Case 6 Flashcards
what kind of measurements are recommended to confirm the diagnosis of hypertension
out of office BP measurements
how many adults had hypertension in 2000
1 billion
percentage of people in Israel with hypertension
23%
percentage of people in Poland with hypertension
62%
what BP confirm hypertension
> 140/90 mmHg
what are primary cases
do not have a specific cause
how many cases are primary
98%
how many cases are secondary
2%
what drugs cause hypertension
NSAIDS
percentage of hyperaldosteronism that is caused by adrenal adenoma
30%
percentage of primary hyperaldosteronism that is caused by adrenal hyperplasia
70%
what is main cause of primary hypertension
over activity of SNS and an underactive PNS
what happens to the heart in hypertension
hypertrophy of the left ventricle
what happens to the kidneys in hypertension
kidneys leak proteins, become granular and will finally fail
what happens in the brain
ruptured cerebral artery and compression of the ventricle
what is diabetic retinopathy
leading cause of blindness in working age adults
what is diabetic neurophathy
leading cause of end stage renal disease
what is diabetic neuropathy
leading cause of non truamatic lower extremity amputations
macrovascular complications
2-4 fold increase in cardiovascular mortality and stroke
heart disease
peripheral vascular disease
what is blood pressure
cardiac output x total peripheral resistance
endothelial cells in the artery
run parallel to the flow in the artery
vascular smooth muscle cells in artery
wrap around the artery and when they contract they squeeze the artery and the lumen shrinks
what reduces contractility in the arteries
when the membrane potential is lowered and the cell becomes hyper polarised because of potassium efflux. the voltage dependent calcium channels become inactivated. less calcium is able to enter the cytoplasm globally and that reduces the contractility.
pressure myography
spontaneous pressure induced constriction or time
measures the diameter of isolated, pressurized arteries to assess the functional activity of smooth muscle and endothelial cells
how does calcium both contract and dilate the arteries
influx of extracellular calcium contracts the artery the the pressure is present. however calcium is also released by vascular smooth muscle events as ‘small release events’ - calcium sparks. these are vasodilatory signals.
contraction mechanism
- intraluminal pressure
- membrane depolarisation
- voltage gated Ca2+ channels
- Ca2+
- pressure induced construction
calcium spark mechanism
both mechanism diagram
vascular ‘see-saw’ diagram
what is key regulator of vascular function
endothelium
what is the function of the endothelium
barrier and vasodilation
what regulates endothelial functions
intracellular Ca2+ levels, the release of nitric oxide, prostaglandins and dilating factors
what are the different vasodilatory pathways
- release of nitric oxide
- endothelial dependent hyperpolarisation
- prostacyclin (cycko-oxygenase pathway)
small arteries regulated by membrane potential diagram
what is the metabolic rate
the amount of energy liberated per unit of time
what happens when same level of exercise is maintained
the rate of oxygen consumption will remain steady
how does lactic acid get removed
converted to glycogen
how does the PO2 level change during exercise
goes from 40mmHg to 25mmHg so alveolar-capillary gradient is raised
what is the value of oxygen entering blood during exercise
4000ml/min
what does brainstem detect
increases in carbon dioxide and to a lesser extent reduction in oxygen In the blood
what does brainstem detection lead to
sympathetic innervation of the heart, lungs and arteries. this increases the heart rate, breathing rate and contraction of the ateries and leads to increase of oxygen in the blood
what happens to curve when you reduce pH
curve shifts to the right and there is increased oxygen delivery to the muscles
what shifts the curve to the right and what is the name of this effect
- temperatures, 2,3-BPG, carbon dioxide and protons
how is BPG produced
by red blood cells during glycolysis
when is the curve shifted to the left
as the blood temperature is reduced compared to the muscles
what do reductions in temperature and increase in blood pH do
will increase the affinity of haemoglobin for oxygen
what does increase in DPG and CO2 in the muscles during exercise do
encourage haemoglobin to release oxygen
what does activation of the SNS cause
arterial vasoconstriction
what does active hyperaemia do
dilation of skeletal muscle arterioles leads to a reduction in total peripheral resistance which reduces the mean arterial blood pressure
where do the baroreceptors send electrical impulses
the medulla oblongata
starlings law explantation
as venous return causes an increase in the load on muscle fibres this increases the stretch on the heart muscle which in turn increases the contractility
At rest and diastolic volume of the ventricle does not cause optimal overlap of actin and myosin
As the venous return increases, the ventricular wall is stretched more and there comes a point where there’s a more optimal degree of overlap between the action and myosin and the stretching of the muscle increases the affinity of troponin C calcium which causes a greater number of cross bridges to form
So an increase in sympathetic tone means the increased noradrenaline increases intracellular calcium and this results in a faster cross bridge formation which causes an increase in conrtactility
This means there’s an increases in stroke volume despite the reduced filling time because the heart rate has increased
what does aerobic exercise training cause
eccentric left ventricular hypertrophy
what does Fick equation state
that oxygen available to muscles increases by increase CO or muscles ability to extract oxygen from arterial blood
haemoconcentration
we get an increase in the hydrostatic pressure across the capillary wall
Means that more blood is squeezed out of the capillaries into the interstitial space surrounding the muscles
Increase in oncotic pressure across the capillary wall and this is because metabolites leak out of the muscle and into the interstitial space and this increase in oncotic pressure also helps to drive fluid out of the muscle cell capillaries
And because of this loss of fluid there is effectively an increase in the concentration of red blood cells and that increases concentration gradient of oxygen from the capillaries to the muscles and this therefore speeds up diffusion
Muscles are more efficient at extracting oxygen from capillaries
diagram for haemoconcentration
when does greatest contractile force occur
when there is less overlap between actin and myosin. as cardiac muscle stretches the degree of overlap between actin and myosin is reduced
average VO2 max in men and women
men is 40-50 and women is 30-40
UK physical guidelines advice (LEARN)
what is blood pressure
cardiac output x total peripheral resistance
what is the cardiac output
stroke volume x heart rate
what is the stroke volume explanation
volume of blood ejected per beat. it is equal to the end diastolic volume. this is the volume of blood in the ventricles at the end of diastole.
