A&p Ii Chapter 20 Heart

Three layers:

** Epicardium (Outer layer): contains Visceral Pericardium, Fibroelastic and Adipose CT

** Myocardium (Middle layer): contain Cardiac muscle

** Endocardium (Inner layer): Contains Endothelium; simple squamous epithelium overlying CT

** Auricle: Increases capacity of Atrium

** Sulci: Contain coronary blood vessels and adipose CT

** Receives blood from Right Atrium

** It pumps blood through Pulmonary Semilunar Valve into Pulmonary Trunk

Pulmonary Trunk- divides into right and left Pulmonary Arteries to the Lungs

** Thickest chamber**

** Pumps blood through Aortic Semilunar Valve into Ascending Aorta; blood flows to Coronary Arteries, Arch of Aorta, Descending Aorta

** Valves open and close in response to pressure change as Heart contracts and relaxes

** One way flow of Blood

** Atrioventricular: Right side of heart has Tricuspid valve; Left side of heart has Bicuspid valve aka Mitral valve

** Semilunar: Right side: Pulmonary valve Left side: Aortic valve

** When AV is open, rounded ends of cusps project into Ventricles

** Ventricles are Relaxed > Papillary Muscles are Relaxed > Chordae Tendineae are Loose > Blood moves from higher pressure in Atria to Lower pressure in Ventricles

** Once Ventricles contract > Pressure of blood pushes cusps upward > Cusps close

** Papillary Muscles contract > Chordae Tendineae are tight this prevents opening of Cusps into Atria

**When Ventricles contract > free borders of cusps project into Arteries Cusps open > Blood is pumped into Arteries

** When Ventricles relax > Back flowing blood fills Valve cusps then Valves close

** Blood flow of deoxygenated: start at the Right Atrium from Superior Vena Cava, Inferior Vena Cava, and Coronary Sinus

** From right atrium to Tricuspid valve to Right Ventricle

** From right ventricle to Pulmonary Valve to Pulmonary Trunk

** From Pulmonary trunk to Pulmonary Arteries to Lungs

** Blood from Left Atrium flow from Pulmonary veins from Lungs

** From Left Atrium to Bicuspid valve to Left Ventricle

** From Left Ventricle to Aortic Valve to Aorta to Arteries through entire Body

** Branch from Ascending Aorta to supply the heart with Oxygenated blood

Two main coronary arteries: Right and Left Coronary Artery

** Anterior interventricular: Supplies both ventricles; aka LAD: Left Anterior descending artery

** Circumflex: Supplies left atrium and ventricle

** Presence of gap junctions allow impulses to spread rapidly from cell to cell so the Myocardium contracts as a single unit

** Electrical events: Generation and transmission of electrical impulses through Myocardium

** Mechanical events: Pressure changes, Volume changes, and Valve changes during Cardiac Cycle

** Sinoatrial Node (SA) depolarizes, the wave of depolarization spreads through Atria

** Atrioventricular Node (AV) depolarizes, AV bundle transmits wave of depolarization to Bundle branches

** The bundle branches transmit depolarizing wave to Apex of Ventricles

** Purkinje Fibers transmit depolarizing wave to Ventricular Muscle cells

** Systole: Muscular contraction and pumping of blood out of a chamber

** Diastole: Muscular relaxation and filling of blood into a chamber

*** Note Atrial diastole occurs at same time as Ventricular Systole

** Atrial Systole: contraction of the atrial walls and ejection of blood into ventricles

- Right or Left Atrium to Right or Left Ventricle

** Atrial Diastole: Relaxation of atrial walls and filling of atrial chambers

- SVC, IVC, and Coronary sinus to Right Atrium

- 4 Pulmonary veins to Left Atrium

** Ventricular Systole: contraction of Ventricular walls and ejection of blood into the outflow tracts

- Right ventricle to Pulmonary Trunk

- Left ventricle to Aorta

** Ventricular Diastole: relaxation of ventricular walls and filling of ventricular chambers

- Right atrium to right ventricle

- Left atrium to left ventricle

** When Atrial are contracting, ventricles are relaxed

** During Atrial systole, pressure increases in Atria

** At beginning of Atrial diastolic period, 130mL of blood in each ventricle (End-diastolic volume)

** When Ventricles contract, Atria are relaxed

** During Ventricular systole, pressure increases in ventricles

** When left ventricular pressure rises more than 80mmHg, the Semilunar valve opens and ejection of blood begins; More contraction pressure rises to 120mmHg

