Cardiovascular Physiology

systole

heart contraction phase

diastole

heart relaxation phase

contraction

tightening of cardiac muscle that pumps blood

autorhythmic

cells that generate their own electrical signals without nervous input

edema

swelling from fluid buildup in tissues

hypertension

high blood pressure

systemic

pertaining to circulation throughout the body

arteriosclerosis

hardening of arteries due to plaque

endothelium

inner lining of blood vessels

vasodilation

widening of blood vessels

vasoconstriction

narrowing of blood vessels

perfusion

delivery of blood to tissues through capillaries

hemorrhage

excessive bleeding from a ruptured vessel

myocardial infarction

heart attack; caused by blocked coronary artery

depolarization

change in electrical charge inside a cell that triggers contraction

repolarization

return to resting electrical state after depolarization

Heart disease

a general term for conditions affecting the heart

Coronary artery disease

narrowing/blocking of arteries that supply the heart

Heart attack

occurs when blood flow to a part of the heart is blocked

Main Function of the Cardiovascular System

1. transport oxygen

2. carbon dioxide

3. nutrients

4. wastes

5. hormones

6. immune cells

7. electrolytes

Unique Feature of the Cardiovascular System

cardiac muscle cells contract independently of the nervous system due to the pacemaker activity

Heart composed of

- autorhythmic cells

- contractile cells or cardiomyocytes

- connective tissue

autorhythmic cells

generate/conduct impulses

contractile cells (cardiomyocytes)

perform pumping

connective tissue

provides insulation, support, and valve structure

cardiomyocytes

cardiac muscle cells

Cardiac muscle cells

- specialized type of striated muscle cells

- intercalated discs

- myoglobin

- lots of mitochondria

- contract in response to action potentials generated by pacemaker cells

intercalated discs

the joining between two cells

desmosomes

holds cells together

gap junctions

enable electrical communication

myoglobin

binds to oxygen

lots of mitochondria

aerobic respiration

connective tissue

1. provides electrical separation or insulation

2. provides physical support

3. structure and support of valves

sinoatrial (SA) node

pacemaker of the heart, determines heart rate

atrioventricular (AV)) node

conducts the impulse to the bundle branches

internodal pathways

specialized tracks of conducting cells that carry the electrical impulse from the SA node to the AV node through the walls of the atria

AV bundle

the only electrical conenction between the atria and the ventricles

bundle branches

after the impulse passes through the AV bundle, it splits into right and left bundle branches which travel down either side of the interventricular septum

Purkinje fibers

branch from the bundle brances and spread throughout the ventricles, conducting the impulse rapidly so both ventricles contract at the same time from the bottom up — efficiently pumping blood out of the heart

bradycardia

slow heart rate

tachycardia

fast heart rate

Cardiac cycle

one heartbeat (contraction-relaxation)

diastole

relaxation

systole

contraction

In the Cardiac Cycle

- blood flows from high pressure to low pressure

- valves open when the pressure on the contracting side is higher than the pressure on the relaxed side

Atrial and ventricular diastole

both atria and ventricles are relaxed, and blood passively fills the heart chambers

Atrial systole

the atria contract to actively push blood into the ventricles

Atrial distal / Ventricular systole

atria relax while ventricles contract

Isovolumetric contraction

ventricles contract, all valves close

ventricular ejection

blood pushed out

ventricular diastole

ventricles relax

isovolumetric relaxation

ventricles relax, valves closed

heart murmurs

abnormal valve sounds

Cardiac Output (CO)

amount of blood pumped by each ventricle in one minute

CO

Strove Volume (SV) x Heart Rate (HR

- ex. 70 ml/beat x 75 beats/min

Stroke volume (SV)

amount of blood pumped out of a ventricle during a contraction

The importance of equal output by the two ventricles:

Unequal Pumping Causes:

- pulmonary edema (left side fails)

- systemic edema (right side fails)

- hypertension (high blood pressure)

So how do we change cardiac output to meet the oxygen demands of the body?

Change HR and SV

Factors that alter stroke volume

- venous return and filling time

- ventricle contractility

- afterload

venous return and filling time

more blood returning to the heart stretches the ventricles, increasing stroke volume

ventricle contractility

stronger heart contractions pump more blood per beat

afterload

the pressure the heart must overcome to eject blood; higher afterload can reduce stroke volume

Factors that affect heart rate

- autonomic nervous system

- parasympathetic

- sympathetic

- hormones/chemicals

- physical factors

parasympathetic

decreases heart rate

sympathetic

increases heart rate

hormones/chemicals

- calcium and potassium imbalances

- caffeine: stimulates HR

blood vessels

basic comparison of arteries, veins and capillaries

arteries

carry blood away from heart

pulsatile flow

rhythmic, wave-like movement of blood through the arteries that occurs as a result of the heart's regular pumping action

aneurysm

a bulge in a weakened blood vessel wall that can burst and cause bleeding

capillary beds

networks of tiny blood vessels where exchange of gases, nutrients, and wastes occurs between blood and tissues

filtration

movement of fluid and small solutes from blood into tissues

reabsorption

movement of fluid from tissues back into the blood

venous valves

flap-like structures inside veins that prevent blood from flowing backward

varicose veins

swollen, twisted veins caused by weak or damaged venous valves that allow blood to pool

Hydrostatic pressure

the force of blood against the vessel wall is blood pressure

Systolic pressure

during ventricular contraction

Diastolic pressure

during relaxation

EFFECTS OF VARIOUS FACTORS ON BLOOD PRESSURE

Arterial blood pressure is related to the cardiac output and the peripheral resistance

Peripheral Resistance

the amount of friction or resistance to flow the blood encounters as it travels through the blood vessels

Diameter of blood vessel

smaller = more resistance

blood volume

more volume = more pressure

viscosity

thicker blood = more resistance

cardiovascular regulation

Tissue perfusion must be maintained at all times or tissue death results within minutes (at normal body temperature)

How is cardiovascular function altered?

- neural mechanisms

- endocrine mechanisms

- antidiuretic hormone (ADH): increases water retention

- Renin-Angiotensis II - Aldosterone: raises blood pressure

cardiogenic shock

Pump Failure

decreased cardiac output

low venous return shock

low blood volume

vascular shock

widespread vessel dilation