PHYS TOPIC 11 pt. 2

Blood Pressure

• = hydrostatic P exerted by blood on wall of vessel (slinically on the walls of the arteries) results when F is opposed by R

• systolic pressure = produced by vent. contraction against vascular restistance

• diastolic pressure = produced by elastic arteries against vascular resistance (when vents. are relaxed)

• what we measure in an artery: 120/80 - syst./diast.

• pulse pressure = systolic - diastolic

• mean arterial pressure (MAP) = regulated by the body i.e. what the body measures

  • = average of blood P through cardiac cycle BUT diastole us longer than systole, so;

  • MAP = diast P +1/3 pulse P

MAP Regulation

• F= change in P/r, therefore change in P = F xR

  • change in P = F x R

  • MAP = cardiac output (HR x SV) X Total peripheral resistance (TPR) (= resistance in all arterioles)

• chnage in P = MAP - venous P (P in veins ~ 0, therefore change in P = MAP)

• MAP is regulated by controlling;

  • Cardiac Output

  • TPR (arteriolar radius)

  • Blood Volume (affects venous return which impacts SV; also MAP directly)

Extrinsic Regulation of MAP - Neural Control

• baroreceptor reflexes - short term changes e.g. standing

  • stretch receptors - monitor MAP in:

    • carotid sinus (brain bp)

    • aortic arch (systemic bp)

• chemoreceptor reflexes

  • peripheral chemoreceptors - respond to pH, CO2, O2

  • found in aortic arch and carotid sinus (called “bodies”)

  • involved in regulation of respiration, but affect bp

Extrinsic Regulation of MAP - Hormonal Control

• epi

  • incr. HR, force of contraction which results in incr CO2 = incr. MAP

• renin-angiotensin system:

  • angiotensin II causes:

    • incr. vasocons. and venocons. therefore incr. MAP

    • incr. aldosterone, ADH which act to incr. renal Na+, H2O absorption and incr. thirst which incr. blood volume = incr. MAP

• atrial natriuretic peptide(ANP) causes:

  • decr. renin (therefore decrease angiotensin II) decrease aldosterone, ADH, all contribute to incr. urine production which will decrease blood volume

  • decrease vasoconstriction

  • so overall = decrease in MAP

Capillary Exchange

• between blood and ISF

• solutes enter and leave caps. by:

  • diffusion = major route (except brain)

    • CO2, O2, Ions, aa, glucose, hormones, etc.

    • usually between endothelial cells

  • Vesicular transport - large proteins (antibodies)

    • occurs via transcytosis

      • = endothelial from blood into cell, then exocytosis from endothelial cell into ISF

  • mediated transport - requires a memb. carrier protein

    • important mainly in brain

Capillary Exchange - Fluid

• (h2) enters (absorption) or leaves (filtration) capillaries by:

  • osmosis

  • bulk flow - due to pressure differences

    • 4 pressures involved

      • blood hydrostatic P (BHP) = blood pressure

      • blood osmotic P (BOP) - mainly due to plasma proteins

      • ISF hydrostatic pressure (IFHP) = 0mmHg

      • ISF osmotic pressure (IFOP) - mainly due to ISF proteins

Net Filtration Pressure (NFP)

• sum of hydrostatic and osmotic pressures acting on the capillary

• in the body:

  • 90% of filtered fluid reabsorbed to blood

  • 10% enters lymph

  • therefore ISF volume remains relatively constant

• clinical apps. Edema

  • = accumulation of fluid in the tissue (ISF) causing swelling

  • due to:

    • high BP

    • leakage of plasma proteins into ISF → inflammation (incr. IFOP)

    • decr. plasma proteins (malnutrition, burns) (decr. BOP)

    • obstruction of lymph vessels - elephantiasis, surgery

Circulatory Shock

• inadequate flood flow (decr. O2, nutrients to cells)

• types:

  • hypovolemic shock

  • vascular shock

Circulatory Shock Types

• hypovolemic:

  • decrease blood volume

  • due to: blood loss, severe burns, diarrhea, vomiting

• vascular shock:

  • blood vol. normal, but vessels expanded

  • due to: systemic vasodilation of blood vessels = decr. bp

  • examples:

    • anaphylactic shock- allergic reactions

      • due to lot of histamine released from mast cells

    • septic shock

      • due to bacterial toxins

    • cardiogenic shock

      • pump failure = decr. CO

      • heart cannot sustain blood flow

Stages of Shock

• compensatory

• progressive

• irreversible

Compensatory Shock Stage

• mechanisms can restore homeostasis by themselves

• involves:

  • baroreceptors

  • chemoreceptors

  • ischemia (lack of O2) of medulla

• all trigger SNS:

