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408 Cards in this Set
- Front
- Back
What are the goals of the Cardiovascular system?
|
1)Mediates movement of the fluids
2)Transports Waste (oxygen, nutrients, CO2, waste, hormones, and cells) 3. Mediates temperature |
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What are the two components to the cardiovascular system?
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1. Blood vascular system (heart, arteries, and veins)
2. Lymph vascular system (returns lymph from tissues to the blood vascular system - no pump) |
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Layers throughout the cardiac system?
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Tunica intima (endothelium, basement membrane, and fibrous tissue)
Tunica media- muscular layer Tunica adventitia - outer supportive layer |
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Layers in the heart?
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endocardium
myocardium epicardium (includes the coronary arteries) |
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Purkinje FIbers
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apart of the special conducting system within the heart
The SA node (autonomically generated) spreads through atria then to AV node then through ventricles via the atrioventricular bundle to the Purkinje Fibers |
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What forms the heart valve
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The base is from myocardium
consists of a tough fibrous sheet lined by endothelium |
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Describe how the pericardial sac surrounds the heart?
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The Pericadial Sac is divided into fibrous and serous pericardium
Serous pericardium is divided into parietal and visceral pericardium Parietal and visceral are separated by the pericardial cavity that contains the fluid The epicardium is part of the visceral pericardium |
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epicardium is lined by what?
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mesothelium, which is supported by a thin layer of fibroelastic tissue
|
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how is the epicardium connected?
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it is connected to the myocardium by a broad layer of adipose tissue
|
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what is the purpose of mesothelium?
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it provides lubrication fluid between two layers which ultimately provides movement
- visceral serous pericardium lubrication |
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What is blood forced into the arteries?
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the forcing action causes the arteries to expand
|
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What is the purpose of the elastic recoil during diastole?
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this maintains the pressure in the arteries - helps maintain the force that keeps the blood pushing forward
|
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Three major types of vessels:
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elastic/ muscular/ arterioles
*as vessels get smaller the elastic content decreases and the smooth muscle increases |
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elastic aorta layers?
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intima (endothelium/base memb./minimal supportive tissue)
media - mostly elastic adventitia - connective tissue contains the vasa vasorum |
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what is the vasa vasorum
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like the coronary arteries they feed oxygen to the outer wall of the aorta
|
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Layers of a muscular artery?
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Intima
Internal Elastic tissue Media External elastic tissue Adventitia |
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what is the importance of arterioles
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they are important in regulating systemic blood pressure
|
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The layers of arterioles?
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thin intima
media = 6 layers or less adventitia - merges with surrounding elastic tissue * there is no external elastic lamina |
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what is microcirculation?
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consists of network of capillaries and venules
exchanges gases, fluids, nutrients, and waste |
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How is the flow into the capillary bed controlled?
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Controlled by the arterioles and muscular sphincters
|
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what are larger diameter capillaries called?
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Sinusoids
liver, bone marrow, spleen, and lymph nodes |
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What are Pericytes and what are their function
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flattened cells that embrace the capillary endothelial cell
also have a contractile function |
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What isn't contained in microcirculation?
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Media or adventitia
because you want the exchange to occur as easily as possible |
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what are the functions of endothelial cells?
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1. acts as permeability barrier - tight junctions
2. synthesizes collagen for the basement membrane 3. make and secrete pro-throbotic agents 4. secrete vasoactive factors 5. mediates inflammation 6. produces growth factors |
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The three varying connections for endothelium?
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1. continuous (most common)
2. fenestrated (pores) 3. discontinuous (only in liver) |
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Properties of Continuous connections?
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- exchange can occur:
1. passive diffusion (small molecules and gases) 2. pinocytosis ( active process) 3. across intercellular bridges |
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What is fenestrated epithelium?
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opening between endothelium to outer area = "windows"
- exchange for larger molecules - areas of thinning within a cell and between cells |
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Where is fenestrated endothelium found?
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found in tissues where extensive exchange occurs (small intestine, endocrine, and kidney)
permits rapid passage of macromolecules surrounded by basement membrane |
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what is the pathway for venules?
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from capillaries to postcapillary venules, collecting venules, and muscular venules
|
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The characteristics of the venous system
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-functions as a low pressure collecting system for blood
-blood flow passively assisted with: inspiration and contraction of skeletal m. -valves counter the effects of expiration and gravity -major portion of total blood volume present in venous system -devoid of elastic lamina and media has very little smooth muscle |
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Does the vein contain elastic lamina?
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NO it does not contain internal or external elastic lamina
|
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Large muscular veins?
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femoral, renal, and venae cavae
(in the venae cave the muscle is longitudinal) * no internal elastic tissue |
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Functions of the lymph vascular system?
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Drains excess fluid from the tissues
returns lymph to blood vascular system via thoracic duct and right lymphatic duct - consist of thin endothelial cell layer with little basement membrane |
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How does fluid reach the tissue surrounding the vessel that is later collected by the lymphatic system?
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Hydrostatic pressure is created by blood pushing up against the walls of the vessel
this makes fluid leak out into connective tissue - there are also proteins in the blood (albumin) that help with oncotic pressure to suck fluid back in - Hydrostatic > Oncotic |
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Where does the main pressure drop occur?
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The main pressure drop occurs in the small arteries and arterioles
|
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what is the relationship between area and velocity
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there is an inverse relationship between cross-sectional area and velocity
|
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Characteristics of Arterioles
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-contain very little blood
-chief site of peripheral resistance - stopcocks for circulation - arteriole pressure is decreased significantly why they act like stop cocks |
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Relaxation of the cardiac muscle...purpose and how is this accomplished?
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purpose:
- reduce blood flow to heart - decrease the force of contraction - affect the speed of relaxation *Ca taken up by SR (receptor) *Ca is also extruded into the extra cellular space - |
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pulmonary circulation
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the right ventricle to propel blood through the lungs fro exchange of CO2 to O2
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Systemic circulation
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the left ventricle to propel blood to all other tissues of the body
|
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What happens during Systole?
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more blood is ejected inot the arota than runs off through the peripheral resistance located in the more distal small arteries and arterioles causing the walls of the aorta and its branches to be distended outward.
|
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What happens during diastole?
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the recoil of these walls inward during ventricular relaxation propels blood through the peripheral circulation thereby dampening the pulsatile flow created by the heart and provides a continuous blood flow at the capillary level.
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Why are arterioles called the stopcocks of circulation?
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because the arteriolar smooth muscle tone can be adjusted through neurohormonal and metabolic mechanisms to regulate bp
|
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Do arterioles have the ability to adjust blood flow
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Yes! they have the ability to adjust blood for the needs of different organ systems
|
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What is cardiac output controlled by?
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chiefly through the control of tone in the veins, which controls the amount of blood returning to the right side of the heart = preload
|
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Pre-load
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increase myocardial fiber length as occurs with an increase in ventricular filling during diastole
- results in the increased force of ventricular contraction *the heart gets its pre-load from systemic vessels |
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Contractility
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performance of the heart at a given preload and afterload, and is chiefly determined by intracellular calcium
|
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Afterload
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the "load" against which the ventricle contracts, is chiefly regulated by changes in the amount of peripheral resistance present in the arterioles
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Stroke volume
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determined by preload, after load and contractility
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On the V-V /V-P graph the end diastolic volume doesn't exceed zero for a while, why is this?
