Blood pressure Flashcards
Series
2 paths in a row
Flow in both paths is the same
Pressure is higher in the first path than the 2nd path
b/c energy is lost as blood experiences friction/resistance
Parallel
Branching paths
Flow is split between 2 paths
Pressure is same at start of both paths.
If paths have identical resistance same pressure
Pmean
Pdiastolic + (Psystolic - Pdiastolic)/3
Stroke volume
Volume of blood pumped out of a ventricle during one beat of the heart
70ml
Cardiac output
Volume of blood pumped out of a ventricle per minute
4.9L/min
End Diastolic Volume
Volume of blood in a ventricle at the end of filling (diastole). EDV is associated with “pre-load”, how stretched the muscle is.
120ml
End Systolic Volume
Volume of blood remaining in a ventricle at the end of contraction (systole). So: SV = EDV – ESV
50ml
Ejection Fraction
Percentage of ventricular volume pumped out during a heart beat: SV / EDV
55-70%
vasoconstriction
Smaller radius
- > higher resistance
- > lower flow rate
Dilation and constriction of BV causes
Central regulation: CNS, Autonomic, Endocrine
Exercise
Local regulation of pressure
Immune
Haemostasis
Excercise
peripheral vasodilatation
muscle/skin
vasoconstriction
splanchnic circulation
Increase HR and systolic BP
Decrease diastolic BP
Standing
Initially a drop in BP
- then compensatory recovery (ie increase back to normal):
peripheral vasoconstriction
- Arterial + venous
- & Increased HR
Systemic BP control
Local - Endothelial - Nitric Oxide (NO) Neurological – the autonomic system - Sympathetic: noradrenaline Humoral – renal / pituitary / adrenal - The kidney is central to Blood Pressure
Local Vasomotor control
Endothelial cells release vasodilator compounds
- Nitric Oxide
- Causes smooth muscle relaxation
- Vasodilatation
Controlled by local blood flow conditions Hydrostatic pressure Shear force - Made greater by laminar flow - Shear force is atheroprotective
Baroreceptors
Detect pressure and feed back to the brain
Located in the transverse aortic arch and the carotid sinuses of the left and right internal carotid arteries
Activity —> decreased BP
Chemoreceptors
Detect when O2 levels are low & feed back to the brain
Located in the carotid bodies and aortic bodies
Frank-Starling
The stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end diastolic volume)
Venous return
The volume of blood flowing back to the heart through the veins
Preload
The initial stretching of the cardiac myocytes during diastole (prior to contraction). Depends on venous return
Volume Overload
Results when preload becomes too large
Afterload
The resistance that the chambers of the heart must overcome in order to eject blood out of the heart
Resistance during systole
Increased by back pressure
from Aorta or pulmonary arteries
Increases if the exit valve fails to open completely
Pressure Overload
Results from elevated afterload
Thoracic Pump
“Pulls” the blood (from below) towards the right atrium.
during inspiration
intrathoracic pressure is negative
abdominal pressure is positive (compression of abdominal organs by diaphragm).
Creates a pressure gradient
Muscle Pump
Rhythmical contraction of limb muscles
as occurs during normal locomotor activity
Squeezes blood out of nearby veins
Venous valves assure one-way flow toward heart
Pulmonary Circulation
High Capillary Density
Low Vascular Resistance
Acts as Blood Reservoir
Endocrine control of BP (ACE)
Acts as Filter
Pulmonary Circulation - O2, CO2 and pH
O2, CO2, pH effects opposite those in systemic circulation
If O2 is low in a region of the lung, the arterioles constrict
(likewise if CO2 or H+ are high, vasoconstriction)
Poor ventilation reduced perfusion
This minimises the amount of blood that is poorly oxygenated
Coronary Circulation
Cardiac Muscle has High Demand
Most Flow occurs during Diastole
Obtains blood almost before aorta
Hypertension
High blood pressure
esp. high diastolic pressure
Often Asymptomatic
May result in coronary artery disease and MI
Hypertension caused by
Mismatch between blood volume and circulatory capacity
Most cases are idiopathic Hormones (Ang II) Brain Medulla (NTS)
2ndary to Kidney disease
Cardiogenic shock - failure to compensate
Low urine output Hypotension Syncope Confusion Acidosis
Cardiogenic shock - compensatory mechanisms
Tachycardia
Tachypnoea
