Which of these is not a common symptom of hypovolemic shock?
Low urine output due to reduced kidney end-organ oxygenation
Cardiogenic shock arises from [blank_start]pump[blank_end] failure. This causes decreased contractility, which therefore reduces SV and therefore reduces the Cardiac Output. Poor forward flow will eventually cause a back-log of pressure into the venous system which can lead to an [blank_start]elevated[blank_end] CVP/JVP.
CVP is used as a surrogate for preload and is normally between 15-25mmHg?
The 3 mechanisms in which preload increases force of contraction via the Frank-Starling Law of the heart are:
-Increased [blank_start]length[blank_end]-tension relationship placing cardiac muscle in place of best contraction (due to optimal actin-myosin cross bridges).
-Increased Calcium sensitivity of the [blank_start]filaments[blank_end]
-Increased [blank_start]tension[blank_end] on the stretch-activated calcium channels, thereby increasing Ca2+ entry. Calcium is increased intracellularly resulting in more cross-bridge formation.
Which of these is not a benefit of gelofusine?
Similar properties to blood
Half life of 4-5 hours
Don't need to know blood type
Good for intracellular shock
Normal saline distributes about 25% of the solution into the vascular compartment
Dextrose can be used to treat low blood sugar, insulin shock or dehydration, as it is rapidly taken up by cells and is useful to replenish intracellular fluids.
Arteries consist of 3 layers (tunica intima, [blank_start]tunica media[blank_end] and tunica externa). The tunica intima consists of [blank_start]squamous[blank_end] epithelium and a basement membrane (thin fibrous, non-cellular Laminin, protein, collagen).
The Internal [blank_start]elastic[blank_end] membrane separates the tunica intima from the tunica media.
The tunica media consists of SMC's, [blank_start]collagen[blank_end], elastin and proteoglycans
The next structure is the external elastic membrane which separates the tunica media from the tunica externa.
-The outermost structure is the adventitia or tunica externa, which consists of [blank_start]fibroblasts[blank_end], collagen and elastin.
What prominent structures on arteries are not a feature of veins?
Single layer of endothelium
Atherosclerosis is not associated with?
Chronic Endothelial Injury
Increased permeability with monocyte and leukocyte adhesion
SM emigration from tunica media to intima and macrophage activation
Macrophages and SMC's engulfing lipid
Smooth muscle proliferation, collagen and other ECM deposition.
Aortic dissection involves a split in the intimal layer, which allows blood to enter the wall of the vessel.
Peripheral Vascular disease is [blank_start]atherosclerotic[blank_end] build up in the lower limbs. The stenosis occurs through repeated endothelial injury. During exercise a [blank_start]reduced[blank_end] blood flow leads to the requirement for anaerobic sources of metabolism, this creates [blank_start]lactic acid[blank_end] which is sensed by nerves as noxious stimuli. Once the patient rests and oxygen demand reduces, the pain leaves.
Peripheral venous disease is normally due to epithelial damage?
Chronic venous [blank_start]insufficiency[blank_end] is due to valve dysfunction which causes the normal pressure ([blank_start]20[blank_end]mmHg) to rise above 40mmHg. This sees fluid driven [blank_start]out[blank_end] the venous vascular circuit and [blank_start]into[blank_end] the tissues.
In varicose veins, the [blank_start]leaflets[blank_end] of the valves no longer meet properly and this causes a back-log of blood into the veins which become distended and not aesthetically pleasing.
Adrenaline binds to [blank_start]B1[blank_end] adrenoreceptors on the heart to cause an increase release of cAMP. This increased cAMP will lead to activation of Ca2+ channels and increased Ca2+ will enter the cytosol. This will increase the amount of actin-myosin cross brides formed and therefore increase the force of contraction. NA also binds to a1 adrenoreceptors on blood vessels to cause vasoconstriction.
These can both increase MAP by CO x SVR.
A person with a blood pressure of 143/ 95 is grade 2 hypertensive?
Ohm's Law = P/ R.
The [blank_start]3[blank_end] forces of pressure through the body are hydrostatic, driving pressure and [blank_start]transmural[blank_end] pressure.
In Pouseuille's law- F = P x r4....therefore flow is directly proportional to pressure and [blank_start]radius[blank_end] but inversely proportional to vessel length and viscosity.
The following parameters of blood are in line with Poiseulle's assumptions?
Fluid must be incompressible
Viscosity of fluid must be constant
Flow must be steady
Velocity at the wall must be zero
Tube must be straight, rigid and cylindrical
Flow must be laminar
Laminar flow is [blank_start]silent[blank_end], whereas turbulent flow is [blank_start]noisy[blank_end].
Aneurysms result in laminated thrombus as the blood flows more [blank_start]slowly[blank_end] through the vessels resulting in a slow viscous blood near the edges of the lumen. This can cause an aggregation of platelets and a thrombus will form.
In ath[blank_start]erosclerosis[blank_end], the reduce cross-sectional area will cause an increase in velocity which can further damage the vessels due to the turbulent nature of flow.
The baroreceptor reflex is found in the carotid sinus and aortic arch. If blood pressure is low, there will be less afferent firing to the medullary cardiovascular centre. This will lead to a decrease in parasympathetic activity and an increase in sympathetic activity. This will cause B1 adrenoreceptors to increase HR and contractility and increase SVR via a1 adrenoreceptors. This mechanism can become sustained after?
The 2 mechanisms of intermediate blood pressure control are:
Transcapillary volume shift--> low pressures will drive fluid from interstitium into plasma (2 x more effective than baroreceptor reflex)
Reverse stress relaxation mechanism: tightening of blood vessels by vascular tone secondary to low stress on the vessel wall.