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Cardiology > Cardio- Embryology and Physiology > Flashcards

Cardio- Embryology and Physiology Flashcards

1
Q

Truncus Arteriosus

A

Gives rise to ascending aorta and pulmonary trunk

Issues with this can cause transposition of great vessels

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2
Q

Right common cardinal vein and right anterior cardinal vein

A

Gives rise to SVC

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3
Q

Cardiac looping

A

Begins at 4 wks of development

Dynein defects (Kartagener- ciliary dyskinesia)- can lead to dextrocardia

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4
Q

Septation of chambers- Atria

A
  1. Septum primum
  2. Foramen secundum
  3. Septum secundum
  4. Foramen ovale
  5. Septum secundum and primum fuse (forming atrial septum)- failure of fusion: patent foramen ovale
  6. Foramen ovale closes due to increased LA pressure
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5
Q

Separation of chambers- Ventricles

A

Endocardial cushions separates atria form ventricles and contributes to atrial and membranous portion of interventricular septum

VSD: most common congenital cardiac anomaly
Usually occurs in membranous septum

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6
Q

Conotruncal abnormalities

A

Associated with failure of neural crest cell to migrate

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7
Q

Valves

A

Derived from endocardial cushions
Outflow tract- A&P
AV canal- M&T

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8
Q

Fetal circulation

A

Two main circuits to the aorta:

Mom –> Umbilical vein (oxy blood from mom) –> ductus venosus –> IVC –> foramen ovale –> LA –> LV –> aorta –>

brain + body –> back through IVC & SVC –> RA –> RV –> Pulmonary artery –> Ductus arterioles –> Aorta –>

Aorta –> Umbilical arteries –> Mom

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9
Q

Ductus Arteriosus- steroids vs. prostaglandins

A

Indomethacin (NSAID)- closes PDA

Prostaglandins (E1 and E2)- kEEp PDA open

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10
Q

Umbilical arteries and veins

A

2 umbilical arteries, one umbilical vein (think smiley face)

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11
Q

AllaNtois

A

Carries gas and waste

Become mediaN umbilical ligament

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12
Q

UmbiLilcal arteries

A

Become mediaL umbilical ligaments

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13
Q

RCA (Right coronary artery)

A

Supplies SA and AV node (can cause heart block if damaged)
More common for PDA (posterior descending artery) to come from RCA- called” right-dominant circulation”, but can come from LCA or both (co-dominant)

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14
Q

LAD (Left anterior descending)

A

More common site of coronary artery occlusion

Supplies anterior LV

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15
Q

Most posterior part of heart

A

LA; enlargement can cause dysphagia (compression of esophagus) and hoarseness (compression of the left recurrent laryngeal nerve)

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16
Q

Pericardium

A

3 layers: parietal, visceral, and fibrous

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17
Q

Oxygen extraction

A

Highest in myocardium (coronary arteries)

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18
Q

3 main features of heart circulation

A
  1. Muscle perfused in diastole
  2. High O2 extraction
  3. O2 demand and coronary blood flow are tightly coupled
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19
Q

Cardiac output

A

= SV * HR = rate of O2 consumption (aka VO2)/ (a. - v. O2 content)
Early exercise: CO maintained by increased HR and SV
Late exercise: CO maintained by increased HR only (SV plateaus)

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20
Q

Increased HR

A

Diastole preferentially shortened (less filling time –> decreased CO)

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21
Q

MAP

A

= CO * TPR = 2/3 diastolic pressure + 1/3 systolic pressure

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22
Q

Pulse pressure

A

Systolic - diastolic pressure

Proportional to SV, inversely prop to compliance

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23
Q

SV

A

EDV - ESV

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24
Q

Increased pulse pressure

A

Hyperthyrodism, aortic regurg, aortic stiffening, obstructive sleep apnea

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25
Q

Decreased pulse pressure

A

Aortic stenosis, cardiogenic shock, tamponade, HF

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26
Q

SV

A

Increased with increased:
Contractility and preload

Increased with decreased:
Afterload

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27
Q

Contractility

A

Increased with:
Catecholamines (increase Ca2+ release)
Decreased Na+ extracellularly
Digitalis (increases Na+ and Ca2+ intracellularly)

Decreased with
B1 blockers
HF with systolic dysfunction
Acidosis
Hypoxia/ hypercapnea
Non-DHP Ca2+ blockers (verapamil and diltiazem- mainly target heart)
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28
Q

Myocardial oxygen demand- CARD

A

Increased by:

Increased CARD: Contractility, After load, heart Rate, Diameter of ventricle

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29
Q

Tension

A

= PR(Radius) / (2t(wall thickness))

