5. Cardiac System 2 Flashcards

1
Q

What is contractility?

A

Inotropic state of heart
Defined as property of the contractile myocytes that account for the strength of contraction
Related to the intrinsic cellular mechanisms that regulate interaction between actin and myosin

Independent of preload and afterload and sarcomere length

Epinephrine increases contractility which increases stroke volume

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2
Q

What are the 7 parameters that can be used to evaluate the cardiac performance of the heart?

A
  1. Ventricular end-diastolic pressure
  2. Cardiac index
  3. Stroke volume
  4. Ejection fraction (EF)
  5. Peak rate of ventricular pressure development (peak +dp/dt) during isovolumic contraction
  6. End-systolic pressure-volume relationship (ESPVR)
  7. Maximum velocity of muscle shortening (Vmax)
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3
Q

How is ventricular end diastolic pressure used to evaluate cardiac performance?

A

Any inadequate systolic emptying will lead to an increase in ESV, increasing EDV (preload)
Increase EDV increases EDP regardless of compliance
Hypertrophic heart will generate higher EDP and dilated heart will generate lower EDP
Failing heart has very high EDP

EDP can be used as an index for ventricular function (performance)

Slides 5-10 Sept 26

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4
Q

How is cardiac index used to evaluate cardiac performance?

A
Cardiac output can be used as a measure of the overall cardiac performance
Cardiac index (CI) is defined as the cardiac output (CO) divided by body surface area (BSA)
CI=CO/BSA

Increase contractility increases SV increases CI

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5
Q

How is stroke volume used to evaluate cardiac performance?

A

Stroke climate indirectly reflects the extent of ventricular fiber shortening
Shorter fiber length, smaller ventricular chamber size, lesser volume of blood remains at end of ventricular systole

SV can be influenced by ventricular loading (preload or afterload) in addition to contractility
SV can be reduced despite cardiac output is normal due to tachyarrythmia

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6
Q

How is ejection fraction (EF) used to evaluate cardiac performance?

A

Defined as the fraction of end-diastolic volume ejected from ventricle during each systolic contraction
EF=SV/EDV
Normally EF is greater than 55% but depends on variation of afterload

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7
Q

How is peak rate of ventricular pressure development during isovolumic contraction used to evaluate cardiac performance?

A

It is the value corresponding to the rate of pressure rises (Δpressure/Δtime) in ventricular chamber during isovolumic contraction

Stronger force of contraction, steeper the slope

Highest +dp/dt usually occurs at the moment just before the opening of the semilunar valves
+dp/dt can be influence by contractility, loading, and heart rate

Slides 14-15 sept 26

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8
Q

Look over the treppe (staircase) phenomenon or Bowditch effect on slide 16 sept 26?

A

Ok

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9
Q

How is end-systolic pressure-volume relationship (ESPVR) used to evaluate cardiac performance?

A

Any increase in inotropy (contractility) will shift the ESPVR upwards to the left with a steeper slope

Slide 17 sept 26

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10
Q

How is maximum velocity of muscle shortening (Vmax) used to evaluate cardiac performance?

A

It is the true indicator of contractility at a given inotropic state
Vmax cannot he measured
Can only be extrapolated

When contractility if the ventricle is increased, it will cause a parallel shift of the force-velocity curve up and to the right (increases both Vmax and maximal tension development)

Slide 18 sept 26

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11
Q

What are the effects of contractility on stroke volume?

A
At a given loading condition (EDV or preload), increases in Vmax means increase in contractility
Which;
Increase ejection velocity
Increase stroke volume
Reduce ESV
Reduce ESP

With increase in stroke volume and a decrease in ESV, ejection fraction is increased

Overall increase in stroke volume (SV)

Slides 19-21 sept 26

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12
Q

What is aortic stenosis?

A

Narrow opening of aortic valve (resistance to flow)
No problem with valvular closure

Increase flow velocity of blood (velocity is proportional to 1/cross sectional area) through the stenotic valve causing turbulence flow and generating systolic murmur (murmur between S1 and S2)

Aortic stenosis causes an increase in LVP (much greater than the aortic pressure) due to increase in afterload (resistance to flow) cause by the stenosis
Increase afterload cause huge increase ESV
Decrease strove volume
Slides 23-27 sept 26

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13
Q

What is mitral stenosis?

A

Increase resistance to flow across the mitral valve during ventricular filling (gives rise to the elevation of left atrial pressure)
Could lead to huge reduction in LVEDV which decreases SV and CO
Also leads to small reduction in aortic pressure (afterload) which leads to small decrease in ESV
Creates a diastolic murmur between S2 and S1 due to higher velocities of blood flow

Slides 28-30 sept 26

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14
Q

What is aortic insufficiency?

A

Effect of valvular insufficiency in cardiac function
Incomplete closure of aortic valve (regurgitation)
Blood movement between aorta and left ventricle at all times
No true ventricular isovolumic relaxation or contraction phase in an aortic regurgitated heart
Increases EDV which increases force of contraction through frank-starling mechanism

Slides 32-34 sept 26

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15
Q

What is mitral insufficiency?

