Chapter 17: The Heart -Lecture Flashcards

Question

Tachycardia

Answer 1

- abnormally fast heart rate- >100beats/min | - can be caused by changes in body temp, stress, drugs or heart disease

Answer 2

- heart rate < 60beats/min - can be caused by drugs, low body temp, parasympathetic activation - in trained athletes: the HR is often as low as 40bpm because the heart has hypertrophied and SV has increased, allowing resting HR to be lower and still provide the same CO

Answer 3

- heart can't pump efficiently enough to meet the demands of the tissue - can be caused by : coronary athersclerosis(clogged artery vessels), persistent high blood pressure, multiple myocardial infarctions, dilated cardiomyopathy, DCM(ventricles stretch and become flabby and myocardium deteriorates)

Answer 4

-excess of watery fluid collecting in cavity or tissues of body

Answer 5

- failure of the LEFT side of the heart; fluid builds up in the lungs(pulmonary edema) - right side keeps sending blood

Answer 6

-failure of right side of the heart; blood stagnates in organs and edema occurs in extremities

Answer 7

1. Na+ influx from extracellular space, causes positive feedback opening of voltage-gated Na+ channels; membrane potential quickly depolarizes (-90 to +30 mV); Na+ channels close within 3 ms of opening. 2. Depolarization causes release of Ca++ from sarcoplasmic reticulum (as in skeletal muscle), allowing sliding actin and myosin to proceed. 3. Depolarization ALSO causes opening of slow Ca++ channels on the membrane (special to cardiac muscle), further increasing Ca++ influx and activation of filaments. This causes more prolonged depolarization than in skeletal muscle, resulting in a plateau action potential, rather than a "spiked" action potential (as in skeletal muscle cells).

Answer 8

1. All-or-None Law - Gap junctions allow all cardiac muscle cells to be linked electrochemically, so that activation of a small group of cells spreads like a wave throughout the entire heart. This is essential for "synchronistic" contraction of the heart as opposed to skeletal muscle. 2. Automicity (Autorhythmicity) - some cardiac muscle cells are "self-excitable" allowing for rhythmic waves of contraction to adjacent cells throughout the heart. Skeletal muscle cells must be stimulated by independent motor neurons as part of a motor unit. 3. Length of Absolute Refractory Period - The absolute refractory period of cardiac muscle cells is much longer than skeletal muscle cells (250 ms vs. 2-3 ms), preventing wave summation and tetanic contractions which would cause the heart to stop pumping rhythmically.

Answer 9

- slow Ca2+ channels open allowing Ca2+ from the EXTRACELLULAR SPACE. - this triggers Ca2+ channels in SR to be opened; allowing more into the cell, this keeps cell depolarized because few K+ channels are open, then creates plateau - this allows for the sustained contraction necessary to eject blood from heart

Answer 10

1. SINOTRIAL(SA) NODE- in right atrium- The heart's main pacemaker; sets heart rate by generating impulses at about 75bpm; called sinus rhythm. 2. ATRIOVENTRICULAR NODE(AV)-in R.atrium- Impulse is delayed here for about 0.1 s to allow atria to complete their contraction before the ventricle contracts, slows down signal. 3. ATRIOVENTRICULAR(AV) BUNDLE OF HIS- in Atrialventricular septum- Only electrical connection between the atria and ventricles. 4. RIGHT&LEFT BUNDLE OF BRANCHES-conducts impulses through the Interventricular septum. 5. PURKINJE FIBERS-in Ventricular Walls-Depolarize the contractile cells of the ventricles(both)

Answer 11

- the SNS releases NOREPINEPHRINE which results in increased HR. - also speeds up Ca2+ movement to cells, which increases contractility and speeds relaxation. SV(stroke volume) is increased

Answer 12

- the PNS uses ACETYLCHOLINE Ach, will reduce heart rate, but does not affect contractlity. Ach opens up channels to start AP.

Answer 13

closing of the heart valves

Answer 14

1. VENTRICULAR FILLING:MID-TO-LATE DIASTOLE: ventricles fill and contract; AV valves open, your semilunar valves are closed 2. VENTRICULAR SYSTOLE-atria relax, ventricles begin to contract; ventricular blood pressure forces AV valves closed, leading to ISOVOLUMETRIC CONTRACTION - when the pressure in the ventricles rises above that in the large vessels leaving them; the SL valves open and blood is expelled into the aorta and pulmonary trunk during the VENTRICULAR EJECTION PHASE 3. ISOVOLUMETRIC RELAXATION: EARLY DIASTOLE-ventricles relax, ventricular pressure drops rapidly and blood in the aorta & pulmonary trunk flows back toward the heart; closing the SL valves. *during isovolumetric contraction and isovolumetric relaxation both AV and SL valves are closed

Answer 15

Blood is just going to the lungs , Vs. the aorta that goes to the whole body

Answer 16

- CR is the difference between resting and maximal cardiac input - NONATHLETE- 20-25L/min(4-5X resting CO) - ATHLETE-up to 35L/min (7X resting CO) - * CO is variable & increases to special demands-ex.running to catch bus

Answer 17

1. PRELOAD(degree of stretch of heart muscle before contraction)- Cardiac muscles are normally shorter than optimal length, so stretching can increase contractile force. - Venous Return- amount of blood returning to the heart can affect muscle stretch- slow HR &exercise increase volume or speed of venous return and this increase EDV and SV 2. CONTRACTILITY-contractile strength achieved at a given muscle length - this depends on the amount of Ca2+ entering the cytoplasm - increased contractile strength can be caused by:hormones, drugs, sympathetic stimulation>positive inotropic agents - decreased contractile strength can be caused by: acidosis, high extracellular potassium, some drugs> negative inotropic agents 3. AFTERLOAD-back pressure exerted on atrial blood. In people w/ hypertension(high BP) afterload can reduce the ability of ventricles to eject blood, increasing ESV & decreasing SV.

Answer 18

Fetus- fastest (140-160 beats/min) Women- (72-80 beats/min) Men- (64-72 beats/min)