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BIOL 112 > Lecture 2 CVS: the heart > Flashcards

Lecture 2 CVS: the heart Flashcards

1
Q

what is an electrocardiography

A

process of monitoring the electrical events of the heart over a given period

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2
Q

what is an electrocardiograph

A

a device that detects electrical currents generated by an transmitted through the heart

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3
Q

what is an electrocardiogram (ECG)

A

-a graphical representation of electrical changes that accompany each heartbeat
-obtained by placing electrodes at specific locations on body surface
-a composite of all APs

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4
Q

what do abnormal patterns of an ECG show

A

they are used to diagnose damage
cardiomegaly, defective cardiac conduction system, heart and chest injuries/pain etc.

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5
Q

what does an ECG show

A

there are three waves of each heart beat and intervals

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6
Q

what are the 5 steps shown on an ECG (slide 5&6)

A
  1. atrial depolarization, initiated by SA node which causes the P wave
  2. with atrial depolarization complete, the impulse is delayed at the AV node
  3. ventricular depolarization begins at the apex, causing the QRS complex and atrial repolarization occurs
  4. ventricular depolarization is complete
  5. ventricular repolarization begins at the apex, causing the T wave
  6. ventricular repolarization is complete
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7
Q

what does an enlarges P wave show

A

enlargement of the atria

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8
Q

what does an enlarged Q wave show

A

myocardial infarction (heart attack)

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9
Q

what does an enlarged R wave show

A

enlargement of ventricles

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10
Q

what is the P-Q interval

A

-start of P wave to start of QRS complex
-start of atrial excitation to start of ventricular excitation

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11
Q

what is the S-T segment

A

-end of S wave to the beginning of T wave
-depolarization of ventricular contractile fibers during plateau phase

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12
Q

what is the Q-T interval

A

-the start of the QRS complex to the end of the T wave
-from the start of ventricular depolarization to the end of ventricular repolarization

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13
Q

what does increased/ decreased P-Q interval show

A

CAD, rheumatic fever

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14
Q

what does increased/decreased S-T interval show

A

myocardial infarction

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15
Q

what does increased/decreased Q-T interval show

A

myocardial infarction, ischemia, defective cardiac conduction system

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16
Q

what is a summary of an ECG

A

tracks the electrical activity of the heart
-P wave: impulse across atria; atrial depolarization
-P-R interval: time taken for cardiac impulse to travel from the atria to the ventricles
-QRS complex: ventricular depolarization; spread of electrical impulses throughout the ventricles
-S-T segment: end of ventricular depolarization and the beginning of ventricular repolarization
-T wave: ventricular repolarization

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17
Q

what is the cardiac cycle

A

-period from the start of one heartbeat to the beginning of next
-one cardiac cycle consists of the contraction (systole) and relaxation (diastole) of both atria, rapidly followed by the systole and diastole of both ventricles
-blood pressure in each chamber: rises during systole, and drops during diastole
-blood flows from an area of higher pressure to one of lower pressure, it is controlled by timing of contraction, and directed by one-way valves

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18
Q

how many bpm does the heart do and how long does the cardiac cycle last

A

at 75 bpm, the cardiac cycle lasts ~800 msec (0.8 sec)

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19
Q

what are the two phases of the cardiac cycle

A

-systole: atrial and ventricular systole
-diastole: atrial and ventricular diastole

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19
Q

what happens to the cardiac cycle when heart rate increases

A

all phases of the cardiac cycle shorten, particularly diastole

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20
Q

what does atrial systole and diastole show

A

-atrial contraction begins, tricuspid and mitral valves are open
-atria eject blood into the ventricles
-atrial systole ends, and atrial diastole begins
-ventricles contain maximum blood volume known as end-diastole volume (EDV)

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21
Q

what does ventricle systole show

A

-ventricles contract and build pressure-> causes the AV valves to close, producing Isovolumetric Contraction
-ventricular pressure is greater then (>) arterial pressure, semilunar valves open, allowing blood to exit= ventricular ejection
-amount of blood ejected= stroke volume (70-80 ml of blood)
-as ventricular pressure falls: semilunar valves close, ventricles contain end-systolic volume (ESV)

