Chapter 3: Cardio (not everything, mainly equations) Flashcards
Velocity of blood flow can be expressed as
V= Q/A
Q= Flow ( mL/Min) A= Area (cm^2)
As blood flow goes up so does velocity.
As cross sectional area goes up, velocity decreases. (Low in capillaries since they have the largest cross sectional area)
Q = dP/R
Flow = Change in Pressure / Resistance (TPR)
dP= MAP -Right Atrial Pressure
Analogous to ohms law: I (flow) = V(voltage or Pressure) / R (resistance)
Poiseulles law
To determine Resistance
R = (8 x Viscosity x Length) / pi x r^4
In this, changes in radius have the larges effect on resistance.
The larger the radius the less resistance (by exponent 4)
Really just remember R= Viscosity x L / R^4 (the other crap won’t change but these will)
Is resistance in the vascular system in series or in parallel ?
Parallel (like the capillary bed)
With excetption of going from one organ to the next (series), blood flow is set up in parallel
Blood flow where there is no leading edge, fluid moves in a solid wall
Laminar
When Reynolds Number is increased, is there an increased or decreased chance of turbulence ?
Increased
As blood viscosity decreases, is there an increase or decreased chance of turbulence ?
Increased
As velocity of blood flow decreases is there an increased or decreased chance of turbulence ?
Decreased
Capacitance
The distensibility of a vessel (ability of a vessel to accommodate increased volume with minimal increases in pressure)
C= V/P
Capacitance = Volume/ Pressure
decreases with age
Is capacitance higher in veins or arteries ?
VEINS (of course, did i really need to ask ?)
Where in the vascular system is the decreases in blood pressure most pronounced ?
Across the ARTERIOLES !
Aorta: 100 mmHg
Arterioles: 50 mmHg
Capillaries: 20 mmHg
Vena Cava: 4 mmHg
Pulse Pressure
Systolic - Diastolic
Mainly determined by STROKE VOLUME
Decreases in capacitance leads to pulse pressure increases
MAP
Diastolic + 1/3(Pulse Pressure)
Pulse pressure = Systolic - Diastolic
P Wave
Atrial Depolarization
Atrial Repolarization
Burried in the QRS
PR interval
Beginning of P-wave to beginning of Q
R = QRS complex, they just don’t want to say it.
PR interval varies with conduction velocity through the AV Node
QRS Complex
Depolarization of the Ventricles
QT Interval
Beginning of the Q wave to the End of T-wave.
Represent Ventricular Depolarization and Repolarization
ST Segments
End of the S-wave to the beginning of the T-wave
T-wave
Ventricular Repolarization
What ion determines the resting membrane potential ?
K+ (the equilibrium potential of -94 is close to resting membrane potential)
In general, inward current of ions should _______ the cell
depolarize ( I, know this isn’t necessarily true, only with Cations)
Outward flow generally hyperpolarizes the cell
Phase 0 is mediated by opening of which Voltage Gated channel ?
Na+ ( leads to an inward current) and depolarization of cell
Phase I is mediated by
Brief depolarization when Na+ gates close and K+outflow
Phase II
Plateaus mediated by outflow of K+ and inflow of Ca++
Phase III
Reolarization
K+ outflow and Ca++ channel closing
Phase IV
Resting membrane potential
Where inward an outward K+ channels equal each other
The Atria, Ventricles and Purkinje system have the same resting membrane potential , what is it ?
-90
What is the pacemaker of the heart
SA node (membrane potential at around -65 mV)
Along with the SA node, what other portions of the heart can be considered pace makers ?
AV node, His-Purkinje system (When the normal pacemakers are insufficient or absent)
Phase O of SA Node
Fast upstroke mediated by Ca++ influx
Phase 3 of SA node(yes, there are no phases 1 and 2)
Repolarization
Outward K+
Phase 4 of SA Node
Slow depolarization
Reason for autonomous pacemaker ability of SA node
I-f (
What causes an upstroke in the action potential for the AV node ?
Ca++ (Just like the SA node, unlike the other portions of the heart in which phase O is Na+ mediated)
An increase in the inward current will lead to an __________ in the conduction velocity of excitation in the hard.
Increase
Where is the conduction velocity the greatest in the heart ?
Purkinje System
Where is the conduction velocity the slowest in the heart ?
AV node.
This is the P-R interval (beginning of P to beginning the QRS complex).. Slowing in the AV allows for ventricular filling before contraction and ejection.
Excitability
The ability of cardiac cells to initiate AP’s in response to inward currents.
Depends on the ability of the cells to recover from previous depolarization.
Absolute Refractory Period
Period in which another AP cannot be generated , even with increasing stimuli
Begins with the upstroke (0) of the AP and ends at the end of the plateau phase (2)
Effective Refractory Period
Slightly longer than ARP (conducted action potential cannot be elicited)
Relative Refractory Period
Just after the ARP , point at which a higher than normal stimulus can elicit an action potential.
