Blood Vessels - Class Flashcards

Question

Effects of Physical Activity on Venous Return

Answer 1

*Effects of Exercise on Venous Return* - ↑ Heart rate and contractility → ↑ cardiac output and blood pressure - Vasodilation of vessels in muscles, lungs, and heart → ↑ blood flow - ↑ Respiratory rate → enhances thoracic (respiratory) pump - ↑ Skeletal muscle activity → activates skeletal muscle pump *Venous Pooling with Inactivity* - Venous pressure alone is insufficient to move blood upward - Prolonged standing may reduce cardiac output enough to cause dizziness - Prevented by: - **Tensing leg muscles** → activates skeletal muscle pump - **Pressure suits** (e.g., for jet pilots) → support venous return

Answer 2

- **Veins** hold ~**64–70%** of total blood volume → Act as **volume reservoirs** due to high distensibility → Can expand **~8× more** than arteries at same pressure - **Arteries + capillaries** hold only **30–35%** of total volume - Arteries: ~15% - Capillaries: ~5% - Blood distribution is **uneven**: most is stored in **systemic veins**, not evenly across all vessels

Answer 3

- The **force of blood** distending arterial walls 1. **Systolic Pressure** - **Highest pressure** in arteries - Occurs during **ventricular contraction** (systole) 2. **Diastolic Pressure** - **Lowest pressure** in arteries - Occurs during **ventricular relaxation** (diastole) 3. **Blood Pressure Reading** - Reported as **systolic/diastolic** - Normal: **120/80 mmHg** 4. **Korotkoff Sounds (Cuff Sounds)** - Cuff inflated above systolic pressure → **no sound** (no flow) - **1st sound = systolic pressure** (turbulent flow begins) - **Sounds disappear = diastolic pressure** (laminar flow restored) - Used during auscultatory blood pressure measurement

Answer 4

- Average pressure in arteries over a full cardiac cycle - Reflects **driving force** of blood through the vasculature **Pulse Pressure (PP)** - PP = **SBP − DBP** **Formulas to estimate MAP** - *At rest* (diastole lasts longer): **MAP = DBP + (SBP − DBP) / 3** - *During exercise* (systole and diastole nearly equal): **MAP = DBP + (SBP − DBP) / 2** **Clinical relevance** - Important for assessing tissue perfusion, especially in critical care - Normal MAP ≈ **70–110 mmHg** - Minimum of **60 mmHg** needed to perfuse vital organs

Answer 5

1. **Cardiac Output (CO)** - CO = **Stroke Volume × Heart Rate** - ↑ CO → ↑ BP 2. **Peripheral Resistance** a. **Vessel Diameter**: - Vasoconstriction ↑ resistance → ↑ BP - Vasodilation ↓ resistance → ↓ BP b. **Blood Viscosity**: - ↑ viscosity (e.g. polycythemia) → ↑ resistance → ↑ BP c. **Total Vessel Length**: - ↑ vessel length (e.g. obesity) → ↑ resistance → ↑ BP 3. **Arterial Blood Volume** - More blood in arteries → ↑ pressure against vessel walls 4. **Arterial Compliance / Vessel Elasticity** - ↓ compliance (stiff arteries) → ↑ systolic pressure - Elastic vessels buffer pressure fluctuations

Answer 6

- *CO = HR × SV* - ↑ **Cardiac Output** → ↑ **Systolic BP** - ↓ **Cardiac Output** → ↓ **Systolic BP** - ↑ HR or SV = ↑ CO → proportionally increases BP *(as CO ↑, BP ↑ if resistance is constant)* **Frank-Starling Law** - ↑ **Venous return** → ↑ **EDV** (end-diastolic volume) - ↑ EDV → ↑ **stretch** of ventricular wall (↑ **preload**) - ↑ Stretch → ↑ **cross-bridge formation** in sarcomeres - ↑ Cross-bridges → ↑ **force of contraction** - ↑ Force → ↑ **SV** → ↑ **CO** → ↑ **BP** - *Proportional relationship*: More filling = more ejection = higher pressure - *Moderator band* limits overexpansion of right ventricle

