cardiovascular and lymphatic systems

circulatory system structures

• blood vessels (complex array of tubing)

• heart (pump)

circulatory system function

• deliver oxygen, nutrients, and other substances to all body cells

• remove waste products of cellular metabolism

intrinsic regulators of circulatory system

• nervous system

• endocrine system

supply nutrients

interaction between circulatory system and digestive system

• supply oxygen

• remove carbon dioxide

• maintain acid-base balance

interaction between circulatory system and respiratory system

• waste removal

• fluid, electrolyte

• acid-base balance

interaction between circulatory system and renal system

pulmonary circulation

right heart pumps deoxygenated blood to the lungs for gas

systemic circulation

left heart pumps oxygenated blood to the rest of the body for delivery of oxygen & nutrients and removal of wastes & carbon dioxide

arteries

carry blood away from heart

capillaries

allow closest contact and exchange between blood and interstitial space or the cellular environment

veins

carry blood toward the heart

lymphatics

carry plasma from interstitium to heart

heart

• weighs < 1 lb, about size of fist

• lies obliquely at an angle in the mediastinum (above diaphragm and between lungs)

heart wall/fibrous skeleton

• enclose and support heart

• divides it into 4 chambers

• valves and great vessels

valves

indentations of endocardium that direct flow

• separate atria from ventricles & ventricles from aortic/pulmonary arteries

• open and close with pressure changes within chambers

great vessels

conduct blood to and from heart

coronary circulation

arteries and veins serve metabolic needs of heart cells

heart’s nerves/muscle cells

direct rhythmic contraction and relaxation → propel blood through pulmonary and systemic circuits

pericardium

double-walled membranous sac that encloses heart

parietal pericardium

outer layer; surface layer of mesothelium over a thin layer of connective tissue

visceral pericardium

aka epicardium (inner layer), folds back and is continuous with the parietal pericardium

• allows large vessels to enter/exit the heart w/o breaching layers

pericardial cavity

fluid-containing space between visceral and parietal pericardium

pericardial fluid

secreted by cells of mesothelium to lubricate membranes and minimize friction as the heart beats

pericardium functions

• prevents displacement of heart during gravitational acceleration/deceleration

• provides physical barrier against infection/inflammation from lungs and pleural spaces

• contains pain and mechanoreceptors that elicit reflex changes in BP and HR

myocardium

• cardiac muscle

• anchored to heart’s fibrous skeleton

thickness of myocardium

varies from one chamber to another

• r/t amount of resistance muscle must overcome to pump blood from different chambers

endocardium

internal lining composed of connective tissue and squamous cells

• continuous w/ endothelium that lines arteries

• creates a continuous closed circuit

atria

• smaller w/ thinner walls

  • R = 2mm, L = 3-5mm

• serve as storage units and conduits for blood

• offers little resistance of flow of blood into ventricles

ventricles

• thicker myocardial layer and make up bulk of heart

• must propel blood through pulmonic and circulatory systems

15 mmHg

mean pulmonary pressure

92 mmHg

mean arterial pressure

left ventricle

• 13-15mm, most muscular

• larger, bullet shaped and pumps blood through large valve opening into the higher-pressure systemic circulation

right ventricle

• 3-5mm

• crescent/triangle shaped and acts like a bellows to propel large volumes of blood through a small valve into the low-pressure circulation

interatrial septum

separates R and L atria

interventricular septum

separates R and L ventricles

• an extension of fibrous skeleton of the heart

atrioventricular valves

• open at the beginning of systole and allow blood to fill ventricles

• close at beginning of ventricular contraction to prevent backflow of blood into atria

semilunar valves

• open at end of ventricular contraction when the pressure in the ventricles exceed the pressure in the pulmonary artery & aorta

• close at the beginning of ventricular relaxation as the pressure in the chambers drops below the pressure in the pulmonary artery & aorta to prevent backflow of blood into the ventricles

chordae tendinae

connect valve leaflets or cusps to papillary muscle

papillary muscle

extensions of myocardium that pulls cusps together and downward at beginning of ventricular contraction

• prevent backward expulsion of AV valves into atria

tricuspid valve

AV valve with 3 cusps (largest diameter)

mitral valve

AV valve with 2 cusps — left heart, resembles a cone shaped funnel

aortic/pulmonic valves

• have 3 cup-shaped cusps

• behave like one-way swinging doors

• pulmonic is thinner than aortic

superior/inferior vena cavae

enter the right atrium

pulmonary artery

carries deoxygenated blood from right ventricle to the lungs

pulmonary vein

carries oxygenated blood from lungs to the left atrium

aorta

delivers blood to systemic vessels which carry it to the rest of the body

diastole

relaxation phase, blood fills ventricles

systole

contraction phase, blood pumped out of the ventricles into the circulation

• ejection on right occurs slightly earlier than left d/t pressure changes

R atrial contraction

blood enters the atria from inferior and superior vena cavae and coronary sinus

L atrial contraction

blood enters through 4 pulmonary veins (2 from each side)

atrial contraction

• atria fill and distend → opens AV valves

• blood passively fills ventricles

• provides “atrial kick” → actively pumps additional blood into ventricle

cardiac cycle phases

phase 1: isovolumetric contraction

phase 2

phase 3: isovolumetric relaxation

phase 4

phase 1

ventricular volume is constant

• increase in ventricular pressure closes AV valves

phase 2

increase in ventricular pressure opens SL valves and blood is ejected to the circulation → intraventricular volume and pressure decrease

phase 3

decrease in ventricular pressure closes SL valves

• ventricles continue to relax

phase 4

decrease in ventricular pressure opens AV valves

• permits ventricular filling from atria

diastole: isovolumetric ventricular relaxation/filling

(0.4 sec)

• as the ventricles relax following systole, the pressure drops below that in the arteries and the semilunar valves close.

