Physiology Flashcards
The Fick principle please
CO = rate of O2 consumption/ (arterial O2 content - venous O2 content)
describe what happens in the early stages of exercise
Co is maintained by increased HR and increased SV
what maintaines CO in late stages of exercise?
CO is maintained by HR only because SV platueas
what increases pulse pressue
a) hyperthyroidism (decreased compliance = increased PP)
b) aortic regurgitation
c) aortic stiffening - isolated systolic hypertension in elferly (decreased compliance = increased PP)
d) obstructive sleep apnea - increased sympathetic tone (decreased compliance = increased PP)
e) exercise - transient
what decreases pulse pressure
aortic stenosis
cardiogenic shock (decrease SV)
cardiac tamponade
advanced heart failure (decreased SV)
relationship of PP with a) SV and b) arterial compliance
PP is proportional to SV
PP is inversely proportional to arterial complaince
describe effects of a) contractility b) preload and c) afterload on SV
Sv is increased by increased contractility
SV is decreased by increased afterload
SV is increased by increased preload
list what increases contractility
catecholamines
intraceullar Ca
decreased extracellular Na (less Na to move into the cell to kick Ca out)
digitalis (blocks Na K ATPase - less Na out of cell to move CA into the cell)
list what decreases contractility
b1 blockade (decreased cAMP) HF with systolic dysfunction (eccentric hypertrophy, in series; increased preload) acidosis** hypoxia/hypercapnia** non-dihydropyridine CCBs
what increases myocardial oxygen demand
increased contractility
increased afterload (proportional to arterial pressure)
increased heart rate
increased diameter fo ventricle (increased wall tension)
Laplace’s law
wall tension = (pressure x radius)/(2x wall thickness)
what approximates EDV?
prolaod
what does preload depend on?
venous tone
circulating blood volume
effects of nitroglycerin on preload?
decrease - venodilation
what is used to approximate afterload?
MAP
increased afterload - increased pressure - increased wall tension via laplace - increased O2 use (contractility, afterload, heart rate too)
what do vasodilators do?
decreased afterload
what do ACEi and ARBs do/
decreased afterload and preload
what does the ejection fraction represent?
ventricular contractility
normal is > 55%
what type of heart failure has a normal EF?
diastolic dysfunction (heart cant relax but can pump out ) --> normal ejection fraction systolic dysfunction (heart is relaxed, but cant pump) --> low ejection fraction
EJECTION FRACTION SI DECREASED IN SYSTOLIC HF (heart can relax, but cant pump ie dilated cardiomyopathy - decreased contractility)
EJECTION FRACTION IS NORMAL IN DIASTOLIC DYSFUNCTION (heart cant relax, but can pump)
frank starlign law
force of contraction is proportional to EDB of cardiac muscle fibre ie preload
formula: resistance =
(8 x viscosity x lenfth) / (pi resistance ^4)
what does viscosity depend most on?
hematocrit
when does viscosity increase?
hyperproteinemic states - multiple myeloma
poycythemia
when does viscosity decrease?
anaemia
describe the result on the vardiac and vascular function cruevs if inotropy
changes in contractility - altered CO for a ive RA pressure
describe the result on the cardiac and vascular function curves of venous rerun
changes in circulating colume or venous tone - altered RA for a given CO
describe the result on the cardiac and vascular function curves of TPR
changes in TPR - altered CO at a five RA pressure, however the mean systemic pressure is unchangesd
qhat causese the mean systemic pressure to change?
altered blood volume or venous tone
what is S3?
early diastolic
normal in chidren and pregnancy
abnormal when have increased filling pressures ie mitral regurgitation, HG, dilated ventricles (systolic dysfunction)
what is the a wave?
atrial contraction
absent in atrial fibrillation
when does the mitral valve close in relation to the jugular venous pulse wave?
low pressure point between a and c wave
what is the c wave?
rapid ejection of ventricular systole and tricuspid pushed up int othe atrium
what is the x descent
ventricle is platuea - occurs beore the t wave
blood still leaving ventricle, but its not squeezing at max
no tricuspid buldge
what is the v wave?
atrila is filling and the ventricle is relaxed,
mitral valve is closed
when does the mitral valve open in relation to the jugular venous pulse wave?
between the v and y wave
what is the y descent?
when mitral valve opens and blood enters the ventricle from the atrium
describe the phases of the myocardial action potential that occurs at the myocardium, bundle of HIs and purkinje fibres
phase 0 - rapid upstroke, depol, vg Na
phase 1 - initial repol 0 inactivation of vg Na, vg K start to open
phase 2 - platuea - vg Ca channels balance K efflux. Ca -induced calcium release from the sarcoplasmic reticulum
phase 3 - rapid repol - slow vg K open
phase 4 - resting potential - high K perm through leak channels
describe the action potential phases in the pacemaker
phase 0 = upstroke - vg Ca channels. (fast vg Na are permanently inactivated bc resting membrane potential is about -70 too high to reactivate). results in a slow conduction veloscity that is used by the V node to prolong transmission from the a to the v for filling
phase 1 - absent
phase 2 - absent
phase 3 - inactivation fo CA channels and increased activation fo K channels - increased K efflux
phase 4 - slow spontaneous diastolic depol as na conductancec increased (If). accounts for automaticity of SA and AV nodes.
