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Universities » University of Alabama - Birmingh.. » BY - Biology » 409 - Principles of Human Physio.. » Flash Cards

Final - Flashcards

Flashcard Deck Information

Class:	BY 409 - Principles of Human Physiology
Subject:	Biology
University:	University of Alabama - Birmingham
Term:	Spring 2011

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INCORRECT

CORRECT

Click Card to flip

The smooth muscle is found in the walls of viscera

Click Card to flip

The smooth muscle forms ciliary and iris muscles of the eye and pilorector muscles of the skin

Click Card to flip

Smooth muscle is 2-5 um in diameter

Click Card to flip

Smooth muscle is 20-500 um in lenght

Click Card to flip

Smooth muscle is composed of cells with a single nucleus

Click Card to flip

Smooth muscle contains actin and myosin as contractile filaments

Click Card to flip

Smooth muscles are not organized into sacromeres and myofibrils

Click Card to flip

Smooth muscles have no striations

Click Card to flip

In smooth muscle, actin attaches to proteins called dense bodies

Click Card to flip

In smooth muscles actin has tropomysoin attached to it; NO TROPONIN

Click Card to flip

In smooth muscle the tropomyosin does not cover the actin binding sites

Click Card to flip

Smooth muscle has no t-tubules

Click Card to flip

The smoot muscle has a poorly developed sarcoplasmic reticulum

Click Card to flip

In the smooth muscle, the action potential running along the smooth muscle cell membrane causes an increase in ICF Ca++

Click Card to flip

In the smooth muscle most Ca++ enters from the ECF in the smooth muscle, although some is released from the SR.

Click Card to flip

Ca++ binds to intracellular Ca++ receptors, calmodulin

Click Card to flip

Ca++ malmodulin complex activated the enzyme myosin kinase

Click Card to flip

Myosine kinase activates myosin

Click Card to flip

Myosin binds to actin and undergoes power stroke

Click Card to flip

Smooth muscle produces a slower and more prolonged contraction

Click Card to flip

Smooth muscles also used LESS energy than skeletal muscles

Click Card to flip

Some smooth muscle forms an electrical SYNCYTIUM

Click Card to flip

Smooth muscles are connected by GAP junctions that allows ion flow

Click Card to flip

By GAP junctions the depolarization of one cell will initiate depolarization in adjacent cells.

Click Card to flip

Some smooth muscle is capable of generating action potentials without neuronal stimulation

Click Card to flip

Some smooth muscle is autorhythmic

Click Card to flip

Verapamil

Calcium channel blockers

Click Card to flip

Verapamil

Blocks the influx of Ca++ into the smooth muscle cell

Click Card to flip

Verapamil

decreases smooth muscle contraction in blood vessels

Click Card to flip

Verapamil

causes vasodilation of blood vessels

Click Card to flip

Verapamil

Used to lower blood pressure; increases vasodilation

Click Card to flip

Verapamil

Can increase blood flow through coronary arteries, thus reducing ANGINA

Click Card to flip

Cardiac muscle

Found only in the heart

Click Card to flip

Cardiac muscle

Similarities to both skeletal and smooth muscle

Click Card to flip

Similarities to skeletal muscle: contains myofibrils, Ca++ activated contraction by bindining to troponin C. It has a well developed SR and t-tubules. Quick/strong contractions

Click Card to flip

Similarities to smooth muscle; connected through GAP junctions, electrical syncytium, capable of being autorhythmic, it can spontaneously generate action potentials at an endogenous rate

Click Card to flip

Cardiac muscles have short branched muscle fibers which contain 1-2 nuclei

Click Card to flip

In cardiac muscles individual cells are connected to one another by intercalated discs

Click Card to flip

Intercalated discs

In cardiac muscles they are specialized cell membranes separating muscle cells.