• when the pressure in the ventricles drops below that in the atria, the AV valves open and allow for ventricular filling.

• toward the end of diastole, the atria contract and eject 0-30% more blood volume into the ventricles (0.1 sec)

systole: isovolumetric contraction/ejection

(0.3 sec)

• as the pressure in the ventricles becomes greater than the atria, the AV valves shut

• isovolumetric contraction of the ventricles

• as the pressure increases and becomes greater than the arteries, the SL valves open → blood is ejected into the pulmonary and systemic circulation

first heart sound

AV valves shut at beginning of systole due to increasing pressure in the ventricles

• surrounding tissue vibrates and blood flow becomes turbulent = sound

second heart sound

SL valves shut at end of systole due to falling pressure in the ventricles

• physiologic split

physiologic split

aortic valve precedes pulmonic valve closure by 0.02-0.04 sec during expiration and 0.04-0.06 sec during inspiration

valve closure and cardiac cycle

third heart sound

may be heard if ventricular wall compliance is decreased and structures in ventricular wall vibrate

• can occur in congestive heart failure or valvular regurgitation

• may be normal in those younger than 30

fourth heart sounds

may be heard on atrial systole if resistance to ventricular filling is present

• abnormal

causes of S4

cardiac hypertrophy, disease or injury to ventricular wall

blood flow

coronary circulation

branch that supplies heart; done by vessels of systemic circulation

• blood within chambers does NOT supply oxygen and nutrients to heart cells

coronary arteries

receive blood through aortic openings (coronary ostia)

• traverse epicardium and branch several times

R coronary artery

supplies blood to

• posterior septum

• posterior heart

• SA, AV node

cardiac veins

empty into the right atrium through another ostium called the coronary sinus

conus

(R coronary artery) supplies blood to upper right ventricle

marginal branch

(R coronary artery) traverses right ventricle to apex

posterior descending

(R coronary artery) supplies smaller branches to both ventricles

left anterior descending artery

(L coronary artery) blood to portions of R and L ventricles and much of the interventricular septum

• anterior septum, anterior L ventricle

circumflex artery

(L coronary artery) supplies blood to left atrium and lateral wall of left ventricle

collateral arteries

connections or anastomoses between 2 branches of same coronary artery OR connections of branches between R and L coronary arteries

• circulation protects the heart

collateral artery locations

• interventricular/interatrial septa

• apex of heart

• anterior surface of R ventricle

• around sinus node

• more in epicardium than endocardium

gradual coronary occlusion

results in growth of coronary collaterals under effects of nitric oxide and endothelial growth

coronary capillaries

(3000 per mm², or 1 capillary per muscle cell) where exchange of oxygen and nutrients takes place

ventricular hypertrophy (coronary)

capillary network does not expand with muscle fiber size → same # of capillaries must perfuse larger area → decreased exchange of oxygen and nutrients

coronary veins

• most venous drainage occurs through veins in visceral pericardium

• smaller veins feed into great cardiac vein → empties into R atrium through coronary sinus

coronary lymphatic vessels

• drain fluid to lymph nodes in the anterior mediastinum that eventually empty into superior vena cava with cardiac contraction

• impt for protecting myocardium

conduction system

specialized cells that enable heart to generate its own action potentials w/o stimulation from nervous system

• muscle fibers uniquely joined so that action potentials pass very quickly

cardiac action potentials

transmission of electrical impulses, affects cardiac cycle

• electrical impulse → fibers shorten → muscular contraction → systole

• after action potential → fibers relax → return to resting length → diastole

nodes

concentrations of specialized cells in the heart

factors that affect conduction system

• ANS provides regulation that affect HR and diameter of coronary vessels

• nutrition/oxygen needed for survival and normal function

• hormones/biochemicals affect strength and duration of myocardial contraction/relaxation

pacemakers

• sinus (SA) node → 70-75 bpm

• AV node → 50 bpm (atrial contraction)

• bundle of his

• bundle branches → R and L

• purkinje fibers → 15-30 bpm (ventricular contraction)

depolarization

(activation) inside of cell becomes less negatively charged

repolarization

deactivation of action potential, becomes more negative again

membrane potential

electrical (voltage) difference across the cell membrane

• r/t changes in permeability of cell membranes (Na+ and K+)

threshold

point at which the cell membrane’s selectively permeability to Na and K is temporarily disrupted → depolarization

• determined by Ca2+

hyperpolarization

resting membrane potential becomes more negative aka hypokalemia

pacemaker cells

more permeable to Na and start off more positively charged → reach threshold and fire sooner

depolarization (cardiac AP)

• voltage-sensitive Na channels open & allow rapid influx of Na then rapidly close

• K channels close then reopen slowly

• voltage-sensitive Ca channels have delayed & slowed opening relative to Na

• Ca responsible for contraction of cardiac muscle

• normal circumstances: < max amt of Ca released which permits modulation of contractile strength

repolarization (cardiac AP)

• return to resting membrane potential is delayed

• makes it impossible to fire a second action potential before the first is complete

• prevents summation and tetany

60-100 bpm

normal heart rate

> 100 bpm

sinus tachycardia

< 60 bpm

sinus bradycardia

increased heart rate

= less time for the heart to fill and cardiac output decreases aka increased oxygen consumption

sympathetic stimulation

releases norepinephrine →

• increased HR

• increased conduction speed through AV node

• increased atrial & ventricular contractility, & peripheral vasoconstriction

stimulation occurs when a decrease in pressure is detected