Cardiovascular 5 Flashcards
Sympathetic modulation of contraction (SV): 4 steps
- Phosphorylation of CA2+ channels increases calcium conductance during an AP
- Phosphorylation of ryanodine receptors enhances sensitivity to Ca2+, increasing release of Ca2+ from SR
- Increases rate of myosin ATPase (binds faster)
- Phosphorylation of SERCA increases speed of CA2+ reuptake, increasing Ca2+ storage
-that can be used for next contraction
Increasing sarcomere length increases
Force of Contraction (SV)
2 Reasons why increasing sarcomere length will increase force of contraction
- Increases the Ca2+ sensitivity of Myofilaments
-a stretched sarcomere has a decreased diameter, can reduce distance Ca2+ needs to diffuse
-increases probability of cross bridging - Additional tension on stretch activated Ca2+ channels
-increases Ca2+ entry from extracellular space
-increasing Ca2+ induced Ca2+ release
-increases tension
The degree of myocardial stretch prior to contraction is known as
The preload on the heard
-load on ventricles before contraction
Increase preload= increase contractility
Frank- Starling Law of the Heart
Stroke volume increases with increasing EDV
The amount of force developed by cardiac muscle of ventricle (SV) depends on the initial stretch oof the ventricle walls (ventricular filling)
How is EDV determined
Normally by Venous return
-increased venous return increase venous pressure
-results in increased atrial filling and leading to increased ventricle filling
Factors affecting Venous Return: (3)
- Skeletal Muscle Pump
- Respiratory Pump
- Sympathetic Constriction of Veins
How does the Skeletal Muscle Pump affect venous Return
Skeletal muscle activity compresses veins in the extremities, pushing blood back to the heart
-increased muscle activity of the extremities can increase venous return
-through one way valves it returns
-pressure in veins usually low at rest
How does the Respiratory Pump affect Venous Return
During inspiration, the chest expands and diaphragm moves down
-creates a subatmoshperic pressure in the thoracic cavity
-draws blood into the vena cava that exist within
Basically makes thoracic cavity bigger and creates a negative reassure to stretch internal viscosities more
-also during inspiration veins in the abdomen are compressed -forces blood back to the heart
How does sympathetic constriction of veins affect Venous Return
-decreases their volume squeezing blood back towards the heart
-Fromm norepinephrine -pressurized blood to increase return
What is after load
The end load against which the heart contracts to eject blood
3 factors that affect SV of the heart
Preload. After load, COntractility
How is afterload determined
By the combination of the EDV and the pressure in the outflow artery, prior to contraction
Afterload can be increased how
Increased arterial blood pressure, decreased aortic compliance, chronic hypertension, echocardiography, altered ejection fraction
Hypertrophy in the Ventricles means
The muscle around it (wall) gets thicker
-this causes the ventricles to lose elasticity and compress the coronary arteries
-results in a lower SV as the ventricle can’t stretch to fill
Heart rate is determined by
The rate of depolarization in autorhytmic cells
Cardiac Output is determined by:
Heart rate and Stroke volume
-about 5L/min
Heart rate decreases due to
Parasympathetic innervation
Heart rate increases due to
Sympathetic innervation and epinephrine
Stroke Volume is determined by
Force of contraction in ventricular myocardium
Stroke Volume is influenced by
Contractility, EDV, Afterload
Contractility is increased by
Sympathetic innervation and epinephrine
EDV varies with affect from
Venous return
-respiratory pump and skeletal muscle pump
An increase in afterload causes a what in SV
A decrease in SV
Each side of the heart…
Functions as an independent pump and loop
Elastic systemic arteries are a pressure reservoir that
Maintain blood flow during ventricular relaxation
The arterioles are the site of
Variable resistance
-choose where blood is constricted to or allowed to
Gas exchange between the blood and cells takes place
ONLY at the capillaries
Systemic veins serve as
An expandable volume reservoir
-half the blood in the body sits in the systemic veins
Progressive branching of vessels pathway:
Aorta> Arteries > Arterioles > Capillaries > Venules ? Veins > Vena cavas
All vessels contain what inner layer
An inner layer of thin endothelial cells
-can be wrapped in a combination of elastic tissue, smooth muscle, or fibrous tissue
Endothelial Cells are important in: (4)
Secreting Paracrines
Regulation of BP
Blood Vessel Growth
Absorption of Materials
In most vascular smooth muscle, there is always a state of
Partial contraction
-can be influenced by neurotransmitters, hormones, paracrines (Sympathetic Input)
-these bind receptors, resulting in increased cystitis Ca2+ release, causing contraction
Systemic circuit begins with
The aorta (single), branches off to major arteries
Arteries walls breakdown:
Walls are both stiff and springy (pressure reservoir)
-thick smooth muscle layer and large amount of elastic and fibrous connective tissue
Arteries branch into
Arterioles
-that mainly have vascular smooth muscle
Microcirculation
Smallest place where circulation takes place
-arterioles, capillaries, venules
-across you have metarterioles which are bypass vessels (also for WBCs)
Capillaries breakdown
-smallest venules in the CV system
-majority of exchange of O2 between blood and interstitial space happens
-single think endothelial layer surrounded by basal lamina (extra cellular matrix)
-gases normally passively diffuse across endothelial cells
Capillaries are linked by
Interendothelial junctions -also aid in transport of small solutes and water
-they are like tight junctions (transmembrane proteins that link adjacent cells together)
-
What are Fenestrations in Capillaries
Membrane lined pores running through them to allow the transport of substances between plasma and interstitial fluid
Capillaries are often surrounded by
Pericytes (BBB)
-periocytes and astrocytes
-prevents substances from the plasma to interstitial fluid of the brain (which is good)
Main types of Capillaries: (3)
- Continuous Capillary
- Fenestrated Capillary
- Discontinuous (sinusoidal) Capillary
Continuous Capillaries
Most common
-seen in brain
-thicker endothelial cells that don’t contain fenestrations
-only allow passage of water and small ions through intercellular junctions
-least amount of transport
Fenestrated Capillaries
-found in Kidneys, GI Tract
-thin endothelial cells-perforated with fenestrations (pores)
-small molecule passage
-increased amount of transport
Discontinuous Capillaries
-least common
-found in liver, spleen, bone marrow
-lack a basal membrane
-large open fenestrations
-gaps between endothelial cells
-large proteins for large gap
Methods of Transport in Capillaries: (3)
- Transcellular Transport
- Paracellular transport
- Transcytosis
Transcelluar Transport in Capillaries
-diffusion or osmosis across endothelial cell membrane
-gases, small lipid soluble molecules, water (aquaporin channels)
-some facilitated diffusion
Paracellular Transport in Capillaries
-diffusion through inter endothelial junctions, pores, or fenestrations
-water, small water soluble, small polar molecules
Transcytosis in Capillaries
-combo of endocytosis, vesicular transport, and exocytosis
-transport macromolecules (bigger) across endothelial cells
