l25-l32: cardiovascular system

cardiovascular system

consists of blood and the means of moving blood around the body

blood

specialized connective tissue containing plasma (aqueous matrix), cells, and platelets

plasma

more than half of the volume of blood and consists of water, dissolved substances, and proteins

• considered an extracellular fluid, but it has far more protein than other extracellular fluids in the body

albumin

plasma protein responsible for transport and fluid balance

globulin

plasma protein responsible for immune (antibodies) and transport

fibrinogen

plasma protein responsible for clotting

formed elements

cells or cell fragments found in blood which help carry out its various functions

red blood cells (erythrocytes)

cells that transport dissolved gases and wastes

• make up >99% of all formed elements

• notable features: biconcave shape, lack of a nucleus, lack of mitochondria and other organelles

• lifespan of ~4 months then contents are recycled into new RBCs, and/or excreted

white blood cells (leukocytes)

cells that defend against pathogens and toxins

platelets

cells that defend against fluid loss

• survive for 9-12 days in the bloodstream

• lack organelles and are constantly recycled by phagocytic cells (primarily in the spleen) and replaced

complete blood count (CBC)

determines the number and distribution of formed elements and measures of RBC health

mean corpuscular hemoglobin (MCH) and mean corpuscular volume (MCV)

measures of RBC maturity and size

cell counts

measure which formed elements are present

hematocrit

packed red blood cell volume (% of RBCs in whole blood)

hemoglobin (Hb)

protein that enables the transport of oxygen by RBCs

hemostasis

physiological processes that limit or halt blood loss through damaged blood vessels

serum

fluid that is left after blood clotting

• contains water, solutes, and blood proteins that are not related to clot formation

vascular phase of hemostasis

cells in the blood vessel wall undergo rapid contraction and increased endothelial ‘stickiness’

platelet phase of hemostasis

platelets aggregate at exposed endothelial surfaces to plug the broken vessel

• attach to the sticky endothelia cells and basement membrane and become activated

• change shape and release chemicals that attract other platelets and help them stick to each other

coagulation phase of hemostasis

fibrin mesh network forms around platelets, producing a clot

• involves a cascade of enzymes that catalyze the formation of fibrin from soluble fibrinogen

• triggered by tissue damage or exposed connective tissue

• takes at least 30 seconds after vessel damage to begin

fibrin

protein which binds aggregated platelets (and blood cells) into a clot

common pathway

1. Factor X → Factor Xa
   catalyzes

2. Prothrombin (Factor II) → Thrombin (Factor IIa)
   which catalyzes

3. Fibrinogen (Factor I) → Fibrin (Factor Ia)

fibrinolysis

dissolves the clot after the vessel wall is repaired

1. tissue plasminogen activator (t-PA) is released from the repaired vessel wall

2. t-PA converts plasminogen (a plasma protein) to plasmin

3. plasmin degrades fibrin

red bone marrow

found in the space around spongy bone and produces blood cells and platelets

megakaryocytes

remain in bone marrow, shedding membrane packets containing structural proteins and enzymes (platelets)

erythropoietin (EPO)

hormone secreted by the kidneys in response to hypoxia

• stimulates RBC progenitors to divide and differentiate, enhancing RBC production

RBC formation

1. myeloid stem cells

2. erythroblasts

3. ejection of nucleus

4. reticulocyte enters bloodstream

5. RBC maturation is completed

pulmonary circuit

moves blood from the heart to the lungs and back

systemic circuit

moves blood from the heart to all other organs in the body and back

unidirectional sequence of blood flow

heart → arteries → capillaries → veins

• exception: portal veins connect capillaries to other capillaries

vasodilation

relaxation of smooth muscle cells in the vessel wall

vasoconstriction

contraction of smooth muscle cells reduces lumen diameter

artery structure

• intermediate lumen diameter

• thick smooth muscle layer

• tight endothelial layer

capillary structure

• smallest lumen diameter

• absent smooth muscle layer

• leaky (gaps) endothelial layer

vein structure

• largest lumen diameter

• thin smooth muscle layer

• tight endothelial layer

heart

pump that creates the pressure gradients which propel blood through blood vessels

• wall has multiple layers, and most of the thickness comes from layers of striated striated cardiac muscle cells

heart valves

fibrous connective tissue structures that open in response to pressure build-up in the proximal chamber

cardiac cycle

1. relaxation

2. atria contract: atrial pressure rises

3. ventricles contract: ventricular pressure rises, AV valves close

4. relaxation: ventricular pressure falls, SL valves close

systole

contraction of a heart chamber

diastole

relaxation of a heart chamber

full diastole

both sets of chambers being relaxed

• lasts for ~half the duration of each cardiac cycle

cardiac myocytes

branching, mononucleate cells that contain myofibrils

• have reduced T-tubules and sarcoplasmic reticulum

• lack specialized neuromuscular junctions

intercalated discs

physically link the plasma membranes of two cells

gap junctions

allow ions (and thus membrane potential signals) to flow between cells

cardiac action potentials

• have a prolonged plateau of depolarization

• slower, and last ~200x longer

• involve the opening of L-Type voltage-gated calcium channels

cardiac excitation-contraction coupling

1. some calcium ions enter the cytoplasm from the ECF

2. the elevated [Ca²⁺]_i triggers the release of much, much more calcium from cellular stores (the SR)

conduction pathways

run through the heart wall, and synchronize the excitation and contraction of heart chambers

• formed from highly modified cardiac myocytes that lack myofibrils but are highly excitable and connected by gap junctions

sinoatrial (SA) node

cardiac rhythm begins when its cells spontaneously depolarize and repolarize

SA node cell

• pacemaker cell

• V_m is never at rest

• generates its own (intrinsic) rhythm of regular depolarization and repolarization