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because until there is a certain volume in the ventricles (50mL) has been added the shape of the ventricle will not be "rounded out" which needs to occur before stretching can occur
|
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Unstressed Volume
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The volume needed to round the ventricle out before stretching can occur
|
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Left ventricular end-diastolic volume (LVEDV)
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The point on this diastolic p-v curve to which the ventricle fills before it contracts
|
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venomotor
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controlling dilation or constriction in the veins
|
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What does preload depend on?
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Venomotor - controls the amount of blood returning to the heart
|
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pericardial effusion
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when excess fluid accumulates in the pericardial sac
= reduces the ventricular volume at which the pericardium becomes a limiting membrane. In severe case (shock or death) = cardiac tamonade |
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pericardial constraint
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when the pericardium around the heart becomes stiffer due to increased filling of the LVEDV - limiting the pressure-volume relationship
|
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Compliance
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change in volume / change in pressure
|
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Two situations that decrease compliance?
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1.when ventricle is stiff - decreased relaxation during diastole - decreased compliance
2. coronary artery thrombosis or blood pressure in aorta high -no matter what pre-load is the max pressure is reduced |
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what does ventricular afterload depend on?
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varies according to the peripheral resistance which is chiefly regulated through the modulation of smooth muscle tone in the arterioles
|
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ejection fraction
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ratio of stroke volume TO end- diastolic volume
a reduction in this = sign of impaired cardiac function |
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stenosis
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abnormal narrowing of blood vessels
|
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Atrial systole
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begins shortly after the electrical activation of the atrium
-indicated by P wave on EKG - a wave on jugular tracing - atrial contraction propels blood through mitral and tricuspid |
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atrial kick
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contributes very little under resting conditions 10% but with increased HR and decrease in time for ventricle diastole or when ventricle is stiff - more important
|
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What is the time period for isovolumeric contraction?
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time period between closing of AV valves and opening of semilunar valves
-ventricular pressure is constant |
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how is the c wave formed
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due to the constant pressure on the valves during isovolumic contraction
|
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What is rapid ejection?
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early short phase of the ventricular ejection
- characterized by rapid increase in aortic flow and rapid decrease in LV volume - left atrial pressure also falls due to atrial stretch from rapid descent of base of heart |
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what occurs during reduced ejection?
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blood flow from the aorta to the periperhy exceeds blood flow from the LV to the aorta = causes the pressure in the aorta to drop
- The pressure in aorta will still exceed that of the ventricle due to the storage of potential energy in the distended aorta |
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What rises during reduced ejection?
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blood flow into LA and venous pressure increase during reduced ejection as blood flows into them and within them
|
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How is the "v" wave formed?
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when LA is filling with blood and when venous pressure rises as blood flows within the veins
|
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when does the aortic valve close?
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once the LV pressure falls below that aortic pressure
*this is indicated by a notch or incisura on the aortic pressure graph |
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What does the aortic valve closing mark?
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the end of ventricular systole
|
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What is the isovolumic relaxation?
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-ventricular pressure falls rapidly
- ventricular volume remains constant - left atrial and venous pressure begin to rise throughout this period - atrial pressure and venous pressure exceed the rapidly falling ventricular pressure - mitral valve open |
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What gets the mitral valve to open?
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when the artrial pressure and the venous pressure exceeds the rapidly falling ventricular pressure
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Rapid Ventricular filling?
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blood flow from the LA to LV- aided by the suction from the LV due to LV still relaxing
|
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What is Diastasis?
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gradual increase in LA, LV, and venous pressures due to blood continually returning to the heart from pulmonary and systemic circulation
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What does S1 indicate?
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S1 - lub - closer of the AV valves
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What does S2 indicate?
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S2- dub - closer of semilunar valves
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What does S3 indicate?
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normally can't hear but it is due to the rapid filling of the ventricle with sudden termination of ventricular destension and deceleration of blood
*can be heard on some child * adults with LV failure |
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What does S4 indicate?
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normally not heard
atrial contraction *can hear when there is an abnormally stiff LV or when there is LV hypertrophy (caused by years of high blood pressure) |
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How do murmurs form?
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from valves that are narrow or incompetent
|
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How can you judge right atrial pressure superficially?
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By placing person at 45 degree angle with head turned slightly and observing their jugular vein
|
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How is cardiac output calculated?
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CO = HR x SV
Heart rate x stroke volume |
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What is one way to measure cardiac output?
|
By using a pulmonary artery catheter in a technique called the indicator dilution technique
and looking at thermodilution curve. |
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Characteristics of Slow Cardiac APs
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originate at the SA node (automaticity)
AV node- delay conduction to ventricles graph is less dramatic |
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Characteristics of Fast Cardiac APs?
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propagate through atrial muscles via gap junctions
rapidly depolarize Purkinje and ventricular muscle more dramatic/steep graph |
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What are the 5 phases of Fast response AP in Cardiac muscle?
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0- rapid depolarization (Na)
1-Early partial repolarization- (K) 2- Plateau (LTCC and out K) 3- Repolartization - (delayed rectifier K) 4- Resting (K out and small Na in) |
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What are the phases of the slow cardiac AP?
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0- Depolarization - (LTCC)
*Pacemaker cells don't contain Na channels 3- Repolarization - (outward delayed rectifier) *tend to be slower than the channels in fast AP 4- Gradual depolarization- in funny Na current (LTCC helps @end and K diminish) |
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Effective (absolute) Refractory
|
extends midway phase 3
- cant induce AP - Na channels in recovery - allows for diastole - LTCCs can generate slow upstroke (before Na channels recover Ca channels open = extra heart beats) |
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Relative Refractory
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mid phase 3 - phase 4
-requires stronger stimulus -smaller mag APs -repolarizing K current is diminishing in time |
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3 Key Differences between the cardiac system and skeletal AP?
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1) Plateau - LTCC
2) Cell to cell conduction - gap junctions 3) Automaticity - intrinsic pacemaker activity |
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What is automaticity?
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Natural excitation of the heart
*Cardiac muscle - automaticity and rhythmiticity |
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SA Node
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60-100 bpm
overdrive expression - dominates others (highest frequency of natural excitation) - depolarization spreads across atria = determines HR |
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Ectopic Atrial Foci and Escape Rhythems
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safety atrial foci
- safety back up when SA node fails - can trigger premature atrial depolarization = escape beat - @ rate or faster as SA |
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AV node
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40-60bpm
normally suppressed by atrial beat becomes dominate if SA node isn't working |
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Purkinje Fibers
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30-40 bpm
when conduction of AV node is out |
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What are the idioventricular pacemakers?
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specialized cell with the Purkinje conducting fibers of the ventricles
*occasionally fire at rate > SA node |
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Ischemia
|
restriction of blood supply
|
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What modulates pacemaker rate?
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1. synaptic inputs
2. humoral factors 3. serum ion concentrations 4. cellular hypoxial ischemia 5. antiarrythmic drugs |
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What is electrotonic (passive) conduction?
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the conduction of action potentials through a cardiac muscle fiber over the surface of individual cells as APs. Where one region of the cell depolarizes the adjacent membrane (local circuit conduction)
|
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How is the depolarization reach the next cell in a cardiac muscle fiber
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through gap junctions
- which are made of connexins |
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What determines electrontonic conduction velocity?
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1. resistive/capacitive properties of cell membranes
2. gap junctions 3. cytoplasm |
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conduction velocity?
|
propagating wave of depolarization is proportinoal to the rate of change in membrane potential during Phase 0
*Rapid depolarization favors rapid conduction |
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Is conduction velocity inversely proportional to resting membrane potential during phase 4?
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Yes! with lower membrane potentials resulting in faster conduction velocities
|
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How does the conduction of slow responses occur?
