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Bloc C - Circulation > Physiology > Flashcards

Physiology Flashcards

1
Q

When is the LV at its fullest?

A

At the end of diastole

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2
Q

When is the LV at its emptiest?

A

At the aortic valve closure

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3
Q

During the ventricular diastole, the proper filling of the ventricles depends on 3 conditions:

A
  1. The filling pressure of blood returning to the heart and atria (to push blood into the heart)
  2. The ability of the Atrio-ventricular valves to open fully (i.e. no stenosis)
  3. The ability of the ventricular wall to expand passively with little resistance (compliance)
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4
Q

What is stroke volume?

A

The amount of blood ejected with each beat =

End diastolic volume – End systolic volume

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5
Q

What is the ejection fraction?

A

Stroke Volume / End-diastolic volume

Normal range = 55-70%

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6
Q

What is pulse pressure?

A

Systolic BP – Diastolic BP

Ex. 120/80mmHg; Pulse pressure = 120-80 = 40mmHg

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7
Q

What is Mean arterial pressure (MAP)?

A

Diastolic BP + 1/3 Pulse pressure

Ex. B/P = 125/80mmHg;

Pulse pressure = 45mmHg;

MAP = 80mmHg + 45/3 = 95mmHg

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8
Q

What is the Windkessel effect?

A

The aorta distends during systole as more blood enters the aorta than leaves it. During diastole, the arterial pressure is maintained by the elastic recoil of walls of the aorta and other large arteries. The aorta kid of acts life a pump.

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9
Q

What are the 3 compartments of the total body water?

A
  1. INTRACELLULAR COMPARTMENT (2/3 of TBW) = 30 Liters
  2. EXTRACELLULAR FLUID (1/3 of TBW) = 15 Liters
    A) INTERSTITIAL COMPARTMENT (12 L)
    B) CIRCULATING PLASMA COMPARTMENT (3L)
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10
Q

What are the 2 types of circulation in the body and their advantages?

A
  1. Pulmonary and systemic circulation in series (all the blood that passes in one passes in another)
  2. Organs and in parallel

Advantages

  • Systemic organs receive arterial blood of identical composition
  • Flow through any of the systemic organs can be controlled independently
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11
Q

Equation of Flow (Q)?

A

FLOW (Q) = Pressure difference (Δ P)

Resistance (R)

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12
Q

Poisseuille’s Equation ?

A

Factors determine the resistance: R4 = Inside radius of tube / L = Tube length / η = Fluid viscosity.

Since the ΔP is nearly identical across all systemic organs, cardiac output is distributed among the various organs primarily on the basis of individual resistances to flow.

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13
Q

Describe how are the valves when during systole and diastole

A

Systole

  • When the ventricular pressure exceeds the pressure in the pulmonary artery (right pump) or aorta (left pump), blood is forced out of the chamber through the outlet valve
  • The inlet (AV valve) is closed

Diastole

  • When the ventricular muscles cells relax, the pressure in the ventricle falls below than in the atrium, the AV valve opens, and the ventricle fills
  • The outlet valve is closed
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14
Q

What is cardiac output and how do you calculate it?

A

Cardiac output: The amount of blood pumped out by the heart per minute

  • HR = Heart rate = number of heartbeats per minute
  • SV = Stroke volume = Volume of blood ejected per heart beat = EDV – ESV (end of diastolic – systolic)

CO = HR x SV

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15
Q

Describe the electrical conduction system of the heart

A
  • Sinoatrial (SA) node: The heart’s pacemaker; Initiates the action potential that is conducted through the heart; Controls heart rate
  • Atrioventricular (AV) node: Contains s l o w l y conducting cells that function to create a slight delay between atrial and ventricular contraction
  • Purkinje fibers: specialized for rapid conduction to ensure that all ventricular cells contract at the same instant

+ Participation of the autonomic nervous system via ß2 (SE) and vagus nerve (PSE)

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16
Q

What are the 5 requirements for effective ventricular pumping action of the heart

A
  1. Contraction of individual cardiac muscle cells must occur at regular intervals and be synchronized (not arrhythmic)
  2. The valves must open fully (not stenotic)
  3. The valves must not leak (not insufficient or regurgitant)
  4. The muscle contractions must be forceful (not failing)
  5. The ventricles must fill adequately during diastole
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17
Q

What do all vessels have in common?

A

Vessels have different characteristics but all types are lined by endothelial cells.

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18
Q

As the heart, blood vessels are regulated by the sympathetic nervous system, EXECT 2 types. Which one?

A
  1. arteries
  2. capillaries
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19
Q

Describe blood

A

Complex fluid that serves as medium for transporting substances between the tissues of the body

  • Blood cells (40% Red blood cells, white cells, platelets, all formed in bone marrow)
  • Plasma (60%, liquid component of blood, electrolytes, proteins, serum, transport)
  • Hematocrit = Cell volume / Total blood volume
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20
Q

Name 1 to 6 in this Wiggers Diagram

A
  1. Isovolumic contraction
  2. Isovolumic relaxation
  3. A-V valve opens
  4. A-V valve closes
  5. Aortic valve closes
  6. Aortic valve opens
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21
Q

In a Wiggers Diagram, what are the 2 phases were the volume does not change?

