Cardiovascular System Flashcards by iliana manjon

Determinants of SV

AFTERLOAD: Aortic blood pressure
PRELOAD: end-diastolic volume
CONTRACTILITY: active or passive contraction of ventricular muscles

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Cardiac Output

CO = SV x HR

CO = Pressure gradient/R

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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)

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Preload

The SV cannot increase unless the rate or cardiac filling also increases

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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)

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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

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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

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Systole

Ventricular contraction and blood ejection

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Diastole

Ventricular relaxation and filling

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Chronic topic effects

Effects of the ANS on heart rate

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Fibers from cardioacceleratory center

Sympathetic

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Fibers from the cardio inhibitory center

Parasympathetic

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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

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Chemical influences on Heart Rate and Contractility

Hormones
Hypocalcemia
Hypercalcemia 
Hypernatremia 
Hyperkalemia

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Hormones that increase heart rate and heart contractility

Epinephrine and thyroxine

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Hypocalcemia

Reduced ionic calcium depresses contractility

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Hypercalcemia

Dramatically increases heart irritability and leads to spastic contractions

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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