Click Card to flip

Intercalated discs contain gap junctions, so tissue forms an electrical syncitium

Click Card to flip

Intercalated disks also contain desmosomes

Click Card to flip

Desmosomes mechanically attach to one another

Click Card to flip

Cardiac action potential is unique to cardiac muscle

Click Card to flip

Cardiac muscle cells have long duration action potentials (250 msec)

Click Card to flip

Cardiac action potentials display a plateu

Click Card to flip

Na+ channels open in depolarization phase, massive influz of Na++. Open and close rapidly

Click Card to flip

Increased Ca++ permeability of plateau phase due to slow opening of Ca++ channels, slow to open and close. This causes a steady influc of Ca++ that maintains the positive potential in ICF

Click Card to flip

In plateau phase K+ and NA+ permiability remains low

Click Card to flip

Repolarization phase Ca++ channels close and K+ channels open

Click Card to flip

A porlonged action potential allows for a prolonged contraction of muscle (300 msec)

Click Card to flip

A prolonged action potential allows for a prolonged refractory period

Click Card to flip

A prolonged action potential means a porlonged refractory period that prevents rapid restimulation of the heart and filling of heart

Click Card to flip

Cardiac cycle

beginning of one heart beat to the beginning of the next

Click Card to flip

Diastole

Relazation phase of the cardiac cycle

Click Card to flip

Diastole

The heart is relaxed and filling with blood

Click Card to flip

80 mm of Hg

The blood pressure in artieries during diastolic is

Click Card to flip

Systole

contraction phase of cardiac muscle

Click Card to flip

120 mm Hg

Systolic blood pressure reached a max of

Click Card to flip

Contractile fibers normally do not initiate their own action potentials

Click Card to flip

Heart contraction

autorhytmic tissue, initiation and conductance of AP in heart

Click Card to flip

The heart muscle its autorthymic tissue spontaneously depolarizes because Na+ channels leak

Click Card to flip

In autorhythmic tissue it is extensively throughout the heart

Click Card to flip

SA Node

70-80 depolarizations per minute

Click Card to flip

AV node

40-60 depolarizations per minute

Click Card to flip

AV Bundle

15-40 depolarizations per minute

Click Card to flip

Purkinje Fibers

15-40 deplarizations per minute

Click Card to flip

The SA node is an ellipical strip of tissue in the upper wall of the right atrium

Click Card to flip

Pacemaker of Heart

SA Node

Click Card to flip

SA Node

Depolarizaes before other tissues have the chance to

Click Card to flip

The SA node tissue is continuous with contractile tissue of the right atrium

Click Card to flip

The right atrium depolarizaes immediately after the SA depolarization

Click Card to flip

Depolarization is rapidly conducted to the left atrium via an interatrial pathway so that both atria contract at the same time

Click Card to flip

Nonconductive connective tissue between atria and ventricles block the direct trasfter of action potentials from atria to ventricles

Click Card to flip

Depolarization must go through the AV node before going to the ventricles

Click Card to flip

AV node located at the base of the right atrium and it connects with the AV bundle

Click Card to flip

AV depolarizes then AV bundle depolarizes

Click Card to flip

The AV node slows conductance of action potential into ventricles by .1 second

Click Card to flip

AV nodal delay

0.1 second

Click Card to flip

The AV node has a small diameter fiber and a decreased number of gap junctions

Click Card to flip

AV bundle originates from the AV node

Click Card to flip

The AV bundle extends down and through the interventicular septum

Click Card to flip

The AV bundle has two main branches

Click Card to flip

The AV bundle conveys depolarization down to the bottom of the ventricles to the purkinje fibers

Click Card to flip

Myocardium

muscular portion of the heart wall

Click Card to flip

Purkinje fibers are fast conducting fibers

Click Card to flip

Purkinje fibers rapidly spread the depolarization from end of the AV bundle through the ventricular myocardium

Click Card to flip

Botton-top depolariztion of the ventricles

Click Card to flip

contraction occurs from the bottom up

Click Card to flip

depolarization does not contrinue to spread after the ventricles depolarize-- long refractory period

Click Card to flip

Your basal heart rate is determined by the SA node

Click Card to flip

autonomic nervous system can increase/decrease your basal heart rate

Click Card to flip

Parasympathetic system stimulates the heart via the vagus nerve

Click Card to flip

vagus nerve

tenth cranial nerve

Click Card to flip

Acetylcholine

opens the K+ channels in the heart

Click Card to flip

Acetylcholine

K+ channels open resulting in hyperrepolarization

Click Card to flip

Acetylcholine

hyperrepolarization causes decrease in excitability of SA node which decreases heart rate, decreases conduction speed of AV node

Click Card to flip

Sympathetic

Norepinephrine is releasesed from the sympathetic neurons

Click Card to flip

Norepinephrine

opens Na+ and Ca++ channels in heart tissue

Click Card to flip

Norepinephrine

increased excitability of SA node and AV node causing an increase in heart rate and conduction speed of depolarization