A

With the incomplete closure of the mitral valve, blood flows back to the left atrium during ventricle contraction causing a sharp rise in left atrial pressure during ventricular systole (can open valve fine)
Back flow of blood ti left atrium during ventricular systole creates systolic murmur between S1 and S2

Slides 35-37 sept 26

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16
Q

What is physiological ventricular hypertrophy? (1 of 2 types of ventricular hypertrophy)

A

An adapting change to stress (exercise training) in order to enhance pumping capacity of the heart
Reversible and non pathological

17
Q

What is pathological ventricular hypertrophy? (2 of 2 types of ventricular hypertrophy)

A

Two sub types
a) Afterload related- induces by chronic increase in afterload
Ventricle need to generate a greater pressure chronically to eject blood
Can lead to a DECREASE in SV
b) Preload related- increase in ventricular wall stress in this type of hypertrophy is caused by volume overload
Giving rise to a dilated ventricle
Often associates in systolic dysfunction
Small SV
Slides 4-7 oct 1

18
Q

What are the 2 types of pacemakers?

What about the membrane potential of pacemakers?

A

Sinoatrial node (native pacemaker)- with 70 to 80 bpm

Atrioventricular (latent pacemaker) with 40 to 60 bpm

Pacemaker cells within the heart is responsible for the genesis of automaticity leading to cardiac muscle contraction
Membrane potential of the pacemaker cell does not remain constant at resting state after repolarization
Slides 9-10 oct 1

19
Q

What is autorhythmicity?

A

Refers to the combination of both the automaticity and rhythmicity properties
Automaticity is ability of cell to initiate its own peacemaking activity
Rhythmicity is ability of cell to maintain the regularity of pacemaking activity
Both are intrinsic to cardiac pacemaker

20
Q

What is the ionic basis of automaticity?

A

Membrane slowly depolarizes and drifts toward threshold between action potentials
Pacemaker cells exhibit the slow response in their action potentials
3 phases of the permeability changes for various ions are observed in the AP of the pacemaker cells;
Phase 4
Phase 0
Phase 3
Slide 12 oct 1
Summary slide 17 oct 1

21
Q

What is phase 4 of the permeability changes for various ions?

A

Phase 4- spontaneous gradual depolarization due to ionic influx creating pacemaker current (If), slow leak of Na into pacemaker cells
Rapid decline of K efflux (Ik) die to closing of voltage gated K channels
Followed by Ca influx
Net result: resting membrane potential becomes progressively more positive for pacemaker cells

Slides 12-14 oct 1

22
Q

What is phase 0 of the permeability changes for various ions?

A

Opening of long lasting Ca voltage gated channels after reaching threshold
Depolarization occurs once the threshold potential is reached
No fast Na channel is involved and the slope of upstroke is not as steep as that of the AP for the contractile myocytes

Slide 15 oct 1

23
Q

What is phase 3 of the permeability changes for various ions?

A

Starts with gradual closing of voltage gated Ca channels (Ca influx stops)
Voltage gated K channels are now activated
Repolarization occurs
Once the membrane reaches the maximum diastolic potential (MDP), phase 4 will start again
Slide 16 oct 1

24
Q

What are the 3 variables that can influence cardiac rhythmicity (heart rate)?

A
  1. Rate of diastolic depolarization
  2. Maximum diastolic potential (MDP)
  3. Threshold potential (TP)
25
Q

What is interatrial conduction?

A

Bachmans bundle conducting electrical impulses (generated by SA node) to left atrium

26
Q

How do you go from sinoatrial node to atrionodal conduction?

A

Through intermodal pathways

3 internodal tract: anterior, middle, and posterior

To ensure a secure conduction or impulses from SA node to AV node & subsequent ventricular contraction

Slide 22 oct 1

27
Q

What is the delay of conduction within the AV node?

A

Atrioventricular (AV) node with intrinsic firing rate of 40 to 60 beats per min
Contains 3 regions:
Atrionodal (AN)
Nodal (N)
Nodal-His (NH)
AN and N regions are the principle delay between atrial and ventricular contraction
N region has a slower conduction velocity, but AN has longer length

28
Q

What are the 3 main sections from AV node to the ventricular contractile myocytes?

A
  1. Atrioventricular (AV) bundle- bundle of His, below AV node
    Passes through the fibrous ring that separates the atria and ventricles
  2. Bundle branches- continuation of AV bundle which then divided into the right and left bundle branch (right bundle branch into right ventricle and left bundle branch into left ventricle) (right is longer and thinner than left)
  3. Purkinje fibers- inferior terminal branches of the bundle branches
    Resemblance of cardiac myocytes but with fewer myofibrils
    Fastest rate of conduction at any tissues within the heart
    Slide 27 oct 1
29
Q

What are the 3 possible accessory reacts (abnormal usually not found in individual) for abnormal conducting system of the heart?

A
  1. James Fibers- from atrial internodal tracts that last around AV node and enter inter-ventricular septum
    Induces ventricular pre-excitation
  2. Mahaim fibers- any direct connections between AV node, bundle of His, or bundle branches into the interventricular septum
    Also can give rise to ventricular pre-excitation
  3. Bundle of Kent (atrioventricular pathway)- muscle bundle forming direct connection between atrial and ventricular myocardium
    Can give rise to supraventricular paroxysmal tachycardias and atrial fibrillation