Answer 7

- *Definition*: Friction between blood and vessel walls that opposes flow; BP must overcome PR to maintain circulation - *Affects*: **Afterload** – resistance heart must work against to eject blood **3 Primary Sources of PR:** 1. **Vessel Diameter** - *Smaller diameter = much greater resistance* (inverse to radius⁴) - Flow is slower and more turbulent in narrow vessels → more resistance - Arterioles control this dynamically through vasoconstriction and vasodilation - **Most powerful influence** on PR 2. **Blood Viscosity** - Thicker blood = greater resistance - *Increased by*: dehydration, polycythemia (↑ RBCs), high protein content - *Decreased by*: anemia, dilution with IV fluids 3. **Total Vessel Length** - Longer vessels = more surface area = greater resistance - *↑ Fat tissue* adds capillary length (~200 miles/lb) → raises PR **Systemic Vascular Resistance (SVR)** - Total PR in the systemic circulation - Major regulator: **arterioles**, by changing radius **Summary (Poiseuille’s Law)** - PR is governed by: - **↑ Resistance** if radius ↓ (to the 4th power), viscosity ↑, or length ↑ - **↓ Resistance** if radius ↑ (vasodilation has a major impact) - *Key takeaway*: **Vessel diameter** is the most effective and rapid way to change resistance and blood pressure.

Answer 8

Widespread or localized changes in vessel diameter to adjust **blood pressure** and **flow distribution** 1. **Regulate Systemic Blood Pressure** - *↑ BP*: Via vasoconstriction (narrowing vessels) - Requires **medullary vasomotor center** or **hormonal signals** - *↓ BP*: Via vasodilation - *Clinical importance*: Maintains **cerebral perfusion** during hemorrhage or dehydration 2. **Redistribute Blood Flow (Perfusion)** - *Central control*: Sympathetic NS directs blood away from kidneys/digestive organs → toward muscles during exercise - *Local control*: Metabolites (e.g., CO₂, H⁺, adenosine) in tissues trigger local vasodilation to increase perfusion - No systemic pressure change needed 3. **Localized Vasoconstriction** - *Constriction of one artery*: - ↓ pressure downstream - ↑ pressure upstream - *Effect*: Routes blood away from some organs and toward others based on need

Answer 9

- *Highly variable* depending on activity level - Controlled by both **systemic sympathetic input** and **local metabolite signals** *Receptor Distribution and Function* - **Skeletal muscle arterioles express both**: - **α₁-adrenergic receptors** → vasoconstriction (dominant **at rest**) - **β₂-adrenergic receptors** → vasodilation (activated **during exercise**) *Resting State* - **Sympathetic tone** is mediated by **norepinephrine** from postganglionic sympathetic neurons → binds **α₁ receptors** on skeletal muscle arterioles → causes **vasoconstriction**, ↓ perfusion to inactive muscle → most **capillary beds closed**, total skeletal muscle flow ~**1 L/min** *Exercise State* 1. **Epinephrine** released from **adrenal medulla** into bloodstream → binds **β₂ receptors** on skeletal muscle arterioles → causes **vasodilation**, **overrides α₁ tone** in active tissue → effect is **receptor-selective**: **epinephrine has high affinity for β₂**, unlike norepinephrine 2. **Local metabolites** (↑ CO₂, H⁺, lactate) accumulate in working muscle → trigger additional **vasodilation**, independent of neural control 3. **Sympathetic stimulation to non-muscle organs** (e.g., gut, kidney): → activates **α₁ receptors**, causing **vasoconstriction** → **redistributes blood** to skeletal muscle *Additional Notes* - **β₁-adrenergic receptors** are found in the **heart**, not vessels → ↑ heart rate and contractility → ↑ cardiac output - **Isometric contractions** impede local blood flow → cause **faster fatigue** than isotonic exercise

Answer 10

*Total Cardiac Output* - **At rest**: ~**5 L/min** - **Moderate exercise**: ~**17.5 L/min** *Major Shifts During Exercise* 1. **Skeletal muscle** - At rest: **20%** (~1,000 mL/min) - Exercise: **~71%** (~12,500 mL/min) - ↑ Perfusion via **β₂-receptor activation** and **local metabolites** (CO₂, H⁺, lactate) 2. **Digestive + Renal systems** - Digestive: ↓ from **27%** to **3.4%** - Renal: ↓ from **22%** to **3.4%** - ↓ Flow via **α₁-mediated vasoconstriction** 3. **Cutaneous (skin)** - ↑ Absolute flow: 300 → 1,900 mL/min - Helps dissipate **heat** - %CO increases modestly 4. **Cerebral circulation** - **Constant flow** (~750 mL/min) - % of CO ↓ due to larger CO - Maintained by **tight autoregulation** → *ensures brain perfusion* 5. **Coronary circulation (heart)** - %CO remains **stable** (~4%) - Absolute flow ↑ in proportion to cardiac output - Matches **increased oxygen demand** from myocardium *Key Point* - Exercise redistributes blood to **active muscle and skin**, while maintaining **brain and heart perfusion**, and reducing flow to **kidneys and GI tract**.