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also through electrontonic spread but the slow response within the SA and AV nodes has a much slower conduction (1-4 m/s) vs. .3-1 m/s in fast
|
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Is the firing of the SA node represented in the EKG?
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No- firing localized to small region and this is why you can't measure it on EKG
|
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What part of the heart is associated with slow conduction?
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The SA node
spontaneous but slow |
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What part of the heart is associated with fast conduction?
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Atrial Pathways
- Radial atrial muscle fibers - LA to RA = Bachmann's Bundle - A to V (intermodal band) -Atrial depolarization = p save - AV ring - encircles base of the heart "insulates thus precludes direct A to V spread |
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what is the only pathway from atria to ventricle in a healthy heart?
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Through the AV node
|
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AV involved in slow or fast conduction?
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Slow conduction - imparts delay allows ventricles to fill and time for "atrial kick" (P-R interval)
*firing not reflected on EKG |
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Bundle of His Conduction pathway?
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emerges from the AV node on right side of IV septum
Fast conduction *firing not reflected on EKG |
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Conduction system of Bundle Branches?
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Fast conduction
divides into: LBB and RBB LBB penetrates septum and takes electrical signal to ant. and post. fascicles RBB - takes wave quickly to right ventricle *not reflected on EKG |
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Conduction pathway of Purkinje Fibers?
|
invests ventricular walls
Rapid conduction (4 m/s) = fast response AP -right under endothelium - firing not reflected on EKG |
|
EKG provides indirect/noninvasive assessment that can tell us:
|
1. autonomic state
2. heart thickness/size/orientation 3. conduction system 4. cardiac tissue ischemia 5. non-cardiac disease |
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EKG amplitude depends on what?
|
1. vector magnitude
2.vector direction 3. tissue impedance 4. lead direction |
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EKG duration depends on what?
|
1.AP duration
2. Conduction speed |
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In terms of physics, what does a surface EKG measure?
|
Cardiac dipole moment (magnitude and direction)
|
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What are two properities of the AV node that allow it to delay the signal?
|
1. slow response tissue
2. smaller diameter of the fibers increases the resistance |
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How is the IV septum depolarized?
|
Depolarization occurs due to Bundle of His and depolarizes L to R
|
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How is the anteroseptal region depolarized?
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Via the Bundle branches
|
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How is the myocardium depolarized?
|
from purkinje fibers who depolarize endocardium to epicardium
|
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What is the overall direction of depolarization?
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Apex to base
* with the posterobasal region of the left ventricle as the last region to depolarize |
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Definition of Mean Electrical Axis?
|
Direction of the dipole vector during the peak of the ventricular depolarization (R-wave)
|
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What is Hypertrophy?
|
s the increase in the volume of an organ or tissue due to the enlargement of its component cells
|
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What are the two possible causes of Left Axis Deviation?
|
LV hypertrophy
decrease in RV depolarization |
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What are the two possible causes of Right Axis deviation?
|
Right V hypertrophy
or decrease in LV conduction or depolarization |
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What are the three ways to calculate Mean Electrical Axis?
|
1. Vector Addition Method
2. Equal R-wave method if equal II and III then implies aVF 3. Inspection method if you have an isoelectric lead do perpendicular to lead axis |
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What can Lead II give you a good determination of?
|
R wave
|
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Which lead would you look at for disease in the septum?
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Lead 1 - it is what produces the negative Q wave
|
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What lead would you like at to make a decision about the S wave?
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Lead 3
|
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Where does aVR lie?
|
-150 degrees
|
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Where does aVL lie?
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-30 degrees
|
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Where does lead 1 lie?
|
0 degrees
|
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Where does Lead II lie?
|
60 degrees
|
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Where does aVF lie?
|
90 degrees
|
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Where does lead III lie?
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120 degrees
|
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What do V1 and V2 have a good view for?
|
Right ventricle
|
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What does V3 and V4 have a good view for?
|
Septum
|
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What does V5 and V6 have a good view for?
|
the left ventricle
|
|
What are the steps to clinically approaching an EKG?
|
Rate
Rhythm Morphology Interval/Segments |
|
What is the quick and dirty way of calculating a rate on an EKG?
|
300/ # of big boxes
|
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How many small boxes would the QRS need to cross to be considered prolonged?
|
4 small boxes
|
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What does the ST segment signify?
|
Ventricular depolarization to repolarization
QT needs to be less than 50% of RR interval *varies inversely with HR |
|
What wave is the most sensitive?
|
The T wave
- shows sensitivity to temperature, pH, electrolytes, and ischemia |
|
What is the best lead for the p wave?
|
Lead II
|
|
What is the time duration of a big box on the EKG?
|
.02 secs
|
|
Sinus Tachycardia
|
sinus tachycardia refers to a sinus rhythm emanating from the SA node that is faster than 100 bpm. This can occur in normal autonomic response to exercise. BUT can be significant of hemorrhage, fever, or infection
|
|
What can increase SA node automaticity?
|
Sinus Tachycardia
*looks normal just faster 1) sympathetic stimulation (fight or flight) 2)Hyperthermia 3)Metabolic (thyroid) |
|
Sinus Arrest
|
loss of a SA node is usually diagnosed by a change or loss of the P-wave, signaling the existence of an escape pacemaker
|
|
Premature Atrial Contractions
|
PAC are P-waves which emanate from an ectopic atrial pacemaker in between normal sinus beats.
*odd or inverted p-waves |
|
AV transmission block
|
the conduction of an impulse is blocked when it reaches a region of the heart which is electrically unexcitable. This can occur at a variety of levels between the atria and ventricles or within the conduction system of the ventricle itself
|
|
Primary AV block
|
reflects a slowing of conduction through the AV node
On the EKG, this appears as a long P interval (regular) |
|
Sinus exit block
|
Depolarization from SA node fails to conduct
-can be distinguished from sinus arrest |
|
Sinus block with junctional AV escape rhythm presents how?
|
with an inverted p wave
|
|
primary AV Block
|
reflects slowing of conduction thorugh the AV node
Longer PR interval (>.2 sec or 1 block) *no therapy needed |
|
Secondary AV Block
Type 1 (Wenckeback block) |
progressive prolongation of the PR interval on consecutive beats that is followed by a complete block of AV conduction = dropped QRS complex
*No treatment necessary |
|
Second degree AV Block
Type 2 |
partial block in which the PR interval stays the same but every nth P wave fails to conduct to the ventricles - resulting in a dropped beat
|
|
Third degree AV block
|
The p waves are completely independent of the QRS complex
*no atrial conduction to the ventricles AV DISSOCIATION - NO APPARENT RELATIONSHIP BETWEEN A AND V *QRS is wider and misshapen |
|
Ventricular Conduction Blocks
|
conduction black occurs in the large branches of the His- Purkinje fiber system (bundle branch blocks)
* impulse is left to spread slowly and inefficiently through ventricles by conducting from one myocyte to the next |
|
Right Bundle Branch Block characteristics?
|
-Conduction in RV is slower
- 50% of LV finished depolarizing -last EKG deflection is to the right in V1 -R' >R in V1 |
|
Left Bundle Branch Block Characteristics?
