CP/SL Exam Flashcards
Equation for O2 consumption (VO2)
VO2 = COx(arterial O2 - venous O2)
Cardiac Output/Flow
CO = HRSV or change in P (MAP - CVP)/TPR or vA or (change in P * pi * r^4)/(8Lviscosity)
Normal range of CO
5-6L/min
25L/min with exercise
Sides that pump to systemic vs pulmonary
Left = systemic Right = pulmonary
Normal Blood Volume
5L
Which circulation system is in parallel vs series?
Systemic = parallel (except liver has both) Pulmonary = series
Liver blood sources
Hepatic artery & portal vein from GI system
MAP
about 95mmHg
mean arterial pressure = mean aortic pressure
MAP = DBP + PP/3
CVP
about 2mmHg
central venous pressure = vena cava pressure
Normal systemic BP & pulmonary BP
Systemic 130/80
Pulmonary 25/10
Mechanisms to help pressure drop
- Reduce outflow - increase resistance in organs that do no have high demand for nutrients
- Increase inflow (CO) - increase HR or contractility (SV)
- Increase Volume - short term, veins; long term, kidneys
How much blood does the venous system hold?
about 70%
P of right atrium
2mmHg
P of left atrium
8mmHg
P of right ventricle
25/5mmHg
P of left ventricle
130/10mmHg
P of pulmonary artery
25/10mmHg
Mean = 15mmHg
P of aorta
130/80mmHg
Mean = 95mmHg
P of pulmonary capillaries
8mmHg
P of systemic capillaries
25mmHg
Route of electrical impulse through heart
SA -> AM -> AV -> His/P -> VM
What has fast APs? slow APs?
Fast - His/P, AM, VM
Slow - SA, AV
Fast AP
Phase 0: rapid depolarization, inward Na current
Phase 1: repolarization from inactivation of Na channel, activation of outward K+
Phase 2: plateau - slowly activating inward Ca2+ currents
Phase 3: repolarization from inactivation of Ca2+ currents and activation of IKr & IKs (K channels)
Phase 4: resting potential from inward-rectifying K channels (IK1)
Slow AP
Phase 0: slow depolarization from slow activating Ca2+ channels (NOT NA)
Phase 3: repolarization from Ca2+ inactivation and activation of K channels
Phase 4: slow depolarization
effective refractory period
only single AP can be elicited, not propagated AP
IK,Ach or IGIRK
If
IK,Ach or IGIRK - outward current, hyperpolarizes cell/SA node - PNS
If - inward current, nonselective ion channel (HCN), depolarizes - SNS
Pace of SA node, AV node and His/Purkinje fibers
SA node - 100bpm
AV node - 40-60bpm
His/Purkinje - 30-40bpm
Dromotropic effects
Conduction velocity
Positive - increases (SNS)
Negative - decreases (PNS)
P-wave
atrial depolarization
PR segment
conduction through AV node
QRS complex
ventrical depolarization
Q wave often too small to detect
bundle branch block
QRS widens
ST segment
all ventricular tissue depolarized, plateau phase, beginning of repolarization
T wave
repolarization of ventricles
Lead I
Right arm to left arm
Lead II
right arm to left leg
Lead III
left arm to groin
AVL, AVF, AVR
A = abdomen L = left arm F = femoral artery R = right arm
shifts in MEA with hypertrophy
RVH - clockwise
LVH - counterclockwise
First degree, second degree, third degree AV block
First - PR interval increases
Second - P wave not always followed by QRS
Third - pacemaker is His/P
What happens to ST interval with MI or ischemia?
ischemia, early stages of MI - ST depression
late stages MI - ST elevation
S4
atrial gallop - stiffened ventricle
S3
ventricular gallop - more flexible ventricle
normal in children/young adults
dilated cardiomyopathy in adults
S2
aortic valve closes
S1
mitral valve closes
Normal SV
about 60-100mL
Normal EF
55-70%
Increased preload
Increases EDV, EF, SV, CO
Increased afterload
Increases ESV
Decreases EF, SV, CO
Increased inotropy
Decreases ESV
Increases EF, SV, CO
Largest SA
capillaries
Largest pressure drop
arterioles
due to increase in TPR
Poiseulle’s law
Q or CO = (change in P * pi * r^4)/(8Lviscosity)
factors increasing viscosity
increased hematocrit
loss of plasma
sickle cell anemia
PP
SBP - DBP
Which type of shock do you not want to give a vasodilator?
