First Aid Step 1 Cardiology - Anatomy, Physiology

Front 1

What does the left circumflex artery supply?

Back 1

Lateral and posterior walls of the left ventricle

Front 2

What does the left anterior descending artery supply?

Back 2

Anterior 2/3 of interventricular septum, anterior papillary msucle, and anterior surface of L ventricle

Front 3

What does the posterior descending/interventricular artery supply?

Back 3

Posterior 1/3 of interventricular septum and posterior walls of ventricles

Front 4

What does the acute marginal artery supply?

Back 4

R ventricle

Front 5

What artery usually supplies the SA and AV nodes?

Back 5

RCA

Front 6

Where does posterior descending artery arise from in R and L dominant circulation and which is more common?

Back 6

R-dominant (85%) from RCA.
L-dominant (8%) LCX.
Codominant (7%) LCX and RCA

Front 7

Where is the most common coronary artery occlusion?

Back 7

LAD

Front 8

When do the coronary arteries fill?

Back 8

During diastole

Front 9

What is the most posterior part of the heart?

Back 9

L atrium

Front 10

What other symptoms can you have (outside cardio) if the L atrium enlarges?

Back 10

dysphagia (compression of esophagus) or hoarseness (due to compression of the L recurrent laryngeal nerve - a branch of the vagus)

Front 11

When is transesophageal echocardiogram useful?

Back 11

Diagnosing L atrial enlargement, aortic dissection, and thoracic aortic aneurysm

Front 12

What is the formula for CO?

Back 12

CO = SV x HR

Front 13

What is the Fick principle?

Back 13

CO = (rate of O2 consumption)/(arterial O2 content - venous O2 content)

Front 14

What is the formula for mean arterial pressure?

Back 14

MAP = CO x TPR = 2/3 diastolic pressure + 1/3 systolic pressure

Front 15

What is the formula for pulse pressure?

Back 15

Pulse pressure = systolic pressure - diastolic pressure

Front 16

What is the formula for stroke volume?

Back 16

SV = CO/HR = EDV - ESV

Front 17

What is pulse pressure proportionate to?

Back 17

Stroke volume

Front 18

What happens to CO during the early and late stages of exercise?

Back 18

Early: CO maintained by inc HR and SV.
Late: CO maintained by inc HR only (SV plateaus)

Front 19

What happens if the HR is too high?

Back 19

Diastolic filling is incomplete and CO decreases (ex: ventricular tachycardia)

Front 20

What variables affect stroke volume and how?

Back 20

Contractility, afterload, and preload.
SV increases when PL increases, AL decreases, or contractility increases

Front 21

What increases contractility (and therefore SV)?

Back 21

Catecholamines (inc activity of Ca pump in sarcoplasmic reticulum), increased intracellular Ca, dec extracellular Na (decreases activity of Na/Ca exchanger), Digitalis (blocks Na/K pump) -> inc intracellular Na -> dec Na/Ca exchanger activity -> inc intracellular Ca)

Front 22

What decreases contractility (and therefore SV)?

Back 22

B1 blockage (dec cAMP), heart failure (systolic dysfunction), acidosis, hypoxia/hypercapnea (dec pO2/inc pCO2), non-dihydrohyridine Ca channel blockers

Front 23

In what physical states does SV increase?

Back 23

anxiety, exercise, and pregnancy

Front 24

What is the change seen in SV in pts with failing heart?

Back 24

Dec SV

Front 25

What increases myocardial O2 demand?

Back 25

Increased afterload (proportional to arterial pressure), increased contractility, increased heart rate, increased heart size (increased wall tension)

Front 26

What is preload?

Back 26

Ventricular end diastolic volume

Front 27

What is afterload?

Back 27

Mean arterial pressure (proportioanl to peripheral resistance)

Front 28

What increases preload?

Back 28

Exercise (slightly), inc blood volume (ex: overtransfusion), excitement (inc sympathetic activity)

Front 29

What do venodilators and vasodilators do to preload and afterload?

Back 29

Venodilators (ex: nitroglycerin) decrease preload.
Vasodilators (ex: hydralazine) decrease afterload

Front 30

What is the force of contraction of cardiac muscle proportional to?

Back 30

End diastolic length of cardiac muscle fiber (preload)

Front 31

What is the formula for ejection fraction?

Back 31

EF = SV/EDV = EDV-ESV/EDV

Front 32

What is EF an index for?

Back 32

Ventricular contractility

Front 33

What is the normal EF?

Back 33

>55%

Front 34

What is the change in EF in systolic heart failure?

Back 34

EF decreases

Front 35

What is Ohm's law?

Back 35

change in V = IR

Front 36

What is the formulat for change in pressure?

Back 36

change in pressure = Q x R (Q = flow)

Front 37

What is the formulat for resistance (2)?

Back 37

resistance = driving pressure (delta P)/flow (W) = (8n(viscosity) x length)/pi(r^4)

Front 38

What is the forumula for total resistance of vessels in series?

Back 38

Total R = R1 + R2 + R3...

Front 39

What is the forumula for total resistance of vessels in parallel?

Back 39

1/Total R = 1/R1 + 1/R2 + 1/R3...

Front 40

What does viscosity depend mostly on?

Back 40

Hematocrit

Front 41

What conditions does viscosity increase in?