Answer 11

**Blood Pressure: Arm vs. Leg Exercise** - **All skeletal muscle arterioles** have **α₁ receptors** (vasoconstriction) and **β₂ receptors** (vasodilation) - Sympathetic tone is **systemic** and does **not differ** between arms vs. legs - **Key difference** lies in: - **Local metabolite accumulation** (↑ CO₂, H⁺, lactate) in **active muscles** - → Triggers **vasodilation** in **working muscle**, lowering **total peripheral resistance (TPR)** - **Leg exercise**: - **Large muscle mass** → more local vasodilation - → **Greater ↓ TPR** → **smaller increase in BP** - **Arm exercise**: - **Smaller muscle mass** → less local metabolite production - → **Less vasodilation** → **higher TPR maintained** - → Leads to **greater rise in BP** for the same workload - *Summary*: - BP rise is **greater during arm exercise** due to **less metabolically driven vasodilation**, not because of different sympathetic output

Answer 12

*Definition* - Tissues can regulate their own blood supply based on local conditions *Metabolic Theory* - Inadequate perfusion → accumulation of **CO₂, H⁺, lactate** → **Stimulates vasodilation** → increases local blood flow - Oxygen delivery clears metabolites → Once cleared → **vasoconstriction** resumes *Vasoactive Chemical Control* - **Paracrine secretion** by nearby cells (acts locally, not systemically) - Released by **platelets, endothelial cells, mast cells, perivascular tissue** *Vasodilators* 1. **Nitric oxide (NO)** – from endothelial cells in response to shear stress 2. **Prostacyclin** – inhibits platelet adhesion and promotes dilation 3. **Histamine, bradykinin, prostaglandins** – from mast cells, basophils *Vasoconstrictor* - **Endothelins** – potent constrictors secreted from endothelial cells *Clinical Note* - This **local vasodilation overrides sympathetic α₁-mediated vasoconstriction** during exercise - Especially important in **active skeletal muscle**, ensuring perfusion where needed

Answer 13

Sudden increase in blood flow following a period of ischemia - *Mechanism*: - Occlusion → ↓ flow → metabolite buildup (CO₂, H⁺, adenosine) - Upon restoration → **intense vasodilation** → transient **↑ perfusion above baseline** - *Examples*: Skin flushing after cold exposure, limb reperfusion after compression

Answer 14

Formation of new blood vessels from existing vasculature - *Triggers*: - **Chronic low oxygen** (e.g. exercised muscle, tumor growth) - **Tissue regrowth** (e.g. uterine lining, wound healing, fat, muscle growth) - **Obstructed blood flow** (e.g. coronary collateral development) - *Mediated by*: Growth factors (e.g. **VEGF**, FGF) released by hypoxic or injured tissue

Answer 15

*Sympathetic Vasomotor Tone* - **Sympathetic nerves fire at baseline frequency** to maintain **partial vasoconstriction** ("vasomotor tone") - **↑ Sympathetic firing** → **vasoconstriction** (via **α₁-adrenergic receptors**) - **↓ Sympathetic firing** → **vasodilation** - **NE (norepinephrine)** is secreted by most sympathetic postganglionic neurons *Adrenergic Receptor Distribution* - **Vessel effect depends on receptor type expressed**: - **α₁ receptors** (most systemic arterioles) → **vasoconstriction** - **β₂ receptors** (skeletal muscle, coronary vessels) → **vasodilation** - **Epinephrine** (from adrenal medulla) has high affinity for **β₂**, allowing **vasodilation** in active tissues - **NE** (from sympathetic nerves) favors **α₁**, maintaining **vasoconstriction** elsewhere *Medullary Vasomotor Center (in medulla oblongata)* - Integrates autonomic reflexes that regulate BP: 1. **Baroreflex**: ↑ BP → ↑ baroreceptor firing → ↓ HR, ↓ sympathetic tone (→ vasodilation) 2. **Chemoreflex**: triggered by hypoxia, hypercapnia, or acidosis → ↑ sympathetic output 3. **Medullary ischemic reflex**: ↓ perfusion to brainstem → extreme sympathetic output *Clinical Note* - **Loss of sympathetic tone** (e.g. neurogenic shock) → **dangerous hypotension** - Neural control can **redistribute blood flow**, e.g., shunting from gut to muscle during exercise

