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Flashcards in 8-24 Cardiovascular Pathology Review Deck (96)
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What is laminar blood flow?

concentric layers of blood, with the slowest layer near vessel walls and the fastest near the middle


Turbulence is minimized -> happens more in straight, long vessels


What is the (mechanical/physiological) advantage of laminar flow?

decreased energy losses, minimized viscous interactions between adjacent layers of blood or vessel wall


Physiologically -> pretty sure blood is less likely to clot 


What is turbulence in regards to blood flow?

disrupted laminar flow leading to chaotic flow


When does turbulence happen?

large aa at branch points

diseased/stenotic aa

across stenotic heart valves


How does turbulence change the energy required to drive blood flow? What is the relationship between perfusion pressure, turbulence, and flow?

Increased demand for energy, due to:

friction --> generates heat


turbulence increases perfusion pressure needed to drive a given flow

 - or -

at a perfusion pressure, turbulence leads to decrease in flow


Does turbulence happen gradually?

Turbulence happens when flow is high enough to break laminar layers

 - happens when Reynold's number is exceeded


What is Reynold's number, and what relationship do the different terms of it have with each other?

Re = Vdp/n

V = mean velocity

d = diameter

p/rho = blood density

n = blood viscosity


Reynolds number/threshold for turbulence proportional to velocity, diameter, blood density. Blood viscosity increase will decrease Re/turbulence threshold, vice versa.


What frequent scenarios reduces Re/turbulence threshold?

anemia - makes blood less viscous

high velocity

increased diameter - aneurysm

blood density - increasing RBCs w/ Epo


How is velocity and vessel diameter related?

As diameter of a vessel increases, velocity drops

flow = mean velocity * area(πr2)


How can turbulence be appreciated?

Loss of energy as sound waves = murmurs or bruits


sound energy/murmurs intensify as flow increases


What can increase the sound of murmurs?

Elevated CO - can result in physiological murmurs in pregnant women, or pathological murmurs


What is often the cause of pathological murmurs heard in the heart cycle?

Turbulence of blood flow across a stenotic valve, or movement of blood between heart chambers or into large outflow vessels


Murmurs tend to be low frequency sounds


What are the 2 general classification schemes for murmurs? Give 2 examples of each.

Based on origin:

1. Caused by valve defects

2. Caused by interchamber defects - cause an abnormal flow of blood between chambers


Based on timing in heart cycle:

1. Systolic

2. Diastolic


What is the effect of gravity on venous return prior to compensation?

gravity acts on vascular volume and causes pooling in lower extremities or low points of body

 - partly possible due to large compliance of venous vessels


Shift in blood volume decreases thoracic venous blood volume,

decreases right ventricular filling pressure/preload, 

decline in venous return


What is the effect of gravity on CO before compensation?

Venous return will decrease

Thoracic blood volume will decrease

Cardiac preload will decrease in right atrium

CO will decrease


What is the effect of gravity on BP before compensation?

Since preload in R atrium is lower, there's also less venous return from lungs, creating decreased L ventricular output and decreased CO


Decreased CO will decrease MAP in absence of HR increase


What is the response of the autonomic nervous system that is initiated by increased baroreceptor firing rate?

Less pressure on baroreceptor reflexes will cause increased firing on the SNS, which will increase systemic vascular resistance

decrease stroke volume and preload

increased heart rate


How is Posieuille's law important in hemodynamics? What factors have a big influence on resistance?

Posieuille's law states that resistance is directly porportional to the length & viscosity of the blood, inversely porportional to radius to the 4th power


Whereas vessel length and viscosity do directly influence resistance, these are often fairly fixed entities that don't change much


Radius is under the influence of the ANS, and is subject to change

 - 2x increase in radius = 16x decrease in resistance


What is Ohm's law and how does it impact hemodynamics?

change in pressure is proportional to flow * resistance


Pressure change across stenotic arteries and valves will be much larger due to more resistance

Increased flow can also increase velocity, leading to turbulence and murmurs


What variables can influence vascular resistance?

intrinsic - local blood flow regulation mechanisms

 - i.e. myogenic, NO, endothelin, histamine, bradykinin, arachadonic acid metabolites, hypoxia by-products


extrinsic - originate from outside of tissue, tends to regulate systemic vascular resistance . Tends to be ANS activated or ang II mediated.