Click Card to flip

norepinephrine

increeased contraction strength

Click Card to flip

ECG or EKG

indirect reading of electrical activity of the heart

Click Card to flip

ECG

reading represent a summation of electrical activity occuring in the heart

Click Card to flip

ECG

location of electrodes is important

Click Card to flip

ECG

used is diagnosing abnormal heart rhythms and some cardiac myopathy

Click Card to flip

ECG

reference electrode and a recording electrode that are collectively called a limb lead.. two electrode for each limb lead

Click Card to flip

P wave

atrial depolarization

Click Card to flip

QRS

ventricular depolarization and atrial repolarization

Click Card to flip

T Wave

ventricular repolarization

Click Card to flip

Sinus Rhythm

normal rhythm of heart produced by SA node. 70-80 bpm

Click Card to flip

Tachycardia

Fast heart rate, ECG normal waves but fast, increased sympathetic stimulation, increased body temperature, toxic metabolic conditions

Click Card to flip

Bradycardia

slow heart rate, increased parasympathetic stimulation, result from athletic conditioning, decreased body temperature 15-21

Click Card to flip

submerging the head in water can initiate a parasympathetic response reflex referred to as the mmammalian diving reflex

Click Card to flip

PVC

Ventricles depolarize before SA node depolarizes

Click Card to flip

PVC

usualy the ectopic focus, abnormal location, in the ventricles depolarizes before the SA node

Click Card to flip

Ischemic areas

decrease or lack of blood flow

Click Card to flip

PVC

can initiate ventricular fibrillation

Click Card to flip

Ventricular fibrillation

most life threatening of all arrhythmias

Click Card to flip

Ventricular fibrillation

during normal heart beats, ventricles depolarize in a synchronous fashion and then the entire ventricles are refractory

Click Card to flip

during ventricular fibrilliation, the depolarization continuously propragates around ventricles in an uncoordinated fashion movement of depolarization is relatively slow so it prevents a coordinated refractory period by the entire ventricle

Click Card to flip

during ventricular fibrillation there is no relaxation phase

Click Card to flip

during ventricular fibrillation there is no coordinated contraction

Click Card to flip

during ventricullar fibrillation there is little or no pumping of blood

Click Card to flip

person is usually unconscious in 5 minutes in ventricular fibrillation

Click Card to flip

Electroshock defibrillation

several thousand volt shock over a few milliseconds

Click Card to flip

Electroshock defibrillation

Entire heart is synchronously depolarized. it then becomes refractory. it may regain normal heart beat if the SA node is the first to depolarize

Click Card to flip

After one minute of defibrillation the heart may be too weak due to lack of blood flow, which inturn means lack of ATP

Click Card to flip

CPR

restores oxygenated blood flow, allows heart cells to reproduce ATP, heart cells reestablish membrane potentials

Click Card to flip

cardiac output

Click Card to flip

volume of blood pumped by each ventricle per minute

Click Card to flip

CO is dependent upon

heart rate (72 bpm) and stroke volume

Click Card to flip

Stroke volume

amount of blood pumped each time the ventricle contactes

Click Card to flip

Stroke volume

normally 70 mL each beat

Click Card to flip

Normal CO at rest

5,040 ml per min per ventricle

Click Card to flip

Normal CO at rest

5L of blood per minute

Click Card to flip

Stroke volume

it is a variable and increases with heart rate to a max of about a 50% increase

Click Card to flip

Stroke volume increased due to increased contraction strength due to sypathetic stimulation, this increases the amount of blood ejected by the ventricles

Click Card to flip

stroke volume increases due to increased filling of the ventricles that will stretch muscles closer to optimal length.

Click Card to flip

Heart rate

Resting HR 72 bpm

Click Card to flip

Max HR

220 minus your age

Click Card to flip

During exercise you can have up to 4-5 fold increase in CO

Click Card to flip

During exercise CO output increases up to 20-25L this is due to increased HR and stroke volume

Click Card to flip

Cardiac reserve

Difference between resting CO and max CO

Click Card to flip

cardiac reserve

allows you to greatly increase your activity level

Click Card to flip

Typically exercise increeases your stoke volume and lowers HR

Click Card to flip

Non athlete

at rest stroke volume 70mL

heart rate 72 bpm

CO= 5040 ml/min

Click Card to flip

Non athlete

During exercise

Stroke volume =110mL

HR= 195 bpm

CO=21,400 ml/min

Click Card to flip

Athlete

at rest-

stoke volume 100ml

hr=50bpm

Co=5,000ml/min

Click Card to flip

Athlete

exercise

stroke volume 165

hr=195

CO= 32,175ml/min

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	The smooth muscle is found in the walls of viscera
	The smooth muscle forms ciliary and iris muscles of the eye and pilorector muscles of the skin
	Smooth muscle is 2-5 um in diameter
	Smooth muscle is 20-500 um in lenght

