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SCCM Review Textbook > CV Physiology > Flashcards

CV Physiology Flashcards

1
Q

Name 3 structures located in the morphologically normal RA

A

Limbus of fossa ovalis, snius node, and triangle of Koch (where fibers run to SA node)

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2
Q

LA is the most ____ of all chambers, does not have ______ muscles (like the RA

A

Posterior; pectinate

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3
Q

PFO persists when…

A

The remains of the limbus (septum secundum) and septum primum don’t fuse

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4
Q

Name how the tricuspid valve differs from the mitral v

A
  1. With 2 AV valves and 2 ventricles, TV associated with RV.
  2. TV has 3 leaflets, MV w/ only anterior+posterior
  3. MV chordae attach to 2 distinct papillary muscles
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5
Q

Name 5 features of RV

A
  1. Tripartite: inlet, body, outlet
  2. Heavily trabeculated, thin endocardium
  3. Moderator band near apex
  4. Inlet valve more apical than L AV valve
  5. Smooth outlet (called conus or infundibulum)
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6
Q

Name 5 features of LV

A
  1. Inlet and outlet only
  2. MV is fibrous, continues with AV
  3. Fine trabeculations, smoother endocardium, thicker wall
  4. MV has higher insertion than TV, so LV shares small portion of septum w/ RA
  5. No conus at the outflow
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7
Q

Name the 4 parts of the ventricular septum

A
  1. Inlet (separates TV/MV)
  2. Trabecular (extends to apex, divides LV/RV trabculations)
  3. Outlet (divides outflow tracts)
  4. Membranous (smallest)
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8
Q

Describe the course of ventricular outflow

A

Passive opening and closing of trileaflet semilunar valves to promote unidirectional flow (both ventricles)
PA: rightward, anterior, crosses in front of proximal Ao
Ao: leftward, posterior, crosses over RPA (gives off head/neck vessels) then over left mainstem bronchus, descending goes behind LPA

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9
Q

What does the RCA supply?

A

Coming from Ao sinus, supplies most of the RV, coursing along the AV grove posteriorly
The conal artery is the 1st branch, supplies RV outflow, AV nodes, the posterior descending artery (in R dominance 90%), and sometimes the sinus node

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10
Q

How does the LCA and coronary veins course?

A

Aortic sinus –> transverse sinus –> LAD (–>interventricular groove) or L circumflex –> in 10% supplies posterior descending a.
Veins drain into coronary sinus –> RA

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11
Q

What day gestation does heart heart tube form and when does it start beating?

A

Day 19; within days

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12
Q

Name the mature cardiac segments associated with the following embryonic structures:

  1. Sinus venosus
  2. Primitive atrium
  3. Primitive ventricle
  4. Bulbus cordis
  5. Truncus arteriosus
A
  1. smooth part RA, coronary sinus, oblique v of LA
  2. trabeculated parts of RA/LA
  3. trabeculated parts of RV/LV
  4. smooth parts of RV/LV
  5. Aorta and pulmonary trunk
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13
Q

Once D-looping of primitive tube has occurred, what else must occur in order for 4 chambers to become in series ciruculation?

A

Correct septation
I.e. endocardial cushions grows to separate L and R canals into the future ventricles; conotruncal cushions to septate the ventricular outflow (the truncus)

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14
Q

What defects are associated with conotruncal cushions and why?

A

Craniofacial defects (as in DiGeorge) b/c these cushions include neural crest cells

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15
Q

Names the correlating cardiac defect with the following embryologic abnormality:

  1. Anterior deviation of conal septum, overriding aorta
  2. Persistent left-sided conus, failure of outflow septation
  3. Failure of truncal cushions to spiral, incorrect great vessel septation
  4. Failure of neural crest cell migration, lack of outflow septation, incomplete great vessel septation
  5. Incomplete septation of great vessels
A
  1. ToF
  2. DORV
  3. D-TGA
  4. Truncus arteriosus
  5. Aortopulmonary window
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16
Q

Briefly explain how primum ASD or AVSD occur

A

Roof of common atrium invaginates and eventually fuses with endocardial cushions. Failure of this leads to septum primum not fusing.

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17
Q

Briefly how secundum ASD forms

A

There are perforations of the upper portion of septum primum (for umb v oxygenated blood to shunt R to L). 2nd invagination of atrial roof partially separating atria, creating limbus of foramen. If insufficient, will lead to secundum ASD

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18
Q

Explain how perimembranous VSD forms

A

Intervetnricular foramen closes with outgrowth of endocardial tissue into the muscular septum. If it doesn’t then fuse with the conus septum perimembranous VSD forms (most common congenital heart defect overall)

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19
Q

Explain how Ebstein’s anomaly forms

A

AV valves form after fusion of the endocardial cushions. Ebstein’s forms with incomplete delamination of the septal leaflet of the tricuspid valve.

