Physiology -Block 2 - Part 3

davidwurbel7's version from 2015-07-03 19:33

Electrical activity of the heart

Question Answer
Purkinje fiber innervate this side of the myocardiumEndocardium
This carries impulse signals from the SA node to left atriumBachman's Bundle
An abnormal electrical pathway between the atria and ventriclesAccessary Pathway
This is the only electrical connection between the atria and ventricles normally found in the heartBundle of His
Intrinsic frequency – 60 - 100 AP/minSA Node
Intrinsic frequency – 40 - 60 AP/minAV Node
Intrinsic frequency – 20 - 40 AP/minPurkinje Fiber
Phase of depolarization of atria and ventriclesPhase 0
Phase of initial repolarizationPhase 1
Phase of no net electrical activity (Plateau)Phase 2
Phase of repolarizationPhase 3
Phase of resting membrane potential of atria and ventriclesPhase 4
Phase in which Voltage-gated Na+ channel open, Voltage-Gate Calcium Channels opening, Inward Rectifying Channels (Ik1) close and Delayed rectifying channels (Ik) openPhase 0
Phase in which Voltage-gated Na+ channel closing, Voltage-Gate Calcium Channels open, Inward Rectifying Channels (Ik1) closing and Delayed rectifying channels (Ik) openingPhase 1
Phase in which Voltage-gated Na+ channel closed, Voltage-Gate Calcium Channels closing, Inward Rectifying Channels (Ik1) closed and Delayed rectifying channels (Ik) openingPhase 2
Phase in which Voltage-gated Na+ channel closed, Voltage-Gate Calcium Channels closed, Inward Rectifying Channels (Ik1) reopening and Delayed rectifying channels (Ik) openingPhase 3
Phase in which Voltage-gated Na+ channel closed, Voltage-Gate Calcium Channels closed, Inward Rectifying Channels (Ik1) open and Delayed rectifying channels (Ik) closedPhase 4
Channel that is Always openUngated Potssium Channels
Closed under resting condition. Membrane depolarization quickly open and close. Fast Channel. Once closed, will not respond to a second stimulus until the cell repolarizesVoltage-Gated Sodium Channels
Closed under resting conditions (when the membrane highly negative). Depolarization open (they open more slowly than the sodium channels. Calcium entered through these channels will participate in contractionVoltage-Gate Calcium Channels
Two types - inward rectifying channels and delayed rectifying channelsVoltage-Gated Potassium Channels
Open under resting conditions (negative membrane potential). Depolarization close. Closing during depolarization phase and will be closed during main part of the plateau phase. Reopen during repolarizationInward Rectifying Channels (Ik1)
Control is more like potassium channels in nerve, Open with depolarization. However they very slow to open (delayed). They typically open late in the plateau phase of the action potential to speed repolarization. They close very slowly. They remain opened in to the resting potential and contribute to the extended period of the relative refractory periodDelayed rectifying channels (Ik)
Depolarization of the SA node is due to influx of this ionCa+2
-65 is the resting membrane potential of thisSA Node
Opening of "funny" (leaky) Na+ channel, closure of K+ channels and opening of T-type Ca+2 channel is the reason forUnstable Resting Membrane Potential
The unstable resting membrane potential of the SA Node (AV node and Purkinje fibers) is responsible for this propertyAutomaticity
Channel responsible for prolonging relative refractory periodIK Channels

Cardiac muscle contraction

Question Answer
Entry of calcium from ECF into ICF occurs duringPlateau Phase
Protein that regulates Ca+2 ATPase pump in the SRPhospholambin
Calcium moves from the ICF to ECF through thisNa+ - Ca+2 Exchanger
Calcium is sequestered into the SR by thisCa+2 ATPase Pump
Overall force generated by ventricular muscle during systoleSystolic Performance
Systolic Performance is the same asForce of Contraction
The best index of preload isEnd Diastolic Volume
Another index of preload isEnd Diastolic Pressure
Less reliable indices of this are LAP, PVP, PCWPPreload
Ability of the myocardial cells to develop force at a given muscle length (given preload)Myocardial Contractility
Factors/ drugs that Increase contractility provide more calcium to the contractile machinery more cross- bridge cycling (Increase in force of contraction of the muscle)Inotropic Effect
Increase in myocardial contractilityPositive Inotropic Effect
Sympathetic nerve stimulation, Circulating catecholamines, Cardiac glycosides – digitalisPositive Inotropic Agents
The change of in the ejection fractionIndex of contractility
Increase in thickness of the ventricular wall with a decrease in ventricular luminal volumeConcentric Hypertrophy
Increase in thickness of the ventricular wall with dilatation of the ventricular luminal volumeEccentric Hypertropy
Systemic hypertension or aortic stenosis creates this type of hypertrophyConcentric Hypertrophy
MI can cause this hypertrophy which can create CHFEccentric Hypertrophy