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Koofers.com

	Smooth muscle is composed of cells with a single nucleus
	Smooth muscle contains actin and myosin as contractile filaments
	Smooth muscles are not organized into sacromeres and myofibrils
	Smooth muscles have no striations

Generated by

Koofers.com

	In smooth muscle, actin attaches to proteins called dense bodies
	In smooth muscles actin has tropomysoin attached to it; NO TROPONIN
	In smooth muscle the tropomyosin does not cover the actin binding sites
	Smooth muscle has no t-tubules

Generated by

Koofers.com

	The smoot muscle has a poorly developed sarcoplasmic reticulum
	In the smooth muscle, the action potential running along the smooth muscle cell membrane causes an increase in ICF Ca++
	In the smooth muscle most Ca++ enters from the ECF in the smooth muscle, although some is released from the SR.
	Ca++ binds to intracellular Ca++ receptors, calmodulin

Generated by

Koofers.com

	Ca++ malmodulin complex activated the enzyme myosin kinase
	Myosine kinase activates myosin
	Myosin binds to actin and undergoes power stroke
	Smooth muscle produces a slower and more prolonged contraction

Generated by

Koofers.com

	Smooth muscles also used LESS energy than skeletal muscles
	Some smooth muscle forms an electrical SYNCYTIUM
	Smooth muscles are connected by GAP junctions that allows ion flow
	By GAP junctions the depolarization of one cell will initiate depolarization in adjacent cells.

Generated by

Koofers.com

	Some smooth muscle is capable of generating action potentials without neuronal stimulation
	Some smooth muscle is autorhythmic
Verapamil	Calcium channel blockers
Verapamil	Blocks the influx of Ca++ into the smooth muscle cell

Generated by

Koofers.com

Verapamil	decreases smooth muscle contraction in blood vessels
Verapamil	causes vasodilation of blood vessels
Verapamil	Used to lower blood pressure; increases vasodilation
Verapamil	Can increase blood flow through coronary arteries, thus reducing ANGINA

Generated by

Koofers.com

Cardiac muscle	Found only in the heart
Cardiac muscle	Similarities to both skeletal and smooth muscle
	Similarities to skeletal muscle: contains myofibrils, Ca++ activated contraction by bindining to troponin C. It has a well developed SR and t-tubules. Quick/strong contractions
	Similarities to smooth muscle; connected through GAP junctions, electrical syncytium, capable of being autorhythmic, it can spontaneously generate action potentials at an endogenous rate

Generated by

Koofers.com

	Cardiac muscles have short branched muscle fibers which contain 1-2 nuclei
	In cardiac muscles individual cells are connected to one another by intercalated discs
Intercalated discs	In cardiac muscles they are specialized cell membranes separating muscle cells.
	Intercalated discs contain gap junctions, so tissue forms an electrical syncitium

Generated by

Koofers.com

	Intercalated disks also contain desmosomes
	Desmosomes mechanically attach to one another
	Cardiac action potential is unique to cardiac muscle
	Cardiac muscle cells have long duration action potentials (250 msec)

Generated by

Koofers.com

	Cardiac action potentials display a plateu
	Na+ channels open in depolarization phase, massive influz of Na++. Open and close rapidly
	Increased Ca++ permeability of plateau phase due to slow opening of Ca++ channels, slow to open and close. This causes a steady influc of Ca++ that maintains the positive potential in ICF
	In plateau phase K+ and NA+ permiability remains low

Generated by

Koofers.com

	Repolarization phase Ca++ channels close and K+ channels open
	A porlonged action potential allows for a prolonged contraction of muscle (300 msec)
	A prolonged action potential allows for a prolonged refractory period
	A prolonged action potential means a porlonged refractory period that prevents rapid restimulation of the heart and filling of heart

Generated by

Koofers.com

Cardiac cycle	beginning of one heart beat to the beginning of the next
Diastole	Relazation phase of the cardiac cycle
Diastole	The heart is relaxed and filling with blood
80 mm of Hg	The blood pressure in artieries during diastolic is

