A&P 2 Exam 2 (ch. 18-20)

autorhythmic fibers

Specialized cardiac muscle fibers
Self-excitable
Repeatedly generate action potentials that trigger heart contractions
2 functions
-Act as pacemaker
-Form conduction system

metabolism of cardiac muscle

-Aerobic cellular respiration
-Many mitochondria (Lots of mitochondria help process of ATP production (fuel for heart to beat)
-Can use many different fuels (carbs, fatty acids, lactic acid, AAs, ketone bodies)
-Susceptible to failure in ischemic conditions

intercalated disks

link cardiac muscle cells together

desmosomes

mechanical junctions that prevent cells from pulling apart

gap junctions

tunnels between cells for very fast action potential transmission

describe the heart's pacemaker and internal electrical conduction system

-Your sinoatrial (SA) node is sometimes called your heart's natural pacemaker. It sends the electrical impulses that start the heartbeat
-The SA node depolarizes and is in charge of establishing heart rate
\***if the SA node is damaged, the AV node can take over but it depolarizes much slower**

conduction system of the heart

SA node --\> AV node --\> AV bundle --\> right and left AV bundle branches --\> Purkinje fibers (subendocardial conducting network)

what parts of conduction system are responsible for contraction

-signal sent from SA node: contraction of right and left atria
-signal in purkinje fibers (subendocardial conducting network): contraction of right and left ventricles

nerve supply to the heart

Receives both sympathetic and parasympathetic nerves; Modify heart rate and contraction strength

what establishes fundamental rhythm of the heartbeat

The SA node (APs start here and spread through rest of heart)
normal heartbeat: sinus rhythm

which nerves increase heart rate

sympathetic

which nerves decrease heart rate

parasympathetic

systole

Contraction of the heart
(occurs immediately following depolarization)

diastole

Relaxation of the heart
(occurs immediately following repolarization)

sinus rhythm

normal heart beat

Explain why the SA node fires spontaneously and rhythmically

-The cells of the SA node do not have a stable resting membrane potential
-Their membrane potential starts at about -60mV and drifts upward, showing gradual depolarization called the pacemaker potential (prepotential)
-Results from slow inflow of Na+ without compensating outflow of K+

Nodal APs

Pacemaker potential: due to Na+ channels opening and K+ channels closing
Depolarization: due to Ca2+ influx
Repolarization: Ca2+ channels inactivate, K+ channels open, K+ rushes out

cardiocyte action potential

voltage gated Na+ channels open (depolarization)
Ca2+ channels prolong depolarization of membrane (plateau)
Ca2+ channels close and K+ channels open, rapid K+ outflow (repolarization)

significance of plateau phase

-allows for longer muscle contraction (allows heart to contract in a steady, uniform, and forceful manner)
-very long refractory period: prevents tetanus in the heart

electrocardiogram (ECG)

recording of the electrical changes that occur in the myocardium during a cardiac cycle

p wave

atrial depolarization

QRS interval

atrial repolarization

QRS complex

ventricular depolarization

T wave

ventricular repolarization

The activity of the conduction system

-Your heart (cardiac) conduction system sends the signal to start a heartbeat.
-It also sends signals that tell different parts of your heart to relax and contract (squeeze). -This process of contracting and relaxing

R-R on ECG

one full cardiac cycle

Arythmias

irregular heart rhythms
(due to defects in the conduction system)

fibrillation

-'quivering' of the heart due to irregular contracts
-Heart loses effective pump
-Defibrillation by electrically shocking the heart to 'wipe the slate clean'

How is blood pressure expressed?

millimeters of mercury (mmHg)

Describe how changes in blood pressure operate the heart valves

-Blood flow through the heart is controlled entirely by pressure changes
(High pressure to low pressure)
-Blood flows down a pressure gradient through any available opening
(The reason why valves are so important)

heart sounds

S1 and S2 'lupp-dupp'
Third heart sound (S3): heard in children and adolescents
(If heard in people over 30, may indicate an enlarged and failing heart)

S1

louder and longer

S2

softer and sharper

cardiac cycle

a series of pressure changes that occur in the heart

stroke volume (SV)

amount of blood expelled by ventricles (mL)

End Diastolic Volume (EDV)

the amount of blood that is in the ventricles before the heart contracts
2 factors determine EDV:
-Duration of ventricular diastole
-Venous return