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20
Q

Explain how TAPVR forms

A

Pulmonary veins form from outpouchings of the lungs into a splanchnic plexus, that coalesces into a common vein that links up with back of the LA but if it doesn’t link up, will cause TAPVR

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21
Q

How doe the ductus remain patent in fetal life?

A

Low fetal oxygen tension, circulating prostaglandins (E2) and prostacyclins (I2). With initial inspiration and decreased prostaglandins/cyclins, DA closes in minutes to days.

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22
Q

Explain Ca-induced calcium release

A

In the sarcolemma of the myocyte, voltage gated Ca channels open, plasma Ca influxes, acts on ryanodine receptors on SR to release Ca into cytoplasm. Rapid Ca then blocks SR Ca release and bind troponin C to complete excitation-contraction coupling.

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23
Q

Name the components of the contractile unit cardiac muscle

A

Sarcomere is made up of myosin, think filament (actin, tropomyosin, troponin complex of I, T, and C), thick filaments (myosin and titin); sarcomeres are connected together by the z disk

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24
Q

What does sarcomere length and Ca sensitivity have to do with Frank-Starling relationship?

A

The longer the sarcomere, the more sensitive it is to Ca. This causes increased tension and therefore, when stretched (i.e. more volume at end diastole) the larger the force of contraction and stroke volume

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25
Q

What is end-systolic elastance (Ees) vs vascular elastance (Ea)?

A

Ees: index of contractility, measuring the stiffness of the ventricle
Ea: slope of end-systole to end-diastole on PV loop. Steeper slope indicates increased elastance.

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26
Q

How does CO change as preload (or CVP, EDV) approaches 0 on PV loop?

A

CO approaches 0 too.

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27
Q

How do you calculate end-systolic elastance (E es)?

A

Point at end-systole in cardiac PV loop during different preload and afterload conditions create a line. The slope of this line is E es, an index of contractility. Steeper slope indicates more contractility (i.e. with inotropes).

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28
Q

CVP is solely based on _____ of the _____ (in CVP vs CO curve), with shifts ____ or ____ for increased or decreased volume, respectively.

A

Compliance; venous compartment

Rightward (increased); leftward (decreased)

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29
Q

What is la place’s law?

A

T = Pr; the tension across a thin wall of a sphere is related to the internal pressure and radius of the sphere. In heart, T (afterload) = transmural pressure x radius of chamber / ventricular wall thickness

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30
Q

What is one way sinus rhythm improves CO?

A

Allows for atrial kick to improve ventricular preload.

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31
Q

In addition to HR X SV = CO, how does increased HR improve CO?

A

Force-frequency relationship: increasing frequency of stimulation of myocytes (Ca availability) increases the force of contraction

32
Q

Where are alpha-2 receptors? What does alpha 2 agonism do?

A

Centrally; agonism inhibits sympathetic flow

33
Q

How do beta 1 (and to smaller degree 2) in heart lead to increased CO?

A

Linked to G proteins, increasing cAMP –> increasing Ca influx and uptake in SR. Receptors are dense near SA node, will increase HR.

34
Q

How are neonatal hearts different than adults?

A

Less dense and more disorganized myocytes leads to less ventricular compliance; dependent on HR over SV.
Immature SR doesn’t release as much Ca; dependent on plasma Ca
Sympathetic innervation is less developed, makes them prone to bradycardia.

35
Q

General timing of congenital heart defects

A

Ductal dependent lesions within first week of life (D-TGA, R o L obstructive lesions), while non-obstructive lesions that cause pulmonary over circulation (VSD, ASD) present 4-6 weeks of life.

36
Q

At what ratio of DO2 to VO2 does oxygen become limited (oxygen debt)?

A

2:1

37
Q

What is tissue dysoxia?

A

A cause of increased lactate, where cells at the mitochondrial level cannot use available oxygen. Seen in sepsis or multi-organ failure despite adequate oxygen delivery.

38
Q

What does NIRS try to measure?

A

A calculated venous saturation. Near-infrared apparently penetrates deep tissue.

39
Q

Equations:
Velocity of blood = what?
Flow of blood = what?

A

Q/A; V = cm/s, A is cross-sectional area, Q is blood flow.

