Blood Pressure Flashcards
Mean blood pressure =
(systolic blood pressure +(2x diastolic blood pressure))/3
blood pressure basics
What type of flow in the aorta and large arteries?
pulsatile
What type of flow in the capillaries and veins?
laminar
If systemic arterial blood pressure is too low:
- faint (vaso-vagal attack)
- shock leading to tissue acidosis (pH<7.35)
If systemic arterial blood pressure is too high, leads to tissue damage
too high
Systemic arterial blood pressure is regulated to maintain
adequate tissue perfusion
Humans ideal blood pressure
120/80 mmHg
State the determinants of blood pressure:
- cardiac output
- vascular resistance
State the determinants of blood pressure: Cardiac Output:
- amount of blood pumped by the heart: c. 5L/min
- under hormonal and neurological control
State the determinants of blood pressure: Vascular Resistance:
- predominantly determined by the level of constriction of arterioles
- under hormonal and neurological control
Blood pressure Equation:
cardiac output x stroke volume
Ohm’s Law
V=IR
State 3 physical factors that affect blood pressure:
- gravity
- arterial compliance
- blood viscosity
Physical factors that affect blood pressure: Gravity:
- blood pressure is higher in feet, lower in head when standing upright….
Physical factors that affect blood pressure: arterial compliance:
- arteries stretch and store elastic potential energy in systole
- release energy to maintain flow in diastole
- stiff arteries (eg old age) reduces
compliance and increases systolic blood
pressure
Physical factors that affect blood pressure: blood viscosity:
- contributes to resistance to flow
- high protein/hypercellular blood has high
viscosity - higher pressure to maintain flow
Factors affecting CO and SVR
Cardiac output equation
CO = HR x SV
heart rate is per min
stroke volume is Liters
Usual cardiac output is
c.5L/min
Starling’s Law
- the mechanical energy set free in the
passage from the resting to the active state
is a function of the length of the fiber - fiber length is determined by end diastolic
volume (determined by venous return) - force contraction is translated into stroke
volume
Cardiac pressure volume
Preload is
venous return
preload (venous return)
- circulating blood volume:
- dehydration, major bleeding
- kidney failure, over-transfusion - Venous tone:
- autonomic nervous system
- circulating vasoconstrictors
- local vasoactive substances
Prostacyclin and nitric oxide are
vasodilator substances produced by the endothelium that controls local vascular tone
Endothelin
a vasoconstrictor substance produced by the endothelium that controls local vascular tone
Blood =
cells + plasma
Plasma =
water + salt + proteins
The kidney can affect blood volume.
- aldosterone (adrenal cortex) - salt
retention
- reabsorption in the distal convoluted
tubule - ADH (posterior pituitary) - water retention
- reabsorption in the distal convoluted
tubule and collecting ducts
- released in response to increased
plasma osmolarity
The intrinsic heart rate is
set by the sinoatrial node in the right atrium
Sympathetic nervous system receptors to increase heart rate
Beta-1 adrenogenic
What receptor to slow the heart rate
- parasympathetic
- vagus nerve
- M2 muscarinic receptors
Circulating substances that can affect heart rate?
- adrenaline 9increases) binds to beta-1 receptors
control of systemic vascular resistance
Renin-Angiotensin-Aldosterone System
Local controls
tissue perfusion is autoregulated in response to local need (provide a minimum BP)
- control occurs at arteriole level
- dilation: low O2, high CO2, acidosis, nitric
oxide, prostacyclin
- constriction: endothelin
Circulating Catecholamines
- adrenaline and noradrenaline
- responsible for generalised and sustained
responses to acute changes - receptors:
alpha: systemic arterioles = vasoconstriction (a1)
beta: systemic arterioles - vasodilation
(muscle b2)
heart - increases rate and force of
contraction (b1)
Noradrenaline is predominantly an
alpha agonist
Adrenaline is an
agonist of both alpha and beta receptors
Circulating catecholamines
Sensors involved in blood pressure:
- baroreceptors: aortic arch, carotid body at the carotid bifurcation
- signal the brain via:
- the vagus nerve
- glossopharyneal nerve
Control Centers for blood pressure
- brainstem:
- cardio-accelerator centre
- cardio-inhibitory center
- vasomotor center
Purpose of control centers for blood pressure
integrate sympathetic and parasympathetic responses
Blood pressure: effectors:
- sympathetic nerves:
- noradrenaline (adrenergic)
- vasoconstriction (muscle
vasodilation)
- increased heart rate and force - parasympathetic nerves:
- acetylcholine
- vasodilation
- vagus nerve: decreases heart rate
vasomotor center
Causes of high blood pressure:
- chronic kidney disease
- structural causes:
- renal artery stenosis (narrowing)
- aortic coarctation (narrowing of the
aorta above the kidneys) - Endocrine causes:
- high aldosterone lvels (conn’s
syndrome)
- high catecholamine levels
(phaeochromocytoma)
- high cortisol levels 9cushings)
- high growth hormone (acromegaly) - pregnancy/pre-eclampsia
hypertension is multifactorial:
- poly genetic
- obesity
- high salt intake
- high alcohol intake
- ethnicity
Effects of chronic hypertension
- heart muscle damage leading to heart failure
- large vessel damage
- microvascular damage
Effects of chronic hypertension: Large Vessels Damage:
Aortic aneurysm (and rupture)
Cerebrovascular disease (stroke)
Coronary artery disease (angina, myocardial infarction)
Peripheral vascular disease (claudication, amputations)
Effects of chronic hypertension: Microvascular damage:
Kidney dysfunction (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 haemorrhage
- retinal haemorrhage
Vaso-vagal episodes
- faints
- neurally mediated syncope
- generally reaction to a stressful episode
- disproportionate parasympathetic activation:
- arteriolar dilation
- slow heart rate - above lead to fall in BP
- reduced cerebral perfusion
- transient loss of consciousness
Shock
persistently low blood pressure <90mmHg systolic
state of organ hypoperfusion with resultant cellular dysfunction and death
Shock leads to
reduced perfusion of vital tissues
one inadequate oygen delivery leads to anaerobic metabolism so cellular function declines and can be irreversible leading to death
Symptoms of shock
- altered mental status
- tachycardia
- hypotension
- oliguria
Diagnosis of shock
- clinical
- blood pressure <90mmHg systolic
- measurements of markers of tissue hypoperfusion (blood lactate, base deficit)
treatment of shock
fluid resuscitation
blood products
correction of the underlyign disorder
vasopressors
shock causes
- cardiogenic (large MI) low CO
- sepsis due to low SVR
- anaphylaxis due to low SVR
- low blood volume
- sympathetic activation: blood flow redistributed to head/heat/muscle
- poor tissue perfusion: organ malfunction, acidosis