BLG 111 full midterm 1

cardiovascular system

consists of the heart, blood vessels, and blood

right side of heart

pumps deoxygenated blood to lungs

left side of heart

pumps oxygenated blood to body

pulmonary circuit

carries blood to lungs for gas exchange and returns it to heart

short, low-pressure circulation

systemic circuit

carries blood between heart and body tissues

fast, high-pressure circulation

right atrium

Receives deoxygenated blood from body

left atrium

Receives oxygenated blood from lungs

right ventricle

pumps deoxygenated blood to lungs

left ventricle

pumps oxygenated blood to body

Where is the heart located?

mediastinum, between lungs

Pericardium

Double-walled membrane surrounding heart

fibrous pericardium

fibrous CT

protects heart, anchors heart to surroundings, and prevents overfilling

parietal layer of serous pericardium

lines internal surface of fibrous pericardium

pericardial cavity

fluid-filled cavity that decreases friction between pericardial layers

percarditis

inflammation of pericardium causing pericardial friction rub

Cardiac tamponade

Excess fluid that leaks into pericardial space

can compress heart's pumping abilty

epicardium

visceral layer of serous pericardium

Myocardium

heart muscle

endocardium

Inner layer of heart

What separates the atria?

interatrial septum

What separates the ventricles?

interventricular septum

Fossa ovalis

remnant of foramen ovale of fetal heart

Atria

upper / receiving chambers

superior vena cava

returns blood from body regions above diaphragm

inferior vena cava

returns blood from body regions below diaphragm

coronary arteries

two arteries that supply blood to heart muscle

coronary sinus

returns blood from coronary veins

Ventricles

lower / discharging chambers

trabeculae carneae

muscular ridges on ventricular walls

papillary muscles

anchor chordae tendineae

chordae tendineae

heart strings

prevent cusps everting back into atria

heart valves

ensure unidirectional blood flow

dependent on pressure changes

atrioventricular valves (AV)

prevent back flow into atria when ventricles contract

What is the valve with 3 cusps between the right atria and ventricle?

Tricupsid Valve

What is the valve with 2 cusps between left atria and ventricle?

Mitral valve

What happens when atrial pressure is greater than ventricular pressure?

1. increased pressure opens AV valves

2. ventricles fill

3. atria contracts, forcing more blood into ventricles

What happens when atrial pressure is less than ventricular pressure?

1. ventricles contract, forcing blood against cusps

2. AV valves close

3. papillary muscles and chordae tendineae tighten

semilunar valves (SL)

prevent back flow into ventricles when ventricles relax

What is the SL valve on the right side of the heart?

pulmonary SL valve

What is the SL valve on the left side of the heart?

aortic SL valve

What happens when SL valves open?

1. ventricles contract, increasing pressure

2. pressure forces blood against SL valves, opening them

What happens when SL valves close?

1. ventricles relax, decreasing pressure

2. blood flows back, filling and closing cusps

incompetent valve

Blood backflows so heart repumps same blood over and over

- cause swishing sounds

Valvular stenosis (narrowing)

stiff flaps constrict opening

heart exerts more force to pump blood

What is the shortest circulation in the body?

coronary circulation

angina pectoris

chest pain that results when the heart does not get enough oxygen

myocardial infarction (MI)

heart attack caused by coronary blockage

intercalated discs of cardiac cells

connecting junctions consisting of desmosomes and gap junctions

allows heart to be functional syncytium

differences between cardiac and skeletal muscle

Some cardiac muscle cells are self-excitable

Heart contracts as a unit

Influx of Ca2+ from ECF triggers Ca2+ release from SR

Tetanic contractions cannot occur in cardiac muscles due to longer refractory period

pacemaker cells

heart cells that spontaneously depolarize

intrinsic cardiac conduction system

network of noncontractile cells that initiate and distribute impulses to coordinate depolarization and contraction of heart

what is the sequence of excitation of the heart?