|
V1 is greatly negative due to delayed polarization in lateral left wall
- going away from V1 so that is why it is so largely negative *monomorphic R waves in V6 *monomorphic S waves is V1 |
|
Atrial Fibrillation
|
irregularly irregular
- no discernable p wave - loss of atrial kick - less cardiac output -absence of p waves or numerous p waves - caused by self-perpetuating daughter wavelets due to unidirectional block - can go around circuit many times |
|
Atrial Flutter
|
regularly irregular
best seen in lead II - saw tooth wave front 180-350 bpm - arrive at AV during refractory so they don't conduct |
|
Premature Ventricular Beats
|
= premature ventricular contractions
- common among healthy people (asymptomatic) *wide QRS complexes between normally conducting beats |
|
Ventricular Tachycardia
|
VT is a series of 3 or more PVC
more than 30 sec produces symptoms *large yet stable re-enterent current - when these are quick = cardiac arrest |
|
Ventricular Fibrillation
|
immediate life- threat
leads to complete loss of cardiac output wandering reentrant ventricular circuits causing ventricles to quiver |
|
What system uses two capillary beds in series?
|
Renal circulation
|
|
what system uses capillary beds in series and in parallel?
|
Portal circulation
|
|
Hos does the aorta change the heart's intermittent output into a continuous flow?
|
It contracts during diastole and relaxes during systole
|
|
Why is compliance in the veins important?
|
The compliant reservoir "dampens" (reduces) the influence of changes in volume status on the total volume status on venous return
|
|
What percentage of the storage volume in the veins can be mobilized by the sympathetic nervous system and vaso-pressor drugs?
|
30% is needed to maintain preload in the setting of reduced intravascular volume
|
|
What does changes in the arteriole resistance control?
|
Systemic vascular resistance
|
|
How doe Metarterioles and arterioles differ?
|
Designed a like but the metarterioles don't have an adventitia that is innervated by the autonomic nervous system
|
|
What component is different between capillaries and venules?
|
Venules have fibrous tissue - collagen
|
|
Capillaries are unable to contract BUT what can they do?
|
can change conformational shape
in response to biochemical signals - leaky pores |
|
what does venules provide?
|
capacitance (compliance) and also additional resistance
- this regulates hydrostatic pressure within capillaries |
|
Compliance
|
change in volume that occurs for a given change in pressure
|
|
How do flow rate and blood velocity differ?
|
Velocity = fluid speed expressed distance/ time
Flow rate = volume flux expressed as volume/time |
|
How does Ohm's Law apply to Blood Flow?
|
Resistance = resistance to flow
current - blood flow voltage difference = difference in the pressures at each side = perfusion pressure |
|
Perfusion Pressure
|
The pressure gradient or different
|
|
Systemic Vascular Resistance (SVR)
|
= total peripheral resistance
* total hydraulic resistance to blood flow offered by all of the systemic vasculature between the aortic valve and the right atrium |
|
How to calculate SVR?
|
MAP - CVP / CO
or P(arterial) - P (venous) / CO |
|
What do alterations in SVR primarily reflect?
|
net changes in factors that influence vascular diameter/tone
* influenced by constrictor and dilator influences |
|
How does vasoconstriction and vasodilation affect SVR?
|
vasoconstriction - increase SVR
vasodilation - decrease SVR * constrictors - more influence on larger vessels = maintain vital organ pressure *dilators have a larger influence on smaller vessels |
|
Mean Arterial Pressure
|
time weighted average of arterial pressure = driving force
P (diastolic) + pulse pressure /3 |
|
Pulse Pressure
|
P systolic - P diastolic
|
|
Physical Determinants of Resistance?
|
Length- as length increases:resistance increase
Radius- as radius increases resistance decreases (by factor of 4) *as viscosity increase - resistance increases |
|
Why can't blood be measured as a newtonian fluid?
|
Due to blood being a suspension, blood viscosity depends greatly on the density of the suspension (hematocrit ratio)
|
|
Anemia
|
lower blood viscosity
due to decrease in RBC |
|
Polycythemia
|
increased RBC - increase viscosity
|
|
Interesting property of blood?
|
Blood velocity decreases as vessel radius decreases
(viscosity would normally increase with decreased radius due to decreased velocity) BUT not here = SHEAR THINNING |
|
What happens to viscosity with:
- decreased flow rate? - increased hematocrit? -decrease temp? -increase deformity? |
decreased flow = increase viscosity
increased hematocrit = increase viscosity decrease temp= increase viscosity increase deformity = increase viscosity |
|
What happens to viscosity at low flow rates?
|
the resistance increases
|
|
Blood viscosity (and thus vascular resistance) is impacted by:
|
1) hematocrit
2) radius - vessel diameter 3) RBC deformity 4) temp |
|
What does turbulence depend on?
|
Velocity, viscosity, and fluid density
*higher velocities enhance turbulence |
|
Total flow (Qt) through the circuit of the body is summed up how?
|
it is the sum of all the individual flow rates within the circuit
|
|
The total resistance of network is defined by?
|
in parallel... sum of 1/R
* the sum of the network is less than individual resistant elements |
|
Hydraulic conductance
|
reciprocal of resistance
*using conductances we can see that the total conductance is the sum of individual conductances |
|
large increases in resistance within an individual branch will or will not have a relatively small impact on total resistance?
|
Will have a relatively small impact on overall resistance due to parallel arrangement
*thus little impact on BP |
|
What does the body due in a shock state
|
it will shunt the blood away from the organs by dramatically increasing the resistance of non-vital tissues
|
|
how can the cardiovascular system be simplified?
|
as a two pump/ two exchanger system
|
|
Microcirculation
|
The exchange of gases, water, and solutes between vascular and interstitial compartments by arterioles, capillaries, metarterioles, and venules
|
|
How is blood flow regionally regulated?
|
through dynamic changes in pre-capillary resistance through hydraulic pressure
|
|
What is the function of Vascular Smooth Muscle Cells (VSMC)
|
VSMC wrap thickly around arteries and arterioles and are innervated by autonomic nerve endings
|
|
Passive stretch of arterioles
|
decreases vascular resistance
|
|
Decrease in pressure
|
produces passive recoil = increased resistance
|
|
What is SVR essentially controlled by?
|
local (autoregualtion) and centralized (autonomic) mechanisms
* importance in the balance between central vs. local depends on the tissue |
|
What makes capillaries efficient?
|
Single cell layer
small diameter short length vast numbers |
|
what is capillary hydrostatic pressure?
|
25-35 mmHg
|
|
Transmural pressure
|
defined as the difference between hydrostatic lumen pressure and external (interstitial) pressure
|
|
Autoregulation allows for what?
|
relatively constant tissue blood flow across a wide range (20-120) of mean arterial pressures (perfusion pressures)
|
|
What don't capillaries rupture under this extreme amount of pressure?
|
capillary diameter
* under same transmural pressure the pressure in the aorta will be 5000X greater than in the capillary |
|
What is the myogenic mechanism in terms of auto-regulatory mechanisms of local control?
|
smooth muscle in precapillary vessels responds to increase in transmural pressure
* arterial pressure changes are met with vascular resistant changes = constant blood flow - NOT dependent on endothelium |
|
What is the endothelial release of NO mechanism in terms of autoregulation of local vascular control?
|
increase velocity - increase shear stress- increase NO- vasodilation(decreases resistance) - decreases velocity
|
|
What is vasodilation mediated by?
|
Nitric Oxide
and prostacyclin *released by endothelial cells so the shear stress mechanism can't occur without the endothelial layer |
|
What is the metabolic mechanism in terms of autoregulation of local vascular control?
|
arterioles maintain basal tone (certain amt of vasoconstriction)
|
|
active hyperemia
|
an increase in metabolic rate increases the production of vasodilators and produces a subsequent increase in tissue blood flow referred to as active hyperemia
|
|
metabolic "wash out"
|
when at constant metabolic rate - increased blood flow leads to "wash out" of basal metabolites leading to - vasoconstriction
|
|
reactive hyperemia
|
during periods of reduced blood flow or tissue ischemia - metabolite build up promotes vasodilation
|
|
3 ways autoregulation occurs (intrinsic) ?