A
  1. Isovolumetric contraction phase = Period between mitral valve closure and aortic valve opening
  2. Isovolumetric relaxation phase is the interval between aortic valve closure and mitral valve opening
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22
Q

What is the difference between the righ and the left ventricle in termes of pressure, volume and resistance?

A
  • Same stroke Volume
  • Synchronized
  • All less pressure but same shape of curve in Wiggers
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23
Q

States the origin of the heart sounds

A
  1. S1 = Closure of the atrioventricular valves (mitral and tricuspid)
  2. S2 = Closure of the semilunar valves (aortic and pulmonic)
  3. S3 = Extra sound heard in early diastole when there is exaggerated early diastolic filling (can sometimes be normal)
  4. S4 = Extra sound heard when there is atrial contraction into a stiff, non-compliant ventricle (usually abnormal)
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24
Q

Bruh, what is the pressure-volume loop?

A

The pressure-volume loop is a graphical representation of the changes in intraventricular pressure which occur during the cardiac cycle as the ventricle fills and empties

  • On the x axis is the intraventricular volume
  • On the y axis is the intraventricular pressure
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25
Q

What are the 2 curves of the pressure-volume loop?

A
  1. EDPVR = End- diastolic pressure volume relation
    Indicates the pressure volume relationship during cardiac filling
  2. ESPVR = End-systolic pressure-volume relation
    Indicates the pressure-volume relationship at END SYSTOLE (at aortic valve closure)
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26
Q

What is Startling’s law?

A

When you ↑ demand of the heart, the heart will follow the demande and the end systemic volume will be the same. In other words, it will work harder to acheive the demand. With all other factors equal, stroke volume increases as cardiac filling increases, until a plateau effect or heart failure.

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27
Q

What are the determinants of stroke volume?

A
  1. Ventricular Preload
    Amount of blood in the heart at the end of the filling period (i.e. end diastolic volume)
  2. Ventricular Afterload
    The pressure against which the heart contracts during ejection (proportional to mean arterial pressure)
  3. Ventricular Contractility
    Inherent strength of the heart’s contraction during systole
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28
Q

What happends when there is an increase in the preload in the pressure-volume loop?

A
  • An increased end-diastolic volume
  • An unchanged end-systolic volume
  • An increased stroke volume

On the contrary, a decrease in the preload results in:

  • A decrease in the end-diastolic volume
  • An unchanged end-systolic volume
  • A reduced stroke volume
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29
Q

What happens to the pressure-volume loop when you increase afterload?

A
  • An unchanged end-diastolic volume
  • An increased end-systolic volume
  • A decreased stroke volume

On the contrary, a decrease in the afterload results in:

  • An unchanged end-diastolic volume
  • A decreased end-systolic volume
  • An increased stroke volume
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30
Q

What happens in the pressure-volume loop when you increase ventricular contracibility?

A
  • An unchanged end-diastolic volume
  • A reduced end-systolic volume
  • An increased stroke volume

On the contrary, a decrease in the contractility results in:

  • An unchanged end-diastolic volume
  • An increased end-systolic volume
  • A decreased stroke volume
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31
Q

What are the determinants of cardiac output?

A

A positive chronotropic effect is one in which the HEART RATE is INCREASED (and inversely)

A positive inotropic effect is one in which the CONTRACTILITY is INCREASED (and inversely)

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32
Q

How do you measure caradiac output?

A

1. Fick’s principle

CO = VO2

Ca – Cv

CO = Cardiac output

VO2 = Oxygen consumption

Ca – Cv = Arterial oxygen concentration – Venous oxygen concentration

2. Thermodilution Method

Saline of a known temperature is injected rapidly through a catheter side port into the right side of the heart, at a specific distance from the distal tip of the catheter. The cardiac output is proportional to the rate of the temperature change and is automatically calculated by the equipment

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33
Q

What are the 4 pressures we need to know?

A

Minimum: diastolic pressure

Maximum: systolic pressure

Pulse pressure = systolic-diastolic (height of the pulse)

Mean arterial pressure MAP = diastolic + 1/3 pulse = should be around 100 mmHg

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34
Q

True or false, all the reflexes happening in our body (concerning BP regulation) have the same range of BP gains.

A

False : every reflex has a different speed of operation and strength of reflex. They operate over different ranges of BP (ex, tel reflexe va s’en meler quand on atteint tel threshold de BP) and different gains.

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35
Q

Where are baroreceptors located?

A

In the carotid sinus. Every heartbeat causes stretching in the walls of that sinus.

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36
Q

Explain the afferent/efferent things happening concerning the baroreceptors.

A

Afferent:if BP increases, baroreceptors will feel it and sense it to the brain, which is going to process it.

Efferent: it is the motor part of the reflex. They will send an order to the organ to react to that input.

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37
Q

What does the body want to do when BP decreases?

A
  1. Increase HR
  2. Increase ventricular contractility
  3. Increase vasoconstriction (increase sympathetic output to almost all vessels in the body. Squeezing down veins = greater pressure in veins).
  4. Increasing arteriolar constriction (since it’s a resistance vessel. Increasing TPR means that BP will go up).
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38
Q

What does chronotropic effect mean?

A

Anything that increases the heart rate

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39
Q

What is the buffer reflex (baroreceptors)?

