Exercise & CVS Flashcards

1
Q

What is hypertrophy?

A

= Cardiomyocytes (cells that do all the work in the heart) get bigger
o Because they divide very sparingly
o Very little division from when your heart is fully grown

  • Only way that cardiomyocytes can deal with increased workload is to get bigger
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2
Q

What is the formula for wall stress?

A

Wall stress = P(pressure) * r(radius of heart) / h (wall thickness)
{Pr/h}

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3
Q

What is the equation for elasticity?

A

Elastance = ∆P/∆V

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4
Q

How is increased workload defined?

A

Increased workload defined in 2 ways:
1. Increased Pressure: Myocytes thicken -> concentric left-ventricular hypertrophy (walls get thicker evenly, no shape change)
o Thicken by laying down sarcomeres in parallel (on top of each other)
2. Increased Volume: Myocytes lengthen -> eccentric left-ventricular hypertrophy (heart gets bigger)
o Lengthen by laying down sarcomeres in series

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5
Q

Athletes Heart physiology

A
  • Increased Heart Mass
  • Normal or increased Cardiac Function
  • Reversible – i.e. if people stop exercising it can be reversed
    o This is the difference between physiological and pathological
-	3 types:
	o	Endurance athlete: 
		•	Thickening of LV walls
		•	LV dilation
	o	Strength athlete:
		•	Thickening of LV walls
		•	Mild LV dilation
	o	Combination athlete:
		•	Gross thickening of LV walls
		•	LV dilation
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6
Q

What are the dimensions of an athletes heart?

A
  • Elite athletes have around 10-20% increase in LV wall thickness & cavity diameter
  • Small percentage have dimensions that overlap with cardiac disease dimensions
  • Most pronounced in cycling/rowing/X-country skiing
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7
Q

What is Fick’s Principle?

A
  • VO2 = CO(CaO2 – CvO2)
    o CO = Cardiac output
    o CaO2 = incoming blood in pulmonary vein, highly oxygenated
    o CvO2 = returning deoxygenated blood to the heart
    o CO is what changes when you exercise
  • CO = SV (stroke volume) x HR (heart rate)
  • Max Heart Rate = age dependent
  • Stroke volume = exercise dependent
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8
Q

What is the result of volume overload due to dynamic/endurance exercise?

A
  • Increase Atrial/ventricular inotropy (ability of heart to contract)
    o Increases sensitivity of B1-adrenergic receptors to norepinephrine
    o Means LV can eject more blood on each cycle
  • Increased Lusitropy – ability of heart to relax
  • Increased Peripheral vascular dilation
    o Reduces peripheral resistance so blood flows more easily
  • Increased Skeletal & abdominothoracic (respiratory) pump activity
  • Increased Venous constriction
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9
Q

What is the respiratory/abdominothoracic pump?

A

o In the interpleural cavity (inside your chest)
o Negative pressure inside
o Breathing in expands chest, diaphragm goes down -> pressure drops -> venous dilation -> more blood in right atrium

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10
Q

What is venous compliance?

A

o Sympathetic nerve activity increased during exercise -> venous constriction
o Results in amount of blood that can be held in venous system decreasing -> blood pushed out into rest of the system

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11
Q

What is the result of Pressure Overload due to static/strength exercise?

A
  • Minimal increase in CO
  • Decrease pump activity
    o No rhythmic activity
    o Valsalva manoeuvre
  • Increased Peripheral resistance
    o Mechanical compression
    o Muscle contraction around arterioles and capillaries -> blocks blood flow
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12
Q

What makes theCVS adaptations to exercise physiological and not pathological?

A
  1. Reversible
    o Somewhat related to signals that drive it – seems to be related to IGF
  2. Increased mitochondrial load as energy requirements increase – doesn’t happen in pathological
  3. Increased blood vessel supply – doesn’t happen in pathological
  4. Essentially the system is more balanced
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13
Q

What happens during physiological hypertrophy during pregnancy?

