heart a&p

Heart

location

blood vessels

deoxy vs oxy blood

base and apex

Muscular pump to carry out blood all throughout blood vessels

in thoracic cavity

blood vessels: tubes that blood flows through

oxygenated blood: red

deoxygenated blood: blue

base: where major heart vessels enter/ex it

apex: points inferiorly, anteriorly, to the left

average beats per minute/lifetime

heart vs. intense exercise heart pumps

average 72 beats per minute, 75 years=3 billion beats per lifetime

at rest, heart pumps 5 liters of blood per minute, during intense exercise= 25 L

Heart layers/muscles

endocardium: thin cellular lining in cavities of the heart

myocardium: cardiac muscle, meat of heart

parietal later: fibrous, attach to underlying tissue

in between pericardial cavity: serous fluid, lets heart beat without letting heart beat against tissue its surrounded by

visceral layer

pericardium: thick, fibrous sac holds heart in chest

right atrium

pulmonary artery

blood gets collected

blood to lungs

cardiomyocytes

striations

branching

central nucleus

intercalated disc (important for interconnecting all cardiomyocytes in heart, lets whole heart tissue act as one muscle)

contains gap junctions

Trabeculae carnea

Papillary muscles

Chordae tendenae

Intraventricular septum

waffle life muscular ridges in ventricles, gives the wall structure

anchor AV valves in ventricles, attached to chordae tendenae (strings)

only in AV bc this is where the blood rushes out bc of pressure and valves bellow out, strings hold them in place

in between right and left side of heart

Heart Valves

precent backflow of blood when heart pumps

tricuspid valve: right atrium and right ventricle, pushes blood through

Pulmonary semilunar valve: right ventricle and pulmonary artery + left ventricle and aorta

Bicuspid (mitral) valve: left atrium and left ventricle

Aortic valve: left ventricle and aorta

Blood Flow

superior/inferior vena cava sends deoxygenated blood to

right atrium (deoxygenated blood flowing back to heart from body) to tricuspid valve to right ventricle to pulmonary artery/semilunar valve to lungs

back to heart is oxygenated blood, released CO2:

left atrium (from pulmonary veins) to bicuspid valve to left ventricle to semilunar valve to aorta to body (a lot bigger)

in pulmonary arteries

in pulmonary veins

blood gets reoxygenated, deoxygenated blood pumps to lungs through pulmonary arteries

blood is now oxygenated and comes back to the heart into left atrium via pulmonary veins

Pulmonary circuit

Systemic circuit

transports blood to and from the lungs, where it picks up oxygen and delivers carbon dioxide for exhalation

transports oxygenated blood to virtually all of the tissues of the body and returns relatively deoxygenated blood and carbon dioxide to the heart to be sent back to the pulmonary circulation

deoxygenated blood vessels

oxygenated blood vessels

right/left pulmonary artery, superior/inferior vena cava, coronary sinus, pulmonary trunk

ascending/descending aorta, aortic arch, left/right pulmonary vein

Contractile cells

Pacemaker cells

(99%) responsible for contractions

(1%) initiate depolarization of heart, don’t need nervous system stimulation, specialized adaptation to keep depolarizing

Functional Syncytium

all as one, contraction of all cardiac myocytes ensure effective pumping action

Action Potential Generated Within Myocyte

sustained contraction ensures efficient ejection of blood, longer refractory period prevents tetanic contractions (push as much blood as possible)

Steps of Heart Beat

1) depolarization: opening multiple Na+ channels

2) plateu phase bc of slow Ca2+ channels, keep depolarized bc most K+ channels closed

3) repolarization: Ca2+ channel inactive, K+ channel open, back to resting voltage

Coordinated Heartbeat is function of

presence of gap junctions (allows unique conduction system so you can contract atria first, then break, then blood into ventricles)

intrinsic cardiac conduction system: initiate + distribute impulses to coordinate depolarization/contraction of heart

Action Potential initiation by pacemaker cells

have unstable membrane potentials, called pacemaker potentials or prepotnetials

1) pacemaker potential has slow depolarization bc of open Na+ and close K+, reach threshold on very constant basis

2) depolarization, quickly, Ca2+ influx

3) Repolarization, Ca2+ inactivate, K+ open, go back down

Heart’s Pacemaker

cardiovascular system contracts without nervous system command

SA: provides electrical contraction 70-80 times per minute on average

electrical signals move through atria, stops at AV node, causes atrial contraction, blood flows to ventricles

signal travels from AV node then spreads signal to ventricles via specialized Purkinje fibers

Impulse Conduction

1) SA node activity and atrial activation begins (time=0)

2) stimulus spreads across atrial surface and reaches AV node (time-50 msec)

3) 100 msec delay at AV node, atrial contraction begins, delay allowed fluid in atrial to drain through AV valves

4) impulse travels along the interventricular septum within AV bundle and bundle branches to Purkinje fibers to the papillary muscles to right ventricle (time=175 msec)

5) impulse is distributed through Purkinje fibers and relayed throughout ventricular myocardium. atrial contraction is completed, and ventricular contraction beings (time-225 msec)

electrocardiogram (ECG/EKG)

graphic recording of electrical activity

records all action potentials (during ventricular depolarization, atrial repolarization also happening)

1. P Wave: depolarization of SA node and atria

2. QRS Complex: ventricular depolarization and atrial repolarization, big one

3. T Wave: ventricular repolarization

4. P-R interval: beginning of atrial excitation to beginning of ventricular repolarization

5. S-T segment: entire ventricular myocardium depolarized, squeezed tight

6. Q-T interval: beginning of ventricular depolarization through ventricular repolarization

Diastole

Systole

Steps

ventricle open, blood flowing in, heart at rest

when ventricles are relaxed (diastole), valves between atrial and ventricles are open (bicuspid and tricuspid)

heart is beating

when ventricles are contracted (systole), valves between the atria and ventricles are closed (bicuspid and tricuspid)

