Module 2: Cardiac Physiology (Weeks 2-3) Flashcards by Kianelys Heredia

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Module 2: Video Reviews

Excitation-contraction coupling
The cardiac cycle

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C2: Electrophysiology & amp; ECC Slides

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Cellular Level
Definitions:
The inside is different (more negative with different concentrations of ions) than the outside

Polarized

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Cellular Level
What cells in the heart are polarized?

Cardiac cells

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Cellular Level
How is polarization created?

By ions with different concentrations & charges
- This polarization creates a transmembrane potential
- Transmembrane resting potential = -80 to -90 mV

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Opening of ion channels is going to result in, what?

Depolarization

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Returning back to the polarized state is going to result in, what?

Repolarization
(back to neg. state)

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When there is a trigger within each individual cardiac cell, ion channels open/close creating what?

Action Potential

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Cardiac Conduction Cells
Definition:
Contractile cells of the atrium & ventricle

Cardiomyocytes

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Cardiac Conduction Cells
Definition:
Specialized conduction cells

Purkinje cells
- Don’t contract but allows current to spread to the heart very quickly

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Cardiac Conduction Cells
Definition:
- Sinoatrial (SA or sinus)
- Atrioventricular (AV) node

Pacemaker Cells

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Action Potentials Types
What do Cardiomyocytes & Purkinje cells use for depolarization (Phase 0)?

Na+ channels

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Action Potentials Types
What do Automatic (pacemaker) cells use for depolarization (Phase 0)?

Slow Ca2+ current

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Action Potentials Phases
Fill in the blanks:
1. Phase 0: _________
2. Phase 1: _________
3. Phase 2: _________
4. Phase 3: _________
5. Phase 4: _________

depolarization
brief repolarization
repolarization
resting membrane potential

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How is the resting membrane potential (RMP) determined?

Channels pump ions in a way that creates an ion gradient
- Sodium-Potassium ATPase
- 3 Na+ moved out (extra-cellular)
- 2 K+ moved in (intra-cellular)
Overall net negative inside the cell

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Resting Membrane Potential
There is typically high concentration of _____(1)________ inside the cell and high concentration of ___(2)___ outside the cell

Potassium
Sodium

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Action Potential: Cardiomyocyte and Purkinje
Fill in the blanks for the phases of the action potentials:
- Phase 0:____________
- Phase 1:____________
- Phase 2:____________
- Phase 3:____________
- Phase 4:____________

Na+ channels open (in) => depolarization
K+ channels open (out) => brief repolarization
Ca2+ channels open (in) => plateau
K+ channels open (out) => repolarization
returns to RMP

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Action Potential: Pacemaker Cells
Fill in the blanks for the phases of the action potentials:
- Phase 4: ____________
- Phase 0: ____________
- Phase 3: ____________

RMP with automatic “drift” => depolarization
Ca2+ channel open (in)
K+ channels open (out) => repolarization

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Sodium Channels
What determines the cell-to-cell conduction velocity?

Slope of Phase 0

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Sodium Channels (Phase 0)
Is a type of Na+ channel blocker that helps treat arrhythmias

Lidocaine

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Definition:
Heart rhythm disturbance

arrhythmia

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(T/F) Ca2+ is extremely important in all cardiac cells

True

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Calcium Channels
- T-type (transient) - activated 1st (-60/-50 mV)
- L-type (long-lasting) - activated 2nd

Voltage-gated

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Calcium Channels
- Norepinephrine and Epinephrine

Ligand-gated
- Beta-receptor stimulation increases Ca2+ influx

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Drugs: - *Directly* block L-type Ca2+ channels - *Diltiazem* (heart & vascular) -> treat arrhythmias - *Amlodipine* (vascular) -> treat high blood pressure

Ca2+ channel blockers

Drugs: - *Indirectly decrease* Ca2+ influx and catecholamine effects n the heart - Aten*lol*,, esmo*lol*, carvedi*lol*, many others -> treat arrhythmias and other heart diseases

Beta-blockers

List the Functions of Potassium Channels:

- Help regulate RMP and *repolarization*

What channels determine the *speed of repolarization & the effective refractory period (ERP)*?