A

Reflex preventing us from labile hypertension. However, the MAP is unchanged in this situation - which means that something else is controlling the MAP .

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40
Q

What can carotid body tumor cause?

A

Loss of Butter reflex.

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41
Q

What will the kidney release to, in the end, increase BP?

A

Renin

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42
Q

What does renin do to the body (steps until the release of anti-diuretic hormone)?

A

Renin will transform Angiotensinogen into Angiotensin 1.

Angiotensin 1 goes to the lungs.

ACE enzyme will convert it into Angiotensin 2.

First action: Angiotensin 2 will circulate in the body, and has effect on constriction of arterioles -increasing of BP.

Second action: angiotensin 2 goes to the brain & release of ADH (vasopressin) will induce constriction. Will also induce more production of anti-diuretic hormone.

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43
Q

What does the release of more anti-diuretic hormone do?

A

Less renal Na+ and H20 secretion

More plasma volume

More blood volume

More venous pressure

More venous return

More end-diastolic volume

More stroke volume

More Cradiac Output

INCREASE IN BP WOUHOU

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44
Q

What is the third action of Angiotensin 2 on the body (not on the arterioles, not on the brain secreting ADH)?

A

Angiotensin 2 creates an increase in quantity of aldosterone –> goes to the kidneys –> decrease the amount of sodium excretion –> same physiology than 2nd action with ADH secretion.

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45
Q

What are the 4 types of antihypertensive drugs acting on the RAA system and explain a bit of their mechasnisms plz?

A
  1. Aldosterone-receptor antagonists (blood volume falls –> BP falls)
  2. At-II-receptor blockers (blocks the receptor on adrenal, arterioles, brain: stopped the action of Angiostensin 2, BP falls)
  3. ACE inhibitors: amount of angiotensin 2 drops, BP drops.
  4. Renin Inhibitors: Inhibit the action of renin on angiotensinogen, so less amount of angiotensin 1, so less angiotensin 2, so BP drops.
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46
Q

As the pressure in renal artery goesup, the renal output goes …

A

UP

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47
Q

What is the difference of analyzing an isolated VS an intact kidney (on a graph of urinary output & MAP)?

A

When considering the renal output in an intact kidney (inside a body), the slope is a lot steeper: a tiny increase in arterial blood pressure is going to change by a LOT the renal output - BP falls.

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48
Q

What is the most popular drug to treat hypertension?

A

Anti-diuretics

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49
Q

What are the 4 autonomic control of the CV system?

A

Heart rate

Ventricular contractility

Vessel diameter

Adrenal hormones

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50
Q

To control the heart rate, what is innervated and by which system?

A

The SINUS NODE and it is innervated by both para and sympathetic systems.

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51
Q

What does the parasympathetic system release on the SA node & on which receptor?

A

ACh on muscarinic receptor

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52
Q

What does the sympathetic system release on the SA node and on which receptor?

A

NE on B1-adrenergic receptor

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53
Q

What does para and sympa do on the SA node?

A

Para: slows it down

Sympa: speeds it up

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54
Q

When we talk about ventricular contractility control by ANS, where are the receptors? What system and what receptors? What are the 2 main effects?

A

On the ventricular muscles. Only sympathetic system. B1-adrenergic receptors.

First major effect: speeding up heart rate

Second major effect: increase force of contraction

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55
Q

Why would someone change vessel diameter?

A
  1. To set appropriate flow for each organ
  2. To maintain Mean blood pressure
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56
Q

Size of vessels is controlled by 4 things: what?

A

ANS

Hormones in the bloodstream

Endothelium (the innermost layer can have effects).

Waste products (they surround the vessel and can act on the SM).

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57
Q

Which vessels of the body are not controlled by sympathetic nervous sytem?

A

Capillaries –> no smooth muscle

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58
Q

What is homeostasis?

A

Maintaining the constancy of our internal environement - whether it is for temperature, O2 concentration, pH, ionic composition, osmolarity

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59
Q

What are the 2 compartments of veins?

A

Peripheral venous compartment (large & diverse)

Central venous compartment (small, intrathoracic, vena cava + RA)

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60
Q

IF we assumed there was no pressure/flow in our system (blood was static), where would most of the blood be? What would be the volume?

A

Peripheral venous compartment, 3650ml.

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61
Q

What are the most compliant vessels?

A

Peripheral venous comparment.

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62
Q

What vessels have the most resistance?

A

Arterioles

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63
Q

What is the normal blood volume? Why is it different than the 3560 ml?

A

4.5L. The vessels are inflated - an extra 1L of blood creates a pressure on the vessels.

140 ml of blood = 1 mm Hg. So this volume creates a 7 mmHg internal pressure : the mean systemic filling pressure. Pressure we would have in the absence of flow.

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64
Q

What are the 2 variables influencing the Mean Systemic Filling Pressure?

A
  1. Circulating blood volume
  2. State of the peripheral venous vessel tone (compliance)
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65
Q

Constriction of the vessels of the large venous compartment creates what? Does it have the same effect for arterioles?

A

It increases the pressure throughout the system.

Has almost no effect if arterioles do because there is almost no blood (compared to veins). Also, capillaries & arteries do not actively change their volume.

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66
Q

What is the central venous compartment?

A

Volume enclosed by the right atriumand the great veins in the thorax.

