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ICU > Cardiac Physiology > Flashcards

Cardiac Physiology Flashcards

1
Q

Define Cardiac output and its determinants

A

Volume of blood ejected by the heart per unit of time. Usually expressed as HR x SV with units L/min

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2
Q

What is Fick’s Principle?

A

VO2 = (CO x Pa-oxygen content of art) - (CO x Pv-oxygen content of vein)

CO = VO2/Pa-Pv

can be used to calculated CO as VO2 = 3.5mLO2/kg/min

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3
Q

SV is a function of what factors?

A

Preload, Afterload and contractility

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4
Q

Define Preload, how is it approximated?

A

Myocardial sarcomere length just prior to contraction

Approximated by EDV (or worse by EDP)

because we are interested in the length using a surrogate with dimensions (volume) is better than the force (pressure) which creates that length

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5
Q

How can preload clinically be estimated?

A

EDV measured by echo

EDP (worse estimate) by CVC for RVEDP and PAC for LVEDP

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6
Q

What are the two main determinants of preload?

A

When preload is defined in terms of volume (EDV):

  1. Pressure filling the ventricle
  2. Compliance of the vetricle
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7
Q

What factors effect the pressure filling the ventricle?

A

CO (forward pressure)

Mean Systemic Filling Pressure (MSFP) -which has its own determinants: total venous blood volume and venous vascular compliance

Intrathoracic pressure (effect on venous return)

Atrial pressure/Atrial kick (Atrial contractility and rhythm, valve competence, ventricular ESV, ventricular compliance)

right atrial pressure (less accurately CVP)

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8
Q

What factors effect the compliance of the ventricle?

A

a. Pericardial compliance (walls and contents)

b. Ventricular wall compliance (duration of diastole, wall thickness, lusitropic properties, ESV (Afterload)

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9
Q

describe the effect of IPPV on the RV and pulmonary circulation

A

IPPV increases intrathoracic pressure (ITP)

Raised ITP is transmitted to central veins and the RA and decreases RV preload

Raised ITP is transmitted to the pulmnary arteries and increases pulmonary vascular resistance which leads to increased RV afterload

net effect is deccreased preload and increased afterload decreasing RV SV

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10
Q

describe the effect of IPPV on the LV and systemic circulation

A

IPPV increases intrathoracic pressure (ITP)

Raised ITP decreased preload by decreasing pulmonary venous pressure

Raised ITP decreases afterload by decreasing LV transmural pressure

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11
Q

What net effect does IPPV have on CO and myocardical O2 demand

A

Decreases both

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12
Q

How does IPPV decrease afterload

A

Afterload = wall stress

Laplaces law: wall stress = (LV transmural pressure x r)/LV wall thickness

in spontaneous breathing (NPV) LV transmural pressure is LVP - ITP so 90mmHg - -10mmHg = 100mmHg

in IPPV with PEEP of 10 LV transmural pressure is 90mmHg - 10mmHg = 80mmHg

using laplaces law there is decreased wall stress

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13
Q

What is normal coronary blood flow? How does this change with exercise? How does myocardial oxygen extraction change with increased myocardial work?

A
  • Normal is ~250ml.min-1 (~5% of resting CO)
  • May increase 4x during strenuous exercise
  • Myocardial work may increase up to 9x, though as myocardial oxygen extraction is unchanged efficiency is actually improved during exercise.
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14
Q

What are the determinants of coronary blood flow?

A

CBF = (PAorta−PCavity(or RAP)) / CVR

CBF= coronary blood flow

CVR= Coronary vascular resistance

Coronary perfusion pressure: The difference between aortic root pressure and the greater of RAP or intracavity pressure
-Note that the pressure gradient is usually Aorta-Cavity rather than Aorta-RA
This is because the pressure in the ventricle acts as a Starling resistor - coronary flow is independent of RAP whilst RAP

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15
Q

What are the two broad categories of control of coronary blood flow?

