What are the 2 major divisions of the cardiovascular System?

-Where are they and what do they do?

1.Pulmonary Circuit: right side of the heart

-carries blood to the lungs for gas exchange

2.Systemic Circuit: left side of the heart

-supplies blood to all organs of the body

1.Parietal Pericardium: outer,tough, fibrous layer

2.Parietal Cavity: filled with pericardial fluid

3. Visceral Pericardium: inner, thin, serous layer, covers the surface of the heart

1.Epicardium (Visceral Pericardium): serous membrane that covers the heart

2.Myocardium: thick muscular layer,

-contain the fibrous skeleton: which is a network of collagenous and elastic fibers

-myocardium provides structural support and attachment for cardiac muscle

-important in coordinating contractile activity

3.Endocardium: smooth inner lining

Left and right atria: which recieve blood returning to the heart

Left and right ventricles: pump blood into arteries

1.Interatrial septum: seperates left and right atria

2.Pectinate muscles:internal ridges of myocardium in right atrium and both auricles

3.Interventricualr septum:seperates left and right ventricles

4.Trabeculae carneae:internal ridges in both ventricles

Heart Valves

Atrioventricular Valves: Explain about the right and left AV valves and the chordae tendineae

Right AV valve: has 3 cusps (tricuspid valve)

Left AV valve: has 2 cusps (bicuspid valve)

Chordae tendineae: cords connect AV valves to papillary muscles

Heart Valves

Semilunar Valves

-major function

-what are the 2 semilunar valves and where are they?

-control flow into great arteries

-Pulmonary: right ventricle into pulmonary trunk

-Aortic: from left ventricle into aorta

What are the AV valve mechanics?

-when they contract and relax

Ventricles relax: pressure drops, semilunar valves close, AV valves open, blood flows from atria to ventricles

Ventricles contract: AV valves close,pressure rises, semilunar valves open, blood flows into great vessels

Coronary Circulation

Left Coronary Artery

-give funtions of the anterior interventricular branch and circumflex branch

Anterior Interventricular Branch:supplies blood to interventricular septum and anterior walls of ventricles

Circumflex Branch: supplies left atrium and posterior wall of left ventricle

Coronary Circulation

Right Coronary Artery

-give functions of right marginal branch and posterior interventricular branch

Right Marginal branch:supplies right atrium and ventricle

Posterior Interventricular Branch: supplies posterior wall of ventricles

-partial obstruction of coronary blood flow that causes chest pain

-pain is caused by ischemia, often activity dependent

-heart attack

-complete obstruction causes death of cardiac cells in affected area

-pain or pressure in chest that often radiates down left arm

Venous Drainage of the Heart

-20% drains directly into right atrium and....

-80% returns to right atrium via....

-ventricle via thebesian veins

-great cardiac vein, middle vein, left marginal vein, coronary sinus (collects blood and empties into right atrium)

Nerve Supply to the Heart

Sympathetic Nerves: where, what they do

Nerve Supply to the Heart

Parasympathetic Nerves

-vagus nerves and vagus tone

-right vagus nerve to SA node

-left vagus nerve to AV node

-vagus tone: slows heart rate to 70-80bpm

-myogenic:heartbeat originates within heart

-autorhythmic: regular spontaneous depolarization

1.SA node: pacemaker, initiates heart beat, sets heart beat

2.AV node: electrical gateway to ventricles

3.AV bundle: pathway for signals from the AV node

4.Right and Left Bundle Branches: divisions of AV bundle that enter interventricular septum

5.Purkinje fibers: spread througout the ventricular myocardium

Structure of the Cardiac Muscle

-physical characteristics?

-decreased sarcoplasmic reticulum and T tubules, what action do they perform?

-intercalated disks joining myocytes end to end, what do the interdigitating folds mechanical and electrical junctions do?

-short, branched cells, one central nucleus

-admits more Ca2+ from ECF

-Interdigitating folds: increase surface area

-Mechanical junctions: tightly joins myocytes (fascia adherens:actin anchored to plasma membrane; transmembrane proteins link cells

-also contains desmosomes

-Electrical Junctions: gap junctions that allow ions to flow

-aerobic respiration

-rich in myoglobin and glycogen

-large mitochondria

-Organic fuels: fatty acids, glucose, ketones

-fatigue resistant

Explain Cardiac rhythm

-systole and diastole

Systole: ventricular contraction

Diastole: ventricular relaxtion

Cardiac Rhythm

-Explain Sinus Rhythm

-normal heart beat set by SA node at 60-100 bpm

-adult at rest is 70-80bpm

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-extra systole

-caused by hypoxia, electrolyte imbalance, stimulants, stress

Cardiac Rhythm

-What is a ectopic foli?

-produces slower heart beat

-set by AV node, 40-50bpm

-falls before pacemakers potential

-20-40bpm

-failure of conduction system

-damage to AV node

Depolarization of SA node

-SA node has no...?

