Advanced A&P - Unit 5 Study Guide: Cardiovascular Physiology

aorta

the coronary arteries emerge from the _____

marginal branch

• from right coronary artery

• supplies blood to walls of R atria & R ventricle

posterior interventricular artery

• from right coronary artery

• supplies to posterior walls of both ventricles

circumflex branch

• from left coronary artery

• supplies blood to walls of L atria & L ventricle

anterior interventricular artery

• from left coronary artery

• supplies to walls of both ventricles

• also referred to as the “widow maker” (blockages are often sudden and fatal)

pathway of blood through coronary circulation

aorta → R & L coronary arteries → branches → capillaries → veins → coronary sinus → R atrium

systole

contraction of heart chambers

diastole

relaxation of heart chambers

cardiac cycle

events that happen with each heartbeat

atrial systole

the ventricles are in diastole & blood is moving from atria into ventricles; the AV valves are open to allow this blood movement and the SL valves are closed

ventricular systole

the ventricles are contracting & blood is moving out the pulmonary trunk and aorta; the SL valves are open to allow this blood flow movement and the AV valves are closed to prevent backflow into the atria

relaxation & filing

atria & ventricles are in diastole; the AV valves are open so blood can flow from the atria into the ventricles; SL valves are closed to prevent backflow

S1 (lubb)

when AV valves close

S2 ( dupp)

when SL valves close

murmur

caused by turbulent blood flow; sounds like a “whooshing”

cardiac conduction system

system of specialized cardiac muscle fibers that conduct cardiac impulses from SA node throughout myocardium; coordinates the events of the cardiac cycle

SA node

the pacemaker; initiates the hearts rhythmic contractions; generates impulses at about 100 bmp but parasympathetic system usually decreases firing rate to 70 bmp

atrial syncytium

stimulates atria to contract

AV node

provides the only normal conductivity pathway between atrial and ventricular syncytia

AV bundle

group of specialized muscle fibers that conducts impulses from AV node to purkinje fibers in the ventricular muscle of the heart; right and left branches

purkinje fibers

conduct the impulse to distant regions of ventricular myocardium rapidly; impulse turns upward

ventricular syncytium

impulse travels through walls of ventricles, stimulating walls to contract

path a cardiac impulse

SA node → atrial syncytium → junctional fibers → AV node → AV bundle → bundle branches → purkinje fibers → ventricular syncytium

ECG

recording of the electrical changes in the myocardium

P wave

first upward reflection of on ECG: shows atrial depolarization (firing of SA node and impulse spreading through the atrial syncytium, which results in atrial contraction)

QRS complex

small downward deflection (Q) followed by sharp upward spike (R) and then another downward deflection (S); shows ventricular depolarization (firing of AV node and impulse traveling through rest of conduction system in ventricles, which results in ventricular contraction)

T wave

last upward deflection that shows ventricular repolarization; electrical “reset”

atrial repolarization

occurs during QRS complex but is hidden by the ventricle contraction

atrial fibrillation

not life threatening, blood is still pumping

ventricular fibrillation

often deadly; can be caused by an obstructed coronary artery, toxic drug exposure, electric shock, or traumatic injury to chest wall/heart

tachycardia

fast heartbeat, usually more than 100 bmp at rest

bradycardia

slow heart rate, usually fewer than 60 bmp

cardioaccelerator

will cause an increase in heart rate due to an increase in sympathetic impulses to heart

cardioinhibitor

will cause a decrease in heart rate due to an increase in parasympathetic impulse to heart

aortic arch & carotid sinus

baroreceptors here detect pressure leaving heart

superior & inferior vena cava

baroreceptors detecting pressure returning to heart

vagus nerve

parasympathetic impulses sent out along _____ _____ to decrease heart rate

accelerator nerves

sympathetic impulses sent out along _____ _____ to increase heart rate

hypercalcemia

causes an increase in heart action

hypocalcemia

causes a decrease in heart action

hyperkalemia

causes heart rate to decrease

capillaries

extensions of the inner linings of arterioles in that their walls are endothelium; exchanges of gas, nutrients, waste, and fluid between blood and tissue cells

hydrostatic pressure

• pressure of blood pushes water, ions and other substances through capillary

• increased at arteriolar end, decreased at venular end

• always higher to lower

osmotic pressure

• force exerted by solutes that cannot move across membrane

• plasma proteins draw water into capillary

• remains constant at arteriolar end to venular end

• always low to high

• if more fluid accumulates than can be drained away, results in edema

blood pressure (BP)

• the force blood exerts against the inner walls of the blood vessels

• normal is 120/80

• brachial artery is preferred use to measure

• BP = CO x PR

systolic pressure (SP)

reflects the highest pressure during ventricular contraction and resistance in the vessel

diastolic pressure (DP)

reflects the lowest pressure during ventricular relaxation

cardiac output (CO)

• the amount of blood pumped from a ventricle each minute (measured in milliliters/min)

• CO = HR (heart rate) x SV

stroke volume (SV)

• volume of blood that enters arteries with each ventricular contraction (milliliters / beat)

• SV = EDV (end diastolic pressure) - ESV (end systolic pressure)

Relationship between blood volume (BV) and blood pressure (BP)

if BV increases, SV increases → if SV increases, CO increases = BP increases

peripheral resistance

• the resistance to blood flow through. vessels to friction; higher the PR = higher BP!

• influenced by blood vessel diameter (increase sympathetic impulse - constriction - increased PR or decreased sympathetic impulse - dilation - decreased PR)

• influenced by viscosity of blood (thinner- less resistance, thicker - more resistance)

  • changing levels of RBCs and plasma proteins can affect viscosity

factors that can increase BP

increased BV, HR, SV, viscosity, resistance

Sterling’s Law

the force of the heart’s contraction is directly proportional tot he initial length (stretch) of its muscle fibers. this means: as the volume of blood enter the heart increases, the walls of the heart stretch. this optimal stretch enhances the heart’s ability to contract and eject a larger volume of blood (SV) during the heart beat, automatically matching output to input

mechanisms for lowering BP

• ventricles beat less forcefully

• HR decreases

• decreasing PR can decrease BP

pulse

• surge of BP felt through walls of arteries due to contraction of heart ventricles

• can be felt @ temporal, facial, carotid, brachial, radial, femoral, popliteal, dorsal pedis, and posterior tibial arteries

pulse pressure (PP)

PP = SP - DP; normally about 40 mm Hg

median arterial pressure (MAP)

MAP = DP + 1/3PP; minimum must be 60 mm Hg

central venous pressure (CVP)

• pressure in R atria

  • normal value = 0 mm Hg

why Av valve close

contraction of the ventricles forces blood against the valves pushing them closed

occurs during ventricular diastole

• ventricles are filling

• AV valves open

• ventricular pressure decreases

occurs when ventricles relax

• pressure decreases

• AV valves open

• SL valves close

arterioles

exerts the greatest control over peripheral resistance and blood flow

lymphatic capillaries

return excess tissue fluid out of the capillary networks back into venous system