  • incr. HR, generalized vasoconstriction (except to heart, brains) = incr. BP

  • decr. blood flow to kidneys tiggers renin release - get angiotensin II, aldosterone and ADH release which causes: vasoconstriction; incr. Na+ and H2O retention (to maintain blood volume) , incr. Thirst

Progressive Shock Stage

• mechanisms inadequate to restore homeostasis - requires intervention

• decr. CO, decr. BP in cardiac circ. which will decr. cardiac activity

• decr. blood to brain will decr. the ability of the brains to exert cardiovascular control

• damage to viscera due to decr. blood flow, especially kidneys (can lead to renal failure)

Irreversible Shock Stage

• decr. CP = too little blood to heart = decr. CO

• self-perpetuating cycle - leads to death

Blood Contains

• plasma

  • H2O

  • proteins

  • electrolytes (ions)

  • other solutes

• formed elements

  • RBCs

  • WBCs

  • platelets

Plasma

• H2O (90.5%)

  • transport medium and carries heat

• proteins (7%)

  • albumins (58%)

  • globulins (38%)

  • fibrinogen (4%)

  • functions

    • produce osmotic pressure (especially albumins), buffer pH (7.35-7.45) - keep it from changing

    • α, β globulins - transport lipids, metal ions, hormones

    • (gamma) globulins = antibodies

    • clot formation

• electrolytes (ions)

  • functions: memb. excitability, buffers (HCO3)

• other solutes

  • nutrients, wastes, gases, hormones

Formed Elements in Blood

• Red Blood cells

• white blood cells

• platelets

Red Blood Cells

• functions:

  • transport - O2 on iron of heme; CO2 on globin

  • buffer - globin binds to H+ reversibly

  • carbonic anhydrase (CA) - important for CO2 transport in blood

• hemoglobin:

  • hb= 4 hemes +4 globins (protein)

  • 1 Fe/heme, therefore 4 Fe/Hb

  • broken down by macrophages into:

    • heme

      • Fe removed and stored (liver, muscle, spleen)

      • from stores (or diet) = bone marrow cells make heme → RBCs

      • non iron portion → bilirubin→ excreted in bile from liver

    • globin

      • converted to amino acids - recycled

• NOTE RBCs → no nuclei/mitochondria → anaerobic resp. only

White Blood Cells

• granulocytes

  • neutrophils

    • phagocytic

    • 1st to enter infected area

  • eosinophils

    • attack parasites

    • break down chemicals released in allergic reactions

  • basophils

    • secrete histamine (increases inflammation)

    • secrete heparin (inhibits local clotting)

• agranulocytes

  • monocytes

    • enter tissues, enlarge to become phagocytic macrophanges

  • lymphocytes

    • T lymphocytes - Helper T (TH) + cytotoxic T (CTLs) lymphocytes

    • B lymphocytes - when activated give rise to plasma cells - secrete antibodies

    • natural killer cells - attack foreign cells, abnormal cells (non specific)

Platelets

• cell fragments from megakaryocytes

• functions:

  • form platelet plug - prevents excess blood loss

  • contain granules = coagulation factors (proteins/chemicals involved in clotting)

Hemostasis

• process of stopping bleeding

• involves:

  • vascular spasm

  • platelet plug formation

  • clot formation

  • clot retraction

  • fibrinolysis

• thrombus = a stationary clot in undamaged vessel

• embolus = free floating clot

• hemophilia = clotting abnormal/absent

  • about 83% Type A - lack clotting factor VIII

Hemostasis Vascular Spasm

• = vasoconstriction of damaged arteries, arterioles - decr. blood flow (minutes to hours)

Hemostasis Platelet Plug Formation

• platelets stick to damaged blood vessel, release chemicals (factors) which:

  • cause more platelets to stick (+ feedback)

  • promote clotting

  • begin healing

• neighbouring healthy endothelial cells release a chemical preventing spread of plug

• plug formation requires a prostaglandin - inhibited by aspirin

Hemostasis Clot Formation

• 3 stages:

  • production of prothrombin activator by:

    • extrinsic pathway - uses factors released by damaged tissues

    • intrinsic pathway - uses factors contained in blood → usually both occur together - require Ca²+, tissue, platelet and/or plasma factors

  • prothrombin converted to thrombin (using activator)

  • fibrinogen converted to fibrin (using thrombin, Ca²+)

• thrombin - + feedback to incr. its own formation

• NOTE: ~2 doz. factors involved

  • from diet, liver (plasma proteins), damaged tissue, platelets

  • e.g. vit. K required for synthesis of 4 factors

Hemostasis Clot Retraction and Repair

• retraction - blood vessel edges pull together

• repair - fibroblasts form new CT, new endo. cells repair lining

Hemostasis Fibrinolysis

• clot dissolution

• fibrin digesting enzyme = plasmin

• phagocytes then remove clot in clumps

• plasminogen —→ (using factors) —→ plasmin (breaks down clot)