A
  • VO2 increases 33%
  • Blood volume increases 40%
  • CO increases 50%
  • Total peripheral resistance falls
  • Reversible (Because physiology)
    o Some women don’t go back to due issues in angiogenesis (vessel supply to cardiomyocytes)
    o Results in peripartum-cardiomyopathy
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14
Q

What is heart failure?

A

Inability of the heart to produce sufficient CO to profuse the body sufficiently for it to function

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15
Q

What are the 2 types of heart failure?

A
  1. Forward failure: Decreased CO = heart overflowing
  2. Backwards failure: Increased venous pressure
    o Results in edema (fluid leaking out of circulatory system into tissue)
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16
Q

What are the acute causes of heart failure?

A

Myocardial infarction (heart attack):
- Caused by sudden & complete blockage of a cardiac artery
- Unstable plaque ruptures exposing blood to thrombotic surface due to removal of endothelial surface which causes sudden and catastrophic blockage by thrombosis and fibrin forming fibrinogen clot
- Zone of perfusion becomes ischemic (doesn’t get blood supply)
- Zone of perfusion immediately becomes compliant (unable to contract)
o Compliant means increased P -> increased stretching
- Cardiomyocytes start to die within 2hrs
- If blockage isn’t removed, zone of necrosis (dying cells) grows – starting on endocardial side
o Very thin layer of safe tissue on endocardial side due to diffusion of highly oxygenated blood in the left ventricle
- Increased P after systole -> Dyskinesis -> decreased SV -> volume overload
o Initially compensatory mechanisms acts via increased preload (V of blood in heart at end of diastole)
o Places increased workload on surviving cardiomyocytes

17
Q

What is the zone of perfusion?

A

Area that would have been supplied by the now blocked vessel in the endothelium
o Area of risk during myocardial infarction

18
Q

What are the chronic causes of heart failure?

A
  • Valvular disease
  • Cardiomyopathies
    o Bacterial, viral
    o Alcohol
    o Idiopathic
  • Myocarditis (inflammation)
  • Hypertension (leading to increased pressure)
  • Increased body demands
19
Q

What is preload?

A
  • The initial stretching of cardiomyocytes prior to contraction ( in diastole)
  • Increase in preload -> more rapid generation of tension = contracts to same final length over same period of time
  • EDV (end-diastolic volume)
20
Q

What is afterload?

A
  • The load against which a heart must contract to eject

- Combination of Blood pressure & Wall stress

21
Q

What is inotropy?

A

Cardiomyocyte contractility

22
Q

What is the effect of inotropy on a Pressure-Volume loop?

A
  • Increased inotropy = Shift to left & steeper curve - i.e. higher P at any loading V
  • Decreased inotropy = Shift to right & lower curve - i.e. Decreased P
23
Q

Characteristics of chronic heart failure due to systolic dysfunction

A
  • ↓inotropy: likely due to impaired excitation-contraction coupling
  • ↓ ESPVR
  • Increased ESV -> increased EDV
  • EDV increases less than ESV
  • EDP can rise causing increased pulmonary venous P
  • Edema
  • Decrease in Ejection Factor (EF) is a marker of a poor prognosis
24
Q

Characteristics of chronic heart failure due to diastolic dysfunction

A
  • Impaired filling
    o Hypertension; hypertrophic cardiomyopathy, old age
    o Thickened wall, scarred wall
  • EDPVR shift up and to left
  • Reduction in SV
  • If EDP increases too much results in edema
25
Q

What is an edema?

A

Puffiness caused by excess fluid trapped in the body’s tissues

26
Q

What is the systemic response to heart failure?

A
  • Baroreceptors sense CO drop
  • Sympathetic tone increases:
    o Norepinephrine, resulting in:
    • Increase HR, inotropy, lusitropy
    • Via B1 adrenoreceptors
    o Long term increased workload/O2 consumption
  • RAAS (slower response)
    o AngII (potent vasoconstrictor) increases MAP (mean arterial pressure) and preload
    o Aldosterone/vasopressin
    o Increased fluid retention
    o Compensatory mechanisms
    o Long term increased workload/O2 consumption
    o Edema