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45 Cards in this Set
- Front
- Back
Describe the pressure changes in the heart which cause the valves to open and close.
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- high press in ventricles (systole) = mitral and tricuspid valves close, SL valves open
- low press in ventricles (diastole) = mitral and tricuspid valves open, SL valves close |
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Identify the three main phases of the cardiac cycle.
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Atrial systole - ventricles filled 70% already due to passive flow; contraction causes ventricles to acheive their end diastolic volume (EDV)
Ventricular systole - atria relaxed, ventricles contract, and end up with end systolic volume (ESV) of blood Relaxation period - ventricular press falls, AV open, SL closed |
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Descrive the events associated with each of hte phases of the cardiac cycle, making note of changes in atrial & ventricular pressure, opening/closing of valves, ventricular volume changes.
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Atrial systole - atrium contracts (higher press) while ventricles are in mid/late diastole; AV valves open; higher ventricular volume (120 ml)
Ventricular systole - ventricles high press; AV valves close, SL valves open; blood ejected from heart so volume decreases Relaxation period - ventricular press falls lower than atrial, no change in vent. volume until AV valve opens |
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Define and give a normal value for end diastolic volume (EDV).
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- 120 ml of blood in ventricles
- at end of atrial systole (beforehand, heart only filled 70%) - at end of ventricular diastole |
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Define and give a normal value for end systolic volume (ESV)
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- 50 ml of blood in ventricles (down from 120 at EDV)
- occurs at end of ventricular systole |
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Define and give a normal value for stroke volume (SV).
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- the volume of blood pumped by the ventricle per beat
- EDV-ESV - appx. 70 ml of blood (120-50) |
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Which heart valves are open during isovolumic relaxation? During isovolumic contraction?
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Relaxation - SL valves have closed, but AV valves haven't opened yet; no change in ventricular volume; when AV valves open diastole begins
Contraction - volume remains the same, all valves closed; ends when aortic/pulmonary valves open, and blood begins to leave the heart; pressure is building during this time |
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Describe the first and second heart sounds. Which sound marks the beginning of diastole? Systole?
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- first sound (S1) - longer and louder, closure of AV valves, indicates beginning of ventricular systole
- second sound (S2) - SL valves close, indicates beginning of ventricular diastole |
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What is the contribution of atrial contraction to ventricular filling?
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- before atrial contraction, ventricles filled about 70%
- atrial contraction finishes filling them (the EDV - 120 ml of blood) |
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Define cardiac output and know how it is calculated.
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- the voume of blood ejected from each ventricle per minute
- CO = SV (stroke volume) - HR (heart rate) Stroke volume - EDV-ESV; volume pumped per beat; 7- ml Heart rate - heartbeats/min Total CO - about 5 L/min (pretty much the whole volume in the body!!!) |
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What is cardiac reserve?
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- the ratio between the maximum CO (cardiac output) an individual can achieve and his/her resting CO
- Normal - up to 20-25 L/min as max CO - reserve = max/resting = 4-5, but in athletes can be 7-8 |
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How is stroke volume calculated?
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- vol of blood pumped by ventricle per beat
- EDV- ESV = about 70 ml blood |
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Define ejection fraction and know how it is calculated.
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- how much of the blood in the heart is actually ejected
- SV (stroke volume)/EDV x 100% = 60% |
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Define the terms preload and afterload.
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Preload - the degree of stretch on the heart muscle before it contracts; w/in physiological limits, the more the heart is filled in diastole, the greater the contraction force during systole
Afterload - the pressure that must be exceeded before ejection of blood from the ventricles can begin; the resistance that must be overcome before the SL valves open |
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What is the relationship between stroke volume and venous return (ie preload)?
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- more veinous return stretches heart more, so contraction during systole is stronger (to a certain point)
- Frank-Starling law of the heart - fibrous skeleton prevents too much preload when fibers stretched beyond optimal contraction length |
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Hos does afterload influence stroke volume?
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- increased afterload = decreased CO = decreased stroke volume
- because more resistance must be overcome - HTN increases afterload/resistance |
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How does contractility influence stroke volume?
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- amount of force produced during contraction (@ given pre/afterload)
- stronger contraction creates greater stroke volume - refers to a force that is independent of pre/afterload - affected by CA ions in cytoplasm |
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How do changes in sarcoplasmic Ca2+ levels influence contractility?
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- greater influx from ECF causes greater release from SR
- frees up active sites on actin so that myosin heads can attatch - pulls off the troponin |
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What effects do the sympathetic and parasympathetic divisions of the ANS have on heart rate?
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Sympathetic - increases contractility; associated with cardioacceleratory center in medulla region of brain stem; when activated, the fibers innervate SA and AV nodes and myocardial contractile fibers; SNS fibers also release norepinepherine
Parasympathetic - decrease in contractility; associated with cardioinhibitory center; fibers are in Vagus nerves to SA/AV nodes; release ACh (opens K channels to hyperpolarize membrane), ACh quickly broken down to prevent the heart from stopping; heart normally exhibits vagal tone @ rest |
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What effect does the symathetic division have on contractility?
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increases contractility by releasing norepinepherine, also innervate SA and AV nodes
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Identify other chemical and physical factors that influence heart rate (besides SNS and PNS fibers).
