreased O2/wastes causes vasodilation, too much blood flow and endothelin’s cause vasoconstriction
myogenic controls of blood flow- vascular mm responds to stretch with increased tone causing vasoconstriction, vice versa
Veins VS Arteries anatomy- veins have thinner walls (deal with lower BP), vein’s have endothelium folded to form one-way valves, smooth mm in veins is thinner
veins physiology- reservoirs, up to 65% of blood supply in veins at any given time
respiratory pump- increased respiration directly related to increased circulation
skeletal muscle pump- milks blood upwards and vales prevent back flow
Cardiovascular
Membranes/Linings of the heart - Fibrous CT (anchors, protects), Parietal Pericardium, Visceral Pericardium (aka epicardium)
Heart Wall Layers - Epicardium, myocardium (autorrhythmic), endocardium (smooth mm to prevent clots)
Pulmonary Artery- carries deoxygenated blood from heart (right ventricle) to the lungs
Pulmonary Vein - carries oxygenated blood from lungs to heart (left atrium)
Auricles- appendages that increase atrial volume, right’s posterior wall is smooth, anterior is ridged
Pulmonary circuit - Right side of heart
Systematic circuit - Left side of heart
Left side of heart anatomy - higher BP because pushing to more extremities, walls thicker to have stronger contractions
Blood supply of Myocardium - coronary circulation
Coronary vessels deliver blood to the myocardium when - heart relaxed
Extra pre-existing pathways for blood - anastomoses
Extra created pathways for blood - angiogenesis
Sinoatrial node - natural pacemaker for heart w/out extrinsic factors,
Atrioventricular node - special cardiac mm that slows conduction to allow complete atrial atria
Bundle of HIS/AV Bundle- receives and transmits impulses to bundle branches.
Purkinje fibers- transmit impulses to ventricular myocardium
Atria and ventricle is NOT connected by- gap junctions
P wave - depolarization of atria
QRS complex - depolarization of ventricles + depolarization of atria
T wave - depolarization of ventricles
systole - contraction
diastole - relaxation
atrial diastole - blood flows into atria
atrial systole - blood moves PASSIVELY into ventricles
ventricular systole - blood moves ACTIVELY into semilunar valves
Lubb- long slow 1st sound, contraction of ventricles/closing of AV valves
dubb- short sharp 2nd sound, closing of semilunar valves
What Is the slight pause in a heartbeat called? - quiescent period
Cardiac output formula- (stroke volume x heart rate)/1000
Cardiac output- amount of blood going through body in 1 minute
Stroke Volume- amount of blood pumped by ventricle in 1 beat (60-80 ml)
Starling’s law of the heart- the more stretched the heart mm @ start of contraction, the stronger contraction is
untrained exercise effects on heart - CO increases due to HR/SV increasing, SV plateau’s but HR increases
trained exercise effects on heart- athlete’s develop greater SV due to mm efficiency. CO increases and HR decreases
Heart rate responds to input from - aortic arch and carotid sinuses
raises heart rate - anger, anxiety, fear, exercise, hormones, warm blood
lowers heart rate - grief, pain, cold blood
tunica intima- smooth to prevent clotting, innermost
tunica media- smooth mm and elastic CT, changes vessel’s diameter, maintains normal BP, regulated by SNS
tunica externa- fibrous ct w/nerve fibers. lymph vessels, some elastin, holds vessel open/prevents ruptures
elastic (conducting) arteries- thick walled arteries near heart, contain more elastin, expand as blood ejected, pressure smoothing effect
muscular (distributing) arteries- thickest tunica media. more active in vasoconstriction, less stretchy
arterioles- lose tunica externa as they get smaller, mainly tunica media, determine blood flow into capillary beds
anastomosis- pre-existing alternate pathways for blood, not adequate supply
angiogenesis- new alternate pathways for blood
continuous capillaries- least permeable, most common, abundant in skin/mm
fenestrated capillaries- some have pores, found wherever active absorption/filtration occurs (ex. kidney, small intestine)
sinusoids of sinusoidal capillaries- leaky, in liver as macrophages, spleen as phagocytes, destroy/remove pathogens
places with poor capillary supply- tendons, ligaments, cartilage, cornea, lens
simple diffusion- O2 Co2
intercellular clefts/fenestrations- small water soluble solutes (amino acids, sugars)
pinocytotic vesicles/caveole- larger molecules (proteins)
Metabolic controls of blood flow- decreased O2/wastes causes vasodilation, too much blood flow and endothelin’s cause vasoconstriction
myogenic controls of blood flow- vascular mm responds to stretch with increased tone causing vasoconstriction, vice versa
Veins VS Arteries anatomy- veins have thinner walls (deal with lower BP), vein’s have endothelium folded to form one-way valves, smooth mm in veins is thinner
veins physiology- reservoirs, up to 65% of blood supply in veins at any given time
respiratory pump- increased respiration directly related to increased circulation
skeletal muscle pump- milks blood upwards and vales prevent back flow