CV A&P: APs, DO2, Flow Flashcards
Ventricular myocytes
RMP vs TP
How does K & Ca affect RMP & TP?
↑K = ↑RMP
↑Ca = ↑TP
the wave of depolarization is facilitated by
gap junctions
Ventricular myocytes have (less/equal/more) mitochondria than skeletal.
more
automaticity vs excitability
Automaticity: generate AP spontaneously
Excitability: respond to an electrical stimulus by depolarizing and firing an AP
How do K levels affect signal propigation?
↓K = (-) RMP = resist depolarization
↑K = (+) RMP = easier depolarization
to an extent! severe hyperK can block depolarization
In excitable tissue, the primary job of the sodium-potassium ATPase
restore the ionic balance towards RMP
cardiac myocyte O2 consumption at rest
8-10 ml/O2/100g/min
What makes cardiac muscle similar and different to neural and skeletal tissue?
- like neurons: can generate a RMP & propagate an AP
- skeletal: have actin & myosin contractile elements
- unique: intercalated disc junctions = fxnl synctium, gap jxns, more mitochondria
no net ion movement
equilibrium potential
charges inside = charges outside
conductance
ability to transmit electrical current
open ion channels increase it, while closed ones decrease it
The 4 “-tropies”
- Inotropy: myocardial contraction force
- Chronotropy: heart rate
- Dromotropy: conduction velocity (velocity = distance / time)
- Lustropy: rate of myocardial relaxation
RMP is determined by 3 things:
- Chemical force (concentration gradient)
- Electrostatic counterforce
- Sodium/potassium ATPase
T/F:
At rest, nerve cells continuously lose positive charge.
True
continuously leaks K+
T/F:
A cell can only depolarize from Na+ influx.
False
Ca influx also works
Which part of the cycle is the “all or nothing” phenomenon
depolarization
T/F:
In excitable tissue, an AP reults in depolarization.
FALSE
depolarization results in an action potential
(so long as TP is achieved)
When does the cell repolarize?
When K leaves or Cl enters
T/F:
After repolarization, the cell typically hyperpolarizes for a very short time.
True
T/F:
A hyperpolarized cell can be depolarized.
True
more difficult tho
the 2 actions of the Na/K/ATPase
- removes Na that entersed during depolarization.
- returns K that left during repolarization
the positive inotrope that inhibits Na/K/ATPase
Digoxin
Severe hypoK makes MRP more negative, so its harder to depolarize. How does severe hyperK have the same effect?
severe hyperK inactivates Na channels (remain closed-inactive state)
When is hyperK purposely induced? Why?
- Potassium containing cardioplegia solution used during cardiopulmonary bypass arrests the heart in diastole.
- This prevents repolarization & locks the Na channels in their closed-inactive state.
How do Ca levels affect conductivity?
- HypoCa = TP more (-) = depolarize easily
- HyperCa = TP more (+) = resist depolarization
K will have the opposite effect on ease of depolarization
How does IV calcium reduce the risk of dysrhythmias in hyperkalemia ?
increases the gap between RMP and TP
hyperK increases RMP = more depo
more Ca increases TP = less depo
Which phase of the ventricular action potential is associated with the
GREATEST calcium conductance?
2
What gives myocytes time to contract?
their AP has a plateau phase which prolongs depolarization
(unlike neurons)
These structures do not have a plateau phase
SA & AV nodes
Which parts of the EKG correspond to each AP phase?
Which current is responsible for spontaneous phase four depolarization in
the SA node?
The funny current (I-f)
the primary determinant of the pacemaker’s intrinsic heart rate.
AKA it sets the rate of spontaneous phase four depolarization in the SA node.
The order of the cardiac conduction system
SA Node → Internodal Tracts → AV Node → Bundle of His → Left & Right Bundle Branches → Purkinje Fibers
The heart rate is determined by
intrinsic firing rate of the SA node
(its rate of phase 4 spontaneous depolarization) & autonomic tone
Disease or hypoxia of the SA node impairs its function as the dominant pacemaker. In this situation, which cells takeover?
next highest rate of **spontaneous phase 4 depolarization **
Volatile anesthetics depress the automaticity of the SA node, which explains why these drugs can cause…
junctional rhythm
The SA and AV node action potential consists of 3 phases:
- Phase 4 = Spontaneous depolarization: Nat in (I-f) and then Ca in (T-type)
- Phase 0 = Depolarization: Ca in (L-type)
- Phase 3 = Repolarization: K+
No phase 1 or 2!