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Hormones:
- catecholamines from adrenal medula mimic SNS; - thyroid hormones increase beta adrenergic receptors in membranes to bind to catecholamines - increase in resting HR Ions: - Calcium - hyper = prolonged plateau phase, irritable membranes, arrhythmias/fatal; hypo - lower Ca influx, decreased contractility - Potassium - most deadly; hyper - down HR, repolarization more difficult; hypo - heart beat weak; arrhythmias - Sodium - hypernatremia disrupts # of Ca ions flowing into cell = dec. in HR and contractility Other Factors: - Age - HR = 220 - age - Gender - faster in women to compensate for less blood volume/less EPV - Athletic training - decreased HR - Body temp - fever = inc. HR; hypothermia = dec HR |
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Heart failure is a condition in which the pumping ability of the heart is low and as a result, blood does not circular effectively. Explain how heart failure can result in pulmonary edema.
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- left ventricle can't keep up with the amt of blood pouring into it from the pulmonary circuit
- result: blood backs up in the capillaries in the lungs and some seeps through into the air sacs in the lungs, creating fluid filled lungs |
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Positive inotropic agents
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- factors/substances that increase contractility of the heart
- sympathetic NS - NE and epinepherine - inc. Ca in ECF - drugs: digitalis |
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Nagative inotropic agents
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factors/substances that decrease contractility
- decrease in sympathetic SN stimulation - acidosis = dec in pH in ECF - inc. K ion conc. in ECF - drugs: calcium-channel blockers |
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Positive chronotropic factors
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- increase HR
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Nagative chronotropic factors
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- decrease HR
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Tachycardia
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HR = more than 100 bpm
causes: exercise, fever, hyperthyroidism, pregnanacy, drugs - prolonged causes ventricular fibrillation (V-fib!) |
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Bradycardia
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HR = less than 60 bpm
causes: atheleticism/fitness, hypothermia, drugs, age related changes in SA node - less than 50 bpm is hard for normal people to sustain CO |
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vagal tone
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- what the heart exhibits at rest
- heart rate is being controlled by the parasympathetic nervous system; part of dual innervation - w/o this innervation, the SA node would depolarize 80-100 bpm - the fibers release ACh which opens K ion channels and hyperpolarizes the membrane, decreasing HR |
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chemoreceptors
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- monitor blood chem
- cardiac centers in medulla oblongata receive input - how the ANS provides neural control of heart rate |
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baroreceptors
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- monitor BP
- cardiac centers in medulla oblongata receive input - how the ANS provides neural control of heart rate |
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Frank-Starling law of the heart
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- describes relationship b/w preload and contraction strength
- as preload/stretch on heart muscle increases, the force of contraction increases - only up to the optimal contraction length of the muscle fibers |
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heart murmurs
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- unusual or abnormal heart sounds
- systolic murmurs: aortic stenosis, mitral valve prolapse, aortic obstructions - diastolic murmurs: mitral valve stenosis, regurgitation from aorta/pulmonary trunk |
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valve prolapse
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- cusps don't close tightly
- blood can regurgitate |
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extopic focus
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- an excitable group of cells that causes a premature heart beat outside the normally functioning SA node of the human heart.
- Acute occurrence is usually non-life threatening, but chronic occurrence can progress into tachycardia[1], bradycardia or ventricular fibrillation[2]. In a normal heart beat rhythm, the SA node usually suppresses the ectopic pacemaker activity due to the higher impulse rate of the SA node - malfunctioning SA node its inactivity allows the ectopic pacemakers to generate their rhythm |
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ectopic pacemaker
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- an excitable group of cells that causes a premature heart beat outside the normally functioning SA node of the human heart.
- Acute occurrence is usually non-life threatening, but chronic occurrence can progress into tachycardia[1], bradycardia or ventricular fibrillation[2]. In a normal heart beat rhythm, the SA node usually suppresses the ectopic pacemaker activity due to the higher impulse rate of the SA node - malfunctioning SA node its inactivity allows the ectopic pacemakers to generate their rhythm |
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look at pic p 683
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look at pic p.50 in notes
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Define ECG.
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- a composite of all that action potential generated by nodal and contractile cells at a given time
- NOT a tracing of a single action potential |
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Name the three important waves/deflections of a normal ECG tracing and describe what each represents.
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- P wave (first) - lasts .08 s; depolarization wave from SA node through atria; .1 s after P wave, the atria contract
- the QRS complex (large one) - ventricular depolarization; precedes ventricular contraction; avg. time = .08 sec - T wave - ventricular repolarization; lasts about .16 sec; slower, so wave is more spread out Note: atrial repolarization wave is obscured by the large QRS complex |
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What is the duration of a normal PR interval?
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- the time from the beginning to atrial excitation to the beginnig of ventricular excitation
- usually about .16 seconds |
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What might a prolonged P-R interval indicate?
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- the time from the beginning to atrial excitation to the beginnig of ventricular excitation
- prolonged may indicate an AV node block, so signal not being passed on as quickly to ventricle |
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What is the duration of a normal QRS complex?
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- ventricular depolarization (preceds ventricular contraction)
- usually lasts about .08 sec, but varries depending on the size of the ventricle in relation to the other ventricle |
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What might a prolonged QRS complex indicate?
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- ventricular depolarization (preceds ventricular contraction)
- prolonged indicates impaired conduction w/in ventricles - possibly a bundle branch blocked |
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What cardiac event/activity is represented by the S-T segment?
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- when the action potentials of the ventricular myocytes are in their plateau qhases
- during this phase, the entire ventricular myocardium is depolarized |
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What is the clinical significance of an elevated or depressed S-T segment?
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- when the action potentials of the ventricular myocytes are in their plateau qhases
- during this phase, the entire ventricular myocardium is depolarized Elevated or depressed: indicates cardiac ischemia (ie. possibly an MI) |