K+ channels

What would happen to the ERP when you block K+ channels?

*Increases* the ERP & *slows* repolarization

What represents the *sum* of all the individual cells' electrical activity?

ECGs

A brief intro to ECG: What waveform is the following describing? *Atrial depolarization*

P wave

A brief intro to ECG: What waveform is the following describing? *Ventricular depolarization*

QRS wave

A brief intro to ECG: What waveform is the following describing? *Ventricular repolarization*

T wave

Serum potassium affects potassium channels:

go back

What creates an RMP?

Polarization of cardiac cells - polarization allows cells to become activated (depolarized) and inactivated (repolarized) by movement of different ions across channels

What creates the *automatic drift in pacemaker cells*?

Funny current

(T/F) High extracellular K inactivates Na channels

True

What is responsible for the repolarization of Purkinje/cardiomyocytes and pacemaker cells?

Potassium

(T/F) *Parasympathetic* activity increases heart rate and AV nodal conduction

False, *Sympathetic* activity increases heart rate and AV nodal conduction

(T/F) Ultrastructural components and channels of the sarcomere control *calcium influx* and ultimately myocardial contraction

True

What is the main ion responsible for the repolarization of Purkinje/cardiomyocyte cells?

Potassium (moving out of the cell)

Enhanced *sympathetic tone* causes: A. pacemaker cells to fire more rapidly B. slows AV nodal conduction C. pacemaker cells to fire more slowly D. slower heart rate

A. pacemaker cells to fire more rapidly

What is the main ion responsible for the depolarization of Purkinje/cardiomyocyte cells?

Sodium (moving into the cell)

(T/F) The resting membrane potentials for Purkinje cells and pacemakers cells are normally negative

True

Which is true regarding hyperkalemia and the action potential? A. Hyperkalemia causes the resting membrane potential to be more negative (hyperpolarized). B. Hyperkalemia speeds up pacemaker activity. C. Hyperkalemia causes sodium channels to become inactivated. D. Hyperkalemia causes repolarization to occur more slowly.

C. Hyperkalemia causes sodium channels to become inactivated.

The following sequence of events are related to *excitation-contraction coupling* in cardiomyocytes. Arrange the following events in the correct sequence from start to end: 1. calcium ions move into the sarcoplasmic reticulum 2. sodium enters into the cell during ventricular activation 3. intracellular calcium stores are released via activation of the ryanodine receptor from the sarcoplasmic reticulum 4. calcium ions move inward across the L-type calcium channel 5. binding of calcium by cTnC allows actin-myosin interaction

2 -> 4 -> 3 -> 5 -> 1

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Myocardial Contraction Definition: Associated with increased muscle tension & pumping of blood into the systemic circulation

Period of *contraction* (= systole)

Myocardial Contraction: Period of *contraction* (= systole) List the Essential components:

- Actin - Myosin - ATP (O2) - *Calcium* => absolutely important

Definition: Containing tight junctions and gap junctions link adjacent cells

*Intercalated discs* - Allows *rapid spread of electrical signal for simultaneous regional contraction*

What is the *Functional unit of the myocardium*?

Sarcomere - Hypertrophic cardiomyopathy (in cats) => Sarcomere mutation

Myocardial contraction: *Thin actin* filaments slide between *thick myosin* filaments as a result of what?