Generated by

Koofers.com

Systole	contraction phase of cardiac muscle
120 mm Hg	Systolic blood pressure reached a max of
	Contractile fibers normally do not initiate their own action potentials
Heart contraction	autorhytmic tissue, initiation and conductance of AP in heart

Generated by

Koofers.com

	The heart muscle its autorthymic tissue spontaneously depolarizes because Na+ channels leak
	In autorhythmic tissue it is extensively throughout the heart
SA Node	70-80 depolarizations per minute
AV node	40-60 depolarizations per minute

Generated by

Koofers.com

AV Bundle	15-40 depolarizations per minute
Purkinje Fibers	15-40 deplarizations per minute
	The SA node is an ellipical strip of tissue in the upper wall of the right atrium
Pacemaker of Heart	SA Node

Generated by

Koofers.com

SA Node	Depolarizaes before other tissues have the chance to
	The SA node tissue is continuous with contractile tissue of the right atrium
	The right atrium depolarizaes immediately after the SA depolarization
	Depolarization is rapidly conducted to the left atrium via an interatrial pathway so that both atria contract at the same time

Generated by

Koofers.com

	Nonconductive connective tissue between atria and ventricles block the direct trasfter of action potentials from atria to ventricles
	Depolarization must go through the AV node before going to the ventricles
	AV node located at the base of the right atrium and it connects with the AV bundle
	AV depolarizes then AV bundle depolarizes

Generated by

Koofers.com

	The AV node slows conductance of action potential into ventricles by .1 second
AV nodal delay	0.1 second
	The AV node has a small diameter fiber and a decreased number of gap junctions
	AV bundle originates from the AV node

Generated by

Koofers.com

	The AV bundle extends down and through the interventicular septum
	The AV bundle has two main branches
	The AV bundle conveys depolarization down to the bottom of the ventricles to the purkinje fibers
Myocardium	muscular portion of the heart wall

Generated by

Koofers.com

	Purkinje fibers are fast conducting fibers
	Purkinje fibers rapidly spread the depolarization from end of the AV bundle through the ventricular myocardium
	Botton-top depolariztion of the ventricles
	contraction occurs from the bottom up

Generated by

Koofers.com

	depolarization does not contrinue to spread after the ventricles depolarize-- long refractory period
	Your basal heart rate is determined by the SA node
	autonomic nervous system can increase/decrease your basal heart rate
	Parasympathetic system stimulates the heart via the vagus nerve

Generated by

Koofers.com

vagus nerve	tenth cranial nerve
Acetylcholine	opens the K+ channels in the heart
Acetylcholine	K+ channels open resulting in hyperrepolarization
Acetylcholine	hyperrepolarization causes decrease in excitability of SA node which decreases heart rate, decreases conduction speed of AV node

Generated by

Koofers.com

Sympathetic	Norepinephrine is releasesed from the sympathetic neurons
Norepinephrine	opens Na+ and Ca++ channels in heart tissue
Norepinephrine	increased excitability of SA node and AV node causing an increase in heart rate and conduction speed of depolarization
norepinephrine	increeased contraction strength

Generated by

Koofers.com

ECG or EKG	indirect reading of electrical activity of the heart
ECG	reading represent a summation of electrical activity occuring in the heart
ECG	location of electrodes is important
ECG	used is diagnosing abnormal heart rhythms and some cardiac myopathy

Generated by

Koofers.com

ECG	reference electrode and a recording electrode that are collectively called a limb lead.. two electrode for each limb lead
P wave	atrial depolarization
QRS	ventricular depolarization and atrial repolarization
T Wave	ventricular repolarization

Generated by

Koofers.com

Sinus Rhythm	normal rhythm of heart produced by SA node. 70-80 bpm
Tachycardia	Fast heart rate, ECG normal waves but fast, increased sympathetic stimulation, increased body temperature, toxic metabolic conditions
Bradycardia	slow heart rate, increased parasympathetic stimulation, result from athletic conditioning, decreased body temperature 15-21
	submerging the head in water can initiate a parasympathetic response reflex referred to as the mmammalian diving reflex

Generated by

Koofers.com

PVC	Ventricles depolarize before SA node depolarizes
PVC	usualy the ectopic focus, abnormal location, in the ventricles depolarizes before the SA node
Ischemic areas	decrease or lack of blood flow
PVC	can initiate ventricular fibrillation