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67
Q

What is entering/leaving the central venous compartment? Are these volume equal?

A

Venous return goes in, cardiac output goes out. They are normally equal - otherwise it means there is an accumulation of blood in Central venous compoartment or peripheral vasculature.

*There are however some small temporary differences.

68
Q

What is venous return?

A

Blood flow from the peripheral venous compartment to the central venous comparment.

69
Q

What is the other pressure name that is equivalent to Peripheral venous pressure?

A

Mean systemic filling pressure

70
Q

What is the formula to calculate the Venous Return?

A

VN = (Mean systemic filling pressure - Right atrial Pressure) / Venous resistance

71
Q

What do the 3 points represent on this graph?

A
  1. When there is no flow, MSFP = CVP. In other words, no flow so the pressures are the same.
  2. If the inlet pressure (peripheral) remains at 7 mmHg, decreasing RAP (outlet) will increase DeltaP (P inlet - P outlet) –> increase the venous return. So, venous return increases as RAP decreases.

3. if RAP is below the intrathoracic pressure, the thin-walled veins of the thorax are compressed and collapse,limiting venous return. Flat part means that at this point, lowering the RAP won’t increase venous return.

72
Q

What change in PVP would have the same effect as a drop in CVC on the venous return?

A

An increase in PVP

73
Q

What are 2 ways to change peripheral venous pressure?

A
  1. Changing blood volume
    - Less blood if blood loss, loss of body fluis by vomiting, sweating, vomiting –> reducing PVP

-Transfusion, fluid retention by kidney, transcapillary fluid reabsorption –> increasing PVP

  1. Changing venous tone

Usually done by increasing/decreasing the activity of the sympathetic: pvp increases when activity of sympathetic increases.

Also could be tone by increasing in force compressing the veinson the outside (ex, exercise or elastic socks)

74
Q

What would shift the venous return curve up or down?

A

Up: increased blood volume or venous tone (PVP increased)

Down: blood less or less venous tone (PVP decreased)

75
Q

Would the resistance in veins be able to shift the Venous return curve?

A

No - only change the slope.

Higher slope = decreased resistance, increase in venous return

Reduced slope = increased resistance, decrease in venous return

76
Q

What are the 2 variables that CVP affect?

A

Cardiac output and venous return.

77
Q

What are the 3 main things that can affect the Cardiac Function curve?

A

Afterload, contractility, HR

78
Q

Anything that affects the venous function curve or the cardiac function curve will change the intersection point on a graph, SO will affect…

A

THe right atrial pressure and the cardiac output

79
Q

True or false, CO and VR rarely change.

A

False. They are constantly changing to meet needs of the body.

80
Q

How can we try to have an idea about the CVP?

A

Measure the internal jugular veins pressure, by measuring the # higher than the angle of Louis.

81
Q

Curve-wise, what can cause an abnormally high CVP?

A

Depressed cardiac function curve (shift to the right) or right-shifter venous function curve

82
Q

Curve-wise, what can cause an abnormally low CVP?

A

Shift to the left of the venous curve OS elevated cardiac function curve (to the left)

83
Q

How can we measure the pressure in the left atrium? And why would we do that?

A

We would do that if we have good reasons to think that it is different from RA pressure.

It is done with a specialized flow-directied venous catheter, with a small inflatable balloon.Goes through IVC,RA, RV, PA & then in the pulmonary smaller arteries (in the lungs).

Balloon is deflated, cannula is advanced until it wedges into a capillary/terminal branch. Recorded at this junction and estimates the left atrial pressure.

84
Q
A
85
Q

What is Flick’s Law of diffusion?

A

Flow = Cout - Cin x A

DDM

  • Diffusion is proportional to surface area and inversely proportional to thickness
  • Diffusion is proportional to partial pressure difference (gradient)
  • Diffusion is proportional to the solubility of the gas in the tissue, but inversely proportional to the of molecular weight (diffusion constant)
86
Q

What is the normal volume of blood, stroke volume and unit of blood ?

A

5L (normal total volume)

450 ml (1 unit),

70 ml (stroke volume)

87
Q

How do you calculate the ∆P of vessels in serie?

A

∆P = Flow x (R1+R2)

88
Q

How do you calculate the flow of organs in parallel?

A

Flow = ∆P x 1/R1 + 2/R2

89
Q

How do you calculate the hydrostatic pressure ?

A
  • Hydrostatic pressure = mass x acceleration gravity.
  • 1 mm Hg = 14 mm H2O = 0.13 Pa.
90
Q

How do you calculate perfusion pressure ?

A
  • Perfusion pressure (∆P) = Parterial– P venous Pa >> Pv (100 mmHg vs 5 mmHg).
  • No perfusion pressure = no flow. Pa - Pv = flow.
91
Q

Give examples of physiological (not pathological) arrythmias?

A

Bradycardia in trained athletes or tachycardia during exercise

92
Q

What is an ectopic complexe and tachycardias?

A
  • Ectopic complexes: beat originating in a site other than the sinus node. They can be premature, ex: premature atrial ectopic complexes PAC (different P wave) and PVC (no P wave).
  • Ectopic tachycardias: may be paroxysmal (start and stop abruptly, usually by initiating or terminating factor) or nonsustained or sustained
93
Q

What are the 2 types of after-depolarization induced arrhythmia (predominantly in fast-channel tissue) and their mechanism?