End Systolic Volume (ESV)

volume remaining in ventricle at end of systole

stroke volume calculation

EDV-ESV

ventricular filling

-Atria relaxed, blood passively flows into the ventricle
-Depolarization of SA node
-Atria contract, ventricles are relaxed
-More blood fills the ventricles- end-diastolic volume
-Ventricles depolarize
-Atrial diastole

isovolumetric contraction

-Ventricular depolarization causes systole
-Ventricular pressure rises, forces AV valves to shut (now all 4 valves are closed)\-- isovolumetric contraction
-Heart sound S1

ventricular ejection

-Pressure eventually great enough to force open semilunar valves, blood rushes into aorta and pulmonary trunk
(Stroke volume: volume ejected per beat from each ventricle
Ventricles will not expel all of their blood)

isovolumetic relaxation

-Phase following the T wave
-Ventricles relax, small amount of blood remains
-Ventricular pressure drops, semilunar valves close
--Dicrotic notch: backflow of blood rebounding off aortic SL valve
-During ventricular systole and diastole, atria have been in diastole and filling with blood
--When blood pressure rises high enough, AV valves forced open, ventricular filling begins again

Wiggers Diagram

how is atrial systole related to ventricular filling

Atrial contraction (atrial systole) ejects blood from the atrium and into the ventricle, which is still in diastole, and this completes ventricular filling

AV valves open

atrial pressure greater than ventricular pressure

AV valves close

atrial pressure less than ventricular pressure

SL valves open

pulmonary valve pressure is greater than the aorta and pulmonary trunk

SL valves close

Pulmonary valve pressure is less than aorta and Pulmonary trunk.

Relate the heart sounds to the events of the cardiac cycle

S1- AV valves closing

S2- closing of SL valves

Relate the events of the cardiac cycle to the volume of blood entering and leaving the heart.

Ventricular filling: increase of blood in heart
Isovolumetric contraction: decrease of blood in heart
Ventricular ejection: decrease of blood in heart
Isovolumetric relaxation: increase of blood in heart

Why is it important that the right and left ventricles have the same stroke volume?

Stroke volumes must be equal
-Fluid accumulation in either circuit due to insufficiency of ventricular pumping leads to congestive heart failure
-Causes: congenital defects in cardiac anatomy, chronic hypertension, myocardial infarction, valvular defects

mitral valve prolapse (MVP)

improper closure of the mitral valve
(an insufficiency in which one or both mitral valve cusps bulge into the atrium during ventricular contraction)
-Often hereditary
-Affects about 1 in 40 people (especially women)
-Mainly causes no serious dysfunction but can cause chest pain, fatigue, shortness of breath

congestive heart failure (CHF)

-fluid accumulation in either circuit due to insufficiency of ventricular pumping
-Common causes: myocardial infarction (MI), chronic hypertension, valvular defects, and congenital birth defects in cardiac anatomy

left side CHF

(pulmonary edema)
Left ventricle fails to pump effectively, thus backup into the lungs

right side CHF

systemic edema
Right ventricle fails to pump effectively, thus backup into RA and then into the periphery

Cardiac Output (CO)

:volume of blood ejected from a single ventricle each minute
-Helps keep blood pressure at needed levels and supply brain and vital organs with oxygen-rich blood
-Entire blood volume flows through pulmonary and systemic circuits each minute

cardiac reserve

difference between maximum cardiac output (CO) and CO at rest
-Average cardiac reserve 4-5 times resting value
-Train athletes can generate 7x resting value

Calculate cardiac output given stroke volume and heart rate.

Cardiac output \= stroke volume (SV) x heart rate (HR)

how changes in HR and SV affect CO

Increased heart rate or stroke volume or both will increase cardiac output
Decreased heart rate or stroke volume or both will decrease cardiac output

regulation of stroke volume

Preload
Contractility (inotropic agents)
Afterload

Tachycardia

persistent, resting adult heart rate above 100 bpm
(fast heart rate)

bradycardia

persistent, resting adult heart rate below 60 bpm
(slow heart rate)

vagal tone

steady background firing rate of vagus nerves that holds the heart rate down to its usual 70 to 80 bpm at rest (heart naturally beats around 100 bpm)

Procioceptors

in the muscle and joints provide information on changes in physical activity

Baroreceptors

pressure sensors in the aorta and internal carotid arteries
(detect changes in blood pressure)

chemoreceptors

occur in the aortic arch, carotid arteries, and medulla oblongata
Sensitive to blood pH, CO2 and O2 levels
(More important in respiratory control, but they do influence heart rate)

positive chronotropic agents

increase heart rate
-Sympathetic nervous system
-Epinephrine, norepinephrine
-Thyroid hormone
-Glucagon
-Nicotine, caffeine
-Hypocalcemia

negative chronotropic agents

-decrease heart rate
-Parasympathetic nervous system
-Acetylcholine
-Hypercalcemia
-Hypokalemia
-Beta blockers

How would potassium or calcium excess or deficiency affect heart rate?