|
1) myogenic stretch response
2) flow shear stress 3) metabolic response |
|
Fick's Law states that diffusion rate is dependent on the following:
|
- concentration gradient
- area for exchange - diffusion distance - permeability of the capillary wall |
|
Transcytosis
|
involves creation of pinocytotic vesicles at the luminal or extracellular side of the plasma membrane which get pinched off, shuttle through the cytoplasm and fuse with other vesicles
|
|
how many liters / day are filtered back and forth
|
20 L / day
|
|
Do the venules fine tune capillary pressure?
|
YES! if you increase pressure in veins you see a large increase in capillary pressure as well (vs. artery pressure)
|
|
Water filtration at the arteriolar end of capillaries exceeds reabsorption at the venular end by how much?
|
2 - 4 L/day
25-50% of total plasma proteins/day are returned to the thoracic duct each day muscle contraction aids in this return |
|
What occurs during dehydration?
|
Decrease capillary pressure- decrease outward pressure- increase re-absorption of fluid
|
|
What occurs during malnutrition?
|
decrease oncotic pressure (fewer proteins due to lack of food)- increase outward pressure because fluid will flow out = increase filtration
|
|
Definition of Autoregulation?
|
A local mechanism by which blood flow through a capillary bed is adjusted to maintain homeostasis in response to arterial transmural pressure, blood velocity and changes in tissue metabolic activity. In skeletal muscle, this response allows for relatively constant tissue blood flow across a wide range (20 -120 mmHg) of perfusion pressures. Several mechanisms have been proposed to play a role in this local control system:
1) myogenic 2) endothelial release of NO (shear stress) 3) Metabolic |
|
What does autoregulation provide:
|
- protects vessels
- keeps things constant -optimizes local conditions |
|
What are the two major determinants of cardiac output?
|
cardiac factors and vascular factors
|
|
ANS provides (short term or long term) homeostatic regulation of arterial blood pressure?
|
short term
* links CNS to peripheral sensory organs (baroreceptors) and visceral effectos (veins, arteries, and heart) |
|
ANS responds to sensory input through the regulation of what?
|
- vascular tone
- heart beat - myocardial contractility * thus provides short term control of blood pressure |
|
Cholinergic neurons
|
pre-ganglionic neurons
what the sympathetic and parasympthtic divisions of the ANS are made up of |
|
On the right to be a candidate, what is the standard of review for the following:
[1] Wealth Restriction; [2] Residency Restriction; [3] Property Ownership Requirements; [4] Party Affiliation; [5] Racial Classification; [6] Age Classification; [7] Prohibition on Officeholders from Being Candidates for another office |
On the right to be a candidate, what is the standard of review for the following:
[1] Wealth Restriction: Strict Scrutiny; [2] Residency Restriction: Strict Scrutiny; [3] Property Ownership Requirements: No Articulated Standard; [4] Party Affiliation: Strict Scrutiny; [5] Racial Classification: Strict Scrutiny; [6] Age Classification: Rational Basis; [7] Prohibition on Officeholders from Being Candidates for another office: Rational Basis |
|
Explain how parasympathetic fibers work?
|
Pre-ganglionic fiber that reaches directly to target organ
releases Ach N2 receptors Further release of Ach Bind to M receptor |
|
Explain how most sympathetic fibers work?
|
preganglionic fiber that in ganglion releases Ach to N2 receptor
the post ganglionic fiber releases NE to alpha and beta receptors |
|
Sympathetic response in adrenal medulla?
|
preganglionic fiber releases Ach to N2 receptor on Chromaffin cell
Chromaffin cell then releases Epi which is greater than NE |
|
What are the normal NT or each division of the ANS to release?
|
Sympathetic - NE and Epi
Parasympathetic - Ach |
|
What controls the balance between the parasympathetic and sympathetic tone?
|
Medulla oblongata
- has medullary cardiovascular centers - which integrate sensory "data" from a variety of inputs |
|
Nucleus Tractus solitarious (NTS)
|
principle integrative center for circulatory control, receiving afferent inputs from peripheral sensors (via vagus and glossopharyngeal)
*mediates para and symp outflow |
|
increasing sympathetic stimulation does what to contractility?
|
Increases contractility
* increased contractility = increases stroke volume |
|
Ventricular inotropy is the same as...?
|
ventricular contractility
|
|
Local influences on arterioles?
|
basal tone (inward)
vasodilator metabolites (outward) = sympathetic constrictor nerves (NE) * increase SVR |
|
Influences on Veins?
|
passive distention (outward)
external compression (inward) = sympathetic constrictor nerves (NE) * increase the Pre-load |
|
What are the characteristics of the sympathetic humoral response?
|
Release of Epi>>NE
bind to Beta >> Alpha receptors * increases heart rate and contractility *augments venous return *reduces SVR at low to moderate concentrations * MODERATE INCREASE IN MAP |
|
Sympathetic humoral response where NE>>Epi
|
binds alpha>> beta adergenic receptor
*increases HR and contractility *augments venous return * Increase SVR *substantial increase in MAP |
|
what is the purpose of the hydraulic filtering in aorta?
|
- converts pulsatile flow to continuous
- protects the microcirculation from pressure induced damage - adequate perfusion of heart during diastole |
|
Elastance =
|
change in pressure / change in volume
*increases with age * inverse of compliance |
|
What is BP determined by?
|
Amount of blood in arterial system and compliance
|
|
Does pulse pressure decrease or increase from aorta to capillaries?
|
decreases - want continuous flow at capillaries
*hydraulic filtering |
|
Pulse pressure (increase or decreases) from central to peripheral arteries?
|
increases - looking at same generation this time
and reflection at ankle will come back quicker than the reflection at the aorta |
|
what are the physiological and physical factors that determine arterial blood pressure?
|
Physiological - CO and peripheral resistance
Physical- arterial blood volume and compliance |
|
The body can adjust blood pressure moment to moment by using/measuring arterial compliance or arterial blood volume
|
arterial blood volume
|
|
Pulse pressure and stroke volume and compliance?
|
Pulse pressure is directly related to SV
Pulse pressure is inversely related to compliance |
|
How do arteries and veins differ when it comes to compliance and resistance?
|
Arteries are low compliant but HIGH resistance
Veins are HIGH compliant but LOW resistance |
|
What will occur right after a cardiac arrest?
|
- arterial pressure will fall
- venous pressure will rise - this is due to the fact that blood will go from artery to vein BUT the heart isn't taking blood from vein to artery |
|
Mean circulatory pressure (Pmc)
or Systemic pressure (Pms) defined as? |
the pressure that results when the arterial and venous pressures will become equal.
|
|
Vascular function curve
|
the change in central venous pressure produced by changes in cardiac output can be plotted on this type of graph
How does the compliance of the veins (tone) effect CO |
|
What are two factors that can affect Pms?
|
1) blood volume
2) venomotor |
|
What type of rotation do we see in the vascular function curve (venous return curve) when resistance is increased?
|
see a clockwise rotation with changes in peripheral resistance occur
|
|
Equation for Venous Return
|
= Pms - RA pressure / Resistance to venous return
|
|
What is Resistance to Venous Return?
|
not the same thing as SVR completely
- deals with an impedance that combines the resistance and compliance of the venous and arterial system |
|
Steady State between vascular function and cardiac output?