Chronotropic Effects
Effects on heart rate (usually by modulating phase 4 of the SA node)
Increase or decrease the Ca++ influx
Dromotropic Effects
Cause changes in conduction velocity through the AV node
What phase do negative chronotropic effects work in ?
Phase 4 (of SA node). Inhibits spontaneous depolarization
An negative dromotropic effect will ______ the PR interval
Elongate.
Remember, domotropic events modulate conduction velocity (through the AV normally)
How is the cardiac Sarcomere similar to SkMu ?
Between Z-lines
Has Actin and Myosin filaments (also troponin and tropomyosin)
What special cell communication structures are seen in the intercalated disks of cardiac myocytes ?
Gap Junctions (allows for portions of the heart to act as syncytium
are mitochondria more or less frequent in cardiac muscle as compared to SkMu ?
Cardiac
What is the function of T-tubules ?
To carry the Action potential to the cell interior (more prevalent in ventricles)
During the plateau phase Ca++ enters the cell, what kind of Channels mediate this ?
L-Type Ryanodine Receptors
Like in SkMu what does Ca++ bind to to initiate excitation contraction coupling ?
Troponin C which pulls tropomyosin out of the binding spot allowing for myosin to bind .
Contractility
Intrinsic Ability of cardiac muscle to develop force at a given muscle length.
How is contractility often assessed ?
Via the ejection fraction.
Inotropic effects
Those which modulate contractility
How do sympathetic agents increase contractility ?
- Increase the amount of Ca++ that comes in during phase II of the AP
- Increases the activity of phospholamban which accumulates Ca++ in the SR for subsequent contractions
Ca++ modulates force of contraction
Parasympathetics do the opposite (decrease Ca++ concentrations)
How do cardiac glycoside increase force of contraction ?
Inhibit the Na/K+ pump on myocytes.
This causes a disruption in the Na/Ca++ anti port (Na+ in and Ca+ out) leading to increased Na and Ca++ in the myocyte –> increased contraction
Pre-load
End DIASTOLIC volume (Related to Right Atrial Pressure)
After Load
For the Left Ventricle: Aortic Valve
For the Right Ventricl: Pulmonary Artery Pressure
Frank Starling
increases in stroke volume and cardiac output occur in response to increased venous return and end-diastolic volume
Ventricular Pressure Volume Loop: 1-2
Isovolumetric Contraction
Point 1: Diastole (140 mL) , Mitral vavle is closed when Left Vent P is greater than Right Vent P.
Ventricular Pressure Volume Loop: 2-3
Ejection of ventricle
Volume ejected at this point is the Stroke Volume
Ventricular Pressure Volume Loop: 3-4
Isovolumetric Relaxation
Ventricular Pressure Volume Loop: 4-1
Ventricular Filling
Increased pre-load will lead to an increased ….
Stroke volume
Increased after load will lead to
Decreased stroke volum and an elevated Left Ventricular pressure to overcome increased load
What are two ways in which Mean Systemic Pressure are increasesed
Increases in volume or decreases in compliance.
Shifts the Curve to the right
( Decreased MSP are due to low blood volume or an increase in compliance .. shifts curve to the left)
Equillibrium
Cardiac Output = Venous Return
Venous return can be altered by changing which two variables
Blood volume
Compliance
Increased blood volume or decreased compliance leads to increased veinous return
Decreased blood volume or increased Compliance lead to decreased Venous return
What can you do to alter Cardiac output ?
Give inotropic drugs
Stroke Volume
End diastole - End Systolic
Cardiac Outpute
SV x HR
Ejection Fraction
SV/End Diastolic Volume
Related to Contractility (increased contractility = increased SV and thus larger ejection fraction)
55% is normal Ejection Fraction
Stroke Work
Aortic Pressure x Stoke volume
W = P x V
Primarily run by FATTY ACIDS !
What 4 factors when increased, increase Cardiac Oxygen demand ?
Afterload
Size of the Heart
Contractility
HR
Cardiac Output (FIck Principle)
O2 Consumption /([02 in pulm vein) - [O2 in pulm Artery])
Atrial Systole
Preceded by P Wave (contributes but is not essential for arterial filling)
A-wave on Venous pulse curve
Leads to 4th heart sound
Isovolumetric contraction
Occurs after closure of the AV valves (First Heart Sound)
Pressure in the ventricles force the AV valves shut and when the pressure reaches a point the Semilunar valves are forced open and blood is ejected into the Pulmonary Artery (right vent.) and Aorta (left ventricle)
First Heart Sound
Closure of the AV valves (Lub)
Isovolumetric Relaxation
Repolarization of the ventricles (T-Wave) occurs during this time
Aortic (Pulmonic) Valves close. (2nd heart sound)
What is the event that causes the second heart sound ?
Closing of the Aortic (and pulmonic) Valves
What causes the third heart sound ?
Rapid filling of the ventricle with atrial blood
Normal in kids, not so much in adults.
What is the longest part of the cardiac cycle ?
Reduced Ventricular FIlling (diastasis)
What are the two main ways that the Arterial Pressure is Regulated
Fast Barroreceptor
Slow Renin Angiotensin system
What do barrorecptor respond to ?
