Blood Pressure Basics
What is blood pressure?
→ The force of blood against the vessel wall (Slide 3)
What is vascular resistance?
→ Opposition to blood flow due to friction between blood and vessel walls (Slide 14)
What part of the brain controls short-term regulation of blood pressure?
→ The cardiovascular center in the medulla oblongata (Slide 21)
Which two adrenal hormones increase blood pressure by increasing heart rate and contractility?
→ Epinephrine and norepinephrine (Slide 29)
What condition results from excess fluid in the brain due to high blood pressure?
→ Cerebral edema (Slide 9)
What are the two main values measured when recording blood pressure?
→ Systolic pressure and diastolic pressure (Slide 17)
Name the three main factors that affect resistance.
→ Vessel radius, blood viscosity, and vessel length (Slide 16)
What are the two main centers in the medulla that regulate blood pressure?
→ Cardiac center and vasomotor center (Slide 21)
Which hormone promotes sodium and water reabsorption in the kidneys to raise blood pressure?
→ Aldosterone (Slide 29)
What is a deep vein thrombosis (DVT)?
→ A blood clot forming in a vein, usually in the leg (Slide 10)
What is pulse pressure, and how is it calculated?
→ Difference between systolic and diastolic pressure (Slide 17)
Which factor has the greatest influence on resistance under normal conditions?
→ Vessel radius (Slide 16)
Which cranial nerves carry sensory information from baroreceptors and where are the baroreceptors located?
→ Glossopharyngeal (CN IX) – Carotid Sinus and Vagus (CN X) – Aortic Arch (Slide 25)
What hormone directly stimulates water reabsorption in the kidneys and what does this do to blood pressure?
→ Antidiuretic hormone (ADH), maintenance and increasing BP (Slide 29)
What is a common visible symptom of varicose veins?
→ Bulging, twisted superficial veins, especially in the legs (Slide 12)
What does mean arterial pressure (MAP) represent?
→ The average blood pressure in arteries, weighted toward diastole (Slide 21)
How does vasoconstriction affect resistance and blood pressure?
→ Increases resistance, which raises blood pressure (Slide 16)
How do baroreceptors respond to increased blood pressure?
→ They increase firing, leading to parasympathetic activation (↓ HR) and inhibition of sympathetic tone (vasodilation) (Slide 24)
Which heart hormone lowers blood pressure by promoting sodium and water excretion?
→ Atrial natriuretic peptide (ANP) (Slide 29)
What is circulatory shock?
→ Critically low blood pressure leading to inadequate perfusion (Slide 13)
How do you calculate MAP using systolic and diastolic pressure?
→ MAP = diastolic pressure + 1/3 (systolic – diastolic) (Slide 21)
How does hematocrit affect resistance?
→ Higher hematocrit increases viscosity, which increases resistance (Slide 16)
How do chemoreceptors influence blood pressure regulation and where are they located?
→ They detect changes in CO₂, O₂, and pH, stimulating sympathetic activity to raise BP when needed. Aortic and Carotid Bodies (Slide 26)
What is the primary function of the renin-angiotensin system (RAS)?
→ To increase blood pressure by vasoconstriction and fluid retention, and to stimulate aldosterone and ADH (Slide 30)
Name 2 types of circulatory shock and its cause.
→ Circulatory shock – Obstructed vein or massive vasodilation from toxins or anaphylaxis, Hypovolemic shock – caused by severe blood or fluid loss, Cardiogenic shock – MI, asystole, fibrillation, Neurogenic shock – Trauma to the brainstem resulting in loss of vasomotor tone (Slide 13)
Why is blood pressure higher in arteries than in veins?
→ Arteries are closer to the pumping action of the heart and have greater resistance (Slides 27, 33)
Why is vessel length usually a stable factor in resistance?
→ Vessel length doesn’t change much in adults; only obesity or growth significantly increases it (Slide 16, Supplemental)
What is the primary neurotransmitter released by sympathetic fibers regulating vascular tone?
→ Norepinephrine (Slide 23)
How does angiotensin II increase blood pressure?
→ It causes vasoconstriction and stimulates release of aldosterone and ADH (Slide 30)
How does an aneurysm form?
→ A localized ballooning of a weakened arterial wall (Slide 37)
How does perfusion relate to blood pressure?
→ Perfusion is the delivery of blood to tissues, dependent on maintaining an adequate blood pressure gradient (Slide 11)
Explain laminar vs turbulent flow and their effect on resistance.
→ Laminar flow is smooth and reduces resistance; turbulence increases resistance and decreases efficiency (Slide 16)
Why does activation of α₁ receptors increase blood pressure?
→ α₁ receptors cause vasoconstriction in most blood vessels, raising resistance and blood pressure (Slide 26)
How does ADH affect blood vessels in addition to the kidneys?
→ Causes vasoconstriction at high concentrations (Slide 31)
What are major risk factors for atherosclerosis?
→ High cholesterol, hypertension, smoking, diabetes, obesity (Slide 35)
Explain how blood pressure changes as it moves from arteries → capillaries → veins.