|
when cardiac output = venous return
|
|
What is the equation for venous return?
|
VR = Pms - RAP / RVR
|
|
Does RVR increase or decrease during exercise?
|
RVR decreases during exercise
|
|
What are the defenses for Cardiac Output during hemorrhage?
|
1) venoconstriction - up Pms, up VR
2) up VR, up preload, up contraction 3) increase rate and contractility |
|
What are the defenses for MAP during hemorrhage?
|
arteriolar constriction, increases arterial volume, increasing MAP
*(overlap) - increase CO, up arterial blood volume - increases MAP |
|
What does arteriolar resistance do for a system in hemorrhage?
|
arteriolar resistance defends MAP, but doesn't directly affect CO
|
|
What detects a reduction in MAP and reduction in pulse pressure?
|
baroreceptors in cartoid sinus and aortic arch
carotid sinus>aortic arch |
|
What are chemoreceptors stimulated by?
|
increased hypoxia - stimulates venoconstriction in periphery
increasing venous return |
|
How does venous return increase during inspiration?
|
Inspiration reduces intrathoracic pressure, which reduces arterial pressure and reduces jugular pressure = increase venous return
|
|
After you bleed, one has arteriolar constriction and reduced venous pressure. What does this do to the hydrostatic pressure?
|
reduced capillary hydrostatic pressure on the venous side you get net re-absorption of interstitial fluid back into the lumen
*from this you see your colloid pressure go down but your BP will rise |
|
Responses that take place during a hemorrhage?
|
- baroreceptor reflex
- chemoreceptor reflex - cerebral ischemic response - reabsorption of tissue fluids - release of endogenous vasoconstriction substance. - renal conservation of salt and water |
|
What senses the decrease in MAP during hemorrhage?
|
Baroreceptors in carotid sinus and aortic arch
- see decrease in MAP and pulse pressure * increase sympathetic tone and decrease parasympathetic - up HR, up contractility - up venoconstriction - up Pms and UP VR |
|
What endogenous venoconstrictors are released during hemorrhage?
|
epinephrine, NE, vasopressin (anterior pituitary), and angiotensin II
|
|
Explain Cardiac Dysfunction
|
Many ways that the system tries to defend the MAP and CO, decease the flow through the coronary arteries = leading to further ischemia
|
|
Decompensatory Mechanisms activated during hemorrhage?
|
Cardiac dysfunction
Acidosis (hypoxia) CNS depression Alterations in blood clotting |
|
How much can oxygen consumption increase during exercise?
|
60x
- dramatic increase in metabolic activity leads to dramatic increase in blood flow to exercising muscles |
|
What is Central Command? How is it initiated?
|
cardiovascular response when exercise is initiated
* initiated by cerebral cortex *increase in sympathetic outflow |
|
How are coronaries and skeletal muscle blood flow affected during exercise?
|
release of vasoactive metabolites allows both to increase blood flow
* skeletal muscle dilation decreases peripheral resistance and therefore decreases afterload = increasing SV |
|
What is the response of intramuscular mechanoreceptors and local chemoreceptors?
|
they are stimulated during exercise - increasing sympathetic outflow
|
|
What is venous return aided by:
|
skeletal muscle pumps and respiration (reduction in intrathoracic pressure)
|
|
CO and HR increase during exercise, which is more important?
|
HR seems like the correct answer at first but it has been tested the just increasing HR actually decreases CO (due to decreased filling).
CO controlled by systemic vessels - unaffected by the pace of the heart |
|
How is SV increased during exercise?
|
Increase in VR (skeletal muscles and respiration)
Vasodilation in periphery in skeletal muscles = decreases afterload |
|
How is HR increased during exercise?
|
activation of sympathetics
- Central command - chemo and mechano - receptors |
|
What are the mechanisms of Heat loss?
|
Convection (cutaneous blood flow) and Evaporation (rate of sweat production)
|
|
what are the two types of resistance vessels in the skin?
|
1) Arterioles
2) AV anastomoses |
|
What is the most important influence in Arterioles?
|
Sympathetic control
- also have: local regulator factors reactive hyperemia |
|
Where are AV anastomosis primarily found?
|
in Apical skin
- innervated by sympathetics - DO NOT exhibit: basal tone autoregulation reactive hyperemia metabolic control |
|
What occurs when body temperature increases?
|
dilation of resistance vessels leads to an increase in blood flow to the skin and increased dissipation of heat
|
|
What occurs when body temperature decreases?
|
vasoconstriction - decrease blood flow to the skin - heat conservation
|
|
vasodilation in apical skin differs than the response in non-apical skin...how?
|
vasodilation in apical skin is PRIMARILY from reduction of sympathetics
in non-apical skin reduction is only part of it |
|
What are sweat glands innervated by?
|
Sympathetic Cholinergic Fibers
- Ach is realsed acts on sweat glands leads to: - release of sweat - vasodilation of resistance vessels (bradykinin) - to dissipate heat |
|
Why is the large vascular bed in skeletal muscle important?
|
arterioles in these beds contribute significantly to peripheral resistance
*importnat for vascular tone, regulation of BP, and baroreceptor reflex |
|
What happens to skeletal blood flow when you clamp both carotid arteries?
|
the MAP increases drastically once they are released the blood flow to the skeletal muscle increases drastically
* this is significant because it is show a decrease in peripheral resistance, which will decrease afterload, increase SV |
|
when baroreceptor detect a fall in blood pressure (standing up quickly) what do they do?
|
they increase sympathetic tone causing vasoconstriction
*NE release and activity on alpha receptors |
|
During exercise there is an increased in metabolic demand, how does the body (skeletal muscle) deal with this?
|
releases Epi that acts on Beta receptors = vasodilation and an increase in blood flow by 20x
- decreases SVR and RVR |
|
What is cerebral blood flow controlled by?
|
mostly metabolic factors (CO2 (vasodilator), adenosine, K+)
|
|
How much can food intake affect blood flow?
|
can increase splanchnic blood from 30-100%
|
|
Is splanchnic blood flow a reservoir of blood and site of adjustable resistance?
|
YES!
* skin is also a reservoir of blood |
|
How do the kidneys deal with a decrease in MAP and therefore a decrease in renal perfusion?
|
stimulates renin-angiotensin-aldosterone system
* increased renal sodium - increased retention of fluid *increase in blood volume- increase in MAP= increase in venous return= increases CO |
|
What is the driving pressure for coronary blood flow?
|
Aortic pressure
*also physical, neurohormonal, and metabolic factors that regulate blood flow |
|
What does the left coronary artery divide into?
|
Descending anterior and left circumflex
|
|
What does the right coronary artery divide into?
|
Posterior descending branch of the right coronary artery
|
|
Physical factors regulating coronary blood flow?
|
1) Autoregulation
*perfusion pressure and coronary blood flow have a direct relationship but due to this mechanism stay in a range 2) Mechanical compression *contracting myocardium squeeze the blood vessels coursing through it - why coronary blood flow is highest during diastole |
|
How do the coronary arteries survive during increase in sympathetic tone?
|
the metabolic demand is enough that the resistance vessels dilate
* metabolic demand increases- release of adenosine and NO - opens the K+ATP channels = hyperpolarization and decrease in Ca entry = vasodilation |
|
Which is more sensitive to ischemia...supendocardium or epicardium?
|
subendocardium is more sensitive to ischemia than subepicardium
* greater O2 consumption * greater wall tension * already more dilated - reduced flow reserve |
|
What occurs during myocardial ischemia?
