CV Workshop I, Nov. 8, 1-3PM
All Groups – Lecture Hall Lunch List (meet at noon by the
5th floor elevators)
CV Workshop II, Nov. 9 9-11AM VALLE, EVAN
Groups A & C - Lecture Hall
YESHWANT, SRINATH
CV Workshop II, Nov. 10 9-11AM
Groups B & D – Lecture Hall YU, DIANA
BAYER, KATHERINE
CIRCSIM Monday Nov. 13 9-11AM
Groups A & C – Computer Lab BUCHMAN, RICHARD
CIRCSIM Tuesday Nov. 14 9-11AM CHANG, ALEXANDER
Groups B & D – Computer Lab
CHRUSCINSKI, ELIZABETH
Exam Review Session Wesdnesday Nov. 8 DESAI, PALAK
3-4PM in the lecture hall
DUTMER, CULLEN
FARAG, MARK
Download and install instructions for GANACIAS, KAREN
Hemoflex
FAQ for Hemoflex GREENSPAN, MICHAEL
Lectures 2 & 3 Quizzes
What is the primary determinant of cardiac output?
a. Stroke volume
b. Mean arterial pressure
c. Total peripheral resistance
d. Heart rate
MAP must be regulated. It cannot be allowed to rise too high
or fall too low.
MAP = CO (TPR)
CO = SV (HR)
CO and TPR vary short term.
BV varied long term.
The cardiovascular control center is
located in the medulla. There are a large
number of inputs to it from the cortex and
sensory receptors. Its outputs drive the
sympathetic and parasympathetic
pathways that control the cardiovascular
effectors.
The primary sensory inputs that
determine cardiovascular function are:
a. Baroreceptors
b. Volume receptors
IXth cranial nerve
When the input to the CNS decreases
(signaling that MAP is decreased):
Sympathetic output increases,
parasympathetic output decreases
resulting in:
SA node (pacemaker) → increases HR
Ventricular myocardium → increases
inotropic state Xth cranial nerve
Resistance vessels in renal, splachnic,
skin, and muscle beds (increases TPR)
Capacitance vessels in the splanchnic
circulation → increased circulating BV
The baroreceptor reflex is a negative
feedback system that functions to
minimize changes in MAP (the regulated
variable)
Parameter DR RR SS
IS
CVP
SV
Rv
-
HR
- CO
BV CBV
Art. Res.
CVP
MAP
-
IS SV CO MAP
-
HR TPR
-
Ra
-
BR-CNS
Any disturbance introduced into the system, that produces a
change in MAP (a Direct Response or DR) will give rise to a
Reflex Response (RR), and eventually a new Steady State (SS)
RULES FOR USING CONCEPT MAP
1. Start with the disturbance and propagate the changes to determine the change in
MAP that occurs (the Direct Response).
A variable can change (increases/decreases) only once during any phase of the
response (DR, RR, SS). As the disturbance is propagated to each unchanged cell,
the "first" change that occurs determines the new state of the variable ("later"
changes that arrive at a cell that has already changed can only affect the magnitude
of the initial change not its direction). This rule applies to each of the three phases
of the response.
2. The reflex response generated by BR-CNS will compensate for the original change
in MAP (see Rule 1) by changing the values of Ra, HR and IS.
a. Changing Ra changes TPR (one of the two determinants of MAP).
b. Changing HR changes CO (remember, changes in CO are most often the result
of change in HR). Any change in CO will result in an opposite change in CVP
(and hence a change in SV).
c. The reflex change in IS minimizes the change in SV but doe not reverse the
direction of the change (see Rule 1a).
d. The reflex response will return MAP towards its initial, pre-disturbance level,
but will not fully compensate.
3. The new Steady State that is achieved will be a “sum” of the DR and the RR
responses.
TAKE HOME MESSAGE
MAP is REGULATED (held as constant as possible by active physiological mechanisms.
HR, IS, Ra are CONTROLLED (their values are changed, determined by, the nervous
system so as to minimize the change in MAP). HOWEVER, compensation is essentially
never complete (MAP is never restored exactly to its initial level)
Parameter DR RR SS
IS
CVP
SV
Rv
-
HR
- CO
BV CBV
Art. Res.
CVP
MAP
-
IS SV CO MAP
-
HR TPR
-
Ra
-
BR-CNS
Volume receptors decrease firing in response to decreased volume → increased ADH
→ increased water retension → increased blood volume
Decreased firing from baroreceptors → increased aldosterone, renin → increased
water retension → increased blood volume
Physical Exam
• Vitals in ED
– T. 99.0
– P 104 regular and diminished
– BP 104/62
– R28 labored
– Spo2 89% on room air 94%
on 3L O2
– Weight 132 lbs (increased from
115 lbs documented in clinic 1
month ago)
MAP = 76
Other reflexes
Bainbridge reflex (probably not particularly important in man)
Stimulus: increased atrial volume
Response: increased HR
Magnitude of response depends on balance between Bainbridge and baroreceptor
reflexes
Chemoreceptor reflex
Stimuli: decreased arterial PO2, decreased pH, increased PCO2
Receptors: carotid and aortic bodies (peripheral chemoreceptors)
Primary response is respiratory (increased rate and depth of breathing)
Secondary response is cardiovascular (reflex vasoconstriction, increased heart rate)
Increases CO and MAP
When severe hypoxia is present the resulting cardiovascular response assists in
delivery of oxygen to the tissues, particularly the brain and heart (where
vasoconstriction does not occur)
CNS ischemic response - Cushing reflex
Stimuli: MAP below 50 mm Hg or increased intracranial pressure (stimulates
neurons in CV control centers via as yet unknown agents, possibly decreased O2,
decreased pH, increased PCO2, increased [K+])
Response: massive sympathetic outflow which leads to increased TPR
(vasoconstriction) which gives rise to increased MAP (partially overcomes effects of
increased intracranial pressure); this in turn leads to reflex bradycardia (vagal)
Parameter DR RR SS
IS 0
CVP ↓
SV ↓
Rv
-
HR 0
BV CBV
- CO ↓
Art. Res. 0 ↑
CVP
MAP ↓ ↑
-
IS SV CO MAP
-
HR TPR
-
Ra
-
BR-CNS