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22
Q

what does ventricular diastole show

A

-isovolumetric relaxation occurs
-all heart valves are closed, ventricular pressure> atrial pressure, blood cannot flow into ventricles
-AV valves open; ventricles fill passively-> atrial pressure > ventricular pressure

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23
Q

atrial damage vs. ventricle damage

A

individuals can survive severe atrial damage, however, ventricular damage can lead to heart failure

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24
Q

what is dicrotic notch

A

-closure of aortic valve raises aortic pressure as backflow rebounds off closed valve cusps
-atria continue to fill during ventricular systole and when atrial pressure> ventricular pressure, AV valves open and the cycle begins again

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25
Q

how long do the atrial systole, ventricular systole and the quiescent period last for

A

-artial systole lasts ~0.1 seconds
-ventricular systole lasts ~0.3 seconds
-quiescent period (total heart relaxation) lasts ~0.4 seconds

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26
Q

what type of energy is used for cardiac contractions

A

-Aerobic energy
-from the mitochondrial breakdown of fatty acids and glucose
-oxygen is delivered by circulation
-cardiac contractile cells store oxygen in myoglobin

27
Q

what are the different heart sounds and how do you detect them

A

-they are detected with a stethoscope
-S1 (lubb): loud sound as AV valves close, signals beginning of ventricular contraction
-S2 (dupp): loud sound as semilunar valves close, beginning of ventricular filling
-S3, S4: soft sounds that are hardly heard, blood flowing into ventricle and atrial contractionw

28
Q

what is a heart murmur

A

sounds produced by regurgitation through the valves

29
Q

where can you hear the different valves working

A

-Aortic valve: sounds heard in 2nd intercostal space at the right sternal margin
-Pulmonary valve: sounds heard in 2nd intercostal space at left sternal region
-Mitral valve: sounds heard over the heart apex (in the 5th intercostal space) in line with the middle of the clavicle
-Tricuspid valve: sounds typically heard in the right sternal margin of the 5th intercostal space

30
Q

what is the cardiac output (CO)

A

volume pumped by the left or right ventricle in one minute into the aorta or pulmonary trunk
-CO (ml/min)= HR (beats/min) x SV (ml/beat)

31
Q

what is the stroke volume

A

amount of blood pumped out by each ventricle with each heartbeat, correlates with force of contraction

32
Q

what is the CO and HR at rest

A

HR= 75 beats/min, SV = 70ml
therefor, CO = 5250 ml/min =5.25 L/min

33
Q

what is the regulation of heart pumping

A

-maximal CO is 4-5x resting CO in nonathletic people (20-25 L/min)
-maximal CO may reach 35 L?min in trained athletes

34
Q

what is the cardiac reserve

A

the different between resting and maximal CO
-CO changes (increase/decrease) if either or both SV or HR is changed

35
Q

cardiac output is affected by factors leading to what

A

regulation of stroke volume, and regulation of heart rates

36
Q

what factors determine cardiac output (slide 22)

A
37
Q

how do you calculate stroke volume (SV)

A

SV = EDV - ESV
EDV = end-diastolic volume: the amount of blood in each ventricle at end of ventricular diastole (~120 ml/beat)
ESV = end-systolic volume: amount of blood remaining in each ventricle at the end of ventricular systole (~50 ml/beat)
therefor: Normal SV = 120-50= 70ml/beat

38
Q

what is the ejection fraction

A

the percentage of EDV ejected during contraction

39
Q

what are the three factors affecting stroke volume

A

preload, contractility, and afterload

40
Q

what is preload in the SV

A

-degree of stretch of heart muscle
-changes in preload cause changes in the stroke volume
-cardiac muscle exhibits a length-tension relationship
-at rest, cardiomyocytes are shorter than optimal length-> dramatic increase in contractile force
-most important factor in preload stretching of cardiac muscle is venous return (amount of blood returning to the heart), slow heart beat and exercise increase venous return, increased venous return distends (stretches) ventricles and increases contraction force

41
Q

what is frank-starling law of the heart

A

in a normal heart, the higher the preload, the higher the SV

42
Q

what is contractility in the stroke volume

A

-contractile strength at given muscle length, independent of muscle stretch and EDV

