Disorders of Blood Flow and Alterations in BP Flashcards
list the determinants of systemic blood pressure
blood volume
elastic properties of the blood vessels
cardiac output
Peripheral vascular resistance (PVR)
spongeBob
Eagerly
Called
Patrick
explain: CO=SV X HR
this equation is stating that cardiac output equals the stroke volume times the heart rate.
Your stroke volume is the amount of blood your heart pumps each time it beats, and your heart rate is the number of times your heart beats per minute.
Cardiac output is the term that describes the amount of blood your heart pumps each minute.
explain: BP=CO X SVR
this equation is stating that blood pressure equals the cardiac output (how much blood the heart pumps) times the SVR, or the systemic vascular resistance (resistance to blood flow offered by all of the systemic vasculature, excluding the pulmonary vasculature)
These together help you get the BP
define the terms:
systolic blood pressure
diastolic blood pressure
Systolic blood pressure, the top number, measures the force your heart exerts on the walls of your arteries EACH TIME it beats.
Diastolic blood pressure, the bottom number, measures the force your heart exerts on the walls of your arteries IN BETWEEN beats.
define the terms:
pulse pressure
mean arterial pressure
pulse pressure: Pulse pressure is the difference between the upper and lower numbers of your blood pressure. It represents the force that the heart generates each time it contracts.
mean arterial pressure: MAP, or mean arterial pressure, is defined as the average pressure in a patient’s arteries during one cardiac cycle. It is considered a better indicator of perfusion to vital organs than systolic blood pressure (SBP).
compare changes in cardiac output and systemic vascular resistance and their effect on blood pressure.
changes in cardiac output will either increase or decrease blood pressure.
systemic vascular resistance changes will do the same. If more resistance, there will be a higher blood pressure, and if less resistance there will be a lower blood pressure.
explain the role of baroreceptors and arterial chemoreceptors and their effect on blood pressure regulation as neural mechanisms.
BARORECEPTORS
baroreceptors (pressoreceptors): PRESSURE sensitive receptors located in the walls of blood vessels and the heart.
They respond to changes in the stretch of the vessel wall by sending impulses to the cardiovascular centers in the brain to affect appropriate changes in HR, strength of cardiac muscle contraction, and vascular smooth muscle tone.
this would primarily make bp go up.
explain the role of baroreceptors and arterial chemoreceptors and their effect on blood pressure regulation as neural mechanisms.
CHEMORECEPTORS
chemoreceptors are chemo (CHEMICAL) sensitive cells that monitor blood levels of oxygen, carbon dioxide, and hydrogen ions.
Respond to changes in the concentration of ions, and the main function is to regulate ventilation, can induce widespread vasoconstriction by communicating with cardiovascular centers in the brain.
this would make bp go up
explain the control of blood pressure by the renin-angiotensin system
renin is an enzyme stored in the kidneys that is released when there is increase SNS activity or decreased bp.
After renin leaves the kidney, it enters the blood stream, where it acts enzymatically to convert angiotensinogen to angiotensin I. Angiotensin I is then converted to angiotensin II by the angiotensin converting enzyme (ACE).
Angiotensin II causes blood vessels to constrict and blood pressure to increase.. Together, angiotensin II and aldosterone work to raise blood volume, blood pressure and sodium levels in the blood to restore the balance of sodium, potassium, and fluids. If the renin-angiotensin system becomes overactive, consistently high blood pressure results.
contrast the regulation of bp on a short term and a long term basis.
short term basis
SHORT TERM REGULATION: controlled by the autonomic nervous system–baroreceptors (CANNOT regulate long term bc mechanism that activates baroreceptors resets itself after being activated)
Baroreceptors–> parasympathetic fibers (vagus nerve)—>sympathetic response–>increase in HR/BP
contrast the regulation of bp on a short term and long term basis
long term basis
RAAS System
Renin facilitates the conversion of angiotensinogen to angiotensin I. This is then converted to angiotensin II using angiotensin-converting enzyme (ACE).
Angiotensin II is a potent vasoconstrictor. It acts directly on the kidney to increase sodium reabsorption in the proximal convoluted tubule. Sodium is reabsorbed via the sodium-hydrogen exchanger. Angiotensin II also promotes the release of aldosterone.
this will ultimately increase bp
describe possible mechanisms in the development of atherosclerosis
Fibrous atheromatous plaque: a basic lesion characterized by an accumulation of intracellular and extracellular lipids, proliferation, of vascular smooth muscle cells, formation of scar tissue, and calcification. They increase in size and encroach on the lumen of the artery which may eventually occlude the vessel or predispose to a thrombus formation. Reduction in blood flow can become increasingly greater with disease progression.
One hypothesis of plaque formation suggests that injury to the endothelial vessel layer is the initiating factor. Possible injurious agents include smoking, immune mechanisms, and mechanical stress.
Hemodynamic factors: plaques tend to form where vessels branch and where there is turbulent blood flow
Hyperlipidemia: Elevated cholesterol increases interactions between endothelial layer of the vessel wall and white blood cells particularly monocytes which then become activated macrophages which release free radicals that oxidize LDL which is toxic to endothelium
what are the five types of lipoproteins and which are good/bad?
chylomicrons
very-low-density lipoproteins (VLDL)
intermediate-density lipoproteins (IDL)
low-density lipoproteins (LDL)—BAD
makes up most of your body’s cholesterol. High levels of LDL cholesterol raise your risk for heart disease and stroke.
high-density lipoproteins (HDL)–GOOD
absorbs cholesterol and carries it back to the liver. The liver then flushes it from the body.
list the risk factors for development of primary HTN
NON modifiable:
Age (more common in adults), gender/race (African Americans), family history and genetics
Modifiable: Dietary factors Dyslipidemia Tobacco Alcohol consumption fitness level obesity insulin resistance/metabolic abnormalities obstructive sleep apena
define secondary hypertension and give the etiologies
secondary hypertension is an elevation in blood pressure because of another disease or condition.
most common etiologies (causes):
kidney disease, disorders of adrenal cortical hormones, pheochromocytoma, coarctation of the aorta, and use of oral contraceptive agents