Cardiac Cycle

Question Answer
Cardiac cycle is the period of time from the beginning of one ventricular beat to the beginning of the nextCardiac Cycle
The number phases that occur during ventricular systole3
The number phases that occur during ventricular diastole4
Isovolumetric ventricular contraction. Rapid ventricular ejection. Reduced ventricular ejectionVentricular Systole
Isovolumetric ventricular relaxation. Rapid ventricular filling. Reduced ventricular filling (diastasis). Atrial systoleVentricular Diastole
Isovolumetric contraction and relaxation occur because both _____ are closedValves
70% of the SV is ejected during thisRapid Ejection
30% of the SV is ejected during thisReduced Ejection
This is due to the slight bulging of the aortic valve back in the left ventricleDicrotic notch (Incisura)
The longest phase during diastoleReduced Ventricular Filling
QRS complex proceeds this heart soundS1
Closing of the atrioventricular valvesS1
Closing of the semilunar valvesS2
Rapid filling into a stiff ventricular wallS3
Small volume of blood fills into concentric ventricles creating turbulence which producesS4
Increase in this reduces systolic timesContractility
Increase in this reduces diastolic and to lesser extent systolic timesHeart Rate
Normal splitting of the second heart sound occurs duringInspiration
Caused by opening of mitral valve and rapid filling causing turbulent flowS3
Possibly normal heard in children and young adults below < 35years of ageS3
Pathogenic if this is heard in adult <35 years of ageS3
If heard in adults could be an indicator LV failure or volume over loadS3
Reflects atrial contraction into a noncompliant ventricleS4
Found in Aortic stenosis, hypertension, hypertrophic cardiomyopathyS4
The narrowing or obstruction at the opening of the mitral valveMitral Stenosis
Diastolic murmur appears inMitral Stenosis
Prolonged mitral stenosis can lead toAtrial Enlargement
Increase in the intensity of a murmur just prior to systolePre-Systolic Accentuation
Opening snap and mid diastolic murmur with pre-systolic accentuation is heard inMitral Stenosis
Blood regurgitates from LV to LA during ventricular systoleMitral Insufficiency (Mitral Regurgitation)
Murmur is heard throughout systole with no change in intensityPansystolic (Holosystolic)
There is an increase in this wave seen on pressure graphV Wave
Best heard in the mitral area with possible radiation to the axillary areaMitral Valvular Murmur
Acts as major resistance for flow during ejection which increases the afterloadAortic Stenosis
Prolonged aortic stenosis leads toLeft Ventricular Hypertrophy (Concentric Hypertrophy)
Aortic stenosis is heard as this type of murmurEjection Systolic Murmur
Pressure gradient between left ventricular pressure (LVP) and aortic pressure (AP) during ejection on the graphAortic Stenosis
An incompetent (leaky) aortic valve allows blood to regurgitate from aorta to LV during ventricular diastoleAortic Insufficiency (Aortic Regurgitation)
An elevated left ventricular end diastolic volume and pressure increases this in the left ventriclePreload
High left ventricular pressure (LVP) and aortic pressure (AP) during systole. Low aortic pressure (AP) during diastole. High pulse pressureAortic Insufficiency (Aortic Regurgitation)
In respect to jugular venous pulse, atrial contraction is represented byA Wave
This wave is caused by a bulging of the tricuspid valve into the right atrium during early ventricular contractionC Wave
This wave arises from the pressure produced when the blood filling the right atrium comes up against a closed tricuspid valveV Wave
Decreased right atrial pressure due to relaxationX-Descent
Opening of the tricuspid valveY-Descent
Condition in which A waves will be absent along with no X descentAtrial Fibrillation (A-Fib)
Condition in which the C wave and X descent will be replaced by a large positive waveTricuspid Regurgitation
Condition in which a Large A wave is seenTricuspid Stenosis and Pulmonary Stenosis