Q = delta P / R; delta P is change in pressure, R = resistance – aka MAP - RAp / total peripheral resistance (or SVR)

40
Q

State Poiseuille’s Law

A 
R = (8 n l) / (T pi * r^4)
n = viscosity, l is length of vessel
41
Q

Total resistance for circuit in parallel vs series =

A

Parallel: 1/R total = 1/R1 + 1/R2 + 1/R3 ….
Series: R total = R1 + R2 + R3

42
Q

Name the hormonal control of regional blood flow

A

Histamine and bradykinin (vasodilation), serotonin (vasoconstriction), epi, norepi, ADH/vasopressin
RAAS: renin (converts angiotensinogen to angiotensin)-angiotensin (ACE converts angiotensin I to II)-aldosterone (reabsorbs water/Na)

43
Q

How do changes in PCO2 differ in cerebral vs pulmonary vascular beds?

A

Opposite effects: low PCO2 in brain –> vasoconstriction, high PCO2 (hypoventilation) in lungs –> vasoconstriction

44
Q

How do NO and endothelin work?

A

NO comes from endothelial cells, derived from arginine and oxygen from nitrate by nitric oxide synthase. Acts within tissues. Converts cGTP to cGMP –> smooth muscle relaxation. Sildenafil inhibits degradation of cGMP to prolong NO action.
Endothelin released in vascular injury to cause vasoconstriction and limit bleeding. Bosentan/tezosentan blocks endothelin receptors.

45
Q

Name physical force that determines myocardial blood flow

A

Difference between aortic and RA pressure, specifically during diastole. Subepicardial vessels then subendocardial vessels get perfused.

46
Q

How does hypoxia affect coronary blood flow? What other substances affect it too?

A

ATP –> AMP –> adenosine –> increase coronary blood flow.
NE, epi, bradykinin, angiotensin II, histamine, vaso affect afterload
NO, O2, CO2, H+, K+, prostaglandins. Alkalosis causes constriction (decreased flow; but less than it does in the brain)

47
Q

What is coronary vascular (flow) reserve?

A

The difference in maximal blood flow (ability to decrease resistance, i.e. dilate) and autoregulated blood flow (at a given pressure).

48
Q

W/ respect to coronary flow reserve, what are ways that maximal flow decreases? Ways that autogregulated flow increases? (thus have a net affect of reducing reserve)

A
  1. Tachycardia, coronary artery dz, polycythemia, increased LVEDP or increased contractility
  2. Anemia, increased contractility, hypertrophy
49
Q

How is the RV coronary blood flow different than the LV?

A
  1. Decreased O2 demand (decreased pressure and afterload)
  2. Decreased systemic BP decreases RV coronary pressure withOUT reducing RV work
  3. Dramatic reduction in RV coronary flow in increases in wall stress (i.e. PH, pulmonary embolus) disposing to ischemia very easily
50
Q

How does acidosis affect cardiac function?

A

Reversible cardiac dysfunction by affected Ca metabolism - specifically, reduces myofibrillar responsiveness to Ca. This reduces contractility

51
Q

Name a few IEM derived cardiomyopathies

A

Hypertrophic CM: glycogen storage (Pompe)

Dilated CM: oxidative phosphorylation defects, systemic carnitine deficiency

52
Q

Where does sympathetic and parasympathetic innervation of SA node arise?

A

Sympathetic: right stellate ganglion
Para: right vagus nerve

53
Q

Describe conduction pathways through heart from SA node down

A

SA node –> bachmann bundle (connects SA to atria) OR 3 primary internodal pathways (connects SA to AV) –> AV –> bundle of His –> L and R bundle branch –> Perkinje fibers

54
Q

How does conduction slow down in the SA node? And what purpose does it serve for cardiac function?

A

Increased number of gap junctions between cells, slowing the impulse propagation. It allows for ventricular filling time (diastole)

55
Q

What are the 2 channels are responsible for maintaining the membrane potential across myocyte? What cations are responsible for the resting membrane potential?

A

inward potassium rectifier current (Kir2.1 channel)
Na-K-ATPase
K for intracellular, Na and Ca for the extracellular

56
Q

Where are fast response action potential and what are the phases (0 to 4)?
Where are slow response ap’s and what are the phases (0-4)?

A

Fast: in the perkinje fibres, atria/ventricular myocytes. 0 to fast upstroke and Na inward; 1 is slight repolarization start of K channels opening and K outward; 2 is plateau w/ Ca inward; 3 is early repolarization with K efflux more than Ca inward; 4 late repolarization by K rectifier

Slow: in the pacemaker cells of SA/AV nodes. 0 is Ca inflow; 1 or 2 doesn’t exist; 3 is repolarization w/ K channels; 4 is gradual depolarization w/ gradual Na influx (autonomic nervous system controlled).
Effective refractory period: 0 to 3, until can depolarize again

57
Q

How does heart modulate the automaticity?