Generated by

Koofers.com

Ventricular fibrillation	most life threatening of all arrhythmias
Ventricular fibrillation	during normal heart beats, ventricles depolarize in a synchronous fashion and then the entire ventricles are refractory
	during ventricular fibrilliation, the depolarization continuously propragates around ventricles in an uncoordinated fashion movement of depolarization is relatively slow so it prevents a coordinated refractory period by the entire ventricle
	during ventricular fibrillation there is no relaxation phase

Generated by

Koofers.com

	during ventricular fibrillation there is no coordinated contraction
	during ventricullar fibrillation there is little or no pumping of blood
	person is usually unconscious in 5 minutes in ventricular fibrillation
Electroshock defibrillation	several thousand volt shock over a few milliseconds

Generated by

Koofers.com

Electroshock defibrillation	Entire heart is synchronously depolarized. it then becomes refractory. it may regain normal heart beat if the SA node is the first to depolarize
	After one minute of defibrillation the heart may be too weak due to lack of blood flow, which inturn means lack of ATP
CPR	restores oxygenated blood flow, allows heart cells to reproduce ATP, heart cells reestablish membrane potentials
CO	cardiac output

Generated by

Koofers.com

CO	volume of blood pumped by each ventricle per minute
CO is dependent upon	heart rate (72 bpm) and stroke volume
Stroke volume	amount of blood pumped each time the ventricle contactes
Stroke volume	normally 70 mL each beat

Generated by

Koofers.com

Normal CO at rest	5,040 ml per min per ventricle
Normal CO at rest	5L of blood per minute
Stroke volume	it is a variable and increases with heart rate to a max of about a 50% increase
	Stroke volume increased due to increased contraction strength due to sypathetic stimulation, this increases the amount of blood ejected by the ventricles

Generated by

Koofers.com

	stroke volume increases due to increased filling of the ventricles that will stretch muscles closer to optimal length.
Heart rate	Resting HR 72 bpm
Max HR	220 minus your age
	During exercise you can have up to 4-5 fold increase in CO

Generated by

Koofers.com

	During exercise CO output increases up to 20-25L this is due to increased HR and stroke volume
Cardiac reserve	Difference between resting CO and max CO
cardiac reserve	allows you to greatly increase your activity level
	Typically exercise increeases your stoke volume and lowers HR

Generated by

Koofers.com

Non athlete	at rest stroke volume 70mL heart rate 72 bpm CO= 5040 ml/min
Non athlete	During exercise Stroke volume =110mL HR= 195 bpm CO=21,400 ml/min
Athlete	at rest- stoke volume 100ml hr=50bpm Co=5,000ml/min
Athlete	exercise stroke volume 165 hr=195 CO= 32,175ml/min

