Cardiovascular System Flashcards
Determinants of SV
AFTERLOAD: Aortic blood pressure
PRELOAD: end-diastolic volume
CONTRACTILITY: active or passive contraction of ventricular muscles
Cardiac Output
CO = SV x HR
CO = Pressure gradient/R
Afterload
Ventricles cannot eject blood into the aorta or pulmonary artery until the pressure in the ventricle exceeds the pressure in the artery
(Pressure required to open semilunar valves)
Preload
The SV cannot increase unless the rate or cardiac filling also increases
Contractility
Strength of ventricular muscle contraction
Active contractility: stimulation of the sympathetic nerves to the heart
Passive contractility: the result of changing the length of the cardiac muscle fibers (frank-starling mechanism)
Control of active contractility
Due to actions of norepinephrine (or epinephrine)
- Inc rate or pacemaker activity
- Inc force of cardiac muscle contraction
- inc permeability to Ca => more cross bridge interactions
Sympathetic vs. Parasympathetic Divisions of the ANS
Sympathetic (thoracolumbar): preganglionic releases ACh then postganglionic release NE
Parasympathetic (cranial): preganglionic releases ACh then postganglionic release ACh
Systole
Ventricular contraction and blood ejection
Diastole
Ventricular relaxation and filling
Chronic topic effects
Effects of the ANS on heart rate
Fibers from cardioacceleratory center
Sympathetic
Fibers from the cardio inhibitory center
Parasympathetic
Mechanism of Parasympathetic Control of Heart Rate
ACh release increases K permeability, and the rate of potassium diffusion out of the cells increase.
Results in hyperpolarization (takes more time for membrane potential to reach the threshold for Na channel (atrial contraction) and Ca channels (SA node autorhythmic fibers) activation
Chemical influences on Heart Rate and Contractility
Hormones Hypocalcemia Hypercalcemia Hypernatremia Hyperkalemia
Hormones that increase heart rate and heart contractility
Epinephrine and thyroxine
Hypocalcemia
Reduced ionic calcium depresses contractility
Hypercalcemia
Dramatically increases heart irritability and leads to spastic contractions
Hypernatremia
Blocks heart contraction by inhibiting ionic calcium transport
Hyperkalemia
Too high Ca levels lead to an inhibility to depolarize and leads to heart block and cardiac arrest
Continuous capillary
Most restrictive/ intercellular clefts
Found in lungs, skeletal muscle, connective tissue, BBB
Fenestrated capillary
Pores to let large molecules to pass/ intercellular clefts
Sinusoidal capillary
Intercellular clefts/huge holes to prevent mixing of proteins and blood and to adjust contents in blood
Found in liver, spleen, bone marrow, anterior pituitary gland
Diffusion
Passive process of fluid exchange
Movement of fluid from high to low concentration until equilibrium
Bulk flow
Passive process of fluid exchange
Movement of fluid from a region of higher pressure to one of lower pressure
Transcytosis
Active process of fluid exchange
Blood hydrostatic pressure (BHP)
Pushes fluid OUT through the capillary pores
Interstitial fluid osmotic pressure (IFOP)
“Pulls” fluid OUT via osmosis; this pressure is very small compared to BHP
Blood colloid osmotic pressure (BCOP)
Result of differences in protein concentration between plasma and IFS, which tends to pull water from the ISF and into capillaries (creates constant pull of water into the blood)
Interstitial fluid hydrostatic pressure (IFHS)
Due to pressure exerted by interstitial fluid, but is normal very small
Net Filtration Pressur
Difference between the inward and outward pressures
(BHP + IFOP) - (BCOP + IFHP) = NFP
Outward(Filtration) - inward(reabsorption)
Mean arterial blood pressure
MAP = DBP + 1/3(SBP - DBP)
Pulse pressure
The PP reflects the SV
Vascular resistance
Resistance is the sum of all forces that retard flow
Flow = driving pressure/ resistance
Resistance
R = (viscosity)(vessel length)/ radius to the 4th
Systemic Vascular Resistance (SVR)
Resistance offered by the vessels of the systemic circulation
SVR = (MAP-RAP)/CO
Baroreceptors
High pressure: located in the carotid sinus and aortic arch and enter via cranial nerve IX/X
Low pressure: located in the walls of the right atrium and vena cavae, and enter the CV center via cranial nerve
Chemoreceptors
Located in the carotid sinus (via cranial nerve IX) and in the walls of the ascending aorta via (cranial nerve X)
Respond to inc H content, CO2 and most strongly to hypoxia
Activate the sympathetic div, resulting in inc HR, SV, and vasoconstriction
Catecholamines
Hormonal control of BP
(NE and epinephrine) bind directly to cardiac muscle and blood vessel smooth muscle
Antidiuretic hormone (ADh)
Causes intense vasoconstriction in case extremely low BP
Angiotension II
Causes intense vasoconstriction when renal glands perfusion is inadequate
Aldosterone
Secreted by the adrenal cortex which inc salt and water reabsorption to Cause water retention and inc BP by raising blood volume
RAA System
Kidneys release renin, angiotensinogen converts renin into angiotensin I, concerts to angiotensin II with ACE from lungs
Atrial natriuretic peptide (ANP)
Released by cells in the atria when BP is too high. This hormone causes vasoconstriction and promotes loss of water and salt by the kidneys.
Histamine
Released by mast cells
Cause vasodilation by relaxing smooth muscle
Inc blood flow to inflamed or damaged tissue