Answer 16

- *Sensors*: **Baroreceptors** in **carotid sinus** and **aortic arch** *When BP is high*: 1. Arteries stretch → ↑ baroreceptor firing 2. Signals sent to **medulla oblongata** 3. ↑ **parasympathetic (vagal) tone** → ↓ HR 4. ↓ **sympathetic tone** → vasodilation, ↓ TPR 5. → **↓ Blood pressure** *When BP is low*: 1. ↓ arterial stretch → ↓ baroreceptor firing 2. Medulla increases **sympathetic tone** → ↑ HR, ↑ contractility, vasoconstriction 3. ↓ parasympathetic tone 4. → **↑ Blood pressure**

Answer 17

- *Sensors*: **Chemoreceptors** in **carotid bodies** and **aortic bodies** - *Monitored variables*: **pH**, **CO₂**, **O₂** **Primary role**: - Adjust **respiration rate** to correct blood gas levels **Secondary role**: - Regulate **vasomotion** when chemical imbalance is detected **Triggered by**: - **Acidosis**, **hypercapnia** (↑ CO₂), **hypoxemia** (↓ O₂) **Responses**: 1. Signal to **vasomotor center** → **vasoconstriction** 2. → **↑ BP**, ↑ lung perfusion and gas exchange → enhances **CO₂ clearance**, O₂ delivery

Answer 18

- *Trigger*: ↓ perfusion to **medulla oblongata** (e.g. brain ischemia) **Detection**: - Medulla monitors **its own blood flow** **Response**: - Activates **sympathetic output** from cardiac & vasomotor centers: - ↑ HR and contractility - **Widespread vasoconstriction** **Goal**: - ↑ **BP** to restore perfusion to brain - Short-term emergency reflex to protect **cerebral circulation**

Answer 19

*General Actions* - Hormones regulate BP by: - **Vasoactive effects** (vasoconstriction/dilation) - **Water & Na⁺ balance** → affects blood volume **Angiotensin II** - Formed via **RAAS pathway** from **angiotensinogen (liver)** → Converted to angiotensin I by **renin** (kidney), then to **angiotensin II** by **ACE** - **Vasoconstrictor** → ↑ peripheral resistance → ↑ BP - Stimulates **aldosterone** (adrenal cortex): → ↑ **Na⁺ reabsorption**, water follows → ↑ blood volume and pressure **Aldosterone** - Acts on **distal tubule** & **collecting duct** → ↑ Na⁺ reabsorption, K⁺ excretion → Water retained → **↑ blood volume and BP** **ADH (Vasopressin)** - Secreted from **posterior pituitary** - Promotes **water retention only** via **aquaporins** in collecting duct - At **high levels**, also acts as **vasoconstrictor** → ↑ blood volume and **↑ BP** **Epinephrine and Norepinephrine** - Cause **vasoconstriction** in most vessels via **α₁-adrenergic receptors** - Cause **vasodilation** in **skeletal and cardiac muscle arterioles** via **β₂-adrenergic receptors** → Redistributes blood to muscles during stress or exercise **Atrial Natriuretic Peptide (ANP)** - Released by **atria** in response to stretch (↑ BP/volume) - Promotes **Na⁺ excretion** → water loss - Causes **vasodilation** → ↓ blood volume and **↓ BP**

Answer 20

- **Viscosity** = resistance of fluid to flow; determined by **hematocrit** (RBC concentration) - **Peripheral resistance (PR)** is **directly proportional** to viscosity → ↑ viscosity → ↑ resistance → ↑ BP - **Factors that increase viscosity**: - ↑ **RBC count** (e.g., polycythemia) - **Cold temperature** (slows flow, increases aggregation) → ↑ hematocrit → ↑ viscosity → ↑ BP - **Factors that decrease viscosity**: - **Anemia**, **hemorrhage**, or **increased body temperature** → ↓ hematocrit → ↓ viscosity → ↓ BP

Answer 21

- **Peripheral resistance (PR)** is **directly proportional** to **total vessel length** → ↑ length → ↑ resistance → ↓ flow → ↑ BP (to maintain flow) - **Obesity increases total vessel length**: - ~**200 miles** of new vessels per **1 lb of fat** - ↑ adipose tissue → ↑ number of vessels → ↑ resistance → ↑ BP - Longer vessels increase **friction** against blood flow → heart must generate **higher pressure** to maintain circulation

Answer 22

- **Systolic BP** is **directly proportional** to **arterial blood volume** → ↑ volume → ↑ systolic pressure (due to greater stretch on vessel walls) - **Increased sodium intake** → ↑ blood osmolarity → **Water follows salt** → ↑ blood volume → ↑ BP - **Dehydration or hemorrhage** → ↓ blood volume → ↓ arterial pressure → ↓ systolic BP