Generated by

Koofers.com

List View: Terms & Definitions

Hide All 148 Print

	Front	Back
		The smooth muscle is found in the walls of viscera
		The smooth muscle forms ciliary and iris muscles of the eye and pilorector muscles of the skin
		Smooth muscle is 2-5 um in diameter
		Smooth muscle is 20-500 um in lenght
		Smooth muscle is composed of cells with a single nucleus
		Smooth muscle contains actin and myosin as contractile filaments
		Smooth muscles are not organized into sacromeres and myofibrils
		Smooth muscles have no striations
		In smooth muscle, actin attaches to proteins called dense bodies
		In smooth muscles actin has tropomysoin attached to it; NO TROPONIN
		In smooth muscle the tropomyosin does not cover the actin binding sites
		Smooth muscle has no t-tubules
		The smoot muscle has a poorly developed sarcoplasmic reticulum
		In the smooth muscle, the action potential running along the smooth muscle cell membrane causes an increase in ICF Ca++
		In the smooth muscle most Ca++ enters from the ECF in the smooth muscle, although some is released from the SR.
		Ca++ binds to intracellular Ca++ receptors, calmodulin
		Ca++ malmodulin complex activated the enzyme myosin kinase
		Myosine kinase activates myosin
		Myosin binds to actin and undergoes power stroke
		Smooth muscle produces a slower and more prolonged contraction
		Smooth muscles also used LESS energy than skeletal muscles
		Some smooth muscle forms an electrical SYNCYTIUM
		Smooth muscles are connected by GAP junctions that allows ion flow
		By GAP junctions the depolarization of one cell will initiate depolarization in adjacent cells.
		Some smooth muscle is capable of generating action potentials without neuronal stimulation
		Some smooth muscle is autorhythmic
	Verapamil	Calcium channel blockers
	Verapamil	Blocks the influx of Ca++ into the smooth muscle cell
	Verapamil	decreases smooth muscle contraction in blood vessels
	Verapamil	causes vasodilation of blood vessels
	Verapamil	Used to lower blood pressure; increases vasodilation
	Verapamil	Can increase blood flow through coronary arteries, thus reducing ANGINA
	Cardiac muscle	Found only in the heart
	Cardiac muscle	Similarities to both skeletal and smooth muscle
		Similarities to skeletal muscle: contains myofibrils, Ca++ activated contraction by bindining to troponin C. It has a well developed SR and t-tubules. Quick/strong contractions
		Similarities to smooth muscle; connected through GAP junctions, electrical syncytium, capable of being autorhythmic, it can spontaneously generate action potentials at an endogenous rate
		Cardiac muscles have short branched muscle fibers which contain 1-2 nuclei
		In cardiac muscles individual cells are connected to one another by intercalated discs
	Intercalated discs	In cardiac muscles they are specialized cell membranes separating muscle cells.
		Intercalated discs contain gap junctions, so tissue forms an electrical syncitium
		Intercalated disks also contain desmosomes
		Desmosomes mechanically attach to one another
		Cardiac action potential is unique to cardiac muscle
		Cardiac muscle cells have long duration action potentials (250 msec)
		Cardiac action potentials display a plateu
		Na+ channels open in depolarization phase, massive influz of Na++. Open and close rapidly
		Increased Ca++ permeability of plateau phase due to slow opening of Ca++ channels, slow to open and close. This causes a steady influc of Ca++ that maintains the positive potential in ICF
		In plateau phase K+ and NA+ permiability remains low
		Repolarization phase Ca++ channels close and K+ channels open
		A porlonged action potential allows for a prolonged contraction of muscle (300 msec)
		A prolonged action potential allows for a prolonged refractory period
		A prolonged action potential means a porlonged refractory period that prevents rapid restimulation of the heart and filling of heart
	Cardiac cycle	beginning of one heart beat to the beginning of the next
	Diastole	Relazation phase of the cardiac cycle
	Diastole	The heart is relaxed and filling with blood
	80 mm of Hg	The blood pressure in artieries during diastolic is
	Systole	contraction phase of cardiac muscle
	120 mm Hg	Systolic blood pressure reached a max of
		Contractile fibers normally do not initiate their own action potentials
	Heart contraction	autorhytmic tissue, initiation and conductance of AP in heart
		The heart muscle its autorthymic tissue spontaneously depolarizes because Na+ channels leak
		In autorhythmic tissue it is extensively throughout the heart
	SA Node	70-80 depolarizations per minute
	AV node	40-60 depolarizations per minute
	AV Bundle	15-40 depolarizations per minute
	Purkinje Fibers	15-40 deplarizations per minute
		The SA node is an ellipical strip of tissue in the upper wall of the right atrium
	Pacemaker of Heart	SA Node
	SA Node	Depolarizaes before other tissues have the chance to
		The SA node tissue is continuous with contractile tissue of the right atrium
		The right atrium depolarizaes immediately after the SA depolarization
		Depolarization is rapidly conducted to the left atrium via an interatrial pathway so that both atria contract at the same time
		Nonconductive connective tissue between atria and ventricles block the direct trasfter of action potentials from atria to ventricles
		Depolarization must go through the AV node before going to the ventricles
		AV node located at the base of the right atrium and it connects with the AV bundle
		AV depolarizes then AV bundle depolarizes