What is mean arterial pressure? What relationships does it have with other variables?


 - CVP is central venous pressure, often near 0

Realistically MAP = CO * SVR


What are the 2 most efficient ways to change MAP?

Changes in CO or SVR


All variables regarding MAP are interdependent, changing one will change the rest



In the real world, how is MAP determined?

MAP = Pdias + 1/3(Psys - Pdias)


What affects SVR?

Anything that affects systemic vascular resistance - changing blood viscosity, changing vessel diameter


How can SVR be determined?



What is CO?

Stroke volume of each beat, along with heartrate

CO = SV * HR


Will vary depending on size of person, can use cardiac index instead

 - cardiac index is L/min/m2, denotes amount of blood pumped per min per body surface area


What is ejection fraction?

Fraction of blood ejected by ventricle relative to EDV

EF = (SV/EDV) - 100


How is EF typically measured?

Ejection fraction measured by echocardiography


What can cause EF to change?

Increases - cardiac conditioning, can cause it to increase to 90%+

Normal - >55%



- heart failure (esp dilated cardiomyopathy) due to increased amt of blood left in ventricle after a beat

 - can go down to 20%


What is EF used to assess, clinically?

Inotropic (contractile) status of the heart


Is there a pathology where EF is normal, even though the ventricle is in failure?

Yes - diastolic disfunction caused by hypertrophy, leading to low ventricular compliance

 - Stiff ventricle reduces filling

 - stroke volume and EDV decreased as a result, resulting in a number for EF that still "looks" the same, but isn't normal


Are low EFs associated with systolic or diastolic dysfxn?



What is pulse pressure?

PP = Systolic pressure - diastolic pressure

Reflects the change in aortic pressure during systole


What determines PP?

determined by compliance of aorta and ventricular stroke volume

 - high compliance of aorta dampens pulsatile output of left ventricle

 - larger stroke volume produces a larger pulse pressure at a given compliance



What is the Fick principle?

Reflects O2 extraction of myocardium, with ratio of O2 consumption to coronary blood flow

MVO2 = CBF * (CaO2 - CvO2)

CBF = coronary blood flow, (CaO2 - CvO2) = arterial venous oxygen extraction


How much O2 does the heart extract?

About 1/2 to 2/3 of available O2 under normal conditions

 - heart will tightly control O2 supply and demand to ensure adequate O2 delivery

  -done through local control of coronary blood supply


What are some consequences of CAD?

coronary blood flow and O2 delivery unable to meet demands

 - increased O2 extraction and decreased venous O2 content

 - leads to tissue hypoxia and angina


How is CAD remedied?

If due to fixed stenotic lesion, stent is placed or bypass is done

If due to clot, give thrombolytic

If due to vasospasm, give coronary vasodilators


What is the equation for compliance? What does compliance generally mean?

C = change in volume/change in pressure

 - ability of a vessel to distend and increase volume with increasing transmural pressure



Why can a vein be used in an autograft to bypass an artery?

At lower pressures, compliance of a vein is 10-20x that of an artery

 - however - 

at higher pressurs and volumes, venous compliance is like an artery's


What are the Starling's forces? What are the 4 forces, and is causing the hydrostatic or oncotic pressure for each?

capillary pressure - hydrostatic pressure out of capillaries into tissue

plasma oncotic pressure - pressure into capillaries due to non-diffusable stuff in blood

interstitial fluid pressure - rarely more than capillary pressure, free water and other solutes able to diffuse back into capillaries

interstitial fluid oncotic pressure - tissue pressure pulling solutes back into tissue, usually fairly small


What are the exchange vessels?

capillaries and small post-capillary venules


What are physical factors that can affect the amt of fluid filtered or absorbed per unit time?

Fluid Flux ( or Jv) = Kf*A*NDF


Kf = filtration constant, affected by physical barrier (i.e. fenestrated versus tight jxn endothelium. Frequently affected by hisamine)

A = surface area

NDF = sum of Starlings Forces


What is an equation where you can figure out the sum and vector/directionality of all available Starling Forces?

NDF/net driving force

NDF = (Pc - Pi) - (πc - πi)



+NDF = net fluid filtration

-NDF = net fuid reabsorption


In terms of Starling forces, what is edema?