-Pacemaker potential

-Action Potential, when does is occur? (depolarizing and repolarizing phase)

-Each depolarization creates one heart beat, SA node fires at resting heart rate, how many sec and beats per minute?

-no stable resting membrane potential

-gradual depolarization from -60mV, slow influx of Na+

-occurs at threshold of -40 mV

-depolarizing phase: 0mV, fast Ca++ channels open, (Ca++ in)

-repolarizing phase: K+ channels open, (K+ out),

-at -60mV K+ channels close, pacemaker potential starts over

-.8 sec, 75bpm

Impulse Conduction to Myocardium

-Conduction through the AV node, SA node, AV bundle and purkinje fibers, and Ventricular systole

-SA node signal travels at 1 m/sec through atria 

-AV node slows signal to .05m/sec

                    -thin myocytes with fewer gap junctions

         -delays signal 100 msec, allows ventricles to fill

-AV bundle and purkinje fibers: speeds signal along at 4 m/sec to ventricles

-Ventricular systole: begins at apex, progresses up

Contraction of Myocardium

-What is the stable resting potential for myocytes?

-Explain what happens during depolarization?

-Explain what happens during a plateau?

-Explain what happens during repolarization?

-90mV

-simulus opens voltage regulated Na+ gates, (Na+ rushes in) membrane depolarizes rapidly, action potential peaks at +30 mV, Na+ gates close quickly

-Plateau:(200-250 msec), sustains contraction

               -slow Ca2+ channels open, Ca2+ binds to fast Ca2+ binds to fast Ca2+ channels on SR, releases Ca2+ into cytosol: contraction

-Ca2+ channels close, K+ channels open, rapid K+ out returns to resting potential

1.Na+ gates open

2.rapid depolarization

3.Na+ gates close

4.slow Ca++ channels open

5.Ca++ channels close, and Na+ channels open

ECG

-Explain what happens during the P wave, QRS complex, ST segment, and T wave

P wave: SA node fires, atrial depolarization, atrial systole

QRS complex:ventricular depolarization, atrial repolarization, and atrial diastole 

ST segment: ventricular systole

T wave: ventricular repolarization

ECG

-What happens during the PR interval, QT interval, PQ segment, and R to ST segment?

PR interval:atria contract

QT interval:ventricles contract

PQ segment: atria contract

R-ST segment: ventricles contract

1. Atrial depolarization begins

2.atrial depolarization complete (atria contracted)

3.Ventricles begin to depolarize at apex; atria repolarize (atria relax)

4.Ventricular depolarization complete (ventricles contracted)

5. Ventricles begin to repolarize at apex

6.Ventricular repolarization complete (ventricles relaxed)

-one complete contraction and relaxation of all 4 chambers of the heart

-atrial systole, ventricular diastole

-atrial diastole, ventricular systole

-Quiescent period

Principles of Pressure and Flow

-What does pressure cause

-What is a pressure gradient

-What happens when resistance opposes flow?

-a fluid to flow

-pressure difference between 2 points

-great blood vessels have positive blood pressure

-ventricular pressure must rise above this resistance for blood to flow into great vessels

-First: louder and longer "lubb," occurs with closure of AV valves

-Second: softer and sharper, "dupp," occurs with closure of semilunar valves

Phases of the Cardiac Cycle

Descibe the Quiescent Period

-all chambers relaxed

-AV valves open, and blood flows into ventricles

Phases of Cardiac Cycle

Describe what happens during a atrial systole?

-SA node fires, atria depolarize

-P wave appears on ECG

-atria contract, which forces additional blood into ventricles

-ventricles then contain end diastolic volume of 130 mL of blood

-atria repolarize and contract

-ventricles depolarize

-QRS complex appears in ECG

-ventricles contract

-Rising pressure closes AV valves: S1 heart sound first occurs

-no ejection of blood yet

Ventricular Ejection

-what happens during this?

-rising pressure opens semilunar valves

-rapid ejection of blood

-reduced ejetion of blood (less pressure)

Ventricular Ejection

-What is stroke volume and how much mL is produced at rest?

-amount ejected

-70mL

Ventricular Ejection

What is the Ejection fraction?

-What are the percentages at rest, exercise, and diseased?

-SD/EDV

-54%, 90%, and less than 50%

-T wave appears in ECG

-Ventricles repolarize and relax

-semilunar valves close, second heart sound occurs

-AV valves remain closed

-Ventricles expand but do not fill

1.Rapid Ventricular Filling: AV valves first open

2.Diastolsis: sustained lower pressure, venous return

3.Atrial systole: filling completed

1.Ventricular filling: rapid filling, diastasis, atrial systole

2.Isovolumetric contraction

3.Ventricular ejection

4.Isovolumetric relatation  

Rate of Cardiac Cycle

 What are the rates of the atrial systole, ventricular systole, Quiescent period, and total

-.1 sec

-.3sec

-.4 sec

-total: .8 sec, heart rate 75 bpm

unbalanced ventricular output

Pulmonary edema

-right ventricle output exceeds left ventricle output

-pressure backs up

-fluid accumulates in pulmonary tissue

Unblanced Ventricular Output

Systemic Edema

-left ventricle output exceeds right ventricle output

-pressure backs up

-fluid accumulates in systemic tissue

Cardiac Output

What is Cardiac output?