→ BP decreases steadily; highest in arteries, moderate in capillaries, lowest in veins (Slides 33–34)
Why do arterioles play the biggest role in systemic resistance?
→ They can change radius dramatically and are numerous, giving them the greatest control over total peripheral resistance (Slide 16)
How does β₂ receptor activation affect blood pressure, and where are these receptors located?
→ β₂ receptors cause vasodilation in coronary arteries and skeletal muscle, improving blood flow to active tissues (Slide 26)
Why does ANP act as a counter-regulatory hormone to aldosterone and ADH?
→ ANP decreases blood pressure by reducing volume, opposing sodium/water retention (Slide 32)
How does atherosclerosis impair blood flow?
→ Plaque buildup narrows lumen, increasing resistance and reducing perfusion (Slide 35–36)
A patient has a blood pressure reading of 160/100. Calculate the MAP and explain why it may be concerning.
→ MAP = 100 + (60/3) = 120 mmHg; concern: indicates chronic hypertension and risk of vascular damage (Slide 21, Supplemental)
A patient has polycythemia (abnormally high red blood cell count). Predict how this affects resistance and blood pressure.
→ Increases viscosity → increases resistance → raises blood pressure (Slide 16, Supplemental)
Explain why simultaneous α₁ and β₂ receptor activation during sympathetic stimulation is beneficial.
→ Ensures blood is redirected away from nonessential organs (via α₁ constriction) and toward skeletal muscle/heart (via β₂ dilation) during stress/exercise (Slide 27, Supplemental)
Explain how cortisol can indirectly raise blood pressure.
→ It increases sensitivity of vessels to catecholamines and can promote fluid retention (Slide 29, Supplemental)
Why can untreated varicose veins lead to long-term complications?
→ Pooling of blood increases risk of clots and chronic venous insufficiency (Slide 12, Supplemental)
Why is diastolic pressure more clinically significant than systolic for perfusion?
→ Organs and tissues are perfused during diastole, so diastolic pressure better reflects tissue blood flow (Slide 21, Supplemental)
Compare how resistance differs in systemic circulation vs pulmonary circulation.
→ Systemic circulation has higher resistance due to longer vessels and higher pressure; pulmonary circulation has low resistance for efficient gas exchange (Supplemental)
How does the vasomotor center contribute to venous return?
→ Sympathetic stimulation increases venoconstriction, reducing venous capacity and enhancing return to the heart (Slide 28)
A patient is dehydrated. Which hormones would be elevated to maintain blood pressure, and why?
→ ADH, aldosterone, and angiotensin II → promote vasoconstriction and fluid retention (Slides 29–31)
A patient has recurrent DVTs. Why might they also be at risk for a pulmonary embolism?
→ Clots in deep veins can dislodge and travel to the lungs, blocking pulmonary arteries (Slide 10)
Explain why pulse pressure tends to widen with age.
→ Arteries lose elasticity, causing systolic pressure to rise while diastolic pressure remains relatively stable (Slide 17, Supplemental)
How does atherosclerosis increase resistance and affect blood pressure?
→ Plaque buildup narrows vessel radius, increasing resistance and elevating blood pressure (Slide 46)
Why might neural reflexes be less effective in elderly individuals?
→ Baroreceptor sensitivity decreases with age, impairing rapid blood pressure regulation (Supplemental)
How does the renin-angiotensin-aldosterone system (RAAS) respond to low renal perfusion pressure?
→ Kidneys release renin → converts angiotensinogen to Ang I → ACE converts to Ang II → vasoconstriction + aldosterone release (Slides 30–31)
Why is an aneurysm considered dangerous even if asymptomatic?
→ It can rupture suddenly, causing massive internal bleeding and death (Slide 37)
A patient’s MAP is 58 mmHg. Predict the effect on organ perfusion and identify which organs are at highest risk.
→ Perfusion will be inadequate; brain and kidneys are most at risk due to high metabolic demand and autoregulation needs (Slides 21, 33, Supplemental)
A marathon runner is chronically dehydrated. Explain how this affects viscosity, resistance, and blood pressure, and predict potential consequences.
→ Dehydration thickens blood (↑ viscosity) → ↑ resistance → ↑ blood pressure; long-term can strain heart and reduce perfusion (Slides 16, 46, Supplemental)
A patient loses blood rapidly after trauma. Explain how neural regulation responds to maintain perfusion.
→ Baroreceptors detect ↓ BP → sympathetic activation → ↑ HR, ↑ contractility, vasoconstriction (α₁), venoconstriction → attempt to restore MAP (Slides 24–28)
A patient with chronic hypertension is prescribed an ACE inhibitor. Explain how this lowers blood pressure.
→ ACE inhibitors prevent formation of Ang II → less vasoconstriction and aldosterone release → lower blood pressure (Slides 30–31, Supplemental)
A patient has chronic hypertension and develops both atherosclerosis and an aneurysm. Explain how these conditions are linked.
→ Hypertension damages vessel walls → promotes plaque formation (atherosclerosis) → weakens wall → increases risk of aneurysm (Slides 35–37)