A
  • Autoregulation

- Autonomic control

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16
Q

Describe how CBF is autoregulated

A
  1. Myogenic autoregulation
    Increasing transmural pressure increases the leakiness of smooth muscle membranes, depolarising them
    Resistance increases proportionally to pressure, such that flow remains constant
  2. Metabolic autoregulation
    Anaerobic metabolism results in production of vasoactive mediates such as lactate and adenosine, which stimulate vasodilation and therefore increase flow (and oxygen delivery).
    This is the predominant means for autoregulation in the heart
    Typical myocardial oxygen extraction is 70% and raising this further is difficult
    Therefore, increasing oxygen supply requires an increase in blood flow.
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17
Q

Describe the autonomic regulation of coronary blood flow

A

Direct effects include:
Parasympathetic and sympathetic innervation of coronary vessels, with release of ACh or NA and A decreasing or increasing coronary blood flow

Indirect effects
Are more important than direct effects
Are related to autoregulation occurring with changing levels of myocardial work in response to parasympathetic or sympathetic stimuli

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18
Q

What are the two phases and six stages of the cardiac cycle?

A
  1. Diastole
    -Isovolumetric Ventricular Relaxation
    -Rapid Ventricular Filling
    -Slow Ventricular Filling
    (The cycle begins here).
    -Atrial Contraction
  2. Systole
    - Isovolumetric Ventricular Contraction
    - Ejection
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19
Q

draw a wiggers diagram

A

https://partone.litfl.com/cardiac_cycle.html

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20
Q

describe the slow ventricular filling stage of the cardiac cycle

A
  • MV+TV open, AV+PS closed
  • The ventricle is relaxed completely and fills slowly
  • The ventricles have been mostly filled during rapid ventricular filling and so the pressure gradient is reducing.
  • The pressure in each ventricle is almost zero
  • Arterial pressure is falling, as it is end-diastole
  • CVP is slowly rising as the ventricle and atria fill
  • This period occurs after the y descent.
  • The ECG will show the beginnings of a P-wave at the end of this phase
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21
Q

How much ventricular filling is contributed by atrial contraction?

A

10% of the ventricular filling at rest, but up to 40% in tachycardia

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22
Q

describe the atrial contraction stage of the cardiac cycle

A
  • Arterial pressure is still falling
  • The CVP waveform demonstrates the a wave as atrial -contraction also causes blood to reflux into the SVC
  • The ECG will show the PR interval
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23
Q

describe the isovolumetric ventricular contraction stage of the cardiac cycle

A
  • Ventricular pressure rises, and the AV valves close. This gives rise to the first heart sound, S1.
  • As ventricular pressure is still less than systemic vascular pressure, the semilunar valves remain closed
  • Arterial pressure is still falling
  • The CVP waveform shows the C (closure) wave, as the tricuspid valve herniates back into the RA during ventricular contraction. There is a similar spike in LA pressure as the mitral valve also bulges back into the LA.
  • The ECG will show the remainder of the QRS or the start of the QT interval
  • Atrial repolarisation occurs at this stage, but is typically masked by ventricular depolarisation
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24
Q

describe the ejection stage of the cardiac cycle

A

When ventricular pressure exceeds arterial pressure, the semilunar valves open and ejection occurs. Initial ejection is rapid, but as ventricular pressure falls and systemic pressure rises the gradient falls ejection becomes slower.

During ejection:

  • Arterial pressure rises rapidly, and is slightly less than ventricular pressure during this stage
  • The CVP waveform shows the x descent, as the shortening RV pulls the RA down, rapidly lowering CVP
  • The ST segment shows on the ECG as the ventricles are fully depolarised, though the T wave may appear in late ejection
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25
Q

describe the isovolumetric relaxation stage of the cardiac cycle

A
  • The semilunar valves close
  • This gives rise to the second heart sound, S2, and marks the beginning of isovolumetric relaxation. This occurs when ventricular pressure falls below vascular pressure
  • Arterial pressure begins to fall, interrupted by the dicrotic notch which is a brief increase in arterial pressure as the semilunar valves close
  • The v wave is visible on the CVP waveform. Due to atria filling against closed AV valves.
  • The end of the T wave is visible on the ECG as ventricular repolarisation occurs
26
Q

Describe the rapid ventricular filling stage of the cardiac cycle

A
  • The AV valves open and ventricular filling occurs. This occurs when atrial pressure exceeds ventricular pressure.
  • Arterial pressure is falling
  • The y descent occurs when the AV valves open, causing a rapid drop in CVP as the ventricles fill
  • No electrical activity is produced - the ECG shows the TP interval
27
Q

How does hand grip effect heart murmurs?

