Cardio- Embryology and Physiology Flashcards Preview

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Flashcards in Cardio- Embryology and Physiology Deck (114):
1

Truncus Arteriosus

Gives rise to ascending aorta and pulmonary trunk

Issues with this can cause transposition of great vessels

2

Right common cardinal vein and right anterior cardinal vein

Gives rise to SVC

3

Cardiac looping

Begins at 4 wks of development

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

4

Septation of chambers- Atria

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

5

Separation of chambers- Ventricles

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

6

Conotruncal abnormalities

Associated with failure of neural crest cell to migrate

7

Valves

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

8

Fetal circulation

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

9

Ductus Arteriosus- steroids vs. prostaglandins

Indomethacin (NSAID)- closes PDA

Prostaglandins (E1 and E2)- kEEp PDA open

10

Umbilical arteries and veins

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

11

AllaNtois

Carries gas and waste
Become mediaN umbilical ligament

12

UmbiLilcal arteries

Become mediaL umbilical ligaments

13

RCA (Right coronary artery)

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)

14

LAD (Left anterior descending)

More common site of coronary artery occlusion
Supplies anterior LV

15

Most posterior part of heart

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

16

Pericardium

3 layers: parietal, visceral, and fibrous

17

Oxygen extraction

Highest in myocardium (coronary arteries)

18

3 main features of heart circulation

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

19

Cardiac output

= 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)

20

Increased HR

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

21

MAP

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

22

Pulse pressure

Systolic - diastolic pressure
Proportional to SV, inversely prop to compliance

23

SV

EDV - ESV

24

Increased pulse pressure

Hyperthyrodism, aortic regurg, aortic stiffening, obstructive sleep apnea

25

Decreased pulse pressure

Aortic stenosis, cardiogenic shock, tamponade, HF

26

SV

Increased with increased:
Contractility and preload

Increased with decreased:
Afterload

27

Contractility

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)

28

Myocardial oxygen demand- CARD

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

29

Tension

= P*R(Radius) / (2*t(wall thickness))

30

Preload

Approximated by ventricular EDV (increased preload, increased EDV)

vEnodilators decrease prEload

31

Afterload

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

vAsodilators decrease Afterload

32

Ejection fraction

= SV/ EDV = EDV - ESV/ EDV

Svedv

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

33

Starling curve

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

34

Viscosity of blood

Depends mostly on hematocrit (higher hematocrit, higher viscosity)

35

Arterioles

Account from most of TPR

36

Inotropy

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

37

Venous return

Increased by fluid infusion, sympathetic activity
Decreased in acute hemorrhage or spinal anesthesia

38

Total Peripheral Resistance

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

39

Pressure volume curves

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)

40

S1

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

41

S2

aortic and pulmonic valves close

42

S3

Can be normal in children or adults
Pathologic: dilated ventricles

43

S4 (PHour)

Pathologic always: hypertroPHIC ventricle

44

JVP

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)

45

Normal Splitting of S2

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

46

Wide Splitting of S2

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

Caused by pulmonic stenosis and RBBB

47

Fixed Splitting of S2

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

Paradoxical splitting

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

Inspiration (increases venous return to RA)

Increased intensity of rIght heart sounds

50

Handgrip (increased after load)

Increases MR, AR, VSD (backflow probs)

Decreases hypertrophic cardiomyopathy murmurs

Delays MVP click

51

Valsalva and standing up (decreases preload)

Decreases intensity of most murmurs EXCEPT hypertrophic cardiomyopathy

Early MVP click

52

Rapid squatting (increases preload and after load)

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

Systolic heart sounds

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

54

Diastolic heart sounds

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

55

Aortic stenosis

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

56

Mitral regurgitation

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

Tricuspid regurgitation

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

58

Mitral valve prolapse

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

59

VSD

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

60

Hypertrophic cardiomyopathy

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

61

Aortic regurgitation

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

62

Mitral stenosis

Follows opening snap- OS (mitral valve snapping open)
Rumbling, late diastolic murmur
Increased severity as S2 and OS interval decreases
LA >> 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

PDA

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

64

Myocardial action potential- Phase 0

Sky rocket: Na+ (into cell) channels open

65

Myocardial AP- Phase 1

Dip: K+ (out of cell) channel open

66

Myocardial AP- Phase 2

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

67

Myocardial AP- Phase 3

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

68

Myocardial AP- Phase 4

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

69

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

Knack-Cak-K-K

0. Na (into cell)
1. K (out of cell)
2. Ca (into cell) + K (out of cell)
3. K (out of cell)
4. K (out of cell)

70

Difference from skeletal muscle

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

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

0. Upstroke: Ca2+ (into cell) open

72

Pacemaker AP- Phase 1 and 2 DO NOT EXIST

DO NOT EXIST

73

Pacemaker AP- Phase 3

3. Descent: K+ (out of cell) open, Ca2+ close

74

Pacemaker AP- Phase 4 (Four- Funny)

4. 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

Conduction Pathway

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

76

Pacemaker rates (comparison)

SA > AV > Bundle/Purkinje

77

Speed of conduction

Purkinje > atria > ventricles > AV node

78

P wave

Atrial depol

79

PR

Time from atrial to ventricular depol

80

QRS

Ventricular Depol (+ atrial repol)

81

QT

Time between ventricular deploy and repol

82

T

Ventricular repol

83

ST

Isoelectric, ventricles depolarized

84

U (after T wave)

Seen with hypokalemia and bradycardia

85

Torsades de pointes

Polymorphic ventricular tachycardia

Caused by drugs, decreased K+, decreased Mg2+

Long QT predisposes to this

86

Drugs that induce long QT (ABCDE)

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

87

Torsades de Pointes- tx

magnesium sulfate

88

Congenital Long QT Syndrome

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

Brugada Syndrome- ABCD

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

Wolff-Parkinson-White

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

Atrial fibrillation

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

Afib-tx

anti-coag, rate control, rhythm control, cardioversion

93

Atrial flutter

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

Tx: catheter ablation

94

Vfib

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

95

AV block- 1st degree

PR interval is prolonged (>200ms)

PR is PRo1onged

96

AV block- 2nd degree (Mobitz Type I)

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

97

AV block- 2nd degree (Mobitz Type II)

Occasional missed beat (P that is not followed by QRS)
Tx: pacemaker (to prevent progression to 3rd degree heart block)

98

AV block- 3rd degree

P and QRS are independent of one another

Can be caused by Lyme disease

Tx: pacemaker

99

How to calculate HR

Look at number of boxes between two QRS peaks

300 --> 150 --> 100 --> 75 --> 60 --> 50

100

Atrial Natriuretic Peptide

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

Brain Natriuretic Peptide

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

Net effects of ANP and BNP (3)

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

103

Baroreceptors

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

Cushing reaction

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

Afferent vs. Efferent baroreceptor signals

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

Chemoreceptors- Peripheral

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

107

Chemoreceptors- Central

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

Does NOT directly respond to pO2

108

Normal cardiac pressure

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

109

PCWP (wedge pressure)

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

110

Autoregulation

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

111

Pulmonary vs. systemic vasculature

Pulmonary: hypoxia causes vasoCONSTRICTION

Systemic vasculature: hypoxia causes vasoDILATION

112

Chemicals that help with auto regulation- CHALK

CHALK
CO2
H+
Adenosine
Lactate
K+

113

Normal changes in an aging heart (5)

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

Capillary fluid exchange

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