Cardiac Integration Flashcards

1
Q

Cardiac output and oxygen consumption

A
  • cardiac output increases when O2 consumption increases
  • during exercise cardiac output increases in proportion to the amount of work performed, and also in proportion to the increased consumption of oxygen by the muscles
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2
Q

Factors that increases CO

A

-exercise
-fever
-anxiety
-body weight
-pregnancy
-hyperthyroidism
-compensatory increases;
_chronic anemia
_histotoxic hypoxia
_pulmonary disease with hypoxemia
_mild inspiratory hypoxia

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3
Q

decrease Co

A

-sleep?
-aging
-severe anoxia
-acute hemorrhage
-heart disease:
_acute myocardial infarction
_rheumatic fever
_congestive heart failure

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4
Q

Extracellular Recording of Depolarization and repolarization waves

A
  • first you see the dopolarization wave go as the inside starts changing from negative to positive
  • then all of the inside is positive
  • then the repolarization wave is negative
  • it is about 0.30 seconds apart
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5
Q

Normal electrocardiogram

A
  • P wave- atrial depolarization
  • QRS complex is ventricular depolarization
  • T wave is ventricular repolarization, it is an inverted T wave because of the way the ECG test is made and read on outside of skin
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6
Q

Propagation during PR interval

A
  • depolarization starts with SA node
  • you start seeing P wave when atria depolarizes and then the AV node depolarizes
  • the His bundle, Bundles branches and Purkinje network come next but do not generate voltages big enough to be seen on ECG
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7
Q

ECG and ventricular AP

A
  • the QRS is produces by upstrokes (phase 0) of all the ventricular APs
  • the plateaus phase (phase 2) corresponds to ST segment of ECG
  • T wave is produces by ventricular repolarization (phase 3)
  • the TP segment corresponds to ventricular diastole, at the end of which atrial depolarization produces the P wave of eCG
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8
Q

Ventricular volume during cardiac cycle

A
  • during ejection the volume in the left ventricle falls from 120 mL to 50 mL, SV is 70 and an ejection fraction of 70/120 = 58%
  • most ventricular filling occurs during early diastole as soon as the mitral and tricuspid valves are open
  • atrial contraction (atrial systole) occurs at the end of diastole and produces only a small rise in pressure for both the right and left hearts, and is responsible for only a small increase in ventricular volume
  • atrial diastole occurs during ventricle systole
  • during atrial diastole, atrial pressure rises
  • atrial pressure falls when the mitral valve opens
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9
Q

Dynamic pressure changes

A
  • diastole begins at the dichrootic notch when the aortic valve closes. Shortly after the beginning of diastole after the mitral valve opens, the left ventricular pressure is falling when ventricular volume is increasing
  • the forward momentum of blood entering the ventricles distends the ventricles expanding them and dropping the pressure even though ventricular volume is increasing
  • during systole ventricular pressure is greater than aortic pressure during the rapid ejection phase. However during the slow ejection phase, the pressure falls so rapidly in the left ventricle that the left ventricular pressure actually falls before the aortic pressure
  • blood continues to flow forward from the ventricle to the aorta due to its forward momentum but the flow is decelerated by the reversed pressure gradient
  • so the ventricular contraction gives the blood a push, and it continues to flow forward even when the pressure gradient is reversed
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10
Q

Filling Phase

A
  • ventricles at relatively low pressure
  • AV valves are open: tricuspid (RV), mitral (LV)
  • ventricles fill with blood (50-> 120 mL)
  • P wave of ECG precedes atrial contraction
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11
Q

Jugular Pulse

A
  • follows right atrial pressure
  • A wave: atrial contraction
  • C wave: closure of tricuspid valve
  • V wave: atrial filling and emptying
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12
Q

Heart sounds

A
  • four sounds are produced, but only two normally heard with stethoscope
  • sounds are caused by vibrations of blood flow and closure of valves
  • first heart sound at closure of AV valves
  • second heart sound at closure of aortic and pulmonic valves (semilunar valves)
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13
Q

Isovolumetric Contraction Phase

A
  • QRS complex occurs (ventricular depolarization), ventriclar muscles contract, no immediate volume change so
  • ventricular pressure rapidly increases- AV valves rapidly close (S1- lub)
  • pulmonary and aortic valves then open (destination pressures initially higher
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14
Q

Ejection phase

A
  • once the ventricular pressure exceeds that of the destination vasculature (aorta and pulmonary artery)
  • blood is ejected from the ventricles. The volume of blood that is ejected is called the stroke volume, about 60%
  • dominant event of systole
  • T wave of ECG occurs during end half of outflow phase
  • at the end of outflow phase ventricular pressure decreases leading to isovolumetric relaxation
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15
Q

Isovolumetric Relaxation

A
  • pressure drops rapidly in both ventricles
  • pulmonic and aortic valves close (beginning of diastole) (S2 sound, dub)
  • when ventricular pressure drops below that of the atria: mitral and tricuspid valves open; a new inflow phase (cardiac cycle) begins
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16
Q

Pressure volume loop of left ventricle

A
  • Mitral valve opens at end-systolic volume, and then there is an increase of volume to 120 when you get to end-diastolic volume and the mitral valve closes (filling)- then you get an increase in pressure by isovolumetric contraction
  • then the aortic valve opens and the volume of blood is released and pumped out and then the aortic valve closes when it gets back to 50 mL
  • then there is isovolumetric relaxation
  • the most work of the heart is done in systole
17
Q

Echocardiography

A
  • using ultrasound to image and monitor the heart in real time either 2D or 3D
  • non-invasive (transthoracic) or invasive (transesophageal) assesment of:
  • degree of muscle contraction (ejection)
  • valve function and defects (thombus, stenosis)
  • blood velocity
  • hypertrophy
  • tumors
  • septal defects etc
18
Q

How to increase stroke volume

A
  • both increases contractility (decreased end systolic volume) and increased pre load (increased end diastolic volume) produce an increase in stroke volume
  • stroke volume is EDV- DSV
  • increased contractility- to treat CHF or infarction with positive inotropic drugs
  • increased preload can be an adaptive response to aortic stenosis, ventricular hypertrophy associated with anemias (sickle, B-thalassaemia) and hyperthyroidism
19
Q

Decrease stroke volume

A
  • heart needs to generate more pressure than normal to eject blood
  • increased aortic pressure leads to a decrease in SV (ESV) is increased
  • decreased SV can arise from aortic valve defects and hypertension
20
Q

Mechanisms Regulating SV

A
  • Atrial filling pressure: increase -> impede venous return -> decrease EDV (decrease SV)
  • ventricular filling time: increase -> increase EDV (increase SV)
  • ventricular compliance: increase -> increase EDV (increase SV)
  • HR: increase -> decrease diastole time ->decrease EDV (decrease EDV)
  • EDV (preload): increase -> increase SV (Starling)
  • Afterload: increase-> impedes ejection -> increase ESV, decrease SV