Where net filtration is greater than total net reabsorption (plasma oncotic and tissue hydrostatic pressure) and also more than lymphatics can cope with


What factors precipitate edema?

Increased capillary hydrostatic pressure - gravitational edema, HF, venous obstruction


Decreased plasma oncotic pressure - hypoproteinemia


Increased capillary permeability - proinflamm mediators - histamine, bradykinin - or damage to vascular integrity


Lymphatic obstruction - filiariasis


What is the primary pacemaker of the heart? Why?

Cells in the SA node

 - no true resting potential, generate regular spontaneous action potentials


Why are pacemaker cells considered slow response?

No fast Na+ channels, instead rely on slower Ca++ channels


What happens during the 4 phases of the A.P. of an SA nodal cell?

phase 4 - spontaneous depolarization - triggers AP when threshold is met

phase 0 - depolarization phase of AP

phase 3 - repolarization phase


What is the funny current?

Slow, inward/depolarizing Na+ currents


What initiates phase 4?

If - funny current

- slow depolarization, starts T-type Ca++ channel opening


What currents cause phase 4?

Very negative memb potential at end of repolarization opens If (slow Na+)

T-type Ca++ channels open

L-type Ca++ channels open


What currents cause phase 0?

depolarization due to increased L-type Ca++ channels

 - started to open at end of phase 4


What currents cause phase 3?

repolarization due to K+ channels opening, increasing hyperpolarizing outward K+

 - L-type Ca++ channels close


Why is depolarization considered 'slow' in the SA node?

depolarization through L-type Ca++ channels not rapid, or not as rapid in other cardiac cells


Why does hypoxia in the SA node lead to bradycardia?

Cells unable to reach hyperpolarized state to re-initiate new cycle and AP

 - loss of Na/K ATPases, ATP-dep ion pumps

 - hypoxia depolarizes the cell, resulting in reduced pacemaker rate

Slow decline in outward K+  contributes to depolarized cell


How does sympathetic activity change pacemaker activity?

Release of NE decreases outward K+ flow

increases slow inward Ca++ and Na+ flow

If/pacemaker current enhanced


Increases slope of phase 4, reaching depolarization more rapidly


How does parasym activity change pacemaker activity?

Predominant input - has to be inhibited by SNS to reduce tone


ACh increases outward K+ flow, 

decreases inward Na+ and Ca++

decreases the slope of phase 4, so it takes longer to reach AP

hyperpolarizes cell in phase 4, takes longer to reach AP


How do circulating hormones change pacemaker activity?

hyperthyroidism - tachycardia

hypothyroidism - bradycardia

epinephrine - tachycardia


How do drugs change pacemaker activity?

CCBs - inhibit slow inwards Ca++ channels in phase 4 and 0

Autonomic receptor antagonists/agonist - beta blockers, muscarinic antagonists

Digitalis - bradycardia via increased parasym tone, toxicity will increase automaticity and cause tachyarrhythmias - inhibits Na/K ATPase


What is the effective cardiac refractory period?

Period of time after an AP has been initiated where a new AP cannot be initiated.


Stimulation of cell from adjacent cells will not make an AP

Protective - prevents multiple. compound APs from happening


How do antiarrhythmic drugs work?

Alters ERP, cellular excitability

K+ channel blockers - amiodarone - delays phase 3 repolarization



Why are ectopic beats a frequent feature of ischemic heart disease or following MI?

Hypoxia induced membrane depolarization will inactivate all fast Na+ channels

Inward current is mostly slow Ca++, like in pacemaker cells

cells can then spontaneously depolarize


What is the relative cardiac refractory period?

A new AP can only be elicited under certain circumstances


Explain the effects of a stimulus applied at different time points during the relative refractory period for fast- and slow-response APs. 

APs traveling down a conduction branch can circle back around and travel in a retrograde manner through unidirectional blocks

If it ends up reaching tissue still in the ERP on the other side of the block, the AP stimulus peters out

If it reaches tissue outside of the ERP on the other side of the block, a circular pathway of high frequency impulses can occur and propagate throughout the (usually) ventricles - tachyarrhythmia occurs 


What significantly impacts reentry mechanisms?

changes in conduction velocity/timing and refractoriness - related to ERP


Changes in ANS nerve fxn, antiarrhythmic drugs


What is the pathway typical of WPW?