A

1. Early afterdepolarizations (EADs)
Caused by excessive action potential (AP) prolongation, which allows Ca2+ channels to recover and depolarize the cell, induced by drugs that block K+ channels and favoured byslow HR, long Q-T interval on ECG,
To treat it, you stop drugs that block K+ channels and normalize HR

2. Delayed afterdepolarizations (DADs)

Caused by spontaneous diastolic Ca2+ release, favoured by excess cellular Ca2+ load

94
Q

What is the mechanism of Ca2+ release?

A
  1. Ca2+ enters through Ca2+ channel during phase 2 of the AP
  2. Ca2+ entry triggers release of more Ca2+ through RyR2
  3. Increased free intracellular Ca2+ causes contraction (EM coupling)
  4. Cytosolic Ca2+ removal (essential for relaxation) occurs by 2 mechanisms:
    - Uptake into SR by Ca2+ uptake pump
    - Na+, Ca2+ exchange across cell membrane
95
Q

What is re-entry?

A

To have re-entry, you need 2 paths that go in the same place. One has a short refractory period and the other one has a long one. A premature impulse can find one pathway refractory when the other can conduct because the impulse conducts in the forward (antegrade) direction in the shorter RP path and then retrograde in the long RP. When is goes back to the proximal end of the refractory pathway, it starts again if the conditions are right: if the re-entry time in the circuit is greater than the longest RP.

96
Q

Bradyarrhythmias: types, definition and therapy

A

Pathological bradyarrhythmias cause syncope when clinically significant.

  1. Sick sinus syndrome
  2. Atrioventricular (AV) Block
  3. First-degree AV block
  4. Second-degree AV block
  5. Mobitz Type 1
  6. Mobitz Type 2
  7. Third-degree block

Bradyarrhythmias treatment

  • Acute: atropine and isoproterenol or temporary transvenous pacemaker
  • Chronic: permanent pacemaker
97
Q

Explain Sick sinus syndrome

A

Sinus node intermittently fails to fire, typically causes syncope, not sudden death, occur in elderly.

98
Q

Explain in details the Atrioventricular (AV) Block (Bradyarrhythmias)

A
  1. First-degree AV block: very common, slowing of atrial-ventricular conduction (long PR interval > 0.2), no blocked beats
  2. Second-degree AV block: some beats fail to conduct; divided into 2 subtypes
  3. Mobitz Type 1: progressive PR lengthening on a beat-to-beat basis, until conduction to the ventricles fails (“blocked” P-wave), in the AV, rarely progress in 3rd degree AV block
  4. Mobitz Type 2: blocked P waves occur without gradual PR lengthening, long QRS because the His-Purkinje system is affected, progress in third degree block
  5. Third-degree block: also called complete AV block; no sinus impulses get to ventricles but escape rhythms maintain cardiac activity when peacemaking from above fails, almost always requires pacemaker
99
Q

What is Paroxysmal supraventricular tachycardias (PSVTs)?

A

Is an AV node re-entry and is common in healthy people. Normally, the stimulus comes from the SA node and is regulated by it. The re-entry causes tachycardia because there is more frequent stimulus coming from the re-entry loop.

100
Q

Why do we useAV-node depressing drugs?

A

Stop AV node re-entry

  1. Block Ca2+ channels mediating AV node conduction (CALCIUM CHANNEL BLOCKERS)
  2. Hyperpolarize AV node cells by enhancing K+ current so that their action potentials are further away from threshold (ADENOSINE)

Prevent AV node re-entry

  1. Block Ca2+ channels mediating AV node conduction (oral Ca2+ channel blocker).
  2. Suppress adrenergic enhancement of Ca2+ current (beta blockers)- not as effective.
  3. Suppress premature complexes that initiate tachycardias-not as effective.
  4. Eliminate anatomical basis by burning one AV nodal pathway.

Other uses of AV-node depressing drugs

Reduce ventricular response rate to atrial arrhythmias because consequences of arrhythmia depend on ventricular rate

101
Q

Atrial Fibrillation (AF): mechanisms and therapy

A

Is defined by the Atria firing too fast (400-600 bpm). AF increases risk of stroke due to embolism of clot from static blood pool in fibrillating LA appendage: most common cause of stroke in the elderly (> AGE).

Treatment: restore sinus rhythm

  1. Drugs that increase atrial RP, terminating re-entry (effective for recent AF)
  2. D.C. electrical shock, terminates re-entry by simultaneously depolarizing tissue (>95% effective)

Treatment: maintain sinus rhythm

Challenge because AF tend to reoccur, the choice of treatment is decided by the patient.

  1. Can use drugs that increase atrial RP.
  2. A variety of ablation approaches, targeting atrial zones that are critical in initiating and/or maintaining AF.
102
Q

How do we preditct the risk of stroke with a patient that has AF ?

A

We use the C chronic heart failure (1) H hypertension (1) A age > 75 (1) D diabetes (1) S Prior Stroke/TIA/Thromboembolism(2)

1: 1.5%/yr

3: 6%/yr

6: 8%/yr

103
Q

Atrial flutter: mechanisms and therapy

A

Is defined by a rapid and regular atria firing (240-300 bpm). Need large drug effects (e.g. by up to 200 ms prolongation of RP) before benefit and a bit of exercise may be enough to get abrupt acceleration. Therefore, rate control generally more difficult for atrial flutter versus atrial fibrillation.