Repetitive movements of the myosin head

Definition: The linkage between myosin head and actin

Crossbridge - *Crossbridge cycle* is repetitive attachment | detachment of myosin heads to and from actin filament triggered by arrival of *Ca2+*

Definition: *Rate* (velocity) and *Extent* (tension or force developed) of fiber shortening

Myocardial contractility - *Intrinsic* ability (no outside force) of cardiomyocytes to generate force that is *load-independent*

Definition: Strength of *contraction*

inotropy

Definition: Active, energy-requiring process

Contraction - Transformation of chemical energy -> mechanical work - Splitting ATP by hydrolysis

(T/F) Myocardial contractility can only be assessed using muscle strip preparations (Langendorff technique)

True

Myocardial Contractility - Difficult to measure - Load-independent (inherent) rate & strength of actin-myosin interaction modulated by *Ca2+* availability and sensitivity - Estimated by *velocity* of muscle strip (Vmax) at zero load -- *not measurable in patients* - Inotropy *increases* with increased availability of *Ca2+* - Inotropy *increases* with increased *preload* (fiber stretch, before contraction kicks in) -- proportional - Intropy *decreases* with *increased* afterload (forces opposing contraction) -- inversely proportional - Inotropy *increases* with *increased* heart rate -- proportional

Inotropic State (contractility) - it is all about calcium (and ATP)

(T/F) Normally in a resting state, the Ca2+ concentration in the cardia cytosol during systole is such that the contractile sites are approximately *half activated*

True - *Contractile reserve* => exploited by sympathetic (beta-adrenergic) stimulation which increases Ca2+ release

- Positive inotropy (+ positive chronotropy)

Sympathetic (NE, Epi)

- Negative inotropy (+ negative chronotropy)

PNS (vagus)

List the Effects of *Preload* on myocardial Contractility:

- End-diastolic fiber stretch = preload - Modulates sarcomere (Z-Z) length before contraction - 2 significant effects of increased preload: - increased Sensitivity of cardiac tropin C to Ca2+ - increased Number of cross-bridges - Length- tension relationship (Frank-Starling law of the heart)

Clinical Pointe: What is a variable of preload that influences contractility?

Cardiac chamber size (end-diastolic volume)

Definition: For the *same amount of filling (preload)*, volume pumped per beat is *decreased*

Depressed inotropy

List the Effects of *Afterload* on Myocardial Contractility:

- All *forces* opposing muscle shortening (and thus ejection of blood) - Weight must be overcome and moved as the muscle shortens - The higher Afterload (AL), the higher the *tension* that must develop prior to actual shortening - *increased afterload:* both muscle shortening and duration of contraction decrease

(T/F) Afterload of the intact ventricle is *difficult to measure* force that must be overcome in order to open aortic \ pulmonary valves and eject blood into the arterial system

True

What does Afterload relate to?

Peak wall tension prior to ejection

When does peak wall tension (systolic wall stress) occur?

At the *ONSET* of ventricular ejection

Definition: Volume of blood in ventricles at end of diastole (end-diastolic pressure)

Preload

Definition: Resistance left ventricle must overcome to circulate blood

Afterload

What does increased Heart Rate shorten?

Filling time which *decreases* preload

What is the Shortening fraction?

EDD - ESD/EDD x 100%

Which of the following statements regarding myocardial contraction and relaxation is CORRECT: a. During ventricular filling, the semilunar valves are open, and the AV valves are closed b. During isovolumic relaxation, calcium enters the cardiomyocytes triggering early diastolic cross bridge detachment. c. During the ejection phase, blood is pumped into the ventricles. d. During isovolumic contraction, all 4 cardiac valves are closed and ventricular pressure increases. e. During systole, calcium enters the sarcoplasmic reticulum (SR)and ADP is hydrolyzed. During diastole, calcium leaves the SR into the cytoplasm and is bound to troponin C.

d. During isovolumic contraction, all 4 cardiac valves are closed, and ventricular pressure increases.

