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CV > Microcirculation > Flashcards

Microcirculation Flashcards

1
Q

3 aspects of microcirculation

A 
1. Capillary exchange of solutes
Diffusion 
2. Capillary exchange of water
Starling forces
3. Lymphatics
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2
Q

what is microcirculation

A

The “point” of the circulatory system for multi-cellular organisms
Site of exchange: gases, water, nutrients, waste

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3
Q

What is exchanged by simple diffusion?

A

A. Lipid-Soluble Substances
O₂, CO₂, other non-polar substances
Diffusion across endothelial cells

B. Water-Soluble Substances
Na+, K+, glucose, amino acids, other polar substances
Diffusion across clefts between endothelial cells
Plasma proteins are generally too large to pass

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4
Q

How does tissue metabolism influence concentration gradient? example of oxygen

A

Depletion of cellular O₂ increases gradient to promote increased rate of diffusion, maximizing A-V O₂ difference by increasing O₂ extraction

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5
Q

Capillary Exchange of Fluid: Bulk Flow

A

Water exchange depends on Net Starling Forces across the capillary membrane
Net Hydrostatic Pressure:
Difference between capillary & interstitial fluid pressures:
Net Osmotic Pressure
Difference between capillary & interstitial fluid colloid osmotic pressures (proteins)

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6
Q

Factors influencing net filtration pressure (the 4 Starling forces)

A 
1. Capillary BP (Pc )
	Hydrostatic pressure (BP):  out
2. Plasma-colloid osmotic pressure (πP )
	Osmotic pressure (plasma proteins):  in
  1. Interstitial fluid hydrostatic pressure (PIF )
    Hydrostatic pressure: in (small)
4. Interstitial fluid-colloid osmotic pressure (πIF )
		Osmotic pressure (leaked proteins):  out (minimal)
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7
Q

Net driving force and starling equation

A

NDF = (cappillary P - interstitial P) - sigma (capillary collooid osmotic pressure - interstitial fluid colloid osmotic pressure)

If it’s positive, then filtration is occuring (NDF > 0) (fluid is moving out)
If it’s negative, then reabsorption is occuring

the sigma is not important

BLUF: are the inward pressures greater than the outward pressures? –> reabsorption

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8
Q

What important variable in the starling equation changes most through the course of the circulatory system?

A

Outward pressure from capillary (blood pressure)

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9
Q

Factors impacting filtration & reabsorption (is edema formation promoted or not?)

A

Capillary hydrostatic pressure (promotes filtration)
Plasma-colloid osmotic pressure (promotes reabsorption)
interstitial fluid hydrostatic pressure (typically close to 0)
Interstital fluid-colloid osmotic pressure (promotes filtration)

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10
Q

Factors impacting capillary hydrostatic pressure (which promotes filtration)

A

Increased by:
Arteriolar dilation
Increased venous pressure (causes blood to back up)
Hypertension

Decreased by:
Arteriolar constriction
Hemorrhage/blood loss

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11
Q

Factors impacting plasma-colloid osmotic pressure (which promotes reabsorption)

A

Increased by:
Dehydration (excessive sweating) –>increased protein
Decreased:
Liver failure, protein malnutrition, nephrotic syndrome, pregnancy
Saline infusion

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12
Q

interstitial fluid hydrostatic pressure changes

A

Typically close to zero

Clinically relevant changes involve pulmonary circulation, edema

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13
Q

Interstitial fluid-colloid osmotic pressure factors

A

Increased by:
Chronic Lymphatic Blockage
Burns (increased capillary permeability)

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14
Q

Lymphatic System

A

Accessory route: Filtered fluid & protein  returned to circulation from interstitial spaces
Filtration > Reabsorption
~ 1/10 of fluid enters lymphatics vs. being reabsorbed in capillaries –> 2-4 L/day!
Important in preventing edema
Edema Develops When: Filtered volume > lymphatic capacity
Lymph = interstitial fluid that flows into the lymphatic system

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15
Q

Edema develops when…

A

filtered volume > lymphatic capacity

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16
Q

Factors that increase lymph flow and increase likelihood of edema formation

A
  1. Increased capillary hydrostatic pressure
  2. Decreased plasma colloid osmotic pressure
  3. Increased interstitial fluid colloid osmotic pressure
  4. Increased capillary permeability

Each factor causes the balance of fluid exchange to favor net fluid movement out of the capillary bed and into the interstitium (net filtration), resulting in ↑ interstitial fluid volume, interstitial fluid pressure, & lymph flow. These factors can also promote edema.

17
Q

Coronary blood supply issues

A

Cardiac output distribution: ∼5% ( Skeletal m. (~3000/mm2 vs. ~400/mm2)
Resting cardiac m. O2 consumption almost = exercising skeletal m. per mass

Fiber diameter: Cardiac m.

18
Q

types of coronary arteries

A

Epicardial Coronary Arteries (LCA/RCA) Main coronary arteries on the surface of the heart

Intramuscular arteries Smaller communicating arteries pass through myocardium
Subendocardial Arteries
Deep to the endocardium

19
Q

Coronary blood flow during cardiac cycle

A

Blood flow through coronary arteries depends on:
Perfusion pressure at aortic openings
Extravascular compression due to ventricular contraction (especially left ventricle)

LV Myocardial contraction effectively compresses its own vascular supply
Pressures especially compress subendocardial a.a.