Impulse bypasses AV node via Bundle of Kent

depolarizes ventricular tissues

travels backwards/retrograde through AB node to excite atrial tissue

establishes counter-clockwise global reentry, results in SVT


What causes paroxysmal SVT?

AV nodal reentry tachycardia 

Different conduction velocites and refractory periods in the AV node

Causes signals to travel from atria to ventricles then back to atria via AV node


How do you determine mean electrical axis on an EKG?

Find tracing that is most biphasic, then add 90 degrees or lead that is perpendicular to it with a positive net deflection


Predict the shift in MEA that may occur as a result of obesity, pregnancy, ventricular hypertrophy, or infarction.

Obesity, pregnancy - left axis deviation

ventricular hypertrophy - same axis deviation as whichever ventricle is hypertrophied

infarction - depends on place


What is the hemodynamic consequence of bradycardia?


decreased CO

syncope and other Sx's related to hypotension


What are the hemodynamic consequences of tachycardia?

reduces stroke colume and CO, esp at > 160 bpm

 - decreased ventricular fillint time, decreased ventricular preload

 - reduced ventricular contractility, reduced ejection

 - increased myocardial O2 demand, causing angina esp with CAD

 - chronic state leads to systyolic heart failure


What are the hemodynamic consequences of atrial fibrillation?

- atrial contraction contributes to 10% of ventricular filling at rest, up to 40% at work

 -minor consequence at rest

- reduces normal increases in ventricular stroke volumeand CO during work

- exertional dyspnea, impaired mm perfusion - reduced exercise capacity

 - ventricular hypertrophy, reduced compliance, inhibited passive filling - a-fib will have a big impact

 - THROMBUS - need thinners

- can lead to v-tach if more impulses get through AV node


Try to talk through the different parts of the cardiac cycle. Include heart sounds, systole, diastole, and pressure in the aortic pressure, left ventricular pressure, left atrial pressure, left ventricular volume. 

S1 - Systole - mitral and tricuspid valves shut, aortic and pulmonic valves open

Aortic pressure goes up, left ventricular pressure goes up, left atrial pressure goes down, left ventricular volume goes down

S2 - diastole

Mitral and tricuspid valves open, pulm and aortic valves shut

Aortic & left ventricular pressure go down quick, left atrial pressure goes up a bit

left ventricular volume is down, starts going up in diastole


What is the S1 heart sound caused by?

S1 is caused by closure of the mitral and tricuspid valves at the beginning of isovolumetric ventricular contraction.


S1 is normally slightly split (~0.04 sec) because mitral valve closure precedes tricuspid valve closure; however, this very short time interval cannot normally be heard with a stethoscope so only a single sound is perceived


What is the S2 sound caused by?

S2 is caused by closure of the aortic and pulmonic valves at the beginning of isovolumetric ventricular relaxation.


S2 is physiologically split because aortic valve closure normally precedes pulmonic valve closures

 - splitting is not of fixed duration

 -S2 splitting changes depending on respiration, body posture and certain pathological conditions.


What is an S3 heart sound caused by?

(S3)occurs early in ventricular filling

 - may represent tensing of the chordae tendineae and the atrioventricular ring, which is the connective tissue supporting the AV valve leaflets.


This sound is normal in children, but when heard in adults it is often associated with ventricular dilation as occurs in systolic ventricular failure.


What is the 4th heart sound caused by?

The fourth heart sound (S4)

 - caused by vibration of the ventricular wall during atrial contraction


This sound is usually associated with a stiffened ventricle (low ventricular compliance), and therefore is heard in patients with ventricular hypertrophy, myocardial ischemia, or in older adults.


What 4 basic phases make up a pressure volume loop during the cardiac cycle?

ventricular filling (phase a; diastole)

isovolumetric contraction (phase b; systole)

ejection (phase c; systole)

isovolumetric relaxation (phase d; diastole)


What valves would open and close along the phases of a pressure-volume loop for the left ventricle?

ventricular filling (phase a; diastole) - mitral valve closes at end

isovolumetric contraction (phase b; systole) - aortic valve opens at end

ejection (phase c; systole) - aortic valve closes at end

isovolumetric relaxation (phase d; diastole) - mitral valve opens at the end


How does systolic dysfxn change the pressure volume loop?

impaired ventricular contraction - like chronic heart failure

more preload, but less volume is moved and slightly less pressure achieved

 - shift to right, narrower

- less ejection fraction


What effect does diastolic dysfxn have on pressure-volume loops?