All of the following are characteristics of myocardial contractility, EXCEPT: a. Rate of cross-bridge cycling b. Stretch of myofibers c. Speed (velocity) of contraction d. Extent of fiber shortening e. Myofiber tension developed during contraction

b. Stretch of myofibers

Which of the following statements about myocardial contraction is CORRECT? a. Ca2+ movement into the SR leads to the power stroke b. Activation of the PNS increases contractility c. Ca2+ channel blocking drugs effectively increase Ca2+ sensitivity of troponin C d. Increased end-diastolic fiber stretch increases contractility e. Chronic elevation of afterload increases contractile force via the Anrep effect

d. Increased end-diastolic fiber stretch increases contractility

A dog with chronic mitral valve disease ruptures chordae tendineae of the mitral valve leading to acute, severe mitral regurgitation and subsequent severe left atrial and left ventricular volume overload. All of the following statements regarding changes in LV systolic function are correct, EXCEPT: a. The event causes massive dilation of the LV leading to increased afterload and thus reducing LV systolic function. b. The valve leakage causes an acute increase of preload leading to increased systolic function. c. The SNS will immediately be activated (“fight-or-flight” response) causing increased heart rate and increased cross-bridge cycling. d. The inotropic state of the myocardium will improve via the Frank Starling mechanism and the Bowditch-Treppe effect. e. The sarcomere Z-Z length will increase improving the pumping ability of the myocardium.

a. The event causes massive dilation of the LV leading to increased afterload and thus reducing LV systolic function.

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What is the term used to characterize *Rate* (velocity) & *Extent* (magnitude) of fiber lengthening

Myocardial Relaxation (Lusitropy)

Myocardial Relaxation: Period of cross-bridge ___________ associated with active *relief of muscle tension* followed by filling of the ventricles

Detachment

List the Essential components for Myocardial Relaxation:

- SERCA - Phospholamban - ATP (O2) - NCX - Ca2+ pump

(T/F) Relaxation is very sensitive to hypoxia, ischemia, etc

True

Diastolic Relaxation: Active process (ATP) - O2 It is influenced by ...

- Preload - Afterload - Prior systole - Chamber geometry

When does cardiomyocyte relaxation occur?

Starts after contraction is nearly completed

What expels some Ca2+ out of the cell?

Na+-Ca2+ exchanger

Pumps most of the *free Ca2+* back into sarcoendoplasmic reticulum stores where it is bound to *calsequestrin*

SERCA (sarcoendoplasmic reticulum ATPase)

Where is some calcium temporarily stored?

Mitochondria

Definition: Clinically highly relevant in particular *feline heart muscle disease* & pericardial disease and other conditions

Diastolic Function

Diastolic function: Function that allows adequate *filling* of the ventricles at rest and during exercise without pathogenic elevation of *filling pressure*

Normal diastolic function

Relates *relaxation* and *passive tissue properties* to load & chamber geometry

Diastolic function

(T/F) Diastolic function relates to lusitropy

False, Diastolic function *doesn't equal* lusitropy (relaxation)

Cell lengthening (rate & extent) = _______________ at zero load

Relaxation

The filling phase follows what phase?

Isovolumic (all four cardiac valves are closed) phase

List the phases of Diastole:

- IVR (isovolumic ventricular relaxation) - Rapid Filling - MV open - Slow filling - MV partially open - Atrial contraction - = "atrial kick" - MV open

Ventricular Filling Dynamics: The early diastolic filling provides _______% of LV filling volume

80%

List the effect of preload & Heart rate on diastolic functions:

- increase Preload improves diastolic function (within limits) - increase Heart rate improves relaxation & ventricular suction Caveat: decrease filling time & decrease coronary perfusion

(T/F) If tau goes down, it means there is a better relaxation

True

Which statement about myocardial relaxation is CORRECT? a. It is a passive process related to the early diastolic LA-LV pressure difference. b. It does improve with increased Ca2+ binding to the tropomyosin complex. c. It is facilitated by the binding of phospholamban to SERCA. d. It gets faster and stronger with parasympathetic activation. e. It is a process mainly confined to the isovolumic period in early diastole.

e. It is a process mainly confined to the isovolumic period in early diastole.