1. SA node

2. AV node

3. AV bundle

4. R and L bundles

5. subendocardial conducting network

1. Pacemaker Potential

slow depop due to opening of Na channels and closing of K channels (mp is never a flat line)

2. Depolarization

AP begins when pacemaker potential reaches threshold

depop due to ca2+ influx via ca2+ channels

3. Repolarization

Ca2+ channes inactivate, K channels open

ectopic focus

abnormal pacemaker that takes over pacing

Extrasystole (premature contraction)

ectopic focus in small region of heart generates impulse before SA node causing delay in next impulse

- heart has longer time to fill, thus next contraction is felt as a thud due to larger volume of blood being pumped out

- due to excessive caffeine or nicotine use

heart block

few or no impulses reach ventricles causing them to beat at their own rate

cardioacceleratory center

sends sympathetic signals to increase both rate and force

cardioinhibitory center

sends parasympethic signals to decrease rate

Why do cardiac muscle APs have a plateau?

due to Ca2+ influx through slow Ca2+ channels, keeping cell depolarized

--> prevents tetanus; gives muscle time to contract and relax

Electrocardiogram (ECG)

graphic recording of electrical activity

P wave

atrial depolarization caused by SA node

QRS complex

ventricular depolarization begins at apex, atrial repolarization occurs

T wave

ventricular repolarization begins at apex

P-R interval

beginning of atrial excitation to beginning of ventricular excitation

S-T segment

entire ventricular myocardium depolarized

Q-T interval

from ventricular depolarization to ventricular repolarization

Ventricular fibrillation (V-fib)

abnormal heart rhythm which results in quivering of ventricles

Systole

Contraction of the heart

diastole

Relaxation of the heart

cardiac cycle

blood flow through heart during one complete heartbeat

Ventricular filling: mid-to-late diastole

- Pressure is low; 80% of blood flows from AV valves into ventricles

- atrial depop triggers atrial systole

- atria contracts, pushing remaining 20% of blood into ventricle

- depop spreads to ventricles (QRS wave)

End Diastolic Volume (EDV)

volume of blood in each ventricle at end of ventricular diastole

isovolumetric contraction

- atria relax; ventricles contract

- high pressure closes AV valves AND opens SL valves

Ventricular ejection

- blood rushes into aorta and pulmonary trunk

- pressure of aorta: 120 mmHg

isovolumetric relaxation: early diastole

- ventricles repop (t wave); ventricles relax

- ventricular pressure decreases causing back flow of blood that closes SL valves

- atria fills; when atrial pressure > ventricular pressure, AV valves open = cycle begins again

end systolic volume (ESV)

volume of blood remaining in each ventricle after systole

What is the first heart sound?

closing of AV valves (lub) @ beginning of ventricular systole

What is the second heart sound?

closing of SL valves (dub) @ beginning of ventricular diastole

heart murmurs

abnormal heart sounds

stenotic valve

fails to open completely, restricting blood flow

- high-pitched sound

Cardiac Output (CO)

Amount of blood pumped in 1 minute (~5 L)

stroke volume

the volume of blood pumped out by a ventricle with each heartbeat

cardiac reserve

difference between resting and maximal CO

Preload

degree of stretch of heart muscle before contraction

(affects EDV = more blood is able to fill in ventricle @ beginning)

Frank-Starling Law of the Heart

greater the stretch, the greater the force of contraction

Venous Return (VR)

amount of blood returning to the heart

the higher the venous return =

higher EDV, SV, CO

Contractility of the heart

contractile strength at muscle length

increase contractility/force = increase amount of blood ejected (decreases ESV)

afterload

pressure ventricles must overcome to eject blood

hypertension

pressure in LV << systemic pressure = valves don't open properly = reduced amt of blood ejected

sympathetic nervous system regulation of heart rate

Ne causes:

- pacemaker to fire faster = increase HR

- increases Ca2+ movement = increase contractility

parasympathetic nervous system regulation of heart rate

Ach hyperpolarizes pacemakers by opening K+ channels = decreases HR

vagal tone

slowing of heart rate

What does epinephrine and thyroxine do to HR?

Epinephrine = increases HR and contractility

Thyroxine = increases HR; enhance Ne and E

What specific ions are needed to maintain normal heart function?

Ca and K

Hypocalcemia

depresses heart

Hypercalcemia

increases HR and contractility (can disrupt HR and cause arrythmias)

Hyperkalemia

alters electrical activity = can lead to heart block and cardiac arrest