A

Pacemaker cells: B1 adrenergic receptors –> G protein –> increases cAMP –> opens Ca channels –> more Na inward (phase 4) and faster depolarization
Parasympathetic: release of ACh on inhibitory G proteins –> activates K channels and HYPERpolarizes cell –> decreases slope of phase 4, increased threshold for depolarization

58
Q

Name 2 ways bradyarrhythmias occur (other than congenital abnormalities)?

A
  1. Nodal automaticity issues (sinus brady)

2. Heart block

59
Q

Name the causes of 1st degree heart block (3 acquired, 5 congenital)

A

Rheumatic carditis, electrolyte abnl, digoxin or other drug toxicity, Ebstein’s, ASD, AV septal defects, DORV, corrected TGA. Asymptomatic = no intervention. If symptomatic, treat with atropine or isoproterenol

60
Q

What is atropine’s MOA?

A

Muscarinic receptor antagonist

61
Q

Which mobitz (I or II) always requires further evaluation, i.e. is never normal?

A

Both! Mobitz I is abnormal during activity or awake. Atropine or pacemaker?
Mobitz II is never normal.

62
Q

Name 4 acquired causes of 3rd degree block

A

Surgeries, myocarditis, Lyme disease, rheumatic carditis. If hemodynamically unstable, can use atropine or adrenergic agonists.

63
Q

What is the treatment(s) for atrial flutter? What is an important complication?

A

Digoxin to slow AV node, cardioversion.

Thrombi

64
Q

What is the difference between afib and aflutter? Tx for afib?

A

Afib will have “irregularly irregular” ECG, not “sawtooth” pattern in aflutter.
Tx: beta blockers or cardioversion

65
Q

How does adenosine work in terminating SVT (re-entrant)?

A

Binds to potassium channels and decreases automaticity, nodal hyperpolarization, and duration of action potential.

66
Q

Compare AVRT and AVNRT (age of onset, ECG findings, mechanism)

A
  1. AVRT is usually infants, young; AVNRT young adults
  2. Similar narrow-complex tachycardia, AVRT may have retrograde P waves or delta wave in WPW
  3. AVRT is some accessory pathway –> VA conduction; AVNRT has fast + slow pathway within AV node, when PAC hits at right time will proceed down fast pathway and then retrograde back through slow pathway
67
Q

Class Ia antiarrhymthics: MOA, e.g., unique indications and unique adverse reactions

A

Na channel blocker (reduces speed of depolarization phase 0)
Procainamide, dysopyramide, quinidine
Sustained VT, PAC/PVCs, afib, SVT

68
Q

Class Ib antiarrhymthics: MOA, e.g., unique indications and unique adverse reactions

A

Na channel blocker
Lidocaine, mexiletine, tocainide
Ventricular arrhythmias, NOT atrial
Rash, bone marrow suppression (tocainide), decr sz threshold (lido)

69
Q

Class Ia antiarrhymthics: MOA, e.g., unique indications and unique adverse reactions

A

Na channel blocker, decreases conduction velocity
Flecainide, propafenone, moricizine
Ventricular arrhythmias, SVT, aflutter
Increased mortality after MI, blurred vision (flecainide)

70
Q

Class II antiarrhymthics: MOA, e.g., unique indications and unique adverse reactions

A

Beta receptor blocker (blocks catecholes mainly at SA/AV nodes)
Esmolol, atenolol, nadalol, propranolol
HTN, atrial arrhythmias
Bronchospasm, propranolol hypoglycemia

71
Q

Class III antiarrhymthics: MOA, e.g., unique indications and unique adverse reactions

A

K channel blocker, increases refractoriness and action potential duration
Amiodarone, ibutilide, sotalol
JET, ventricular arrhythmias
Torsades, TFTs PFTs (amio), bronchospasm (sotalol)

72
Q

Class IV antiarrhymthics: MOA, e.g., unique indications and unique adverse reactions

A

Ca channel blocker, causes lower resting potential, decreased depolarization slope in nodes
Diltiazem, verapamil
Afib/flutter, hypertension
Same as all (heart block, heart failure, hypotension, bradycardia)

73
Q

How does RV affect LV in certain disease states? What are some examples?

A

Interdependence from bowing of septum into LV, impeding LV return and outflow.
E.g: tamponade, asthma, tension pneumo and pulsus paradoxus

74
Q

Equation for LV afterload in terms of LV pressure and intrathoracic pressure

A

LV afterload = LVp - ITP

75
Q

Equation for RV preload (or venous return) in terms of CVP and RA pressure

A

RV preload = CVP - RA pressure

76
Q

How do obstructive respiratory diseases lead to poor cardiac output?

A

Large negative intrathoracic forces generated by the patient to overcome the airway obstruction leads to high LV afterload (assuming LV pressure remains the same) and therefore can decrease CO. (i.e. pulsus paradoxus)

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