Vasodilatory/septic
Deviations from poiseulle’s law
- turbulence
- viscosity changes with velocity
- compliance of blood vessels
Reynold’s number
NR = (v*d*density)/viscosity >2000 = turbulent (aortic stenosis)
compliance
change in V/change in P
decreases with increasing wall thickness
Starlings law of the capillary
Q = k*[(Pc + Oi) - (Pi + Oc)]
Local control of blood flow through capillaries
A. metabolic wastes vasodilate
B. myogenic - smooth muscle contracts/relaxes
Central control of blood flow through capillaries
A. Humoral
ANP, AngII, Epi, NO, ET-1
B. Neural
norepi
Atrial Natriuretic Peptide (ANP)
vasodilator
released by atrial myocytes
excretion of Na+ and water
Angiotensin II
potent vasoconstrictor (increases TPR)
retention of Na (increases BV)
stimulates thirst & ADH release
stimulates aldosterone synthesis
Epi
vasodilator in liver, heart and skeletal muscle (B2)
vasoconstriction (a1)
increases HR
NO
EDRF
formed from arginine
vasodilator
produced by endothelium
Endothelin (ET-1)
potent vasoconstrictor
released by endothelial cells
Rate-pressure product (RPP)
RPP = HR * SBP increase = increased O2 demand
Apical skin
hand, feet, ears, nose, & some face
has lots of AV anastomoses
Cerebral Perfusion Pressure
MAP - ICP (intercranial pressure)
Glomerular vs Peritubular capillaries
Glomerular - high P, filter stuff out
Peritubular - low P, reabsorb
Changes in filtration due to changes in AA & EA resistance
AA with low R - increases filtration/flow
AA with high R - decreases filtration/flow
EA with low R - increases flow
EA with high R - decreases flow
Nicotinic receptors
all postganglionic neurons, adrenal medula and skeletal muscle
Muscarinic receptors
effector tissues for PNS & sweat glands (SNS)
PNS vs SNS ganglionic neurons
PNS pre - long post - short SNS pre - short post - long
Alpha1 adrenergic receptors
stimulated by NE and E
radial muscles of eye->dilation
contraction of blood vessels->inc. P
Alpha2 adrenergic receptors
presynaptic
stimulated by NE and E
autoregulatory - inhibits release of NE
Beta1 adrenergic receptors
heart
stimulated by NE and E
increases HR and inotropy
Beta2 adrenergic receptors
stimulated by only E
relaxes bronchi
vasodilates
increases glycogenolysis in liver/skeletal muscle
far vision through dilation of pupil (ciliary muscle relaxes)
Bronchioles
SNS
B2 - increase airway radius
PNS
M3 - opposite
Heart
SNS
B1 - increase HR, contractility, and nodal conductance
PNS
M2 - opposite
Blood vessels
SNS
a1 - vasoconstrict in viscera
B2 - vasodilate in skeletal muscle
Liver
SNS
B2 - increase glycogenolysis/gluconeogenesis
Pupil
SNS
a1 - dilate/increase pupil radius
PNS
M3 - opposite (sphincter muscle)
Ciliary muscle
SNS
B2 - relaxation for far vision
PNS
M3 - contraction for near vision
High Pressure (arterial) Baroreceptors
exposed nerve endings
Carotid sinus - glossopharyngeal nerve (IX) - cerebral blood flow
Aortic arch - vagus nerve (X) - systemic blood flow
Low Pressure (cardiopulmonary) Baroreceptors
cardiac atria and pulmonary artery
A receptors - report on HR (sense atrial wall tension during contraction)
B receptors - report on atrial volume (sense atrial stretch during filling)
Chemoreceptors
CO2 levels
located in carotid fork and aortic arch
Where do the baroreceptors signal?
nucleus tractus solitarius (NTS) in the CV center (in medulla oblongata)
Increase in baroreceptor firing rate
negative signal to Vasomotor Center (lowers SNS - controls HR and SV)
positive signal to Cardioinhibitory Center (increases PNS - controls HR only)
Vasoactive vs nonvasoactive substances
Vasoactive - affect vascular smooth muscle cell contraction and relaxation
Nonvasoactive - affects blood volume
serotonin
vasoconstrictor
histamine
vasodilator
vasopressin
vasoconstrictor at high conc.
increased water reabsorption
Increased renin
due to decreased BP
cleaves angiotensinogen to AngI
ACE
angiotensin converting enzyme
AngI -> AngII
aldosterone
increases retention of Na and water
stimulated by AngII
Does a change in TPR change the mean circulatory pressure?
no
Static exercise
Increase HR, TPR, BP, PP
Decrease SV, CO
Dynamic exercise
Increase HR, SV, CO, BP, PP
Decrease TPR