A

Increased afterload

  • increase intensity of MR, AR, and VSD murmurs
  • decrease hypertrophic cardiomyopathy and AS murmurs
  • MVP: later onset of click/murmur
28
Q

How does valsalva effect heart murmurs?

A

Decrease preload

  • decrease intensity of most murmurs (including AS)
  • increase intensity of hypertrophic cardiomyopathy murmur
  • MVP: earlier onset of click/murmur
29
Q

How does rapid squatting effect heart murmurs?

A

increase venous return, increase preload, increase afterload

  • decrease intensity of hypertrophic cardiomyopathy murmur
  • increase intensity of AS, MR, and VSD murmurs
  • MVP: later onset of click/murmur
30
Q

Describe the phases of the myocardial action potential

A

Phase 0 = rapid upstroke and depolarization—voltage-gated Na+ channels open.
Phase 1 = initial repolarization—inactivation of voltage-gated Na+ channels. Voltage-gated K+
channels begin to open.
Phase 2 = plateau—Ca2+ influx through voltage-gated Ca2+ channels balances K+ efflux. Ca2+
influx triggers Ca2+ release from sarcoplasmic reticulum and myocyte contraction.
Phase 3 = rapid repolarization—massive K+ efflux due to opening of voltage-gated slow K+
channels and closure of voltage-gated Ca2+ channels.
Phase 4 = resting potential—high K+ permeability through K+ channels.

31
Q

contrast cardiac muscle to skeletal muscle

A
  • Cardiac muscle action potential has a plateau, which is due to Ca2+ influx and K+ efflux.
  • Cardiac muscle contraction requires Ca2+ influx from ECF to induce Ca2+ release from
    sarcoplasmic reticulum (Ca2+-induced Ca2+ release).
  • Cardiac myocytes are electrically coupled to each other by gap junctions.
32
Q

Describe the phases of the pacemaker action potential

A

Phase 0 = upstroke—opening of voltage-gated Ca2+ channels. Fast voltage-gated Na+ channels are
permanently inactivated because of the less negative resting potential of these cells. Results in a slow
conduction velocity that is used by the AV node to prolong transmission from the atria to ventricles.
Phases 1 and 2 are absent.
Phase 3 = inactivation of the Ca2+ channels and 􀁱 activation of K+ channels 􀁰 􀁱 K+ efflux.
Phase 4 = slow spontaneous diastolic depolarization due to If (“funny current”). If channels
responsible for a slow, mixed Na+/K+ inward current; different from INa in phase 0 of ventricular
action potential.

33
Q

Which phase of the pacemaker action potential accounts for the automaticity of the SA/AV nodes? Which factors effect the slope of this phase?

A

The slope of phase 4 in the SA
node determines HR. ACh/adenosine decreases the rate of diastolic depolarization and decreases HR, while catecholamines increase depolarization and increase HR. Sympathetic stimulation increases the chance that If channels are open and thus increases HR.

34
Q

How do BNP/ANP work?

A

Acts via cGMP. Causes vasodilation and decreased Na+ reabsorption at the renal collecting tubule. Dilates afferent renal arterioles and constricts efferent arterioles, promoting diuresis and contributing to “aldosterone escape” mechanism.

BNP has longer halflife

35
Q

Where are the major chemo and baro receptors located? What are the afferent nerves for these receptors? Where do the afferent nerves travel to?

A

Baro - Carotid sinus (Glossopharyngeal) + Aortic arch (Vagus)

Chemo - Carotid body (glossopharyngeal) + Aortic arch (Vagus)

carry to nucleus solitarius in medulla

36
Q

What stimulates peripheral and central chemoreceptors?