** Left ventricle ejects 70mL of blood in Aorta; 60mL remain (End Systolic Volume)

** When right ventricle pressure rises more than 20mmHg the Semilunar valve open and ejection of blood begins; More contraction pressure rises to 25-30 mmHg

** Right ventricle ejects 70mL of blood into Pulmonary trunk; 60mL remain (End Systolic volume)

** Two distinct sounds are heard

** S1 or Lubb: First heart sound heard when Atrioventricular valves close (Tricuspid and Bicuspid); it's the beginning of Ventricular Systole

** S2 or Dupp: Second heart sound heard when Semilunar valves close (Pulmonary and Aortic); it's the beginning of Ventricular Diastole

** Pressures increase during Systolic phase of a chamber

** Pressure decreases during diastolic phase of a chamber

Pressure is measured in mmHg

** Measurement of pumping effectiveness

** The volume of blood pumped by a ventricle per minute

** Measured in milliliters per minute

** Calculated: CO= SV x HR

Cardiac output= Stroke volume x Heart rate

** To increase cardiac output: increase stroke volume or heart rate; or increase both

** Volume of blood pumped during each ventricular contraction; Measured as milliliters per beat

** Calculated: SV= EDV-ESV; 130-60= 70 mL

EDV: volume in ventricle at end of relaxation, After ventricle filling

ESV: volume in ventricle at end of contraction, after ejection of blood

** Number of ventricular contractions per minute; measured as beats per minutes

** At rest, 75 beats per minute

** Stroke volume= 70mL per beat

** Heart rate= 75 beats per min

** CO= SV times HR

Once you do the math divide by 1000

** Cardiac output depends on Stroke volume and heart rate; and the factors that affect stroke volume or heart rate will affect cardiac output

1) Preload

2) Contractility

3) Afterload

** Amount of stretch on Ventricular wall

** Greater of Preload, the more forceful muscle contraction then more blood is pumped out of ventricle

** Adding more blood to ventricular chamber, increases stretch in its wall, then more forceful contraction increases stroke volume then increase cardiac output

** Greater end-diastolic volume has increase preload then increase stroke volume then increase cardiac output

** Longer duration of ventricular diastole and more venous return increases EDV

** Forcefulness of ventricular contraction

** Increase in contraction increase in stroke volume

** Decrease in contraction decrease in stroke volume

** Pressure that should be overcome before a semilunar valve can open

** To open semilunar valves, pressure in ventricles should exceed pressure in aorta 80mmHg and Pulmonary trunk 20mmHg

** Higher afterload means lower stroke volume and more blood stays inside ventricles

1) Autonomic nervous system (ANS)

2) Hormones

3) Level of physical fitness

4) Age and Several other factors

** Cardiovascular center: collection of neurons in Medulla Oblongata; that receive input from various areas

** Output is via Sympathetic (Cardiac accelerator) and Parasympathetic (Vagus) nerves

** Higher brain centers: Cerebral cortex, Limbic system, Hypothalamus; Thoughts and feelings affect activity of Heart

** Baroreceptors: Located in walls of Aorta and internal carotid arteries; Detect pressure changes

** Chemoreceptors: Located in wall of Aorta and common carotid arteries; Detect chemical changes

** Proprioceptors: Located in joints; Detect joint movement

** Increases activity of SA and AV nodes that increases heart rate

** Increases strength of muscle contraction that increase pumping effectiveness

** Norepinephrine is neurotransmitter which binds to Beta 1 adrenergic receptor

** Decreases activity of SA and AV nodes that decreases heart rate

** Has little effect on muscular contraction

** Acetylcholine is neurotransmitter which binds to Muscarinic receptors

** Epinephrine and Norepinephrine released from Adrenal glands mimic the effects of Sympathetic stimulation

** Hormones increase SA and AV nodes activity that increase heart rate and contractility

** Athletes develop physiological Cardiomegaly

Increase contractility increase stroke volume

** Heart is lower and resting cardiac output is normal

** Muscle contractions activates proprioceptors in joints

** Then cardiovascular center is stimulated then activates sympathetic nerves

** Sympathetic stimulation increase contractility then increase stroke volume

Increased heart rate and stroke volume increases cardiac output