Blood Pressure- Physiology and Pathology Flashcards
formula for mean BP
(SBP+2xDBP)/3
the difference in flow between the arteries and veins
in arteries and the aorta, the flow is pulsatile and in the capillaries and veins, the flow is laminar
what are the effects of too high or low systemic arterial blood pressure
too low: faint (vaso-vagal attack), shock (tissue acidosis pH<7.35)
too high: tissue damage
therefore, pressure regulated to maintain adequate tissue perfusion
list the determinants of blood pressure
- cardiac output
- vascular resistance
- physical factors (gravity, arterial compliance, blood viscosity)
vascular resistance
predominantly determined by level of constriction of arterioles which is under hormonal and neurological control.
how does arterial compliance contribute to BP?
- arteries stretch and stores elastic potential energy in systole
- releases this energy to maintain flow in diastole
- stiff arteries, e.g., due to old age, reduces compliance and increases systolic BP
how does blood viscosity contribute to BP?
- contributes to resistance to flow
- high protein/hypercellular blood has high viscosity
- therefore, higher pressure to maintain flow
what effect does prostacyclin and NO have on the vascular system?
- vasodilators
- produced by the endothelium that controls the local vascular tone
what effect does endothelin have on the vascular system?
- vasoconstrictor
- produced by the endothelium that controls the local vascular tone
what determines venous return that further affects preload?
- circulating blood volume- can be affected by dehydration-major bleeding, kidney failure-over transfusion
- venous tone- autonomic nervous system, circulating vasoconstrictors (e..g, adrenaline), local vasoactive substances (e.g, NO, prostacyclin, endothelin)
how does aldosterone affect blood volume?
aldosterone produced by the adrenal cortex causes an increase in salt and water absorption in the distal convoluted tubule that increases blood volume and restores BP
how does ADH affect blood volume?
ADH, produced by the posterior pituitary gland, increases water reabosorption in the distal convoluted tubules and collecting ducts by the insertion of aquaporins that transport water through the tubular cells and back into blood, leading to a decrease in plasma osmolarity
what are the different ways the autonomic system controls the heart rate
- sympathetic NS via b1 receptors- increases heart rate
2. Parasympathetic NS via M receptors (i.e., vagus nerve)- increases HR
different factors that affect HR
intrinsic HR (sinus node in right atrium), autonomic controls (SNS, PNS), circulating substances- Adrenaline increases HR via b1 receptors
what factors can cause vasodilation
-low O2/high CO2 -acidosis -NO -prostacyclin
what factors can cause vasoconstriction
-endothelin
what are the causes of high blood pressure
-CKD -Structural causes -Endocrine causes -Preganancy/pre-eclampsia -Essential hypertension
what are the structural causes of high BP
- renal artery stenosis
- aortic coarctation
what are the endocrine causes of high BP
-high aldosterone (Conn’s syndrome) -High catecholamines (phacochromocytoma) -High Cortisol (Cushing’s syndrome) -High growth hormone levels (acromegaly)
What are the essential hypertension causes of high BP
-polygenetic -obesity -high salt intake -high alcohol intake -ethinicity
effects of chronic hypertension
- heart muscle damage
- large vessel damage
- microvascular damage
examples of large vessel damage in hypertension
- aortic aneurysm (and rupture)
- cerebrovascular disease (stroke)
- CAD (angina, MI)
- peripheral vascular disease (claudication, amputation)
examples of microvasculature damage
- CKD
- Brain dysfunction (multi-infarct dementia)
- Exacerbates vascular effects of diabetes (kidneys, eyes and peripheral nerves)
acute effects of severe hypertension
- aortic dissection
- acute heart failure (high afterload)
- confusion (‘encephalopathy’)
- cerebral hemorrhage
- retinal haemmorrhage
explain the pathophysiology of faints
- vaso-vagal episodes
- neurally mediated syncope
- typically occurs as a reaction to a stressful epidoe
- disporportionate PNS activation causes arteriolar dilation and slowing of heart rate which causes a drop in BP
- reduced cerebral perfusion
- tl.c= transient loss of consciousness
explain the pathophysiology of shock
- persistently low blood pressure (<90) which could be due to a range of causes: -cardiogenic (large MI-low CO) -sepsis (e.g. meningitis-low SVR), anaphylaxis (e.g, penicillin or nuts-low SVR), low blood volume (eg., bleeding, burns, diarrhoea- low CO)
- SNS activation- blood flow redistributed to heart, heart, muscle
- poor tissue perfusion can cause organ malfunction, esp in the kidneys and acidosis (lactase)
special circulation in the coronary arteries
- flow occurs mainly in diastole because
- it occurs when there is a pressure difference between the aorta and the small vessels
- during systole, the small (intramyocardial vessels) are ‘squeezed’
- therefore, this pressure difference if highest in diastole.
special circulatin in the pulmonary system
- contains c.20% of the blood volume
- starling’s law ensures the same volume of blood flows through the systemic and pulmonary circulation
- pulmonary arteries respond differently to systemic e..g, pul arteries constrict if there is a high level of CO2 or low levels of O2 to minimise perfusion of non-functional lung tissue
- different sensitivity to vasoactive stimuli, e.g., very sensitive to prostacyclin and endothelin
- pulmonary hypertension is entirely different to systemic hypertension