Treatment

  1. Rate control more difficult
  2. Ablation often simpler, more successful since only 1 macroreentrant circuit
  3. IMPORTANT: Anticoagulation indications are the same for atrial flutter as atrial fibrillation
104
Q

Ventricular tachycardia (VT): definition and treatment

A

Is defined by a rapid rhythm arising from a region in the ventricles, most typically 150-180 bpm. Can be caused by:

  • Enhanced automaticity (acute MI, responds to drugs that block Na+ channels)
  • DADs (cardiac hypertrophy, responds to blockers of Na+ channels in phase 0 activation)
  • EADs (LQT Syndrome, responds to treating underlying condition, ↑ HR and correction serum K+)
  • Re-entry (post MI, responds to drugs that increase refractory period by increasing APD)

Principles of management

  • When mechanistic diagnosis is possible (e.g. congenital syndromes, acquired LQTS, post-MI scar reentry), mechanism-based therapy is possible and appropriate.
  • Direct-current cardioversion should be used to terminate VT when severe hemodynamic compromise is life-threatening
105
Q

Ventricular fibrillation (VF): definition and treatment

A

Is defined by chaotic ventricular rhythm, no effective cardiac pumping. It is Lethal within minutes in the absence of cardiac massage by thoracic compression (requires emergency DC cardioversion).

Treatment

Individuals resuscitated from VF generally require implantation of a defibrillator to prevent recurrence; drug therapy not reliable enough.

106
Q

Summary of arrhythmia properties and treatment

A
107
Q

What are the 2 congenital ventricular tachycardia syndromes and their response to therapy?

A
  • CPVT: usually responds to beta-blocker
  • Long QT syndrome: usually responds to beta-blocker but some recurrences, which requires implantable cardioverter/defibrillator
108
Q

How can the Jugular Venous Pulsations indicate the right heart function?

A

The height of the internal jugular venous column (termed the “jugular venous pressure” or JVP) is an accurate representation of the RA pressure.

109
Q

In the Jugular Venous Pulsations and Assessment of Right Heart Function, identify the letters

A

Two major upward components:

  • a wave RA contraction
  • v wave RA filling

Two descents:

  • x descent (x and x’) RA relaxation and enlargemen
  • c wave tricuspid valve closure
  • y descent atrium empties in ventricle
110
Q

In the Jugular Venous Pulsations and Assessment of Right Heart Function, what would a prominent a wave mean?

A
  • right ventricular hypertrophy
  • tricuspid stenosis
111
Q

In the Jugular Venous Pulsations and Assessment of Right Heart Function, what would a prominent v wave mean?

A

Tricuspid regurgitation (during systole blood is pushed into the right atrium from the right ventricle)

112
Q

In the Jugular Venous Pulsations and Assessment of Right Heart Function, what would a prominent v descent mean?

A

Constrictive pericarditis

113
Q

True or false: if a patient has atrial fibrilation, you can hear an S4

A

BEN NON. If the patient is in atrial fibrilation, there is no contraction of atria !!!

114
Q

What are the 5 mechanisms of heart murmurs?

A
  1. Flow across a partial obstruction (e.g., aortic stenosis)
  2. Increased flow through normal structures (e.g., aortic systolic murmur associated with a high-output state, such as anemia)
  3. Ejection into a dilated chamber (e.g., aortic systolic murmur associated with aneurysmal dilatation of the aorta)
  4. Regurgitant flow across an incompetent valve (e.g., mitral regurgitation)
  5. Abnormal shunting of blood from one vascular chamber to a lower-pressure chamber (e.g. ventricular septal defect [VSD])
115
Q

What are the normal heart sounds and their characteristics?

A
  1. S1 = Closure of the AV valves (mitral and tricuspid)
    Can hear it louder at the of the heart with the diaphragm part of the stetoscope
  2. S2 = Closure of the semilunar valves (aortic and pulmonic)
    Vary with the respiratory cycle: A2 and P2 are normally fused as one sound during expiration. They become audibly separated during inspiration, a situation termed “physiologic splitting”.
116
Q

What are the 2 types of extra systolic heart sounds?

A
  1. Ejection clicks
    Indicate the presence of congenital aortic or pulmonic valve stenosis or dilatation of the pulmonary artery or aorta.
  2. Non-ejection clicks
    Occurring in mid-systole are usually the result of systolic prolapse of the mitral or tricuspid valves. They are loudest over the mitral or tricuspid auscultatory regions.
117
Q

What are the 4 types of extra-diastolic heart sounds ?

A
  1. Opening snap (OS)
  2. Third heart sound (S3) – Ventricular gallop
  3. Fourth heart sound (S4) – Atrial gallop
  4. Pericardial knock
118
Q

What are Opening snap (OS)?

A

Sharp pitch extra diastolic sounds.

Corresponds to mitral or tricuspid opening, caused by valvular stenosis (can’t be heart normally)

119
Q

What are the characteristics of Third heart sound (S3) ?