A

Peripheral—carotid and aortic bodies are stimulated by decreased Po2 (< 60 mm Hg), increased Pco2, and decreased pH of blood.

Central—are stimulated by changes in pH and Pco2 of brain interstitial fluid, which in turn are influenced by arterial CO2. Do not directly respond to Po2!!!

37
Q

What are the pressures throughout the circulatory system

A 
RAP <5
RVP 25/5
PAP 25/10
PCWP 4-12
LA <12
LV 130/10
Ao 130/90
38
Q

What molecules are used throughout the body for vascular autoregulation?

A 
CHALK
CO2
H+
Adenosine
Lactate
K+
39
Q

How does the autonomic nervous system act on the AV node to change condution speed?

A

prolonged by vagal stimulation, which increases potassium permeability and hyperpolarises the cell

Conversely, sympathetic stimulation increases calcium permeability and allows more rapid transmission

40
Q

What is the intrinsic rate of the SA node?

A

There is continual PNS input (“Vagal tone”) via inhibitory ACh GPCR, reducing the SA node from its intrinsic rate of 90-120bpm to a more sedate 60-100bpm.

41
Q

which vagus nerve innervates the SA/AV nodes

A

SA - right

AV - left

42
Q

state the Frank starling law of the heart

A

The strength of contraction is dependent on the initial fibre length

43
Q

Why does additional muscle stretch increase contraction?

A
  • more myofilament crossbridges can interact

- increased myofilament Ca sensitivity

44
Q

Express the frank starling law graphically. demonstrate what increased/decreased inotropy or a failing ventricle would look like

A

ventricular function curve (preload vs SV or CO if HR constant)

45
Q

Define Afterload

A

Afterload is the ventricular wall stress at the onset of systole.

46
Q

What are the determinants of afterload?

A

This is given by the Law of Laplace, θ∝(P×r)/T , where:

θ is ventricular wall stress
r is ventricular chamber radius (EDV)
This is a proxy for ventricular size, or end-diastolic volume.
P is ventricular transmural pressure
T is ventricular wall thickness (increases in response to high afterload to mitigate afterload - HCM)

47
Q

how is transmural pressure calculated?

A

Transmural pressure is the difference between intrathoracic pressure and the ventricular cavity pressure during ejection.

TMP = Vent P - ITP

48
Q

How does positive/negative pressure ventilation affect afterload? Explain how this is implicated in APO

A

Negative intrathoracic pressure will increase afterload, as the ventricle has to generate a greater change in pressure to achieve ejection.

PEEP reduces LV afterload

Negative-pressure ventilation with a high work of breathing increases afterload

This is why APO deteriorates - increased work of breathing increases LV afterload and worsens LV failure, increased pulmonary oedema, causing increased work of breathing…

49
Q

What are the determinants of ventricular cavity pressure during ejection?

A

To facilitate ejection, the ventricle must overcome:
1. Outflow tract impedance - Valvular disease, HOCM

  1. Systemic arterial impedance: Determined by resistance (SVR), inertia, and compliance
50
Q

What are the components of systemic arterial impedance?

A

Determinants of resistance are stated in the Poiseuille Equation:

R=(8.η.l)/ (π.r^4) , where:

η = Viscosity
Affected by haematocrit (e.g. increased in polycythaemia)

l = Vessel length
Essentially fixed.

r = Vessel radius
(Greatest determinant) Function of degree of vasoconstriction of resistance vessels

51
Q

Describe how inertia affects afterload.

A

Inertia is given by the mass of blood in the column. increases afterload in early systole and decreases it in late systole.

Affected by heart rate

52
Q

Describe how changing arterial compliance affects the reflected pressure waves

A

Decreased arterial compliance increases the speed of propagation of reflected pressures waves returning to the aortic root

Wave arrival in diastole augments coronary blood flow

Wave arrival during systole further increases afterload

53
Q

Describe the Windkessel effect

A

in diastole the arteries recoil and blood pressure and flow are maintained

54
Q

How is contractility defined? how is it measured?