		The AV node slows conductance of action potential into ventricles by .1 second
	AV nodal delay	0.1 second
		The AV node has a small diameter fiber and a decreased number of gap junctions
		AV bundle originates from the AV node
		The AV bundle extends down and through the interventicular septum
		The AV bundle has two main branches
		The AV bundle conveys depolarization down to the bottom of the ventricles to the purkinje fibers
	Myocardium	muscular portion of the heart wall
		Purkinje fibers are fast conducting fibers
		Purkinje fibers rapidly spread the depolarization from end of the AV bundle through the ventricular myocardium
		Botton-top depolariztion of the ventricles
		contraction occurs from the bottom up
		depolarization does not contrinue to spread after the ventricles depolarize-- long refractory period
		Your basal heart rate is determined by the SA node
		autonomic nervous system can increase/decrease your basal heart rate
		Parasympathetic system stimulates the heart via the vagus nerve
	vagus nerve	tenth cranial nerve
	Acetylcholine	opens the K+ channels in the heart
	Acetylcholine	K+ channels open resulting in hyperrepolarization
	Acetylcholine	hyperrepolarization causes decrease in excitability of SA node which decreases heart rate, decreases conduction speed of AV node
	Sympathetic	Norepinephrine is releasesed from the sympathetic neurons
	Norepinephrine	opens Na+ and Ca++ channels in heart tissue
	Norepinephrine	increased excitability of SA node and AV node causing an increase in heart rate and conduction speed of depolarization
	norepinephrine	increeased contraction strength
	ECG or EKG	indirect reading of electrical activity of the heart
	ECG	reading represent a summation of electrical activity occuring in the heart
	ECG	location of electrodes is important
	ECG	used is diagnosing abnormal heart rhythms and some cardiac myopathy
	ECG	reference electrode and a recording electrode that are collectively called a limb lead.. two electrode for each limb lead
	P wave	atrial depolarization
	QRS	ventricular depolarization and atrial repolarization
	T Wave	ventricular repolarization
	Sinus Rhythm	normal rhythm of heart produced by SA node. 70-80 bpm
	Tachycardia	Fast heart rate, ECG normal waves but fast, increased sympathetic stimulation, increased body temperature, toxic metabolic conditions
	Bradycardia	slow heart rate, increased parasympathetic stimulation, result from athletic conditioning, decreased body temperature 15-21
		submerging the head in water can initiate a parasympathetic response reflex referred to as the mmammalian diving reflex
	PVC	Ventricles depolarize before SA node depolarizes
	PVC	usualy the ectopic focus, abnormal location, in the ventricles depolarizes before the SA node
	Ischemic areas	decrease or lack of blood flow
	PVC	can initiate ventricular fibrillation
	Ventricular fibrillation	most life threatening of all arrhythmias
	Ventricular fibrillation	during normal heart beats, ventricles depolarize in a synchronous fashion and then the entire ventricles are refractory
		during ventricular fibrilliation, the depolarization continuously propragates around ventricles in an uncoordinated fashion movement of depolarization is relatively slow so it prevents a coordinated refractory period by the entire ventricle
		during ventricular fibrillation there is no relaxation phase
		during ventricular fibrillation there is no coordinated contraction
		during ventricullar fibrillation there is little or no pumping of blood
		person is usually unconscious in 5 minutes in ventricular fibrillation
	Electroshock defibrillation	several thousand volt shock over a few milliseconds
	Electroshock defibrillation	Entire heart is synchronously depolarized. it then becomes refractory. it may regain normal heart beat if the SA node is the first to depolarize
		After one minute of defibrillation the heart may be too weak due to lack of blood flow, which inturn means lack of ATP
	CPR	restores oxygenated blood flow, allows heart cells to reproduce ATP, heart cells reestablish membrane potentials
	CO	cardiac output
	CO	volume of blood pumped by each ventricle per minute
	CO is dependent upon	heart rate (72 bpm) and stroke volume
	Stroke volume	amount of blood pumped each time the ventricle contactes
	Stroke volume	normally 70 mL each beat
	Normal CO at rest	5,040 ml per min per ventricle
	Normal CO at rest	5L of blood per minute
	Stroke volume	it is a variable and increases with heart rate to a max of about a 50% increase
		Stroke volume increased due to increased contraction strength due to sypathetic stimulation, this increases the amount of blood ejected by the ventricles
		stroke volume increases due to increased filling of the ventricles that will stretch muscles closer to optimal length.
	Heart rate	Resting HR 72 bpm
	Max HR	220 minus your age
		During exercise you can have up to 4-5 fold increase in CO
		During exercise CO output increases up to 20-25L this is due to increased HR and stroke volume
	Cardiac reserve	Difference between resting CO and max CO
	cardiac reserve	allows you to greatly increase your activity level
		Typically exercise increeases your stoke volume and lowers HR
	Non athlete	at rest stroke volume 70mL heart rate 72 bpm CO= 5040 ml/min
	Non athlete	During exercise Stroke volume =110mL HR= 195 bpm CO=21,400 ml/min
	Athlete	at rest- stoke volume 100ml hr=50bpm Co=5,000ml/min
	Athlete	exercise stroke volume 165 hr=195 CO= 32,175ml/min

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