A

Extra sound heard in early diastole when there is exaggerated early diastolic filling (can sometimes be normal or with heart failure because of high right ventricle pressure)

It is a dull, low-pitched sound best heard with the bell of the stethoscope at the cardiac apex

120
Q

What are the characteristics of Fourth heart sound (S4)?

A

Extra sound in late diastole heard when there is atrial contraction into a stiff, non-compliant ventricle (abnormal)

Is a low-pitched sound best heard with the bell of the stethoscope at the cardiac apex

121
Q

What is Quadruple Rhythm or Summation Gallop?

A

When a patient has an S3 and an S4 (ça va pas ben son affaire)

122
Q

What are heart murmurs?

A

A murmur is the sound generated by turbulent blood flow.

123
Q

How are described murmurs?

A

Timing

Systole or diastole, or is continuous (begins in systole and continues into diastole).

Intensity

The intensity of the murmur is typically quantified by a grading system (I - VI)

Pitch

High-pitch (high pressure gradient) and low-pitch (less of a pressure gradient heard with bell)

Shape

Crescendo, decrescendo, crescendo-decrescendo, uniform

Location

Aortic, Tricuspid, Pulmonary or Mitrsl

Radiation

From their primary locations, murmurs are often heard to radiate to other areas of the chest depending on the direction of the turbulent flow.

Response to maneuvers

Valsalva, squatting, handgrip, leg raise

124
Q

What are the 3 types of Systolic murmurs?

A
  1. Systolic ejection murmurs
  2. Pansystolic (holosystolic) murmurs
  3. Late systolic murmurs
125
Q

Describe systolic ejection murmurs in detail.

A

Typical of aortic or pulmonic valve stenosis, crescendo-decrescendo murmur

Begins a short time after S1 and terminates before or at S2

  • EX: Innocent systolic murmur: Increased systolic flow across normal aortic and pulmonic valves or flow through a ventricular septal defect
126
Q

Describe pansystolic (holosystolic) murmurs in detail.

A

Caused by regurgitation of blood across an incompetent mitral or tricuspid valve

  1. Mitral: uniform sound, no gab between S1 and murmur, heard best at the apex, is high pitched and “blowing” in quality
  2. Tricuspid: intensity increases with inspiration, radiates to the right sternum but heard in left sternum
  3. Ventricular Septal Defect: associated with a thrill, the smaller the VSD, the higher the murmur
127
Q

Describe late systolic murmurs in detail.

A

Late systole and continue S2

Ex: mitral valve prolapse

128
Q

What are the 2 types of diastolic murmurs?

A
  1. Early decrescendo murmurs
  2. Mid-to-late rumbling murmurs
129
Q

Explain in detail the Early decrescendo diastolic murmur.

A

Decressendo from S2, high pitch (diaphragm)

  • Regurgitant flow through aortic (best heard when leaning foward)
  • Regurgitant flow through pulmonic valve (increases with inspiration, pulmonary area)
130
Q
A
131
Q

Explain in detail Mid-to-late diastolic rumbling murmurs.

A

Decressendo with a little increase at the end, low pitch, left side apex of heart.

Result from either turbulent flow across a stenotic mitral or tricuspid valve or less commonly from abnormally increased flow across a normal mitral or tricuspid valve. If resulting from stenosis, the murmur begins after S2 and is preceded by an opening snap

132
Q

The coronary circulation can be compromised in the systole or diastole?

A

Since the intramural arteries run within the myocardium, they are squeezed during ventricular systole. Thus, the blood flow is greater during diastole in the left ventricle, since the intramural pressure is very high during systole.

Clinical importance: during tachycardia, the diastole time decreases and that can compromise the coronary circulation. In a healthy heart, this effect is counterbalanced by the increased blood flow provoked by the increased metabolic demands. EX: ventricular fibrillation is fatal because of that.

133
Q

What are the 2 mechanisms of blood flow control?

A
  1. Metabolic: local reduction of pO2 and the local accumulation of waste products of metabolism will act to produce arteriolar vasodilation followed by vasoconstriction to go back to normal (Bayliss reflex/effect).
  2. Myogenic: smooth muscle of arteries will contract (myogenic reflex) when Ca2+ ↑
134
Q

How does NO act on vascular tone?

A

NO os induced by ACh through a receptor in the endothelial cells that will release NO, which will diffuse in the adjacent muscle cell and cause vasodilation.

NO is also atheroprotective (iprotects against the development of atherosclerosis)

135
Q

How does ACh act on vascular tone?

A
  1. ACh will bind to a receptor in the endothelial cells that will release NO, which will diffuse in the adjacent muscle cell and vasodilate it.
  2. When ACh binds to a smooth muscle receptor, this causes vasoconstriction.

In healthy people, the endothelial effect (NO release) greater, resulting in a total vasodilation.

136
Q
A
137
Q

What are the risk factors of endothelial dysfunction?

A
  • age
  • family history
  • smocking
  • diabetes
  • obesity
  • hypercholesteremia
  • hypertension

Adverse results are partly reversible when risk factors are removed.

138
Q

What are the determinants of oxygen demand of the heart?

A
  • HR (↑ –> ↑)
  • Wall stress (↑ –> ↑ –> heart failure)
  • Contractility (↑ –> ↑)
139
Q

Describe the blood flow to the brain.