other way to work out stroke volume
end diastolic volume - end systolic volume
what is the preload
the tension in the cardiac myocytes before they contract.
contractility
contraction force of the myocardium for a given preload
what is the after load
the blood pressure in the aorta and pulmonary trunk
what decreases the heart Tate
acetylcholine
cold temp
intense visceral pain
what is the total peripheral resistance effected by
- viscosity of the blood - stable
- vessel length - unchanged
- vessel radius - easily changed
how are blood vessels maintained
in a state of partial vasoconstriction
where is vessel radius controlled
controlled by the vasomotor centre in the medulla oblongata
what are the sensors of blood pressure control;
- baroreceptors
- volume receptors
- chemoreceptors
- osmoreceotpors
neural control of the BP
- automomic nervous system
- directly influence heart and blood vessels
- short term mechanism
humeral control of BP
- circulating hormones
- directly influence heart and blood vessels or alter blood volume
- intermediate and long term mechanisms
where are baroreceptors found
carotid and aortic senses
what nerve is connected to the carotid sinus
glossopharyngeal nerve
what nerve is connected to the aortic sinus
the vagus nerve
where is afferent information take to
the nucleus solitarius in the brain stem. it modulates the activity of the CV centres and sensitivity of the receptors can be altered
accelerator centres in the brain
vasomotor centre and cardiac accelerator are groups of sympathetic neurones in the medulla
inhibitor centre
dorsal motor nucleus of the vagus and the nucleus ambiguous. tonally active - vagal tine
what does vagal tone do
slows heart rate
what happens if BP goes up
increases firing rate to cardiac and vasomotor centres.
- stimulates cardio inhibitory centre, increase in PNS activity to the SA node and therefore decrease in heart rate -
- inhibits cardioacceleratoe and vasomotor centres, decrease in SNS activity snd therefore decreased heart rate and vasoconstriction
what happens f BP falls
there is a decrease in firing rate to cardiac and vasomotor centres
- stimulates the cardioaccelerator and vasomotor centres, then increase in SNS activity to SA node and increase in heart rate which increases the force of contraction and vasoconstriction
- inhibits cardio inhibitory centre therefore decreased PSN activity to SA node and therefore increased heart Tate
what happens if blood volume is not replaced?
- venous return continues to fall therefore decreased EDV
- the heart rate increase therefore less filling time and EDV decreased
- decreased EDV therefore decreases force of contraction (starlings Law of the heaert0
valsalva manoeuvre
humoral control systems
- catecholamines - epinephrine and norepinephrine
- RAAS
- ANP (atrial natriuretic peptide)
- ADH
where are catecholamines released
from the adrenal medulla
alpha 1 vascular smooth muscle cells
vasoconstrictor
alpha 2 presynaptic membrane
negative feedback
beta 1 SA node and cardiac muscle
increased heart rate and contraction force
beta 2 vascular smooth muscle in heart
vasodilator, bronchodilator
beta 3 adipocytes
lypolysis
RAAS system.
atrial natriuretic peptide ANP
ADH production
produced by the hypothalamus, secreted in the pituatary and released by the posterior pituariry
ADH
how would the carotid sinus baroreceptors respond to occlusion of both common carotid arteries and what would be the cardiovascular responses?
physiological response to haemorrhage
are blood vessels innervated?
yes by synthetic fibres only
what is normal LDL:HDL ratio in males
100mg/dl LDL but > 40 mg/dl HDL
In the Stages of Change Model, in which stage do people begin ‘weighing’ up the pros and cons
Contemplation
Approximately what percentage of women aged over 75 have hypertension
65%
By what mechanism do dihydropyridines decrease blood pressure
Increasing natriuresis
What is the main social predic
tor of smoking initiation
Having parents that smoke
what is nitric oxide released in response to
parasympathetic nervous stystem stimulation
direct pathway of NO
the PNS uses NO as a neurotransmitter and has a direct effect on the smooth muscle cells. The drug GTN, once converted into NO, acts directly on the smooth muscle cells
the indirect pathway of NO
the PNS uses acetyl choline as a neurotransmitter and stimulates the endothelial cells to produce NO, which then act on the smooth muscle cells.
how is nitric oxide stimulated in endothelial cells
Nitric oxide synthase (NOS) enzymes in endothelial cells synthesize NO from arginine and oxygen and by reduction of inorganic nitrate.
what does nitric xide activate
Activates guanylate cyclase (G-cyclase).
This increases formation of cGMP, which activates protein kinase G.
This leads to the dephosphorylation of myosin light chains and sequestration of intracellular Ca2+, with consequent relaxation.
what vasocontrictors can stimulate NO
angiotensin II
Endothelin
Endothelin is present in the endothelial cells of all blood vessels.
It greatly increases when the vessels are injured.
After severe blood vessel damage, release of local endothelin and subsequent vasoconstriction helps to prevent extensive bleeding from arteries.