Stretch within the walls of the Carotid Sinus near the bifurcation of the common carotid arteries.
MOST RESPONSIVE TO RAPID DECREASES IN STRETCH. (rapidly decreasing arterial)
(there are also barroreceptors in the Aortic Arch which respond to increased Stretch but not to decreased stretch)…
When there is less stretch in the carotid barroreceptors, there will be _________ firing of the carotid sinus barroreceptor nerves.
DECREASED ( increased stretch leads to more firing which inhibits parasympathetic outflow to the heart)
Note: Firing of the Carotid barrorecetors –> increased parasympathetic tone. In by IX out by X with decreased Sympathetic outflow
The opposite is true for increased stretch.
What is the sent point for the vasomotor center in the brain stem in terms of MAP ?
100 mmHg
Purpose of the Vasomotor center is to decrease MAP back to 100 (increase Parasympathetic outflow if above and decrease PS if below)
What four processes are modulated to increase arterial pressure when Barroreceptors sense low BP ?
Bascially you increase the Sympathetic outflow while decreasing Parasympathetic
INcrease : HR, Contractility (and SV consequently), Vasoconstriction of Arterioles (Alpha 1 receptor activation by NE) , Venoconstriction.
Valsalva Manuever
Increases intrathoracic pressure, thus decreasing Venous Return
What causes a release of Renin ?
Decreased perfusion pressure in the kidney (really its decreased Na+ in the blood outflow)
What rxn does Renin catalyze ?
Angiotensinogen –> AT1 (In plasma)
What catalyzes AT1 –> AT II
ACE (in the lungs)
ARBs block …
Angiotiensin Receptors (Bind Angiotensin II)
What hormone is released in response to Angiotensin II action ?
Aldosterone –> Na+ Reabsorption and K+ excretion
4 Effects of Angiotensin II binding with AT1 Receptor
Releases Aldosterone (Na+ reabsorption in the Distal Tubule)
Increase Na+/H+ exchange (Sodium into blood, H+ into filtrate)
Increased Thirst
Vasoconstriction –> TPR
What is actually sensed in Cerebral Ischemia that leads to increased sympathetic outflow from the Vasomotor ?
Partial Pressure of CO2 (Central Chemoreceptors)
Leads to Vasoconstriction that may be dangerous !
Where are peripheral chemoreceptors located in the body ?
Carotid Body
Aortic Bodies
What are the peripheral chemoreceptors sensitive to ?
Decreases in Partial Pressure of O2
Low P- 02 leads to increased firing o the Chemorecptors, this will lead to vasoconstriction –> increased Arterial pressures ( increases Venous Return ?)
Vassopressin (ADH) is released when BP is decreased due to ..
Hemorrhage or dehydration (DECREASED BLOOD VOLUME)
Which Vassporessin receptors are activated and lead to vasoconstriction ?
V1
Which vassopressin receptors are activated and lead to the implantation of Aquaporins into the distal tubule and collecting ducts ?
V2
ANP is released from ?
Atria (in response to increased blood volume !!)
What is the overall effect of ANP ?
Relaxation of vascular smooth muscle (decreased TPR)
Leads to excretion Na+ and H20
Inhibits Renin Secretion !
Starling Equation
(Pc + Oi) - (Pi + Oc) x Kf
\+= fluid out of the capillary - = fluid into the capillary
What is responsible for the unidirectional flow of lymph ?
One way flap valves.
Edema
when the volume of interstitial fluid is more than can be returned to venous from the lymph
Autoregulation
BLOOD FLOW IS CONSTANT TO AN AREA DESPITE CHANGING ARTERIAL PRESSURES
Active hyperemia
BLood flow to an organ is directly proportional to the its metabolic activity
Reactive Hyperemia
Increased blood flow after an occlusive event . Can cause repercussion injuries.
Myogenic Control
Smooth muscle tends to contract when stretched to a point.
Metabolic Hypothesis
When O2 is low, ATP is low. Lack of ATP leads to build up of vasodilatory substances that causes SM to relax.
What organ has the largest response to sympathetic innervation >
SKIN
PGE’s are VASO….
dilatory
PGF’s are VASO…
Constrictors
Thromboxane A2 is ..
a vasoconstrictor
What controls coronary circulation ?
Local Metabolic Factors (almost entirely)
What are more innervated by sympathetics in SkMu: Arterioles or Venules ?
ARterioles
Alpha I adrenergic stimulation in SkMu leads to ..
Vasoconstriction
Beta 2 stimulation in SkMu leads to ..
Vasodilation.
When does orthostatic hypotension occur ?
When a patients Carotid Barroreceptor reflex is impaired
What occurs in the skin and peripheral tissues during exercise ?
Vasoconstriction so that (resistance increases) –> lowered blood flow to these organs
What are some of the vasodilatory metabolites that are purported in the Metabolic Theory ?
Lactate, K+, Adenosine
How does the Metabolic Theory Play into the Exercise physiology ?
As you exercise your vasodilatory metabolites build up leading to vasodilation in SkMu