Answer 23

- **Inverse relationship** with blood pressure → More compliance = **lower BP**, less compliance = **higher BP** - *High compliance* (young, healthy arteries) → Arteries stretch easily during systole → **dampen pressure surge** - *Low compliance* (aging, arteriosclerosis) → Arteries resist stretch → ↑ systolic pressure → ↑ pulse pressure

Answer 24

- *Definition*: Inadequate cardiac output → insufficient **tissue perfusion** - *Two main categories*: 1. **Cardiogenic shock** → *Pump failure* (e.g., **myocardial infarction**) 2. **Low venous return (LVR) shock** → *↓ preload*, not enough blood returning to heart --- **Types of Low Venous Return Shock** 1. **Hypovolemic shock** - *Cause*: ↓ blood volume from trauma, dehydration, hemorrhage, or **extensive burns** - *Burns*: loss of skin barrier → can't retain water 2. **Obstructed venous return shock** - *Cause*: Tumor or aneurysm compresses a vein → ↓ return to heart 3. **Venous pooling (vascular) shock** - *Cause*: Blood pools in limbs (e.g., long standing or widespread vasodilation) - Subtypes: - **Neurogenic shock**: loss of **sympathetic tone** → systemic vasodilation - **Septic shock**: bacterial toxins → **vasodilation** + ↑ **capillary permeability** - **Anaphylactic shock**: severe allergic response → **histamine** release → vasodilation + permeability

Answer 25

- *Definition*: Inadequate cardiac output → insufficient **tissue perfusion** - *Two main categories*: 1. **Cardiogenic shock** → *Pump failure* (e.g., **myocardial infarction**) 2. **Low venous return (LVR) shock** → *↓ preload*, not enough blood returning to heart --- **Types of Low Venous Return Shock** 1. **Hypovolemic shock** - *Cause*: ↓ blood volume from trauma, dehydration, hemorrhage, or **extensive burns** - *Burns*: loss of skin barrier → can't retain water 2. **Obstructed venous return shock** - *Cause*: Tumor or aneurysm compresses a vein → ↓ return to heart 3. **Venous pooling (vascular) shock** - *Cause*: Blood pools in limbs (e.g., long standing or widespread vasodilation) - Subtypes: - **Neurogenic shock**: loss of **sympathetic tone** → systemic vasodilation - **Septic shock**: bacterial toxins → **vasodilation** + ↑ **capillary permeability** - **Anaphylactic shock**: severe allergic response → **histamine** release → vasodilation + permeability

Answer 26

**Compensated vs. Decompensated Shock** - **Compensated shock**: - Homeostatic mechanisms restore perfusion - E.g., fainting → lying flat lets **gravity** restore cerebral blood flow - **Decompensated shock**: - Fails to correct itself → **positive feedback loops** - ↓ perfusion → MI → ↓ CO → tissue death - Risk of **DIC**: coagulation due to undiluted fibrinogen/thrombin

Answer 27

*Blood Changes* - ↓ **Hematocrit** → ↓ **viscosity** - ↑ Risk of **thrombi** and **emboli** formation - **Venous pooling** in legs due to reduced venous return *Heart Changes* - ↓ **Efficiency** and **elasticity** of myocardium - Formation of **scar tissue** - ↑ Risk of **coronary atherosclerosis** → *Note*: **Estrogen** is protective against **LDL**, so risk ↑ post-menopause *Blood Vessel Changes* - ↓ **Elasticity** → stiffer vessels - **Calcium deposits** damage vessel walls → contribute to arterial stiffness

Answer 28

- *Definition*: Growth of **plaque deposits** (lipids, calcium) inside **arterial walls** - *Mechanism*: - **Hypertension** → ↑ shear stress → endothelial damage → plaque formation - **Plaques** narrow lumen → ↑ resistance → worsens **hypertension** - Establishes **positive feedback loop** of vascular damage - *Consequence*: ↓ perfusion to tissues, ↑ risk of MI and stroke --- **Risk Factors and Complications of Atherosclerosis** - *Risk factors*: - **Diabetes mellitus** - **High-cholesterol/saturated fat diet** - **Estrogen loss** post-menopause (estrogens inhibit atherogenesis) - *Complications*: 1. **Atherosclerosis + hypertension**: - ↓ perfusion to organs (e.g., kidneys) - ↑ risk of **aneurysm** and **stroke** 2. **Coronary atherosclerosis**: - Leads to **angina pectoris**, **myocardial infarction** - ↓ heart wall thickness → ↓ stroke volume, ↓ cardiac output/reserve

Blood Vessels - Class Flashcards

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