Impaired preload - reduced compliance, less ventricular filling

decreased stroke volume

less volume to start, less volume to move, curve shifted to the left


Can lead to pulmonary edema if left ventricle is involved, due to increased EDP


How does mitral stenosis impair the pressure volume relationship?

mitral stenosis impairs left ventricular filling

 - decrease in preload, stroke volume, CO


Less volume moved, pressure is still somewhat similar, shift left


How does aortic valve stenosis impair the pressure volume relationship?

left ventricular emptying impaired due to high outflow resistance

 - smaller valve orifice

-increased afterload, increased end-systolic volume, decreased stroke volume


Smaller volume of blood moved, pressure almost doubled, shift to right and up


How does mitral valve regurg impair the pressure volume relationship?

as ventricle contracts, blood is ejected into aorta and left atrium

- increased left atrial volume and pressure

 - no isovolumetric contraction phase

 - less afterload


Wider volume, slightly less pressure, more rounded - like pusheen


How does aortic valve regurg impair the pressure volume relationship?

blood flows from aorta back into ventricle during diastole

- no isovolumetric relaxation

- enhanced ventricular filling


 Greatly increased volume, slightly increased pressure

rounded, like pusheen


What do cardiac function curves show?

CO plotted against changes in venous pressure/right atrial pressure(Pra)

- as Pra increases, CO goes up

- steep curve, so small increase in Pra = big change in CO



What do systemic vascular function curves show?

CO as a function of different vascular features

 - increased vol or vascular compliance increases CO

- decreased systemic vascular resistance  generally increases CO

- aa & venous constriction will increase mean circulatory filling pressure


What baroreptors have the most influence on BP?

Carotid sinus - travel back through IX, affect ANS outflow in medulla

- nerves are more responsive to MAP, small changes in arterial pressure drastically alters firing

 - responds to pulse pressure and MAP, which can work together in hemorrhagic shock to amplify baroreceptor response


What happens ot the baroreceptors during a sudden reduction in arterial pressure?

decreased aa pressure = decreased baroreceptor firing

increased SNS outflow, decreased vagal/PNS outflow

(baroreceptor firing = tonic PNS outflow, none = SNS disinhibited)

vasoconstriction, tachycardia and + inotropy (increased CO) happens


What does the body do in response to hemorrhagic shock to return blood volume to normal?

Baroreceptor reflexes - increased SNS, CO and vasoconstriction
Chemoreceptor reflexes - acidosis activates these, which increases SNS
Circulating vasoconstrictors - catecholamines
Renal reabsorption of sodium and water
Activation of thirst mechanisms
Reabsorption of tissue fluids


How do gravitational forces affect venous return?

Blood volume shifts into systemic veins

central venous pressure decreases

decreased right ventricular filling pressure/preload

decline in reduced pulmonary venous return

decreased CO and arterial BP


How does the Fick principle illustate extraction of O2 from coronary blood flow and actual coronary blood flow?

MVO2 = CBF × (CaO2 − CvO2)

MVO2 = myocardial O2 consumption

 CBF = coronary blood flow (ml/min)

(CaO2 – CvO2) is the arterial-venous oxygen content difference (ml O2/ml blood).


For example, if CBF is 80 ml/min per 100g and the CaO2-CvO2 difference is 0.1 ml O2/ml blood, then the MVO2 = 8 ml O2/min per 100g


What determines O2 delivery to the myocardium?

O2 Delivery = CBF × CaO2

where CBF = ml/min and CaO2 = ml O2/ml blood


O2 delivery of blood is relatively stable, mostly predicated on coronary blood flow


What pathologies can affect O2 delivery to myocardium?

Stenosis - limits maximal coronary flow, also in-series with microcirculation

Diseased vessels more susceptible to vasospasm

thrombus formation


Which of the following regions of the heart are fed by what vessels:






Inferior  - Right coronary
Anteroseptal - Left anterior descending
Anteroapical - Left anterior descending (distal)
Anterolateral - Circumflex
Posterior - Right coronary artery