43
Q

what is increased contractility (lowers ESV) caused by

A

-sympathetic epinephrine release stimulated increased Ca2+ influx-> more cross bridge formations
-positive inotropic agents- thyroxine, glucagon, epinepherine, digitalis, high extracellular Ca2+

44
Q

what is contractility decreased by

A

-negative ionotropic agents
-acidosis (excess H+), increased extracellular K+, calcium channel blockers

45
Q

what is afterload of the stroke volume

A

-back pressure exerted by atrial blood; it is the pressure ventricles must overcome to eject blood
-back pressure from arterial blood pushing on semilunar valves is a major pressure
-hypertension increases afterload-> increased ESV and reduced SV

46
Q

what is the normal aortic and pulmonary trunk pressures in afterload

A

-aortic pressure is around 80 mm Hg
-pulmonary trunk pressure is around 10 mm Hg

47
Q

what factors affect heart rate

A

autonomic innervation, chemical regulation, age, gender, exercise, and body temperature

48
Q

what is autonomic innervation and how does it affect HR

A

-cardiac plexus innervates the heart
-Vagus nerve (CN X)- parasympathetic fibres to small ganglia in cardiac plexus
-cardiac centers of medulla oblongata

49
Q

what does the cardioacceleratory center do

A

controls the sympathetic neurons that increase heart rate

50
Q

what does the cardioinhibitory center do

A

controls parasympathetic neurons that slow heart rate

51
Q

how does and which chemical/s regulation affect heart rate

A

-Hormones: heart rate is increased by catecholamine- epinephrine
(E) and norepinephrine (NE), thyroid hormone (T3)
-Ions: intra and extracellular ion concentrations (ex. Ca2+ and K+) must be maintained for normal heart function, imbalances are very dangerous to the heart

52
Q

how does age affect HR

A

fetus has the fastest HR; declines with age

53
Q

how does gender affect HR

A

females have a faster HR than males

54
Q

how does exercise affect HR

A

it increases HR, trained athletes can have slow HR

55
Q

how does body temp affect HR

A

HR increases with increased body temperature

56
Q

how does hypocalcemia affect the heart

A

it depresses the heart

57
Q

how does hypercalcemia affect the heart

A

it increases HR and contractility

58
Q

how does hypokalemia affect the heart

A

it results in weak heart beat; arrhythmias, low levels of potassium

59
Q

what is tachycardia

A

abnormally fast HR (>100 beats/min), if persistent may lead to fibrillation

60
Q

what is bradycardia

A

heart rate is slower than 60 beats/min
-may result in grossly inadequate blood circulation in nonathletes
-may be a desirable result of endurance training

61
Q

what is congestive heart failure (CHF)

A

is it a progressive condition: CO is so low that blood circulation is inadequate to meet tissue needs, reflecting weakened myocardium

62
Q

what can weakened myocardium and CHF be caused by

A

-Coronary Atherosclerosis: clogged arteries caused by fat buildup; impairs oxygen delivery to cardiac cells, the heart becomes hypoxic (lacks O2) and contracts ineffectively
-Oersistnet HBP: aortic pressure> 90 mmHg causes myocardium to exert more force, chronic increased ESV causes myocardium hypertrophy and weakness
-Multiple Myocardial Infarctions: heart becomes weak as contractile cells are replaced with scar tissue
-DIlated Cardiomyopathy (DCM): ventricles stretch and become flabby and myocardium deteriorates, drug toxicity of chronic inflammation may play a role

63
Q

what are three common types of congenital heart defects

A

ventricular septal defect, coarctation of the aorta, and tetralogy of Fallot

64
Q

what is a ventricular septal defect

A

the superior part of the interventricular septum fails to form, allowing blood to mix between the two ventricles, more blood is shunted from the left to the right because the left ventricle is stronger

65
Q

what is a coarctation of the aorta

A

a part if the aorta is narrowed, increasing the workload of the left ventricle

66
Q

what is a Tetralogy of Fallot

A

multiple defects (tetra=4)
1. The pulmonary trunk is too narrow and the pulmonary valve stenosed, resulting in
2. hypertrophied right ventricle
3. ventricular septal defect
4. aorta receives blood from both ventricles

BIOL 112 (21 decks)

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