Physiologically, we can increase the heart rate by…
(2)
- increasing the rate of phase 4 spontaneous depolarization
and/or - bringing RMP and TP closer together
Name the internodal tracts
The SA node has a (lower/higher) RMP than a myocyte
higher
The AV node has a slower intrinsic firing rate than a myocyte, as evidenced by…
lower phase 4 slope
The SA node’s membrane is leaky to
Na
I-f current is activated by
HYPERpolarization
Intrinsic firing rates of the conductive tissues
… of the SA node determines the intrinsic heart rate.
The rate of spontaneous phase 4 depolarization
T/F:
All the cells in the myocardium are capable of automaticity (self-generating an action potential).
True
each cell type has its own intrinsic rate of spontaneous depolarization
What determines how frequently the heart depolarizes?
The cells with the fastest rate of depolarization
The ANS modulates HR. Which structures of the SNS and PNS control heart rate?
- PNS: right vagus innervates the SA & left vagus innervates the AV
- SNS: Cardiac accelerator fibers (1-T4)
We can alter the heart rate by manipulating three variables:
- The rate of spontaneous phase 4 depolarization
- Threshold potential
- Resting membrane potential
How do we manipulate phase 4 spont. depo, RMP & TP to increase HR?
- Increase slope of phase 4 depo
- slope constant, but TP more negative
- slope constant, but RMP more positive
Which NTs and receptors of the SNS & PNS affect HR?
SNS:
Norepi @ B1 increases HR by increasing Na & Ca conductance, increasing phase 4 slope
PNS:
ACh @ M2 slows HR by** increasing K conductance & hyperpolarizing** the SA node (↓ RMP & phase 4 slope)
CaO2, DO2, VO2, and CvO2
for a 70 kg adult
- CaO2: Arterial oxygen content = 20 mL/O2/dL
- DO2: Oxygen delivery = 1,000 mL/min
- VO2: Oxygen consumption = 250 mL/min
- CvO2: Venous oxygen content = 15 mL/dL
CaO2
oxygen content
g of O2/dL of arterial blood
DO2
delivery
O2 carried in blood and how fast its delivered to tissues
EO2
extraction ratio (by tissues)
whole body = 25%
VO2
consumption (by tissues)
CvO2
venous oxygen content
15 ml/dL
- brackets = O2 carrying capacity (CaO2)
- 10 is a conversion factor that corrects Hgb g/dL and CO L/min
Example: If CO = 5 L/min and CaO2 = 20 mL/dL, then DO2 = 1,000 mL 02/min.
If CO = 5 L/min and CaO2 = 20 mL/dL, then DO2 = ___
1,000 mL O2/min
External respiration
- Ventilation
- Distribution
- Diffusion
- Perfusion
if PaO2 = 100mmHg, what is SaO2?
98%
CO NR
5L/min
CO= HR x SV
What makes up SV?
- preload
- afterload
- contractility
What makes up interal respiration?
EO2 (extraction)
VO2 (consumption)
PvO2 & SvO2 NR
PvO2 = 40 mmHg
SvO2 = 75%
DO2 comprises of these 2 concepts
- amount of oxygen in blood
- speed of delivery to tissue
Most oxygen is bound to Hgb, while a small amount is dissolved in the blood. The dissolved oxygen follows this law
gas dissolved in a solution = Henry’s law
at a constant temperature, the amount of gas that dissolves in solution is directly proportional to the partial pressure of that gas
factors for
Hgb’s O2 carrying capacity
&
O2 dissolved in blood
2 Laws that can describe flow
Ohm’s
Poiseuille’s (uses Ohm’s, adds vessel diameter, viscosity and tube length)
Ohm’s Law
How does changing the radius increase flow?
Vascular resistance is primarily determined by
the radius of the arterioles
Small changes in vessel diameter can yield profound effects on tissue blood flow.
Reynolds’ number (Re)
predict if the flow is laminar or turbulent
- Re < 2,000: mostly laminar
- Re = 2,000 - 4,000: transitional flow
- Re > 4,000: mostly turbulent
vibrations
murmur vs. bruit
murmur = valvular Dz
bruit = carotid stenosis
Blood viscosity is directly proportional to ___ and inversely proportional to ___.
hematocrit
body temperature
When giving PRBCs, we improve flow by diluting w/ NS & warming device
Ohms equation as it applies to HD
Calculating MAP using CO & SVR
Poiseuille’s Law
How to determine increase in flow from radius
laminar
vs.
turbulent
vs.
transitional
- Laminar: parallel path thru tube
- Turbulent: non-linear & will create eddies
- Transitional: laminar along walls & turbulent in center
Which flow loses energy? and to what?
turbulent
to heat & vibration
Viscosity is the result of
friction from intermolecular forces as a fluid passes through a tube
Blood viscosity is determined by ….. & inversely r/t ….
hematocrit & body T
temperature
(↓T = ↑viscosity ➡️ ↑ resistance)