what determines heart rate
the slow of phase 4.
p wave?
atrial depol
PR interval
3 small squares to 5 small squares
0.12-0.2 sec
atrial depol start to start of ventricular depol
QRS complex
2 small squares to 2.5 small squares
0.8-0.1 sec
ventricular depolarization normally >120 msec
QT interval
ventricular depolarization, mechanical contraction of the ventricles, nventricular repolarization
8 small squares to 11 small squares
0.32 sec to 0.40 seconds
J point
junction between end of QRS complex, and start fo ST segment
ST segment
isoelectic
ventricles depolarized
U wave
caused by hypokalenima and bradycardia
what effect does hypokalemia have on the ECG?
U wave appearance (also occurs in bradycardia)
what predisposes to torsades de pointes?
increased QT interval
normal 8-12 small squares/0.32-0.4 sec
list specific causes of increased QT interval and risk fo trades de pointes
antiatthythmics A (class IA and III, antibiotics B (macrolides), anticycholites C (haloperidol), antidepressnats D (TCAs), antiemetics E (ondansetron)
low potassium
low magnesium
how to treat torsades de pointes
magnesium sulfate
Romano-Ward SYndrome
AD
no deafness
inherited disorder of myocardial repolarization typically due to ion channel defects
increase risk of sudden cardiac death due to torsades de points
Jervell and Lange-Nielsen syndrome
AR
sensineural deafness
inherited disorder of myocardial repolarization typically due to ion channel defects
increasd risk of sudden cardiac death due to torsades de pointes
Brugada SYndrome
ECG changes: pseudo-RBBB and ST elevations in V123
AD
most common in Asian males
increasd risk of ventricular tachyarrhythmias and sudden cardiac deacl
prevent with implantable cardioverter-defibrillator
Wolff-Parkinson-White Syndrome
MOST COMMON ventricular preexcitation syndrome
buncle of kent - bypass AV node delay to ventricles = DELTA wave and widened QRS complex with decreased PR interval
may result in re-entry circuit supraventricular tachycardia
what is associated with atrial fibrillation
hypertension coronary artery disease rheumatic heart disease binge drinking HF valvular disease hyperthyrodisin atrial stasis -- cardioembolic events
list the irregular ECG tracings
atrial fibrillation
ventricular fibrillation
second degree, Mobitz I aka Wenckebacj
list the regular ECG tracings
atrial flutter
1st degree AV block
mobitz II 2nd degree AV block
3rd degree, complete
lyme disease arrhtymia plase
3rd degree block
regulary irregular
2nd degree block Mobitz I
describe role of ANP
released from volume overloaded/increased pressure in atrial myocytes –> acts via cGMP to:
a) vasodilate
b) decrease absorption of Na in collecting ducts
c) dilates afferent arteriole, constricts efferents to promote diuresis
d) aldosterone escape
describe role of BNP
released from ventricular myocytes in respone to increased tension. longer t1/2 than ANP
BNP blood test use to diagnose HF (good NPV)
can be used to treat HF (recombinant form - nesiritide)
a) vasodilates
b) decreased Na reabsorption in the collecting fucts
c) promotes diuresis - dilates afferent and constricts efferent arterioles
d) aldosterone escape
aortic arch baroreceptors respond to?
increased BP only
carotic body baroreceptors respond to?
increased and decreased BP
how does cartodi massage work?
increased pressure on carotid body - mimics increased bp by stretching - increased afferent baroreceptor firing - increased AV node refractory period - decreased HR
what is cushing reaction
increased intracranial pressure contricst arterioles - cerebral iscahemia - increased pCO2 and decreased pH - central reflex sympahteti increase perfusion pressine ie hypertension - causes strcht in barareceptors that increased para sympathetic output
a) hypertension
b) bradycardia
c) respiratory depression
peripheral chemoreceptors are stimulated by?
<60 mmHg of PO2
increased PCO2 and decreased pH
central chemoreceptors are stimulated by?
increasd PCO2 and decreased pH
PCWP measures?
left atrial pressure
pressure in RA?
< 5 mmHg
pressue in RV?
25/5 mmHg
pressure in pulmonary circulation
25/10 = mmHg
PCWP should be what?
<12 mmHg
Pressure in LA
<12 mmHg
pressure in LV
130/10 mmHg
pressure in aorta
130/90
when will PCWP > LV diastolic pressure?
mitral stenosis
autoregulatio in heart
adenosine, NO, CO2, decreased O2
autoregulation in brain
CO2
autoregulation in kidneys
myogenic and tubuloglomerular feedback
autoregulation in lungs
hypoxia causes vasoconstriction **unique shunts blood to hyperox areas
autoregulation in skeletal muscle
@ exercise - H, K, lactate, adenosine
@ rest - sympathetic tone
autoregulation in skin
sympathetic control for temperature control is most importnat
causes of oedema
increased capillary pressure @ HF
decreased plasma proteins @ nephrotic syndrome and liver failure
increased capillary permeability @ toxins, infection, burns
increased interstitial fluid colloid osmotic pressure @ lymphatic blocakge