SA node action potential

• depolarization generated by T-type (transient) VGCCs

• repolarization generated by VGKCs

pacemaker potential

slow depolarization that automatically restarts after every repolarization

• ‘funny current’ (I_f) flows across the cardiac myocyte plasma membrane

funny channel

voltage-gated cation channel that ONLY opens when the membrane is hyperpolarized (allowing Na⁺ to enter the cell)

parasympathetic heart rate

ACh leads to the opening of additional K⁺-selective channels

• hyperpolarization

• slower depolarization

sympathetic heart rate

NE enhances the activation of funny channels

• reduced repolarization

• more rapid depolarization

conducting cells of the internodal fibers

electrically coupled to SA node cells, allowing depolarization to rapidly spread across both atria

AV node

has relatively few gap junctions, which slows down AP transmission between its cells

• causes a 100 ms delay in the spread of depolarization

interventricular bundle and Purkinje fibers

geometry means the apex of the ventricle will be excited (and contract) before the base, allowing for efficient emptying into the arteries

electrocardiogram (ECG)

detects rhythmic electrical activity in the heart wall

ECG P wave

due to the depolarization from action potentials occuring in cardiac myocytes within the atrial wall

ECG QRS complex

large because there are many more myocytes in the ventricle walls and they all depolarize nearly at the same time

T wave

due to the repolarization of the ventricle myocytes

arrythmias

unusual patterns of cardiac electrical activity

sinus arrythmia

interval between heart beats varies 5% during respiratory cycle and up to 30% during deep respiration

premature atrial contractions

occasional shortened intervals between one contraction and the next (frequently occurs in healthy people)

tachycardia

heart rate >100 bpm (normal in babies, and during exercise, but unusual for an adult at rest)

bradycardia

heart rate <60 bpm (common in athletes at rest, but should rise with exercise)

cardiac output

the volume of blood (mL) moved through the heart into the systemic circuit a given time (min)

• CO = SV mL/beat × HR beat/min = mL/min

heart rate

the number of cardiac cycles (beats) per minute (bpm)

• primarily affected by ANS activity and certain hormones

• increases are primarily due to a reduction in diastole

stroke volume

the volume of blood (mL) ejected into the artery during each cardiac cycle (mL/beat)

• affected by muscle activity, vessel blood flow patterns, sympathetic activity, and hormones

ventricular (and atrial) diastole

when passive filling of the ventricles occurs

• all chambers are relaxed

• AV valves are open

atrial systole

completes the filling of the ventricles, which reach their End Diastolic Volume (EDV)

• atria contracting, ventricles relaxed

• AV valves are open

End Diastolic Volume (EDV)

maximum volume achieved when blood is squeezed from atria to ventricles

• affected by the venous return and ventricular filling time

venous return (VR)

volume of blood that is delivered to the right atrium during the cardiac cycle

• affected by CO, constriction of arteries, or compression of veins

filling time

the duration of ventricular diastole, which determines the time the AV valves are open

• ↑HR = ↓filling time

ventricular systole

involves a brief period of isovolumetric contraction and then a period of ventricular ejection

• atria relax, ventricles contract

• AV valves close

• SL valves open

isovolumetric contraction

occurs when pressure is rising but both valves are still closed

ventricular ejection

occurs as long as the semilunar valves are open, allowing the stroke volume to be squeezed into the artery (aorta)

End Systolic Volume (ESV)

remaining blood in the ventricle after ventricular diastole begins

isovolumetric relaxation

occurs when pressure is decreasing with no change in volume (both valves closed)

preload

amount of stretching of the heart wall due to blood volume within the ventricle

• ↑EDV = ↑stretch

afterload

amount of force the ventricle has to generate to open its semilunar valve

• ↑aorta pressure = ↑afterload

• directly affected by resistance (pressure) in the blood vessels

contractility

amount of force produced during a contraction for a given amount of preload

• measures force production regardless of muscle stretching

• altered by sympathetic and hormone activity

rate of blood flow through a vessel

function of the opposing forces of pressure

pressure gradient

produces a force that moves fluid in the direction of lower pressure

resistance

caused by friction between the walls of the tube and the fluid

• increases linearly with vessel length

• inversely related to vessel luminal diameter

  • diameter has a bigger effect than length

• increases in any location where turbulent flow occurs

viscosity

measure of resistance due to interactions among the molecules in the moving fluid

laminar flow

all the liquid is moving in one direction in smooth layers

turbulent flow

layers are disrupted, and the movement is not all unidirectional, so overall flow is reduced for a given pressure gradient

• can occur due to shifts or changes in the geometry of the vessel wall

arterial pressure

fluctuates with the changes in pressure due to the cardiac cycle

• highest during and just after ventricular systole, and lowest during diastole

pulse pressure

difference between systolic pressure and diastolic pressure

mean arterial pressure (MAP)

diastolic pressure plus 1/3 pulse pressure

blood pressure

systolic pressure / diastolic pressure

sphygmomanometer

measures blood pressure by tracking how much external pressure it takes to occlude blood flow

• normal values: 120-130 mm Hg to 70-80 mm Hg

elastic arteries

help to buffer the pulse pressure, reducing the variability in blood flow and pressures in capillaries

average blood pressure

declines as blood passes through the systemic circuit, encountering a series of resistances

• drop-off is largest through the arterioles

cross-sectional area of all blood vessels

highest in capillaries and lowest in elastic arteries

velocity of blood flow

highest in arteries and lowest in capillaries

veins in the limbs

contain valves to help prevent backflow of blood due to gravity

• skeletal muscle contractions provide a secondary pump that helps propel blood toward the trunk

capillary beds

networks formed by capillaries that connect between an arteriole and venules

arteriovenous anastomoses

able to dilate, diverting blood away from the higher resistance in the rest of the capillary bed