What is the cardiac output equation?

What should cardiac output be at rest and during exercise?

What is cardiac reserve and what does it increase and decrease?

-amount ejected by ventricle in 1 minute

-cardiac output=heart rate x stroke volume

-about 4-6L/min at rest

-21 L/min at vigorous exercise

-Cardiac reserve: difference between a persons max. and resting CO

-increase with fitness, decrease with disease

-surge of pressure in an artery

-120bpm or more

-females: 72-80bpm

-males: 64-72bpm

-HR is usually higher than when your an adult

-resting adult heart rate above 100bpm

-stress, anxiety, drugs, heart disease, or increased body temperature

-resting adult heart rate less than 60bpm

-during sleep and endurance trained atheletes

How do positive and negative chronotropic effects affect the heart rate?

-Positive: increases heart rate

-Negative: decreases heart rate

Cardiac Center of Medulla oblongata

What are the 2 centers within the autonomic control center?

-Cardiacceletory center (sympathetic)

-cardioinhibitory center (parasympathetic)

SyNS

It stimulates the cardiac nerves to go the...?

What neurotransmitters and receptors are involved?

Cardiac output peaks at how many bpm for SyNS?

SyNS can increase and decrease what?

-SA node, AV node and myocardium

-norepinephrine which binds to b-adrenergic receptors in the heart

-160-180 bpm

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-can increase HR up to 230 bpm

-SV and CO are decreased

PSNS

PSNS stimulates what cranial nerves and where do the left and right ones go to?

What neurotransmitters and receptors are involved?

What is a vagal tone?

What does maxinum vagal stimulation cause?

-right vagus nerve: SA node, left vagus nerve: AV node

-ACh, and muscarinic receptors

-background firing rate holds HR to sinus rhythm of 70-80 bpm

-decreased heart rate

Inputs to Cardiac Center

Where in the higher brain centers does it affect, and how does it affect it?

-cerebral cortex, limbic system, hypothalamus

-sensory or emotional stimuli

Inputs to Cardiac Center

What do proprioceptors do?

-inform cardiac center about changes in activity, HR increases before metabolic demands arise

Inputs to Cardiac Center

Where are baroreceptors and what are their function?

What happens if the pressure is decreased and increased?

-they signal the cardiac center

-aorta and internal carotid arteries

-decreased pressure: signal rate drops, cardiac center increases HR

-increased pressure: signal rate rises, cardiac center decreased HR

Inputs to Cardiac Center

Chemoreceptors

-where are they located?

-what are they sensitve to?

-What is the function?

-What does increased CO2 cause?

-What does the hypercapnia and acidosis cause?

-aortic arch, carotid arteries and medulla oblongata

-blood pH, CO2 and O2

-primary respiratory control, may influence HR

-causes increased H+ levels, may create acidosis

-cardiac center to HR

Chronotropic Chemicals

-What do they affect?

-what neurotransmitters are involved and what do they do?

-what drugs affect the heart rate and how?

What hormone affects the heart rate and what does it do?

-HR

-Neutrotransmitters-cAMP 2nd messenger, catecholamines (NEand EPI), they are potent cardiac stimulants

-Drugs: caffeine inhibits cAMP breakdown, nicotine stimulates catecholamine secretion

-Hormones: TH adrenergc receptors in heart, sensitivity to sympathetic stimulation HR

Chronotropic Chemicals

Electrolytes (explain about K+, what too much and little Potassium does)

Calcium (hypercalcemia and hypocalcemia)

-Potassium has the greatest affect

-hyperkacemia: myocardium is less excitable, HR slow and irregular

-hypokacemia: cells hyperpolarized, requires increased stimulation

Calcium

hypercalcemia: decreases HR

hypocalcemia: increases HR

1.preload

2.contractility

3.unload

stroke volume

Preload

What is Preload?

What does increased preload cause?

What is Frank-Starling law of heart?

-What is the equation

-What does the law state

-What does the increased pre load cause

Stroke Volume

Contractility

What is contractility in stroke volume?

What do positive inotropic agents cause?

What do negative inotropic agents cause?

-contraction force for a given preload

-Postitive:factors that increase contractility: hypercalcemia,catecholamines, glucagon, digitalis

-Negative: factors that decrease contractility are hyperkalemia, hypocalcemia

Stroke Volume

Afterload

What is afterload?

Increased afterload causes....?

A continuous increase of afterload causes what?

-pressure in arteries above semilunar valves opposes opening of valves

-decreased SV

-hypertrophy of myocardium may lead it to weaken and fail

Exercise and Cardiac Output

How do proprioceptors affect exercise?

How does muscular affect venous return and SV?

-HR increases at beginning of exercise due to signals from joings, muscles

-muscular activity increases venous return and causes increases SV