1) both diastole

2) atrial systole, ventricular diastole (lubb)

3) both systole

4) atrial diastole, ventricular systole (dubb)

Blood Pressure

AV Valves close when ventricular pressure exceeds atrial pressure

Semilunar valves open when ventricular pressure exceeds aortic pressure

Semilunar valves close, pressure drops, blood pushes back against aorta

AV valves open when ventricular pressure drops below atrial pressure

Isovolumetric contractions phase

End diastolic volume

Coronary circulation

ventricles are contracting and building up pressure, not quite to when they can push blood out through aortic semilunar valve

volume of blood in ventricles during end of diastole

blood pumped from heart nourishes heart itself (artery comes out from base into heart itself)

Cardiac Output

amount of blood pumped out by each ventricle in 1 minute

heart rate times stroke volume

Stroke Volume

at rest CO?

volume of blood pumped out by 1 ventricle with each beat

CO (ml/min)= HR (75 beats/min) times SV (70 ml/beat)= 5.25 L/min

Exercise CO difference

maximal cardiac output in 4-5 times resting CO in nonathletic ppl (20-25 L/min)

exercise= increase cardiac output bc muscle tissues use O2 rapidly, burning through fuel

Cardiac Reserve

cardiac output affected by factors leading to

difference between resting and maximal cardiac output

regulation of stroke volume and heart rate

Factors involved in determining cardiac output

exercise and increase ventricular filling time= increase venous return, increase end diastolic volume, increase stroke volume, increase cardiac output

epinephrine and thyroxine (excess Ca2+), increase contractility, decrease end systolic volume, increase stroke volume, increase cardiac output

CNS response to exercise, decrease bp, fright, anxiety= decrease parasympathetic activity, increase heart rate, increase cardiac output

Equation for stroke volume

SV= EDV-ESV

EDV: ventricles at rest, wide open, affected by length of ventricular diastole and venous pressure (how much pressure from vena cava to push blood into right atrium)

ESV: pumped everything out, affected by arterial blood pressure and force of ventricular contraction

3 main factors that affect stroke volume

preload: affected by venous pressure

contractility: chemical messenger

afterload

Preload

volume of blood in ventricles at end of diastole (EDV)

stretch of heart muscle, degree to which cardiac muscle cells are stretched just before they contract

changes in preload=changes in stroke volume (affects end diastolic volume)

cardiac muscles exhibits a length-tension relationship

at rest, cardiac muscle cells are shorter than optimal length, leads to dramatic increase in contractile force

most important factor in preload stretching of cardiac muscle is venous return (amount of blood returns to heart) stretches ventricles and increases contractions

Contractility

contractile strength at given muscle length

lowers end systolic value

epi/norepi increase contractility via 2nd messenger system

Ca2+ channels increase in sarcoplasmic reticulum and increase Ca2+ from extracellular fluid=increase force of contraction

Positive Inotropic Agent

Negative Inotropic Agent

quickly increase contractility, increase heart rate

ex. epi/norepi, thyroxine, Ca2+

acidosis (excess H+), increased extracellular K+, calcium channel blockers

Afterload

Resistance left ventricle must overload to circulate blood

back pressure exerted by arterial blood

pressure ventricles must overload to eject blood

hypertension increases afterload, resulting in increased ESV and reduced SV

what will happen if stroke volume decreases bc of decrease blood volume or weakened heart

cardiac output can be maintained by increased heart rate and contractility

+ chronotropic factors increase heart rate

-chronotropic factors decrease heart rate

how can hr be regulated

autonomic nervous system

chemicals

other factors

Extrinsic innervation of heart

heartbeat modified by ANS via cardiac centers in medulla oblangata

Cardioacceletaory center

Cardioinhibitory center

sends signals through sympathetic trunk to increase rate/force

stimulates SA/AV nodes, heart muscle, coronary arteries

parasympathetic signals via vagus nerve to decrease rate

inhibits SA/AV nodes via vagus nerve

Chemical Regulation of Heart Rate

hormones: epi from adrenal medulla increase heart rate and contractility

thyroxin increase heart rate, enhances effects of epi/norepi

Ions: intracellular and extracellular ion concentration (K+ and Ca2+) must be maintained for normal heart function

Other factors

age: fetus has fastest heart rate, declines with age

gender: female faster

Exercise: increase heart rate, athletes have slow resting hr

body temp: increase body temp=increase heart rate

hypocalcemia

hypercalcemia

hyperkalemia

hypokalemia

depresses heart

increases heart rate and contractility

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

results in feeble heartbeat, arrhythmias

Tachycardia

Bradycardia

Congestive Heart failure

fast heart rate, more than 100 bpm, lead to fibrillation

slower heart rate (inadequate blood circulation)

continously not getting enough blood flow out (reflects weakened myocardium caused by coronary athlerosis, persistent high bp, multiple myocardial infarcts)

What does CHF reflect

Caused by

weakened myocardium

Coronary atherosclerosis: clogged arteries caused by fat buildup

Persistent High Blood Pressure: aortic pressure causes myocardium to exert more force, increased ESV

Multiple Myocardial Infarcts: heart becomes weak as contractile cells are replaced with scar tissue

Dilated cardiomyopathy: ventricles stretch and become flabby, myocardium deteriorates

Either side of heart effected in CHF

treatment

left sided: pulmonary congestion, blood backed up in lungs, can’t pump blood out

right sided: peripheral congestion, blood pools in body organs, causing edema

removal of fluid, drugs to reduce afterload and increase contractility