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45 Cards in this Set

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Describe the pressure changes in the heart which cause the valves to open and close.
- 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
Identify the three main phases of the cardiac cycle.
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
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.
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
Define and give a normal value for end diastolic volume (EDV).
- 120 ml of blood in ventricles
- at end of atrial systole (beforehand, heart only filled 70%)
- at end of ventricular diastole
Define and give a normal value for end systolic volume (ESV)
- 50 ml of blood in ventricles (down from 120 at EDV)
- occurs at end of ventricular systole
Define and give a normal value for stroke volume (SV).
- the volume of blood pumped by the ventricle per beat
- EDV-ESV
- appx. 70 ml of blood (120-50)
Which heart valves are open during isovolumic relaxation? During isovolumic contraction?
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
Describe the first and second heart sounds. Which sound marks the beginning of diastole? Systole?
- 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
What is the contribution of atrial contraction to ventricular filling?
- before atrial contraction, ventricles filled about 70%
- atrial contraction finishes filling them (the EDV - 120 ml of blood)
Define cardiac output and know how it is calculated.
- 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!!!)
What is cardiac reserve?
- 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
How is stroke volume calculated?
- vol of blood pumped by ventricle per beat
- EDV- ESV = about 70 ml blood
Define ejection fraction and know how it is calculated.
- how much of the blood in the heart is actually ejected
- SV (stroke volume)/EDV x 100% = 60%
Define the terms preload and afterload.
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
What is the relationship between stroke volume and venous return (ie preload)?
- 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
Hos does afterload influence stroke volume?
- increased afterload = decreased CO = decreased stroke volume
- because more resistance must be overcome
- HTN increases afterload/resistance
How does contractility influence stroke volume?
- 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
How do changes in sarcoplasmic Ca2+ levels influence contractility?
- 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
What effects do the sympathetic and parasympathetic divisions of the ANS have on heart rate?
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
What effect does the symathetic division have on contractility?
increases contractility by releasing norepinepherine, also innervate SA and AV nodes
Identify other chemical and physical factors that influence heart rate (besides SNS and PNS fibers).
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
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.
- 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
Positive inotropic agents
- factors/substances that increase contractility of the heart
- sympathetic NS
- NE and epinepherine
- inc. Ca in ECF
- drugs: digitalis
Nagative inotropic agents
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
Positive chronotropic factors
- increase HR
Nagative chronotropic factors
- decrease HR
Tachycardia
HR = more than 100 bpm
causes: exercise, fever, hyperthyroidism, pregnanacy, drugs
- prolonged causes ventricular fibrillation (V-fib!)
Bradycardia
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
vagal tone
- 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
chemoreceptors
- monitor blood chem
- cardiac centers in medulla oblongata receive input
- how the ANS provides neural control of heart rate
baroreceptors
- monitor BP
- cardiac centers in medulla oblongata receive input
- how the ANS provides neural control of heart rate
Frank-Starling law of the heart
- 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
heart murmurs
- unusual or abnormal heart sounds
- systolic murmurs: aortic stenosis, mitral valve prolapse, aortic obstructions
- diastolic murmurs: mitral valve stenosis, regurgitation from aorta/pulmonary trunk
valve prolapse
- cusps don't close tightly
- blood can regurgitate
extopic focus
- 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
ectopic pacemaker
- 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
look at pic p 683
look at pic p.50 in notes
Define ECG.
- 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
Name the three important waves/deflections of a normal ECG tracing and describe what each represents.
- 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
What is the duration of a normal PR interval?
- the time from the beginning to atrial excitation to the beginnig of ventricular excitation
- usually about .16 seconds
What might a prolonged P-R interval indicate?
- 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
What is the duration of a normal QRS complex?
- 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
What might a prolonged QRS complex indicate?
- ventricular depolarization (preceds ventricular contraction)
- prolonged indicates impaired conduction w/in ventricles
- possibly a bundle branch blocked
What cardiac event/activity is represented by the S-T segment?
- when the action potentials of the ventricular myocytes are in their plateau qhases
- during this phase, the entire ventricular myocardium is depolarized
What is the clinical significance of an elevated or depressed S-T segment?
- 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)