∼80% of LCA blood flow occurs during diastole

RV develops lower pressure during systole
RCA blood flow is not significantly occluded during contraction

20
Q

Cardiac muscle metabolism

A

Resting myocardial O2 consumption
> 60% fatty acid oxidation
O2 supply (anaerobic/ischemic conditions): Anaerobic glycolysis results in lactic acid production
Possible cause of angina during ischemia

21
Q

Myocardial O2 consumption at rest

A

Rest:
Blood flow: ~ 60 - 80 mL/min of blood per 100 g myocardium
O2 extraction: ~ 70 - 80% of arterial O2 content (∼20 mL/dL)
Very low venous O2 content (∼5 mL/dL)

Key Concepts:
Metabolic signals are key drivers of myocardial O2 delivery

Myocardial blood flow parallels myocardial metabolism
Autoregulation

O2 extraction is near max at rest

22
Q

Myocardial O2 consumption during exercise

A

↑ coronary blood flow: Key to meeting large increases in O2 demand during exercise

**Extraction is near maximal at rest
Minimal capability to meet increased metabolic demands by increasing O2 extraction beyond resting levels

Coronary blood flow: Exercise 
> 250 mL/min per 100 g
Flow may increase > 5x
Coronary Flow Reserve
(using dilation, etc.)
23
Q

Rate-Pressure Product

A

Indirect index of myocardial O2 consumption (how hard is the heart working?)
Non-invasive, reasonable correlation with changes in myocardial O2 consumption

RPP = HR x SBP
Based on cardiac work: Rate and Pressure

24
Q

Myocardial O2 supply and demand

A

Supply: O2 content affected by coronary blood flow:

  • coronary perfusion pressure
  • coronary vascular resistance
  • external compression
  • intrinsic regulation
  • local metabolites
  • endothelial factors
  • neural innervation

Myocardial oxygen demand affected by:

  • wall stress
  • heart rate
  • contractility
25
Q

Autoregulation of coronary blood flow

A

Ohm’s Law: Flow determined by pressure gradient and resistance

MAP: little variation, even with exercise
CBF is relatively stable at perfusion pressures of ∼70 - 150+ mm Hg

↓ resistance in order to ↑ flow to exercising myocardium
Vasodilation
Decreased O2 supply promotes vasodilation of coronary vessels
O2 demand > O2 supply: vasodilation 
Active hyperemia: 
Adenosine
Increased Pco2 
NO
H+
Prostaglandins
26
Q

Adenosine and Coronary Blood Flow

A

↓ Myocardial PO2 → (due to increased metabolic activity or insufficient coronary blood flow) ↑ Adenosine levels

Adenosine acts on vascular smooth muscle cells (VSMC), lowering [Ca2+]i and inducing vasodilation

Inadequate perfusion elevates interstitial adenosine, promotes vasodilation & restores flow to affected region

27
Q

Autoregularion and Neural Input

A

Autoregulation & vasodilation prevail during exercise

Parasympathetic Minimal ACh receptor distribution on coronary vessels, Minimal vasodilatory effect

Sympathetic
α1: vasoconstriction with epinephrine & norepinephrine
Expression: epicardial a.a. > endocardial a.a.
β2: vasodilation with epinephrine and norepinephrine
Expression: endocardial a.a. > epicardial a.a.

28
Q

Coronary Blood Flow: Tachycardia

A

Tachycardia: ↓ time for maximal perfusion during diastole
Impacts CBF, perfusion of LV is especially compromised

29
Q

Coronary Blood Flow: Healthy Heart

A

Coronary vessels autoregulate and adequately dilate

Compensate for shorter diastole

30
Q

Coronary Blood Flow in Coronary Artery Disease

A

Stenosis: restriction of blood flow

Exertional Angina

31
Q

Vasodilator Stimuli: Coronary Steal

A

Vasodilator drugs or exercise:
When atherosclerotic plaque is present in large epicardial a.a.
Tissue distal to stenotic lesion is especially vulnerable to ischemia because arterioles may be maximally dilated at ‘rest’ in effort to compensate for stenosis
There may be insufficient Coronary Flow Reserve capacity to further dilate in order to meet demand with exercise or in response to a vasodilator drug
If arterioles distal to stenosis are maximally dilated, vasodilation can only affect vessels in non-ischemic vascular beds

Coronary/Vascular Steal: Additional reduction in perfusion pressure downstream of stenosis, further compromising blood flow to ischemic tissue

32
Q

Ischemic Heart disease examples

A

Angina pectoris

Myocardial infarction

33
Q

Angine pectoris

A

myocardial hypoxia triggers nociceptive fibers; referred pain
Myocardial infarction: severe or prolonged hypoxia damaging myocardium.
Atherosclerosis is primary cause
- CBF restriction: Subendocardium is generally first to be damaged

CV (15 decks)

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