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30
Q

Preload

A

Approximated by ventricular EDV (increased preload, increased EDV)

vEnodilators decrease prEload

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31
Q

Afterload

A

Approximated by MAP (increased after load, increased MAP, increased wall tension)

vAsodilators decrease Afterload

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32
Q

Ejection fraction

A

= SV/ EDV = EDV - ESV/ EDV

Svedv

EF decreased in systolic failure
EF normal in diastolic failure (harder to tx)

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33
Q

Starling curve

A

Increase in end-diastolic length of muscle fiber increases the force of contraction

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34
Q

Viscosity of blood

A

Depends mostly on hematocrit (higher hematocrit, higher viscosity)

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35
Q

Arterioles

A

Account from most of TPR

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36
Q

Inotropy

A

Contractility
Increased by digoxin, catecholamines
Decreased in uncompensated HF and narcotics overdose

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37
Q

Venous return

A

Increased by fluid infusion, sympathetic activity

Decreased in acute hemorrhage or spinal anesthesia

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38
Q

Total Peripheral Resistance

A

Increased with vasopressors
Decreased with exercise (to perfuse organs) and AV shunt
See page 269 of FA for more details on effect on graph

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39
Q

Pressure volume curves

A

Increased preload: shifts right part of curve further right (same ESV, but higher EDV)
Increased after load: elongates curve (upward) with same EDV, but higher ESV
Increased contractility: shifts left part of curve further left (lower ESV, but same EDV)

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40
Q

S1

A

mItral and trIcuspid valves close (remember- sounds are heard mainly when the door CLOSES not opens)

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41
Q

S2

A

aortic and pulmonic valves close

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42
Q

S3

A

Can be normal in children or adults

Pathologic: dilated ventricles

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43
Q

S4 (PHour)

A

Pathologic always: hypertroPHIC ventricle

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44
Q

JVP

A

a wave- atrial contraction
c wave- tricuspid closure/ RV contraction
x descent- atrial relaXation (absent in tricuspid regard)
v wave- atrial filling (“Villing”)
y descent- RA emptYing into RV (passive)

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45
Q

Normal Splitting of S2

A

During inspiration (I) distance between A2 and P2 closure increase due to increased venous return (caused by decreased intrathoracic pressure)

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46
Q

Wide Splitting of S2

A

Not much difference seen between A2 and P2 closure during I and E; delayed P2 closure

Caused by pulmonic stenosis and RBBB

47
Q

Fixed Splitting of S2

A

No difference between A2 and P2 closure during I or E; delayed P2 closure

Heard in ASD (because larger L–> R shunt causes larger volume in LA and therefore takes longer for LA to empty and P2 to close)

48
Q

Paradoxical splitting

A

Delayed A2 closure; P2 sound occurs before A2 (and paradoxically split is less during inspiration –> as opposed to normally when it is more clear during inspiration)

Caused by aortic stenosis and LBBB

49
Q

Inspiration (increases venous return to RA)

A

Increased intensity of rIght heart sounds

50
Q

Handgrip (increased after load)

A

Increases MR, AR, VSD (backflow probs)

Decreases hypertrophic cardiomyopathy murmurs

Delays MVP click

51
Q

Valsalva and standing up (decreases preload)

A

Decreases intensity of most murmurs EXCEPT hypertrophic cardiomyopathy

Early MVP click

52
Q

Rapid squatting (increases preload and after load)

A

Shunts blood from L –> R; used in pts with Tet to force more blood to go through pulmonary circulation by increasing SVR

Decreases intensity of hypertrophic cardiomyopathy murmur

Increases intensity of AS

Delays MVP click (similar to handgrip)

53
Q

Systolic heart sounds

A 
A & P stenosis
M & T regurg
VSD (heard at T)
MVP
Hypertrophic cardiomyopathy
54
Q

Diastolic heart sounds

A

A & P regurg
M & T stenosis
ASD (heard at T)

55
Q

Aortic stenosis

A

Crescendo-decrescendo
Radiates to carotids
Pulsus parvus et tardus (pulses are weak with delayed peak)
SAD: leads to Syncope, Angina, and Dyspnea

56
Q

Mitral regurgitation

A

Holosystolic, high pitched blowing murmur
Loudest at apex and radiates to axilla
Left sided S3 indicates more severe MR (higher regurgitant volume)
Commonly caused by rheumatic fever

57
Q

Tricuspid regurgitation

A

Holosystolic, high pitched blowing murmer (like MR)
Radiates to right sternal border
Caused by RV dilation
Increases in intensity with inspiration

58
Q

Mitral valve prolapse

A

Late systolic crescendo murmur beginning with mid systolic click (delayed by increased after load, earlier with decreased preload)

59
Q

VSD

A

Harsh, holosystolic murmur
Loudest at T
Accentuated by increased after load (more back flow through hole)

60
Q

Hypertrophic cardiomyopathy

A

Systolic crescendo-decrescendo murmur
Caused by left ventricular outflow obstruction
Increased with valsalva