Which of the following sequence of events during cardiac excitation-contraction-relaxation is CORRECT? 1...Ca2+ binding to cardiac troponin C 2... Ca2+ entry via the L-type Ca2+ channel 3... Power stroke 4... Ca2+ extrusion out of the cytoplasm via the Ca2+ pump 5... Temporary Ca2+ storage in the mitochondria 6... Electrical cardiomyocyte activation 7... Ca2+ triggered Ca2+ release 8... Ca2+ flux into the sarcoendoplasmatic reticulum via SERCA

b. 6-> 2-> 7-> 1-> 3-> 8-> 4-> 5

All of the statements about ventricular diastolic function are correct, EXCEPT? a. Diastolic function is an overarching term to describe ventricular filling. b. Diastolic function can conceptionally be divided into 4 phases occurring in the following sequence: Isovolumic contraction, early filling, late filling, and finally diastasis. c. Rapid ventricular filling occurs in early diastole and is caused by myocardial relaxation associated with the suction of blood into the ventricle reducing LV pressure and thus the early diastolic LV-LA pressure gradient. d. Normal diastolic function allows adequate filling of the ventricles without a pathologic elevation of filling pressure. e. Stiffness (or its reciprocal, compliance) describes the passive diastolic properties of the myocardium (ventricle). The stiffer, the worse is diastolic filling.

A cat with severe, idiopathic thickening of the LV walls and a heart rate of 260 bpm (N: 120-220) is diagnosed with hypertrophic cardiomyopathy in your practice via cardiac ultrasound (we will talk about this common feline condition later in the course). Which of the following statements regarding LV diastolic function in this cat is NOT correct? a. LV compliance will be decreased and thus LV filling reduced. b. Relaxation of the LV will be abnormal due to *increased* myocardial mass. c. High heart rate will make LV filling worse. d. LV stiffness will be increased affecting LV diastolic (filling) properties. e. LV stroke volume will be increased due to increased heart rate and better relaxation and thus, better filling, of this thickened heart.

e. LV stroke volume will be increased due to increased heart rate and better relaxation and thus, better filling, of this thickened heart.

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The Cardiac Cycle - Electrical activity __________ mechanical activity (electromechanical delay)

*precedes*(before)

The Cardiac Cycle How is blood flow predicted?

Pressure differences - "Pressure gradients" - Flows from higher pressure to lower pressure

The Cardiac Cycle Heart valves open and close in response to _____________ on either side of the valves

Pressure changes

Wiggers Diagram: Electrical Activity 1. Starts with ECG & ECG is what?

Basis of timing (basically your x-axis)

Genesis of the ECG 1. Impulse starts in the ___ node

Genesis of the ECG 2. Signal traves through atria and ____ node

Genesis of the ECG 3. Signal travels through ________________ system

His-Purkinje system

Genesis of the ECG 4. __________ depolarization

Ventricular

Genesis of the ECG 5. Ventricular _____________

repolarization

Wiggers Diagram: Mechanical - LV ejection - Isovolumic contraction (IVC) - Isovolumic relaxation (IVR)

Ventricular Pressure/timing

Wiggers Diagram: Mechanical _______ atrial pressure/timing

left

Wiggers Diagram: Mechanical - MC = mitral closure - AO = aortic opens - AC = aortic closure - MO = mitral opens

Valve Motion - Driven by pressure differences

Wiggers Diagram: Think about ventricular *volume* as it relates to ___________ & ___________

timing, pressure - Filling - Ejection - Isovolumic periods

Wiggers Diagram: Changes in volume between what two points represent *stroke volume*?

AO & AC

Wiggers Diagram: Clinical Aspect (Heart Sounds) - Closure of atrioventricular valves

S1 - Systolic heart sounds

Wiggers Diagram: Clinical Aspect (Heart Sounds) - Closure of semilunar valves (aortic & pulmonary valve)

S2 - Systolic heart sounds

Wiggers Diagram: Clinical Aspect (Heart Sounds) - Early/rapid ventricular filling

S3 - Diastolic heart sounds

Wiggers Diagram: Clinical Aspect (Heart Sounds) - Atrial contraction ("atrial kick") - final phase

S4 - Diastolic heart sounds

Average Pressures for Species examined (in mmHg) Systole: 120 Diastole: < 12

Left ventricle

Average Pressures for Species examined (in mmHg) Systole: 25 Diastole: < 5

Right ventricle

Average Pressures for Species examined (in mmHg) Systole: 120 Diastole: 80

Aorta

Average Pressures for Species examined (in mmHg) Systole: 25 Diastole: 12

Pulmonary artery

Clinical correlations: How is pulse pressure determined?

