Clinical cardiac and pulmonary physiology Flashcards
equation: MAP
MAP = SVR x CO
equation: SVR
80 x (MAP-CVP)/CO *80 converts mmHg and L/min into dyne/s/cm^5
relationship between resistance and radius
resistance inversely proportional to r^4
Where is most resistance to blood flow?
arterioles (not capillaries bc large combined area)
equation: CO
HR x SV
normal EF and causes of change
60-70%
increased in hyperdynamic states (sepsis, liver failure)
decreased in poor cardiac function
measures of preload
EDV, LA pressure, PCWP (~LA), PA diastolic pressure
causes of low preload
hypovolemia, venodilation, tension ptx, pericardial tamponade
systolic pressure variation
changes in SBP with tidal breathing or ventilation that may be observed on arterial blood pressure tracing; extreme form is pulsus paradoxus
pulse pressure variation
analagous to SPV, calculated by computer
= (PPpeak-PPnadir)/PPavg
What shifts LV filling pressure vs. CO/SV curve down and to the right?
lower contractility or higher SVR
conditions associated with decreased myocardial contractility as a cause of hypotension
myocardial ischemia, anesthetic drugs, cardiomyopathy, previous MI, valvular heart disease (dec SV independent of preload)
What shifts cardiac cycle loop down and to left on systolic pressure-volume relationship curve?
decreasing SVR
Sympathetics effect on heart
stimulation: activates B1 receptors, increasing HR via AV node conduction; increases contractility
Parasympathetics effect on heart
stimulation: profoundly slowed heart rate via muscarinic ACh receptors in SA and AV nodes
suppression: increased HR, minor effect on contractility
location and activation of baroreceptors
carotid sinus and aortic arch
-increased systemic BP -> stretch receptors signal via vagus and glossopharyngeal to CNS -> parasympathetic-mediated dec in HR and decreased sympathetics = dec contractility and reflex vasodilatation
sensitivity of baroreceptors
varies; altered by longstanding HTN
Bainbridge reflex
atrial stretch -> increased HR, helps match CO to venous return
location and activation of chemoreceptors
carotid sinus
arterial hypoxemia -> sympathetic stimulation
prolonged hypoxemia -> bradycardia, possibly via central mechanisms
oculocardiac reflex
increased ocular pressure -> bradycardia
what reflex occurs with abdominal visceral stretch?
bradycardia
Cushing reflex
bradycardia in response to increased ICP
effect of anesthetic drugs on cardiac reflexes
blunted cardiac reflexes in dose-dependent fashion
percentage O2 extraction in coronary circulation
60-70% (vs 25% of body)
backup mechanism of coronary circulation if O2 supply threatened
vasodilatation
-cannot increase extraction d/t baseline high level
endogenous regulators of coronary blood flow
adenosine, nitric oxide, adrenergic stimulation
critical coronary stenosis %
90%
-coronary compensatory vasodilatation downstream exhausted after this point
determinants of perfusion pressure to left ventricle
DBP - LVEDP
*right ventricle has lower intramural pressure and is perfused in both systole and diastole
Where is resistance to pulmonary blood flow?
larger vessels, small arteries, capillary bed
CVP normal, high, pathologic pressures
nrl: 2-8 mmHg
high: >12
path: >18
PAS normal, high, pathologic pressures
nrl: 15-30 mmHg
high: >30
path: >40
PAD normal, high, pathologic pressures
nrl: 4-12 mmHg
high: >12
path: >20
PAM normal, high, pathologic pressures
nrl: 9-16 mmHg
high: >25
path: >35
PCWP normal, high, pathologic pressures
nrl: 4-12 mmHg
high: >12
path: >20
How does increased PAP or CO affect pulmonary circulation?
distention and recruitment of capillaries, decreasing PVR by increased cross-sxl area
How do lung volumes affect intra- and extra-alveolar vessels?
large lung volumes: intra are compressed, extra have lower resistance
small lung volumes: intra have lower resistance, extra may be compressed
benefit of increased PVR at small lung volumes
divert blood flow from collapsed alveoli, e.g. one lung ventilation
drugs that affect pulmonary circulation
nitric oxide, prostaglandins, phosphodiesterase inhibitors
what is HPV
hypoxic pulmonary vasoconstriction; response to low PAO2 by diverting blood from poorly ventilated areas, decreasing shunt fraction
*normal lung can adapt, but globally hypoxic (apnea, high altitude) -> increased PAP
How do anesthetic drugs affect HPV?
Inhaled anesthetics can impair response
No inhibition with opioids, propofol
*Clevidipine = arterial vasodilator
Causes of pulmonary arteriolar thickening
certain long-standing congenital heart disease, idiopathic, cirrhosis (portopulmonary htn)
change in height vs pressure difference
20cm change in height = 15 mmHg pressure difference
lung zone 1
airway pressures > PAP & PVP
*No blood flow despite ventilation. Normally doesn’t exist, but with positive pressure ventilation or low PAP (blood loss, anesthesia) it may develop
lung zone 2
PAP >= airway pressure > PVP
*Flow is proportional to difference between PAP and airway pressure
lung zone 3
PAP, PVP > airway pressure
*normal blood flow pattern proportional to difference between PAP and PVP
At what pressure does pulmonary edema develop?
PCWP >20 mmHg
- If chronic, may tolerate to higher levels
- May also occur at lower PCWP with capillary leak, as with lung injury (acid aspiration of gastric contents, sepsis, or blood transfusion)
hypoxemia vs hypoxia
hypoxemia reflects pulmonary gas exchange
hypoxia is a more general term including tissue hypoxia and reflects circulatory factors
What is P50 on oxyhemoglobin dissociation curve?
the PO2 at which Hgb is 50% saturated with O2
*normal in adult is 26.8 mmHg
causes of left shift of oxyhemoglobin dissociation curve
P50 < 26.8 mmHg
alkalosis
hypothermia
decreased 2,3-DPG (stored blood)
causes of right shift of oxyhemoglobin dissociation curve
P50 > 26.8 mmHg
acidosis
hyperthermia
increased 2,3-DPG (chronic arterial hypoxemia or anemia)
consequence of left and right shifts of oxyhemoglobin curve
rightward: little change in O2 loading conditions but allows more O2 to dissociate into tissues, improving tissue oxygenation
fetal hemoglobin characteristics
left shifted, to allow more O2 to be carried to fetus
Haldane effect
The process of oxygen binding to hemoglobin and displacing carbon dioxide from the blood, making Hgb a stronger acid
Because of carbon dioxide being displaced from the blood, there is a downward shift in the carbon dioxide dissociation curve that takes place in physiologic settings with higher oxygen levels, such as the lungs. This facilitates the removal of carbon dioxide from the body.