61
Q

Aortic regurgitation

A

High-pitched blowing diastolic decrescendo murmur
Hyperdynamic pulse/ head bobbing when severe/chronic
Wide pulse pressure
Loudest when sitting up and leaning forward

62
Q

Mitral stenosis

A

Follows opening snap- OS (mitral valve snapping open)
Rumbling, late diastolic murmur
Increased severity as S2 and OS interval decreases
LA&raquo_space; LV pressure during diastole (blood is retained in LA and not filling in LV as atria are contracting, due to stenosis of the mitral valve)

63
Q

PDA

A

Continuous (machine-like) murmur
Loudest at S2
Due to congenital rubella or prematurity
Best heard in left infraclavicular area

64
Q

Myocardial action potential- Phase 0

A

Sky rocket: Na+ (into cell) channels open

65
Q

Myocardial AP- Phase 1

A

Dip: K+ (out of cell) channel open

66
Q

Myocardial AP- Phase 2

A

Plateau: Ca2+ (into cell) open while K+ (out) channels remain open

67
Q

Myocardial AP- Phase 3

A

Descent: K+ (out) dominates and Ca2+ channels close

68
Q

Myocardial AP- Phase 4

A

Low plateau: K+ stay open- membrane reaches resting potential

69
Q

Memory tool for myocardial AP: Na-K-Ca-K-K-K

A

Knack-Cak-K-K

  1. Na (into cell)
  2. K (out of cell)
  3. Ca (into cell) + K (out of cell)
  4. K (out of cell)
  5. K (out of cell)
70
Q

Difference from skeletal muscle

A
  1. Plateau: Cardiac has plateau phase due to Ca2+ influx (during K+ efflux)
  2. Ca2+ induced Ca2+ release: Require Ca2+ influx into cell to release Ca2+ from SR (sarcoplasmic reticulum)
  3. Gap junctions: Cardiac myocytes are electrically coupled
71
Q

Pacemaker AP (occurs in SA and AV nodes)- Phase 0

A
  1. Upstroke: Ca2+ (into cell) open
72
Q

Pacemaker AP- Phase 1 and 2 DO NOT EXIST

A

DO NOT EXIST

73
Q

Pacemaker AP- Phase 3

A
  1. Descent: K+ (out of cell) open, Ca2+ close
74
Q

Pacemaker AP- Phase 4 (Four- Funny)

A
  1. Funny: K+ (INTO cell) and Na+ (into cell) via “funny current”

Rate at which ions enter cells determines the HR (via adjusting the number of open funny current channels)
Adenosine/ ACh- decreases HR
Catecholamines- increases HR

75
Q

Conduction Pathway

A

SA node –> atria -> AV node –> Bundle of His –> Right and left bundle branches –> Purkinje fibers –> ventricles

76
Q

Pacemaker rates (comparison)

A

SA > AV > Bundle/Purkinje

77
Q

Speed of conduction

A

Purkinje > atria > ventricles > AV node

78
Q

P wave

A

Atrial depol

79
Q

PR

A

Time from atrial to ventricular depol

80
Q

QRS

A

Ventricular Depol (+ atrial repol)

81
Q

QT

A

Time between ventricular deploy and repol

82
Q

T

A

Ventricular repol

83
Q

ST

A

Isoelectric, ventricles depolarized

84
Q

U (after T wave)

A

Seen with hypokalemia and bradycardia

85
Q

Torsades de pointes

A

Polymorphic ventricular tachycardia

Caused by drugs, decreased K+, decreased Mg2+

Long QT predisposes to this

86
Q

Drugs that induce long QT (ABCDE)

A 
Anti-Arrythmics (Class IA, III)
Anti-Biotics (macrolides)
Anti-Cychotics (haloperidol)
Anti-Depressants (TCADs)
Anti-Emetics (ondansetron)
87
Q

Torsades de Pointes- tx

A

magnesium sulfate

88
Q

Congenital Long QT Syndrome

A

Due to ion channel defects- specifically with K+ channel proteins

Increased risk of ventricular tachy, sudden death

Two types:
Romano-Ward Syndrome: AD- no deafness
Jervell and Lange-Nielsen: AR with deafness

89
Q

Brugada Syndrome- ABCD

A

Autosomal dominant, seen in Asian males

Characterized by pseudo RBBB (presence of R’- QRS split into two humps) and ST elevations in V1-V3

Causes increased risk of ventricular tachyarrythmias

Asian male
Brugada
Cardioverter-defib tx
Dominant

90
Q

Wolff-Parkinson-White

A

Most common ventricular pre-excitation syndrome

Causes by reentrant loop (bundle of Kent) that bypasses the AV node

Characterized by delta wave (shortened PR and widened QRS)