- *Difference* in *systolic* and *diastolic* pressure - *Rate of rise* of systolic pressure

Definition: Is a persistent opening between the two major blood vessels leading from the heart.

Patent ductus arteriosus (PDA) - Bounding Pulses = aortic insufficiency, patent ductus arteriosus - *difference in systolic and diastolic pressure*

Definition: Is a narrowing of the area underneath, the aortic valve, that causes some degree of obstruction or blockage of the blood flow through the heart

Subaortic stenosis (narrowing) - *rate of rise of systolic pressure* - Weak pulses

Clinical correlations: What happens when there's any kind of backup of blood in the *superior vena cava* or in your heart itself?

Distended jugular veins

Clinical correlations: "Cannon waves" with arrhythmias (3rd degree AV block) due to dyssynchrony (atria contracting against closed mitral/tricuspid)

Jugular pulsations

Clinical correlations: Slurring between normal heart sounds - Valve leakage = regurgitation or insufficiency - Valve narrowing = stenosis

Heart Sounds: *Murmurs*

Clinical correlations: - Diastolic sounds (S3 and S4 sound) - Normal in large animals - Abnormal in small animals

Heart Sounds: *Gallops*

What occurs immediately prior to the ejection of blood out into the aorta?

c. isovolumic contraction

List the chambers, and great vessels, and list the normal pressure ranges (in mmHg):

- RA (0-5) - RV (25 / <5) - PA (25 / 12) - LA (0-12) - LV (120 / <12) - Ao (120 / 80)

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Hemodynamics Definition: The study of blood flow in the vascular system

Hemorheology

What is the purpose of the cardiovascular system?

To deliver *oxygen* and *nutrients* to the tissues of the body

Hemodynamics Cardiac output

Flow

Hemodynamics - Ventricular - Atrial - Arterial - Venous - Capillary

Pressures

Hemodynamics - Systemic vasculature - Pulmonary vasculate

Resistances

Ohm's Law

I = V/R Q = P/R

Ohm's Law What is current flow (I) determined by?

- Electromotive force or voltage (V) - Resistance to current flow (R)

Ohm's Law What is the flow of fluids (Q) determined by?

- Pressure gradient (P) - resistance to flow (R)

Hemodynamics: Physical Laws & Determinants Physical Law: Venous return Determinants:

- Plasma volume - Vessel capacity

Hemodynamics: Physical Laws & Determinants Physical Law: Cardiac output (CO) --> *CO = SV x HR* Determinants:

- Stroke volume (SV) => EDV - ESV - Heart rate (HR) - Tissue demands

Hemodynamics: Physical Laws & Determinants Physical Law: Blood pressure (BP) --> *BP = CO x SVR* Determinants:

- Cardiac output (CO) - Systemic vascular resistance (SVR) - Reflexes

Hemodynamics: Physical Laws & Determinants Physical Law: Vascular resistance - Systemic vascular resistance (SVR) - Pulmonary vascular resistance (PVR) Determinants:

- Autonomic nervous system - Hormonal & endothelial (local) regulations --> *PVR = about 1/5 of SVR*

Definition: The flow of blood from the periphery back to the right atrium

Venous return

Venous Return: "Force from the rear"

Cardiac pumping from the *contralateral ventricle* - LV pumping blood into the arterial system

Venous return: "Force from the front"

Force from ventricular contraction creates negative pressure in the atrium

Venous Return: Respiratory Pump Inspiration causes the diaphragm to move downward causing negative pressure in the chest and _________ atrium

Right

Venous Return: Influence of Fluid Therapy How can you improve venous return?

with fluid bolus

Venous Return: Influence of Fluid Therapy What drives blood into the right atrium?