|
decrease O2 - increase lactate (H+)
* Na/H+ exchanger to remove excess H+ * Na increased so Na/Ca exchange *Ca+ overload *cell death |
|
Myocardial infarction
|
Necrosis - occurs when myocardial ischemia is severe
- death of the tissue occurs |
|
Myocardial stunning
|
temporary reduction in myocardial contractility due to brief ischemia - followed by reperfusion
|
|
Myocardial hibernation
|
reduction in performance due to down regulation of metabolism
|
|
Coronary collateral vessels
|
develop in response to gradual and persistent reductions in blood glow
|
|
How is the need for O2 affected by the following:
-Tachycardia - up contractility - up afterload - up preload |
tachycardia- decrease in O2 supply
contractility - need more energy (O2) afterload- has to generate more force (up O2) preload- greater P and increase contractility - increase in O2 need |
|
Characteristics of bronchial circulation?
|
receives approximately 2% of CO
supplies blood to non- gas exchanging regions under systemic pressure (from aorta) |
|
Why does pulmonary circulation require less pressure?
|
only supplies the lungs (high flow and low resistance)
doesn't have to accommodate diverse sites |
|
How do you calculate PVR=
|
PVR = (MPAP- PCWP) / CO *80 *MPAP - inflow pressure
|
|
How is PCWP taken?
|
catheter inserted into subclavian vein and moves through pulmonary artery and eventually lodges into small pulmonary artery
* measures static column of blood that lies between the tip and left atrium *appx left atrial pressure *pulmonary vascular resistance |
|
Where is blood flow greatest in the lung?
|
at the base - due to gravity
|
|
describe the three west zones?
|
Zone I - shut
Zone II- flutters (a>A>v) Zone III- open (a>v>A) |
|
Passive regulation of pulmonary blood flow?
|
Distention and recruitment
*response to exercise increase CO 4x but pulmonary pressure doesn't increase significantly due to this mechanism |
|
Effect on pulmonary arterial pressure on blood flow?
|
Increase arterial pressure - see more pulmonary blood flow this is due to recruitment and distention
|
|
Effect of pulmonary arterial pressure on vascular resistance
|
small increase in Pulmonary arterial pressure - large reduction in PVR and see an increase in blood flow as well
|
|
What are the effects on alveolar vessels and extra alveolar vessels?
|
when you breath in extra alveolar vessels expand due to negative intrapleural pressure
alveolar vessels are compressed by the expanding alveoli * these two oppose each other and resistance is lowest at functional residual capacity |
|
What effect does alveolar hypoxia play?
|
is is a vasoconstrictor
*hypoxic pulmonary vasoconstriction - in isolated lung tissue * hypoxia acts directly on pulmonary vascular smooth muscle cells (inhibit K channels) - depolarization Ca+ influx = contraction **redirect blood flow away from poorly ventilated areas to areas with higher oxygen content |
|
what are the pulmonary vasoconstricting substances? vasopulmonary substances?
|
Vasoconstricting - angiotensin II & endothelin I = proliferation of smooth muscle
Vasodilation - NO and prostacyclin = antiproliferations |
|
2 diseases that raises PVR
|
pulmonary embolism
emphysema |
|
Describe the Hydraulic filter?
|
during systole the walls move outward - store potential energy
during diastole- the walls contract converting the potential energy back into kinetic energy *pulsatile flow to non-pulsatile flow *protects microciruclation *adequate perfusion of heart during diastole |
|
What is elastance?
|
I/ compliance
*elastance increases with age while compliance decreases with age |
|
What determines blood pressure?
|
amount of blood in the arterial system and the arterial compliance
*compliance is relatively constant for a given individual * up CO will up BP if resistance is constant and visa versa |
|
Where does Pulse Pressure increase?
|
Pulse pressure increases from central to peripheral
*reflected wave at ankle comes back faster * in older patients the reflective wave comes back fast no matter where in the body due to stiffer blood vessels so there pulse pressure looks very similar at the ankle and aorta |
|
Does body regulate arterial compliance or arterial volume from min to min?
|
arterial volume
* can't regulate compliance like this because it is pretty constant for a given individual |
|
Equation for pulse pressure=
|
systolic BP- diastolic BP
|
|
Pulse pressure decreases or increases from aorta to large arteries?
|
Pulse pressure decreases from aorta to large arteries
|
|
Pulse pressure ~ stroke volume/ arterial compliance
|
as SV increases pulse pressure increase
as compliance decreases pulse pressure increase |
|
How does Septic Shock affect BP and pulse?
|
BP will be decreased
Pulse will increase (robust) MAP pressure is decreased due to the sepsis induced reduction of peripheral resistance decreasing MAP but increasing stroke volume due to decreased afterload - up pulse * these patients will have warm extremities due to vasodilation |
|
Shock due to Hypovolemia (LV failure)
|
decreased CO
vasoconstriction in periphery = cool extremities sluggish refill narrow pulse pressure |
|
What occurs the moment after cardiac arrest?
|
Venous pressure rises
Arterial pressure falls * no way to get the venous back to the artery side * venous pressure will rise slightly and arterial pressure will decrease drastically |
|
How is the Pms determined?
|
the pressure is determined by the volume of blood in the system and the compliance of the system
flow in cardiac system = 0 |
|
What affects Pms?
|
changes in blood volume and venomotor tone
|
|
Venoconstriction affect on Pms and resistance
|
will have the same Pms but will increase resistance - decrease the venous return
|
|
Equation for Venous Return (VR)=
|
VR= Pms-RaP / RVR
|
|
what increases venous return?
|
increase in Pms or venomotor constriction
|
|
describe what occurs after a reduction in myocardial contractility?
|
reduced CO- transfer blood from the venous side to arterial side will be reduced
- blood volume increase in Venous side = increase in preload= increase CO * new equilibrium point is achieved |
|
What are the mechanisms that compensate for acute blood loss
|
increase in sympathetic tone
venoconstriction increases Pms sympathetically mediated venoconstriction in skin - to bring more blood back to circulation |
|
What is pre-capillary resistance achieved by?
|
small arteries
arterioles pre-capillary sphincters |
|
How is precapillary resistance achieved?
|
Arteries and Arteriole vessels consist of endothelial layers wrapped by thick layers of vascular smooth muscle cells (VSMC) which are innervated by autonomic nerve endings
|
|
what is the main control over pre-capillary sphincters?
|
usually not innervated but are very responsive to local tissue conditions
|
|
Do venules have vascular smooth muscle cells (VSMC)?
|
yes but they are a discontinuous layer
|
|
What is SVR essentially controlled by?
|
A balance between intrinsic (autoregulatory) and extrinsic (autonomic) mechanisms
*skin dominated by autonomic *heart dominated by local |
|
What are the three autoregulatory mechanisms?
|
1) myogenic (stretch)
2) endothelial release of NO 3) Metabolic mechanism |
|
Myogenic response for autoregulation?
|
increase in transmural pressure- smooth muscle contraction- decrease in arteriolar diameter- decrease flow - decrease pressure
|
|
Endothelial release of NO for autoregulation
|
increase in blood velocity - increase shear stress- release NO- vasodilate- decrease flow velocity= decrease in sheer stress
|
|
How does NO cause vasodilation?
|
it freely moves into smooth muscle and inhibits Ca++ release and influx with allows for smooth muscle relaxation
|
|
Metabolic mechanisms for autoregulation
|
Active (exercise) - increase in metabolites- vasodilation
Reactive - decrease blood flow- increase in metabolites - vasodilation- decrease resistance - increase in blood flow |
|
3 different mechanisms for capillary exchange
|
diffusion
filtration transcytosis |
|
What is Laplace's Law?