Blood Pressure Regulation

Question Answer
BP regulatory system that is short term controlBaroreceptor Reflex Mechanism
BP regulatory system that is long term controlRenin-Angiotensin-Aldosterone System
Nerve that carries impulses from the carotid sinus baroreceptor to the brain stem BP regulatory centersGlossopharyngeal Nerve (CN IX)
Nerve that carries impulses from the aortic arch baroreceptor to the brain stem BP regulatory centersVagus Nerve (CN X)
Systolic <120 mm Hg, diastolic < 80 mmHgNormal
Systolic 120-139 mm Hg, diastolic 80-89 mm HgPrehypertension
Systolic 140-159 mm Hg, diastolic 90-99 mm HgStage 1 Hypertension
Systolic 160 mm Hg or greater, diastolic 100 mm Hg or greaterStage 2 Hypertension
Hypertension may develop as a result of environmental or genetic causesPrimary Hypertension
Hypertension due to one or more of multiple etiologies, including renal, vascular, and endocrine causesSecondary Hypertension


Question Answer
Lipid soluble substances (steroid hormones) and gases (Oxygen, CO2) diffuse through theEndothelium
Water soluble substances (Glucose, amino acids, electrolytes) diffuse throughIntercellular Gaps
The pressure pushes water awayHydrostatic Pressure
The pressure that brings water to itOsmotic Pressure
This pressure in the capillaries is favored in filtationHydrostatic Pressure
This pressure in the capillaries is favored in absorptionOsmotic Pressure
This pressure in the interstitial tissue is favored in filtrationOsmotic Pressure
This pressure in the interstitial tissue is favored in absorptionHydrostatic Pressure
Jv = Kf [(Pc - Pi) – (πc – πi)]Starling's Equation
[(Pc - Pi) – (πc – πi)]Net Filtration Pressure
If the net filtration pressure is positiveFiltration
If the net filtration pressure is negativeAbsorption
The product of capillary permeability x the surface area of the capillaryKf
Edema caused by arteriolar dilation, Venous constriction, Increased Venous pressure, Heart failure, or Extracelluar fluid volume expansion is due toIncreased Capillary Hydrostatic Pressure
Edema caused by decreased plasma protein concentration, severe liver failure (failure to synthesize protein), Protein malnutrition, Nephrotic syndrome (loss of protein in the urine) is due toDecrease Capillary Oncotic Pressure
Edema caused by burns and inflammation is cause byIncreased Kf (Increased hydraulic conductance)
Edema caused by standing (lack of skeletal muscle compression of lymphatics), removal or irradiation of lymphatics, or parasitic infection of lymph nodes is due toImpaired Lymphatic Drainage
The lost of greater than 3.5 g/day of protein in the urineNephrotic Syndrome
3.5 g/day of plasma protein is produced hereLiver
Generalized edemaAnasarca
Blood flow regulation in which the mechanisms are entirely within the organ itself. No nerves or circulating substances are involvedIntrinsic Regulation (Autoregulation)
Tissue metabolites regulate flow. Vasodilators dilate arterioles & increase flow when the organ is metabolically more activeMetabolic Theory of Autoregulation
Adenosine, lactic acid, hydrogen ions, hypoxiaMajor Metabolic Vasodilators
This is a mechanism to keep the flow constant in spite of increased perfusion pressureMyogenic Theory of Autoregulation
Mean arterial pressure from 160 to 60 mm of HgAutoregulatory Range
Brain, Heart, Kidneys and skeletal muscle during exercise have this regulatory systemIntrinsic Regulation (Autoregulation)
Control of flow in exercising muscle is mainly due toVasodilator Metabolites
This by binding to β2-receptor activation can contribute to increase in flowEpinephrine
The flow of the coronary artery is subjected to severe mechanical compression of intramyocardial blood vessels during systoleLeft Coronary
The flow of the coronary artery is subjected to modest mechanical compression on intramyocardial vesselsRight Coronary
This organ extracts maximum oxygen from flowing blood (A-V difference ) at restHeart
Any increase in O2 demand has to be met with increased blood flow by thisCoronary Dilation
Approximately 15% of cardiac output is delivered to this organBrain
Under normal conditions, this is the main factor regulating cerebral flowArterial PCO2 (PaCO2)
If PaO2 falls below 100 mm of Hg, this is the main factor regulating cerebral flowArterial PO2 (PaO2)
PaO2 in artery100 mm of Hg
PaCO2 in artery40 mm of Hg
PvO2 in vein40 mm of Hg
PvCO2 in vein47 mm of Hg
This maintains alveolar CO2 (PACO2) at 40 mm of HgAlveolar Ventilation
This is the PAO2 in the alveoli100 mm of Hg
Cerebral blood flow will increase with this ventilation patternHypoventilation
Cerebral blood flow will decrease with this ventilation patternHyperventilation

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