Ch. 13/14 Day 6 Flashcards
BP is affected by?
Affected by blood volume, SV, total peripheral resistance (TPR), and HR
- -increase in any of these will increase BP
- -vasoconstriction of arterioles raises BP upstream in the arteries
BP Equation
BP(arterial) = CO * TPR
CO = SV * HR
- SV comes from blood volume
- HR comes from sympathoadrenal signals
- TPR comes from vasoconstriction and sympathoadrenal signals
BP
The BP of blood vessels is related to the total cross-sectional area
- -capillary BP is low because of LARGE total cross-sectional area
- -artery BP is high because of SMALL total cross-sectional area
Progressive drop in BP as you move throughout the system
–steepest BP drop occurs in ARTERIOLE region
BP Regulation
Kidneys can control blood volume and thus SV
–long-term BP control
Sympathoadrenal system stimulates vasoconstriction of arterioles (raising TPR) and increased CO
Baroreceptor Reflex
Activated by changes in BP detected by baroreceptors (stretch receptors) in the aortic arch and carotid sinuses
Increased BP stretches these receptors, increasing action potentials to the vasomotor and cardiac control centers in the medulla
Most sensitive to drops in BP
Vasomotor center controls vasodilation and constriction
Cardiac center controls HR
Baroreceptor Reflex: Structures
- Baroreceptors (sensors)
- Vasomotor and cardiac control centers in medulla (integrating centers)
- Sympathetic/parasympathetic axons to heart and blood vessels (effectors)
Effect of BP on Baroreceptor Response
Baroreceptors increase action potential firing if BP increases; if BP goes down, the decreased firing is interpreted as a signal by brainstem to increase sympathetic output, HR, contractility, vasoconstriction in arterioles to bring BP back up
Action potentials come from sensory nerve fibers from baroreceptors
Baroreceptor Reflex: Fall/Increase in BP
Fall in BP = increased sympathetic and decreased parasympathetic activity, resulting in increased HR and TPR
Rise in BP has the opposite effects
Good for quick beat-by-beat regulation
–e.g. going from lying down to standing
Atrial Stretch Reflexes
Activated by increased venous return to:
- -stimulate reflex tachycardia (sympathetic) - physiologic significance unknown
- -inhibit ADH (anti-diuretic hormone) release; results in excretion of more urine
- -stimulate secretion of atrial natriuretic peptide; results in excretion of more salts and water in urine
Atrial stretch reflexes respond to ____, not pressure.
Volume
BP Management
Measured in mmHg using sphygmomanometer
BP cuff produces turbulent flow of blood in brachial artery - detected as Korotkoff sounds via stethoscope
1) Cuff inflated to beyond systolic BP to occlude artery;
2) Pressure gradually released, the first (tapping) sound is heard at systole;
3) Second “sound” is the last “tap” before sounds disappear - when pressure in cuff = diastolic pressure
Average BP is 120/80 (systolic/diastolic)
Pulse Pressure
“Taking the pulse” is a measure of HR
Each “pulse” = increased BP in that artery at systole
- -P(systole) minus P(diastole) = pulse pressure
- -e.g. if BP is 120/80, pulse pressure = 120 - 80 = 40 mmHg
Pulse pressure is a reflection of SV
*Think about for exam: How is pulse pressure a reflection of SV?
Because that pulse is created by a given SV, the level of that pulse pressure is going to be directly proportional to the volume that has been ejected in that heartbeat
Mean Arterial Pressure (MAP)
MAP = average pressure in the arteries in one cardiac cycle
Significance: MAP - venous pressure = driving force for blood flow into capillaries
Not a simple arithmetic average, since diastole is longer than systole
Approximated as: diastolic pressure + 1/3 * pulse pressure
–e.g. for BP 120/80, pulse pressure = 40, and MAP = 80 + 1/3*40 = 93mmHg
Hypertension (HTN)
High BP
Incidence increases w/ age
Increases risk of cardiac diseases, kidney diseases, and stroke
Classified as “essential” or “secondary”
Essential or Primary HTN
Most people fall in this category.
Causes not clearly defined in all cases; may include:
- -a) increase salt intake coupled w/ decreased kidney filtering ability
- -b) increased sympathetic nerve activity –> increase HR
- -c) altered responses to paracrine regulators from endothelium
- -d) increased TPR
Secondary HTN
A symptom of another disease, such as kidney disease
Dangers of HTN
Vascular damage w/in organs, especially dangerous in the cerebral vessels leading to stroke
Ventricular overload to eject blood due to abnormal hypertrophy, leading to arrhythmias and cardiac arrest
Contributes to the development of atherosclerosis
Treatments for HTN
Lifestyle modifications:
–decrease salt intake, decrease smoking and drinking, decrease weight, increase exercise
K+ (and possibly calcium) supplements
Diuretics to increase urine formation
Beta blockers to decrease cardiac rate
ACE inhibitors to block angiotensin II production
What is Angiotensin II?
Potent vasoconstrictor
–ACE inhibitors given to block angiotensin II producers in HTN
Circulatory Shock
Inadequate blood flow to match oxygen usage in tissues
Early signs: decrease pulse pressure, decrease in diastolic pressure
Late signs: decrease systolic pressure; cold, clammy skin
Hypovolemic Shock
Due to low blood volume from an injury, dehydration, or burns
Decrease CO and BP
Blood is diverted to the heart and brain at the expense of other organs
Compensation includes baroreceptor reflex, which in response to lower pressure, raises HR, raises peripheral resistance, and produces cold, clammy skin and low urine output
Septic Shock
Dangerously low BP (hypotension) due to an infection (sepsis)
Bacterial toxins (endotoxins) induce nitric oxide (NO) production, causing widespread vasodilation
Mortality rate is high (50-70%)
Other Causes of Circulatory Shock
Severe allergic reactions –> anaphylactic shock due to production of histamine and resulting vasodilation
Spinal cord injury or anesthesia –> neurogenic shock due to loss of sympathetic stimulation
Cardiac failure –> cardiogenic shock due to significant loss of myocardial function
Congestive Heart Failure
CO insufficient to maintain blood flow required by the body
- -a) caused by myocardial infarction (MI; heart attack), congenital defects, HTN, aortic valve stenosis, or disturbances in electrolyte levels (K+ and Ca2+)
- -b) similar to hypovolemic shock in symptoms and response
Types of Congestive Heart Failure
A) Left-Side Failure: raises left atrial pressure and produces pulmonary congestion and edema causing shortness of breath
B) Right-Side Failure: raises right atrial pressure and produces systemic congestion and edema