|
smaller diameter decreases wall tension
* smaller diameter in capillaries are what protect it against the increase in pressure |
|
How much water is filled back in forth in one day between capillary endothelium?
|
20 L /day through aquaporins
*diffusional rate of water occurs at a much higher rate (80,000 L) |
|
How much does the water filtration and the arteriolar end exceed the reabsorption at the venular end by?
|
2 - 4 liters/day
lymphatic system delivers what is lost -25-50% of total plasma proteins/day |
|
How much of the storage volume in the veins can be mobilized by sympathetic nervous system?
|
~30% by sympathetic and vaso-pressor drugs
|
|
How do metarterioles and arterioles differ?
|
They are designed very similar except that metarterioles aren't innervated by autonomic nervous system
|
|
Can capillaries contract and have conformational change?
|
Capillaries can't contract but they can undergo conformational change
|
|
Venules
|
*play a role in regulating hydrostatic pressure
*provide compliance and additional resistance *less abundant nerve innervation |
|
Flow rate =
|
volume flux / time
|
|
Does velocity increase or decrease as a vessel narrows?
|
The velocity will increase
|
|
perfusion pressure =
|
arterial - venous pressure
|
|
MAP=
|
diastolic + (systolic- diastolic)/ 3
|
|
What does Poiseuille's Law state?
|
the flow resistance increases with tube length and blood viscosity
while resistance decreases with increasing tube radius |
|
Since blood is a suspension, what does viscosity depend on?
|
blood viscosity depends greatly on the density of the suspension (hematocrit ratio)
*anemia = decrease RBC = decrease viscosity *polycythemia = increase RBC = increase viscosity |
|
Shear thinning
|
the one way viscosity doesn't follow Newtonian law
as radius decreases = viscosity decreases |
|
How do the following affect viscosity:
-temperature? -flow rate? -shear thinning? -Hemotocrit - RBC shape? |
- temp- increase V
- increase flow rate - decreases V -viscosity decreases - radius down - increase Hemo- increase V -deformed cells - increase V |
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Sinus Tachycardia
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sinus rhythm
faster than 100 beats/min sympathetic stimulation to exercise can also be from: -infection -fever -hemorrhage |
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Sinus Bradycardia
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less than 60 beats/min
parasymathetic *ischemia *hypoxia *beta blockers |
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enhanced automaticity of latent pacemakers
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latent pacemaker tissue develops intrinsic rate > SA node
EKG - starts on way then changes |
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Multifocal atrial tachycardia
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3 or more different p wave
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Sinus arrest
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loss of p wave (loss of SA node during ischemia)
= failure to conduct |
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Premature Atrial contraction
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ventricles will depolarize normally since the signal still has to go through the AV node
*produce odd or inverted p waves |
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primary AV block
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reflects a slowing of conduction through AV node
* longer PR intervals (>.02 sec) |
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secondary AV block
Mobitz type I |
(wenchkebach)
progressive prolongation of PR interval on consecutive beats and the complete block of AV conduction (dropped beat) |
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Seconday AV block
Mobitz type II |
constant from beat to beat but every nth P-wave fails to conduct to the ventricles
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tertiary AV block
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complete AV conduction block
p wave and qrs have no apprarent relationship AV dissociation ventricles firing on their own so the QRS is usually wide |
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Right Bundle Branch Block
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alters the direction and magnitude of the ventricular depolarization vector
* RBBB look at V1 QRS has large dip and R'>R |
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left Bundle branch block
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alters the direction and magnitude of the ventricular depolarization vector
LBBB- look at Lead I and V6 for broad R wave |
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Supraventricular Tachycardias
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"narrow-complex" tachycardias since they display normal QRS duration (above the AV node)
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Atrial Flutter
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Look at LEAD II
Regularly Irregular 180-350 bpm slower ventricular rate due to refractory period of the ventricles saw-tooth like pattern |
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Atrial Fibrillation
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irregularly irregular
no discernible p waves or numerous irregular p waves loss of "atrial kick" = decrease CO *usually around pulmonary veins |
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Premature Ventricular beats
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wide QRS complex then normal again
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Ventricular Tachycardia
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3 or more PVC
-produce symptoms (fainting) Sustained VT =requires termination non sustained = self terminating *reflects large and relatively stable underlying reentrant circuit -sometimes can see multiple ectopic foci |
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Ventricular Fibrillation
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immediate life threat
loss of CO wandering reentrant ventricular circuit ventricles just quiver irregularly irregular |
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Atrioventricular Ring
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what precludes the spread of the atrial impulse directly to the ventricles
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What is a large component of the PR interval?
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The AV node delay
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What all can an EKG tell you?
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HR
rhythm conduction morphology intervals/segments orientation size |
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The isoelectric point after the p wave?
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signifies that the ventricles are yet to be depolarized
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QT segment
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measure start of ventricular depolarization to ventricular repolarization
*interval is sensitive to drugs * inverse to heart rate - 1/2 RR |
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Standard leads
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bipolar and separated by 60 degrees
* measure difference between 2 bipolar electrodes |
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Augmented leads
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starts from the central terminal of WIlson
*unipolar |
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How is the Q wave generated?
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it is inverse because it signifies the septum depolarizes L to R
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R wave
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down the septum and into the ventricles - a large net dipole is created inducing and upward P wave
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S wave
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left ventricle complete depolarization = S wave
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Left axis deviation
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heart in more transverse setting
LV hypertrophy RV depolarization decrease |
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Right axis deviation
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Heart in a more longitudinal setting
RV hypertrophy LV depolarization decrease or decrease in conduction |
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T wave is the most sensitive wave:
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sensitive to temperature/ pH/ electrolytes/ ischemia
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Fast Response Cardiac Tissue
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5 phases:
0- inward Na current (activated in 1-2ms and inactivated in 100-200ms) 1- quick outward current of K+ creates dip 2- Plateau - LTCC inward current and K+ (delayed rectifier) outward current 3- repolarization - delayed rectifier K+ channels win out and outward currents overtake 4- resting -inward delayed rectifiers reach resting potential |
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Slow Response Cardiac Tissue
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0- NO Na+ / Inward Ca+ (LTCC)
why polarization is much less steep *pacemaker cells don't contain Na channels 3- Repolarization - outward delayed rectifier 4- unsteady resting potential -gradually depolarize due to: *inward funny Na current (HCN1) - induced by hyper-polarization in phase 3 *LTCC are triggered at end of phase 4 *K+ outward current diminishes toward the end of phase 4 |
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Where are the cells producing ectopic beats usually found?
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found in and around pulmonary veins
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How do catecholamines affect autonomic synaptic efferents?
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NE released from sympathetic nerves or circulating Epi form adrenal medulla increases pacemaker cells by decreasing conductance of HCN1 channels
*HCNA1 channels are what funny Na+ moves through and what allows for gradual depolarization |
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How do hyperkalemia and hypokalemia affect the SA node?
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hyperkalemia (too much K) : induces bradycardia
Hypokalemia: increases rate of phase 4 and causes tachycardia |
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Digitalis's affect on the heart
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causes bradycardia by increasing parasympathetic flow
BUT at toxic concentrations - increase automaticity = tachycardia |
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How are conduction velocity and depolarization rate related to one another?
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Rapid depolarization favors rapid conduction
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Mechanisms for Cardiac Relaxation?
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1) Ca is extruded into the extracellular fluid by Na-Ca exchanger
2) Ca is sequestered into the SR by SERCA2 3) Ca dissociates from tropnin C |