Mean systemic venous pressure - Mean systemic venous pressure > RA pressure = venous return

List the things that increase (improve) venous return:

- Vasoconstriction - Splenic contraction - Fluids

Definition: - Quantity of blood delivered to the systemic circulation per unit time (L/min) - Converted to cardiac index (CI) - Normalize to patient size (body surface area) - L/min/m^2

Cardiac Output

Cardiac Output: End diastolic (filling) volume - End systolic volume

Stroke volume

Cardiac Output: List the thing that will affect *End diastole volume*:

- Preload - Compliance - Diastolic filling time

Definition: how easily a chamber of the heart or the lumen of a blood vessel expands when it is filled with a volume of blood

Compliance

Cardiac Output: List the thing that will affect *End systolic volume*:

- Contractility (pump function) - Afterload

Cardiac Output: Distending stress in the ventricle at end-diastole; depends on *venous return & ventricular compliance*

Preload

Cardiac Output: What is dependent on HR (autonomic tone)?

Diastolic Filling Time

Cardiac Output: The sum of the forces opposing the ventricular ejection (blood pressure, vascular resistance)

Afterload

List the determinants for Arterial Blood Pressure (*BP = CO x SVR*):

- Blood volume (CO, SV) - Compliance of vessels (vascular resistance) - Baroreceptor arcs (reflexes) - Stabilize *BP* in face of changing *CO*

(T/F) Mean arterial pressure (MAP) more important than systolic/diastolic

True *MAP = 1/3 pulse pressure + diastolic blood pressure (pulse pressure = systolic - diastolic)* ** this is important and you should know **

What are the two ways to measure pressure non-invasive (indirect)?

Doppler & Oscillometric

Arterial Blood Pressure: - Gold-standard - Recommended for *severely hypo/hypertensive patients* to guide therapy

Invasive (direct) way to measure Arterial Blood Pressure

Arterial Blood pressure: - Are important ways that the body can *regulate blood pressure* - Important & normal reflex that occurs

Baroreceptor Reflex

An exaggeration of the normal *baroreceptor reflex* can result in what?

Syncope (collapse) - *Vasovagal syncope* - *Neurcardiogenic syncope* - *Reflex-mediated syncope* * all the same thing --> this exaggeration can cause *severe bradycardia & hypotension*

Vascular resistance equation:

Flow (or CO) = change in Pressure / Resistance

(T/F) Flow (CO) can be reduced, although BP increases

True - *RESISTANCES* can Change

Vascular Resistance: Opposition to flow presented by *pulsatile flow* in an elastic vascular system

Impedance - Wave reflection - difficult to quantify

Vascular Resistance: What percentage does Resistance make up of impedance?

90%

Vascular Resistance: Resistance of the *systemic vascular tree* (arterioles)

Systemic vascular resistance

Vascular Resistance: Resistance of the *pulmonary vascular tree*

Pulmonary vascular resistance (PVR)

Poiseuille’s Law

Resistance = 8 x length x viscosity / pi x radius^4 - *Resistance increases EXPONENTIALLY when vessel radius narrows*

List the factors affecting resistance:

- Autonomic nervous system - Hormonal and endothelial (local) factor

If a vessel diameter decreases by *half*, by what factor would the vascular resistance increase?

(T/F) Flow is inversely proportional to resistance

True

(T/F) Flow is inversely proportional to the pressure difference (pressure gradient)

False

Which statement is true regarding venous return and respiration? a. Inspiration increases overall intrathoracic pressure in the chest causing blood to move out of the right atrium into the vena cava. b. Expiration increases intrathoracic negative pressure causing an increase in venous return. c. Inspiration increases intrathoracic negative pressure lowering the pressure in the right atrium. d. An increase in right atrial pressure as compared to the vena cava causes an increase in venous return.

c. Inspiration increases intrathoracic negative pressure lowering the pressure in the right atrium.

Module 2: Cardiac Physiology (Weeks 2-3) Flashcards

(178 cards)