A

Contractility is the change in peak isometric force (isovolumic pressure) at a given initial fibre length (end diastolic volume).

Measures of contractility include:

ESPVR, which describes the maximal pressure that can be developed by the ventricle at any given LV volume. The ESPVR slope increases with increased contractility.

dP/dT (or ΔP/ΔT), change in pressure per unit time. Specifically, in this setting, it is the maximum rate of change in left ventricular pressure during the period of isovolumetric contraction. This parameter is dependent on preload, but is minimally affected by normal afterload.

55
Q

What are the determinants of contractility?

A

-Preload:
Increasing preload increases the force of contraction
The rate of increase in force of contraction per any given change in preload increases with higher contractility
This is expressed as a change in the slope of the end-systolic pressure-volume relationship (ESPVR)

-Afterload (the Anrep effect):
The increased afterload causes an increased end-systolic volume
This increases the sarcomere stretch
That leads to an increase in the force of contraction

-Heart rate (the Bowditch effect):
With higher hear rates, the myocardium does not have time to expel intracellular calcium, so it accumulates, increasing the force of contraction.

Contractility is also dependent on:

  • myocyte intracellular calcium concentration
  • Catecholamines: increase the intracellular calcium concentration by a cAMP-mediated mechanism, acting on slow voltage-gated calcium channels
  • ATP availability (eg. ischaemia): as calcium sequestration in the sarcolemma is an ATP-dependent process
  • Extracellular calcium- availability of which is necessary for contraction

Temperature: hypothermia decreases contractility, which is linked to the temperature dependence of myosin ATPase and the decreased affinity of catecholamine receptors for their ligands.

56
Q

Define venous return, what are its components?

A

Venous return is the rate at which blood is returned to the heart (in L.min-1). At steady state, venous return is equal to cardiac output, and can be expressed as:
VR= (MSFP−RAP) / RVR , where:

VR is venous return
MSFP is the mean systemic filling pressure
This is the mean pressure of the circulation when there is no flow. It is an indicator of circulatory filling, and is a function of circulating volume and vascular compliance.
Normal mean systemic filling pressure is ~7mmHg
RAP is the right atrial pressure
An elevated RAP reduces venous return.
RVR is the resistance to venous return

57
Q

Express venous return graphically and demonstrate the effects of change in volume, compliance, RVR

A

https://partone.litfl.com/venous-return.html

58
Q

Which factors influence venous return?

A

Factors which affect cardiac output

  • Afterload
  • Contractility

Factors which affect mean systemic filling pressure

  • Total venous blood volume
  • Venous smooth muscle tone/compliance (which affects the size of the “stressed volume”

Factors which affect right atrial pressure

  • Intrathoracic pressure (spontaneous vs. positive pressure ventilation)
  • Pericardial compliance (eg. tamponade, open chest)
  • Right atrial compliance (eg. infarct, dilatation)
  • Right atrial contractility (i.e. AF vs sinus rhythm)
  • Tricuspid valvular competence and resistance

Factors which affect venous resistance
-Mechanical factors
Posture
Intraabdominal pressure
Skeletal muscle pump
Obstruction to venous flow (eg. pregnancy, SVC obstruction)
Hyperviscosity (polycythemia, hyperproteinaemia)
-Neuroendocrine factors
Autonomic tone
Vasoactive drugs (eg. noradrenaline, GTN)

59
Q

What is an action potential?

A

an action potential is a propagating change in the membrane potential of an excitable cell, used in cellular communication and to initiate intracellular processes. It is caused by altering the permeability of a membrane to different ions.

60
Q

how do sympathetic and parasympathetic stimulation affect the AV node ion permeability

A

refractory period is prolonged by vagal stimulation, which increases potassium permeability and hyperpolarises the cell

Conversely, sympathetic stimulation increases calcium permeability and allows more rapid transmission

61
Q

What is Guyton’s curve?

A

superimposed starling and venous return curves demonstrating the operating point of circulation

ICU (4 decks)

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