A
  • While total blood flow to the brain remains more or less fixed, the flow to a particular region of the brain depends on the level of activity in that region (local metabolic control). This is the physiologic basis underlying functional magnetic resonance imagining scans (fMRI).
  • Central Ischaemic Reflex: massive sympathetic activation that vasoconstricts the rest of the body. Th ecentral ischemic reflex is called the Cushing reflex when it is elicited by increased intracranial pressure.
  • Endothelial cells of the brain play an important role in the blood-brain barrier and use a lot of energy.
140
Q

Describe the boold flow to the lungs.

A
  • Low pressure
  • Unlike systemic arterioles, pulmonary arterioles constrict in response to a fall in pO2 (or rise in pCO2). This hypoxic vasoconstriction diverts blood away from underventilated areas of the lung and towards well-ventilated areas, thus matching ventilation to perfusion ratio (V/Q ratio) and maximizing the O2 content of the blood exiting the pulmonary capillaries.
141
Q

Describe the blood flow to the kidneys.

A
  • Low arterio-venous difference
  • Portal system (2 capillary beds in series)
  • Flow regulated by myotonic and metabolic autoregulation.
  • Sympathetic activation will reduce flow to kidneys (explains the necessity of measuring urinary output in patients with shock to guard against the development of ischaemic renal damage)
142
Q

Describe the blood flow to the liver.

A
  • Low-pressure perfusion system
  • Elevation of the central venous pressure can cause a rise in the pressure both in the hepatic vein (causing hepatic congestion) and in the sinusoids (causing extravasation of fluid into the peritoneal cavity.
143
Q

Dedcribe the blood flow to the squeletal muscles.

A

The blood flow to resting skeletal muscle on a unit weight basis is low, since the metabolic requirement of resting muscle is low. The myogenic tone is thus much larger than the neurogenic tone.

144
Q

Describe the blood flow to the skin.

A
  • Cold: ↓ vascularisation (vasoconstriction)
  • Heat: ↑ evaporation (sweating), constant radiation, conduction and convection
145
Q

What happens to the MAP in orthostasis (after a couple of minutes)? Systolic? Diastolic?

A

Does not change. Sistolic falls a bit, diastolic rises a bit.

146
Q

What makes the MAP adapt ?

A

Baroreflex

147
Q

When I stand up, what happens to those things:

Central Blood Volume

Volume of ventricles filling

End-Diastolic Volume

SV

CO

A

All decrease

148
Q

3 effects of sympathetic activation in orthostasis

A

Increase in TPR (BFs fall in forearm, renal, splanchnic)

Increase in contractility of the heart (helps to preserve stroke volume)

Venoconstriction (Increase VP, VR, SV, CO,BP)

149
Q

What is the effect of the contraction of calf muscles?

A

Increase the central blood volume, increase venous pressure, increase MSFP

150
Q

What is the second important effect of the muscle pump (par rapport au plasma)?

A

Muscle pump helps loose less fluid in interstitial space (because capillary beds can leak if pressure is too high in the legs –> so muscle pump helps sending blood back up)

151
Q

What between arteria and veins promote filtration/absoprtion?

A

Arteria = filtration

Veinss = absoroption

152
Q

Elephantiasis is ?

A

Infection of lymph nodes by a parasitic worm.

153
Q

When we exercise, what is the effects on:

HR

SV

CO

A

HR goes up, stroke voulme goes a little bit up (up to a certain point, because at one poitn it decreases), and CO increase to supply muscles.

154
Q

What happens to the a-v difference of O2 during exercise?

what effect does this have on O2 consumptioN?

A

It triples –> so the O2 consumption is 9x, since it depends on the blood flow (here, the CO has tripled) and the a-v difference.

155
Q

What are the 3 organs that will receive more blood flow during exercise?

A

HUGE increase in skeletal muscles

Skin

Heart

156
Q

What are the 3 elements included un neural control of skeletal muscle tone?

A
  1. Adrenal medulla secreting NE in blood (a-receptor for constriction)
  2. Sympathetic activation (a-receptor for constriction)
  3. Adrenal medulla secretes epinephrine in bloo (a-receptor for constriction but Breceptor for dilatation)
157
Q

What control dominates when talking about controolling the skeletal muscle tone - local or neural?

A

LOCAL

158
Q

True or false, we can increase someone’s max CO by training.

A

YAS

159
Q

True or false, an athlete has a higher HR at any given work rate.

A

False, it is lower.

160
Q

True or false, training results in an increase of SV. If so, why (lolzzz subtil)

A

True (in particular resting SV and max SV). This is due to training-induced ventricular hypertrophy.

161
Q

What are the 3 effects of muscle pumping?

A
  1. Exercise: venous valves in arms/legs & pumping blood back to the heart, increasing CO.
  2. Orthostasis: make lose less fluid in interstitial space
  3. Orthostasis: calf muscles contract, sending blood back to the heart.
162
Q

What does mitral stenosis do for people exercising?

A

MS causes a marke reduction in VO2 max, max CO and max SV. It reduces the ability to exercise.

163
Q

Why is the VO2 max higher in athletes?

A

Because of a larger CO.

164
Q

Why is the CO increased in athletes?

A

Because of a higher SV - NOT because of a higher Heart rate.

165
Q
A

Bloc C - Circulation (10 decks)

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