Can result in SVT

91
Q

Atrial fibrillation

A

No discrete P waves, varying RR intervals, narrow QRS complexes

Irregularly irregular pattern; AV node generally determines rate of ventricular contraction

RF: HTN, CAD

92
Q

Afib-tx

A

anti-coag, rate control, rhythm control, cardioversion

93
Q

Atrial flutter

A

Sawtooth pattern
Caused by back-to-back atrial depolarization
Can be due to reentrant loop around tricuspid valve

Tx: catheter ablation

94
Q

Vfib

A

Erratic rhythm with no identifiable waves
Fatal in not tx
Tx: CPR and defibrillation

95
Q

AV block- 1st degree

A

PR interval is prolonged (>200ms)

PR is PRo1onged

96
Q

AV block- 2nd degree (Mobitz Type I)

A

Progressively elongating PR interval, that causes a missed QRS
“Regularly irregular”

97
Q

AV block- 2nd degree (Mobitz Type II)

A

Occasional missed beat (P that is not followed by QRS)

Tx: pacemaker (to prevent progression to 3rd degree heart block)

98
Q

AV block- 3rd degree

A

P and QRS are independent of one another

Can be caused by Lyme disease

Tx: pacemaker

99
Q

How to calculate HR

A

Look at number of boxes between two QRS peaks

300 –> 150 –> 100 –> 75 –> 60 –> 50

100
Q

Atrial Natriuretic Peptide

A

Released from atrial myocytes in response to INCREASED volume to promote natriuresis

Acts via cGMP (like NO)

Dilates afferent arterioles and constricts efferent arterioles to promote filtration and diuresis

101
Q

Brain Natriuretic Peptide

A

Released from ventricular myocytes in response to increased tension

Longer half life than ANP

BNP blood test- to diagnose HF

Nesiritide (recombinant BNP) available for HF treatment

102
Q

Net effects of ANP and BNP (3)

A

Increase GFR
Inhibits renin secretion- Increases natriuresis and diuresis
Prevent reabsorption of Na+ at PCT

103
Q

Baroreceptors

A

General path: baroreceptors detect stretch

Carotid massage
If stretch is detected –> baroreceptors fire –> decreases sympathetic stim and increases parasymp stim –> increases AV node refractory period –> Decreases HR

Opposite for hypotension

104
Q

Cushing reaction

A

Triad of hypertension, bradycardia and respiratory depression

(Mnemonic: CHBE- cushing: HTN, Bradycardia, and decreased Exhalation)

Caused by increased intracranial pressure –> stimulates vasoconstriction of a. to brain –> cerebral ischemia –> increases pCO2 and decreases pH (note: brain does not respond to PO2 changes!!) –> sympathetic reflex increases –> causes HTN –> periphery detects increased stretch –> causes bradycardia

105
Q

Afferent vs. Efferent baroreceptor signals

A

Afferent/ Sensory:
IX: Glossopharyngeal- via carotid baroreceptors (e.g. during carotid massage)
X: Vagus- via aortic baroreceptors

Efferent:
Parasympathetic: via vagus nerve (affects heart- SA and AV nodes)
Sympathetic: via sympathetic chain (affects blood vessel and heart)

Processing occurs in the medulla

106
Q

Chemoreceptors- Peripheral

A

Peripheral: Located in similar regions to baroreceptors (aortic arch, carotid)- stimulated by decreased pO2 and increased pCO2 (decreased pH)

107
Q

Chemoreceptors- Central

A

Central: Stimulated by changes in pH and pCO2 of brain interstitial fluid (affected by arterial CO2)

Does NOT directly respond to pO2

108
Q

Normal cardiac pressure

A

RA: 5
RV: 10
LA (PCWP): 25
LV: 100

109
Q

PCWP (wedge pressure)

A

Estimates LA pressure

Gathered by inflating a balloon in pulmonary artery and measuring downstream pressure

110
Q

Autoregulation

A

Blood flow (flow rate) stays the same despite variation in perfusion pressures

111
Q

Pulmonary vs. systemic vasculature

A

Pulmonary: hypoxia causes vasoCONSTRICTION

Systemic vasculature: hypoxia causes vasoDILATION

112
Q

Chemicals that help with auto regulation- CHALK

A 
CHALK
CO2
H+
Adenosine
Lactate
K+
113
Q

Normal changes in an aging heart (5)

A

Decrease in LV chamber size (apex to base)

Sigmoid shaped ventricular septum

Myocardial atrophy (increases collagen deposition)

Accumulation of cytoplasmic lipofuschin w/in myocytes (product of lipid peroxidation)

Dilated aortic root

114
Q

Capillary fluid exchange

A

Jf (net fluid flow) = Permeability to fluid * (Capillary pressure - Interstitial pressure) - Permeability to protein * (Plasma oncotic (colloid osmotic) pressure - Intestitial oncotic pressure)

Cardiology (3 decks)

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