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arteries
- thicker tunica media
- built to handle high pressure
veins
- thinner walls
- more compliant (act as blood reservoirs)
endothelium
- controls vessel size
- regulates vascular tone
hypetension
causes endothelial stress and dysfunction
tunica media
- composed of smooth muscle
- controls vessel diameter
- regulates: vascular resistance & blood flow
- especially important during exercise
stroke volume
blood ejected per beat
sympathetic stimulation (heart)
- ↑ myocyte contraction force
- ↑ stroke volume
- ↑ cardiac output
preload (Starling's Law)
amount of blood in the heart chamber before contraction
left ventricular end-diastolic pressure
- describes preload
- pressure at the end of diastole
increased venous return --> increased preload
true
1 multiple choice option
decreased venous return
- ↓ LVEDP
- Poor actin-myosin overlap
- ↓ stroke volume
afterload
resistance the heart must overcome to eject blood
systole
ventricular contraction
diastole
ventricular relaxation
LUB
AV valves close
DUB
semilunar valves close
muscle pump
- skeletal muscle contraction compresses veins
- increases transmural pressure
- prevents blood stagnation
respiratory pump
- Inhalation ↓ thoracic pressure
- Helps venous return to the heart
- Faster breathing → increased heart rate
sympathetic vasoconstriction
- smooth muscle contraction stiffens veins
- pushes blood back to the heart
peripheral vascular disease
- Varicose veins
- Blood stagnation in venous system
- ↑ risk for DVT
low preload
- Poor filament alignment
- ↓ tension
- ↓ stroke volume
mitral valve regurgitation
- Blood flows back into atrium during systole
- Stroke volume may be high but effective CO decreases
- ↓ LVEDP
- Pulmonary edema → SOB
aortic valve stenosis
- Narrow valve → harder to eject blood
- ↑ afterload
- ↓ stroke volume
hypertension
- ↑ afterload
- Harder to pump blood out
- ↓ stroke volume
stroke volume resistance depends on
- blood viscosity
- vascular tone
baroreceptor relfex
a reflexive change in cardiac activity in response to changes in blood pressure
aortic arch receptor
transmits via vagus nerve to medulla, responds only to an increase in BP
increased vagal tone to SA node
- decreases HR
- decreases CO
decreased sympathetic tone to vessels
- vasodilation
- decreased resistance
bainbridge reflex
- aka atrial reflex
- atria stretches due to increased venous system
chemoreceptor reflex is triggered by
- hypoxia
- hypercapnia
- acidosis
pulse pressure equation
SBP - DBP
MAP equaltion
DBP + 1/3 (SBP-DBP)
dynamic exercise (contract & relax)
- ↑ venous return
- ↑ preload
- ↓ peripheral resistance
- ↓ afterload
static exercise (contract & hold)
- Sustained muscle contraction
- Muscles compress blood vessels
- ↑ blood pressure
- ↑ peripheral resistance
- Very high afterload
VO2 max
the maximum amount of oxygen the body can take in and use during exercise
sympathetic stimulation or HR
- ↑ ion leak
- Reach threshold faster
- ↑ HR
parasympathetic stimulation for HR
- ↓ ion leak
- Reach threshold slower
- ↓ HR
what two NTs bind to B1 receptors?
- epinephrine
- norepinephrine
epinephrine & norepinephrine bind to B1 receptors which leads to
- increase rate of depolarization
- increase HR
beta blockers
- Block B1 receptors
- Prevent epinephrine & norepinephrine binding
- ↓ HR
- ↓ cardiac output
- ↓ blood pressure
dynamic exercise
- ↓ peripheral resistance
- ↓ afterload
- ↑ venous return
- ↑ preload
- Heart works with more volume
static exercise
- ↑ peripheral resistance
- ↑ afterload
- Heart works with more pressure
dynamic exercise BP
- Systolic BP ↑
↑ venous return
↑ contractility
↑ stroke volume
- Diastolic BP ↓
↓ peripheral resistance
static exercise BP
- Very large rise in systolic BP
- Caused by vessel compression
- ↑ afterload
- Heart must pump against high resistance
Ischemia
- Imbalance between oxygen demand and supply
- Insufficient blood flow → insufficient oxygen
- Tissue shifts to anaerobic metabolism
- Can occur due to:
↑ demand not met
↓ supply not met
infarction
- prolonged ischemia
- tissue death due to lack of oxygen
hypertrophic cardiomyopathy
- enlarged heart
- less efficient pumping
- increased risk of heart failure
- due to chronic exposure to high afterload
P wave
atrial depolarization
QRS complxe
- ventricular depolarization
- atrial repolarization
- large peak due to large ventricular muscle mass
T wave
ventricular repolarization
what happens during exercise?
- increase in command (efferent) signal from motor cortex
- increase in sympathetic activity via neural stimulation and circulating catecholamines
- increased afferent signal from muscle/tendon ergoreceptors
- increased afferent signal from muscle metabolic receptors
oxygen lack theory
tissue metabolism increases --> local O2 levels decline --> insufficient O2 for smooth muscle sphincters to maintain contractino --> sphincter looses tone, blood flow increases --> oxygen arrives, smooth muscle regians ability to contract, blood flow reduced
vasodilator theory
increased metabolism/insufficient O2 delivery --> accumulation of by-products of metabolism in interstitial space --> vasodilation via action on pre-capillary sphincters and arterioles
absolute contraindications to execise testing
- acute coronary syndrome
- arrhythmias
- valvular disease
- inflammatory heart condition
- vascular issues
- heart failure
- respiratory distress
fick equation
VO2 = Q x a-vO2 difference
if you exercise less than 3 times a week...