Excess of deficiency of calcium or potassium would lead to irregular heart beats

preload

degree of stretch on the heart before it contracts

Frank-Starling Law of the Heart

the more the heart fills with blood during diastole, the greater the force of contraction during systole
Preload is proportional to end-diastolic volume (EDV)

venous return

the volume of blood that returns from the veins to the atria each minute

how does venous return effect preload

Increase in venous return → increase in preload (increase in preload will increase the force at which the heart contracts)

Contractility

strength of contraction at any given preload/muscle length
(Positive inotropic agents: increases contractility
Negative inotropic agents: decreases contractility)

positive iontropic agents

increases stroke volume
-Increased preload (myocardial stretch)
-Increased contractility
-Sympathetic nervous system
-Epinephrine, norepinephrine
-Glucagon
-Digitalis
-Nicotine, caffeine
-Hypercalcemia
--Often promote Ca2+ inflow during cardiac AP

negative iontropic agents

decreases stroke volume
-Reduced preload
-Reduced contractility
-Increased afterload
-Hypocalcemia
--Often decrease available Ca2+
--Calcium channel blockers
-Hyperkalemia
--Increased K+ in interstitial fluid

calcium effect on stroke volume

excess calcium (hypercalcemia) causes a slow heartbeat, increasing stroke volume. Calcium deficiency (hypocalcemia) causes an increased heart rate, decreasing the stroke volume

potassium effect on stroke volume

excess potassium (hyperkalemia) causes the heart rate to become slow and irregular, increasing the stroke volume

afterload

pressure (resistance in arteries) that must be overcome before semilunar valves can open
(Increase in afterload causes stroke volume to decrease)
(Hypertension and atherosclerosis increase afterload)

Identify the factors that govern cardiac output.

Heart rate, contractility, preload, afterload

cardiovascular center

area of the medulla at which stimulation will activate the sympathetic nervous system to increase blood pressure, heart rate, and the parasympathetic to decrease heart rate

Atrial (Bainbridge) reflex

Due to respiration (deep breathing) increases thoracic pressure which Increases venous return, atria stretch to accommodate blood, this causes increases in heart rate
(An increase in heart rate due to an increase in central venous pressure)

Describe some effects of exercise on cardiac output.

-Increases cardiac output
-Muscular activity increases venous return (increasing the preload on the right ventricle and left ventricle)
-Increases heart rate and stroke volume

factors affecting cardiac output

blood pressure (BP)

the force exerted by blood on a vessel wall
-Measured with a sphygmomanometer
-Depends on: cardiac output, resistance, blood volume

resistance

-Due to viscosity, length, and diameter
-Most important variable as it can change easily due to changes in vessel diameter

vascular resistance

-Opposition to blood flow due to friction between blood and walls of blood vessels
-Vessel diameter
-Blood viscosity
--Ratio of RBCs to plasma and protein concentration
-Total blood vessel length
--400 miles of additional blood vessels for each 2.2lb of fat

flow

amount of blood flowing through an organ, tissue or blood vessel in a give time
-Volume of blood \= cardiac output
-CO \= HR x SV

flow equation

Flow \= change in pressure/resistance

relationship between flow, change in pressure, and resistance

-Flow is directly proportional to change in pressure (increase in ΔP increases flow)
-Flow is disproportional to resistance (increase in resistance decreases flow)

mean arterial pressure (MAP)

-Mean arterial pressure (MAP)
--Not equal to the mean of systolic and diastolic pressure because diastole lasts longer than systole
-Pulse pressure \= systolic - diastolic pressure
-MAP \= diastolic pressure + ⅓ pulse pressure

systolic pressure

generated by contraction (systole) of the left ventricle

diastolic pressure

the minimum to which the BP falls when the ventricle in diastole

pulse pressure

difference between systolic and diastolic pressure

blood viscosity (factor that affects resistance)

-Stems mainly from its plasma proteins (albumin) and erythrocytes
-A deficiency of erythrocytes (anemia) or albumin (hypoproteinemia) reduces viscosity and speeds up blood flow

vessel length (factor that affects resistance)

the greater the vessel length, the less pressure and flow

vessel radius (factor that affects resistance)

-Effects of radius on blood flow stems from the friction of the moving blood against the vessels walls
-Blood usually exhibits smooth, silent laminar flow
-Large vessel radius \= average velocity of flow is high
-Small vessel radius \= lower average velocity

angiogenesis

Angio \= blood vessel; genesis \= creation
(Important process in embryonic development as well as postnatal wound healing, etc.)

changes in blood pressure relative to distance from heart

Systolic and diastolic pressures are lower and there is less difference between them when they are farther away from the heart
(There is no pulse pressure beyond the arterioles)

importance of blood pressure homeostasis

too low: inadequate perfusion of body tissues (ischemia, necrosis)
too high: blood vessel damage (increased risk of aneurysms