- there will be little to no change in VO2
- possible functional improvement only
general recommendation for frequency of exercise
3-5 days per week
frequent exercise leads to
- ↑ stroke volume
- ↓ resting heart rate
- ↓ submaximal heart rate
- ↑ endothelial function
- ↑ vascular compliance
low intensity
walking slowly
moderate intensity
brisk walking (can talk, but not sing)
vigorous intensity
running (must pause for breath during conversation)
how to measure intensity
- heart rate
- RPE
Physiological Effects of Increasing Intensity
- ↑ heart rate
- ↑ stroke volume (up to moderate intensities;; plateaus at higher levels in most individuals)
- ↑ cardiac output
- ↑ a-vO2 difference
- ↑ sympathetic activation
excessive intensity can cause
- Exaggerated blood pressure response
- Large rise in systolic BP
- Possible abnormal diastolic BP response
recommendation for duration of exercise
- 20-60 minutes per day
- can be continuous or intermittent
- minimum or 10-minute bouts
lower intensity --> duration?
longer duration required (30-60 min)
higher intensity --> duration?
shorter duration sufficient
Physiological effects of time
- Sustains cardiovascular demand
- Influences plasma volume shifts
- Affects thermoregulation
cardiovascular drift
- occurs during prolonged exercise (> 10-15 minutes)
- ↑ HR
- ↓ stroke volume
- caused by: increase skin blood flow & plasma volume depletion (sweating)
excessive HR rise may indicate
- increased sympathetic drive
- low fitness level
systolic blood pressure (SBP) during exercise
- Increases with intensity
~ 10 mmHG per MET
- Due to: ↑ Cardiac output, ↑ contractility, & ↑ stroke volume
diastolic blood pressure (DBP) during exercise
- Remains stable or slightly decreases during dynamic exercise
- Due to: ↓ peripheral resistance & ↓ afterload
- Vasodilation in active muscles
red flags to stop exercise
- SBP fails to rise or drops with increase workload
- Excessive SBP rise (>250 mmHg)
- Exercise should be stopped approaching ~200 mmHg, depending on clinical context
- DBP increase > 10 mmHg during exercise
- Suggest excessive afterload
- Delayed HR recovery post-exercise
conducting zone (anatomical deadspace)
trachea --> primary bronchi (left & right) --> secondary (lobar) bronchi (2 left & 3 right) --> tertiary (segmental) bronchi (10 right, 8 left) --> interlobular bronchioles (<1 mm) --> terminal bronchioles (< 0.5 mm)
respiratory zone (ascini)
respiratory bronchioles (0.5 mm diameter) --> alveolar ducts (lined with alveoli) --> alveolar sacs --> alveoli
conducting zone
- has NO gas exchange
- NOT designed for gas exchange
- first 150 mL you breathe in does NOT get your alveoli for gas exchange
respiratory zone
- gas exchange takes place
- O2 in bloodstream
- CO2 out bloodstream
cartilage rings
- NO gas exchange can happen
- horseshoe shape allows esophagus to expand
what structures have cartilage rings?
- primary bronchi
- secondary (lobar) bronchi
- tertiary (segmental) bronchi
what structure has smooth muscle & elastic tissue?
- interlobular bronchioles (<1 mm)
- terminal bronchioles (<0.5mm)
- respiratory bronchioles
what structure epithelial cells?
- thin & have a massive surface area
- alveolar ducts
- alveolar sacs
- alveoli
the conducting zone has higher resistance because
the cross-sectional area is small
the respiratory zone has lower resistance because
the cross-sectional area is large
autonomic reflexes within the airway
- sympathetic drive
- parasympathetic drive
- irritant reflex
- low PCO2
sympathetic drive
- B2-adrenergic receptors cause relaxation of airway smooth muscle - bronchodilation
- Albuterol
parasympathetic drive
- Acetylcholine receptors cause contraction of airway smooth muscle - bronchoconstriction
- Ipratropium
irritant reflex
Particularly excite airway receptors and induce a bronchoconstriction
low PCO2
direct action on airway smooth muscle
inspiratory muscles
- diaphragm
- external intercostals
- SCM (Accessory Muscles)
- scalenes (Accessory Muscles)
- pectoralis minor (Accessory Muscles)
anterior portion of the diaphragm originates at the
ribs
3 multiple choice options
posterior portion of the diaphragm originates at the
vertebrae
3 multiple choice options
external intercostals
contract and pull the ribs up and outward
expiration is usually passive due to the recoil of the lungs
true
1 multiple choice option
expiratory muscles
- rectus abdominis
- external oblique
- internal oblique
- increase abdominal pressure
visceral pleura
lines the lung
parietal pleura
lines the thoracic cavity
intra-pleural space
fluid-filled space between the parietal and visceral pleura
what two things generate negative pressure in the pleural space?
- recoil of the lung
- spring of the chest wall
inspiration does what to pleural pressure
- Volume ↑
- Intrapleural pressure gets more negative
- Flow & alveolar pressure goes from 0 to more negative