Back 41

Polycythemia, hyperproteinemic states (ex: multiple myeloma), hereditary spherocytosis

Front 42

What condition is viscosity decreased in?

Back 42

Anemia

Front 43

What direction does a pressure gradient drive flow?

Back 43

From high pressure to low pressure

Front 44

What is resistance directly proportional and inversely proportional to?

Back 44

Directly: viscosity and vessel length.
Inversely: r^4

Front 45

What type of blood vessels accounts for most of the total peripheral resistance to regulate capillary flow?

Back 45

Arterioles

Front 46

What causes normal splitting of S2?

Back 46

Inspiration causes a drop in intrathoracic pressure, which increases venous return to the right ventricle. This increases stroke volume of the RV, resulting in inc RV ejection time, which leads to delayed closure of the pulmonic valve. In addition, decreased pulmonary impedance (increased capacity of the pulmonary circulation) also occurs during inspiration, which contributes to delayed closure of the pulmonic valve

Front 47

What is normal splitting of S2?

Back 47

A2 before P2

Front 48

What causes wide splitting of S2? What conditions is it seen in?

Back 48

Delay in RV emptying causes delayed pulmonic sound (regardless of breath). It is basically an exaggeration of normal splitting and is seen in conditions that delay RV emptying (pulmonic stenosis, RBBB)

Front 49

What condition do you see fixed splitting of S2?

Back 49

ASD (L->R shunt) -> inc RA and RV volumes -> inc flow through pulmonic valve. Therefore, regardless of breath, pulmonic closure is greatly delayed

Front 50

What is paraxodical splitting of S2?

Back 50

P2 before A2

Front 51

When do you see paradoxical splitting of S2 and why?

Back 51

Conditions that delay LV emptying (aortic stenosis, LBBB).
The normal order of valve closure is reversed (P2 before A2)

Front 52

What murmurs are heard at thea aortic listening area?

Back 52

Systolic murmurs: aortic stenosis, row murmur, aortic valve sclerosis

Front 53

What murmurs are heard at the L sternal border?

Back 53

Diastolic murmurs: AR, PR.
Systolic murmurs: hypertrophic cardiomyopathy

Front 54

What murmurs are heard at the pulmonic listening area?

Back 54

Systolic ejection murmurs: PS, flow murmurs (ASD, PDA)

Front 55

What murmurs are heard at the tricuspid listening area?

Back 55

Pansystolic murmurs: TR, VSD.
Diastolic murmurs: TS, ASD

Front 56

What murmurs are heard at the mitral valve listening area?

Back 56

Systolic murmurs: MR.
Diastolic murmurs: MS

Front 57

What does inspiration do to heart sounds?

Back 57

increases intensity of R heart sounds

Front 58

What does expiration do to heart sounds?

Back 58

Increases intensity of L heart sounds

Front 59

What does hand grip do to murmurs?

Back 59

Increases systemic vascular resistance -> increases intensity of MR, AR, VSD, MVP.
Decreases intensity of AS, hypertrophic CM

Front 60

What does valsalva do to murmurs?

Back 60

Decreases venous return -> decreases intensity of most murmurs, increases intensity of MVP, hypertrophic CM

Front 61

What does rapid squatting do to murmurs?

Back 61

Increases venous return, preload, and afterload (with prolonged squatting) -> decreases intensity of MVP, hypertrophic CM

Front 62

What are the systolic heart murmurs?

Back 62

Aortic/pulmonic stenosis, MR/TR, VSD

Front 63

What are the diastolic heart sounds?

Back 63

Aortic/pulmonic regurgitation, MS/TS

Front 64

What does MR sound like and where do you hear it the best?

Back 64

Holosystolic, high-pitched "blowing murmur".
Heard loudest at apex and radiates towrads axilla

Front 65

What enhances MR murmur?

Back 65

Maneuvers that increase TPR (squatting, handgrip) or LA return (expiration

Front 66

When do you often see MR?

Back 66

Often due to ischemic heart disease, MVP, or LV dilation. Can also be caused by rheumatic fever or infective endocarditis.

Front 67

What does TR sound like and where do you hear it the best?

Back 67

Holosystolic, high-pitched "blowing murmur".
Heard loudest at tricupsid area and radiates to R sternal border.

Front 68

What enhances TR murmur?

Back 68

Maneuvers that increase RA return (ex: inspiration)

Front 69

What can cause TR?

Back 69

RV dilation. Can be caused by rheumatic fever and infective endocarditis

Front 70

What does aortic stenosis sound like? Where does it radiate to?

Back 70

Crescendo-decrescendo systolic ejection murmur following an ejection click (ejection click is due to an abrupt halting of valve leaflets).

Radiates to carotids/heart base

Front 71

What murmur do you hear pulsus parvus et tardus in and what does it mean?

Back 71

Aortic stenosis. "pulse is small and late" meaning pulses are weak with a delayed peak

Front 72

What 3 symptoms can aortic stenosis lead to?

Back 72

SAD: syncope, angina, and dyspnea

Front 73

What often causes AS?

Back 73

Age-related calcific aortic stenosis or bicupsid aortic valve

Front 74

What does the murmur of VSD sound like? Where is it loudest?

Back 74

Holosystolic, harsh-sounding murmur.

Loudest at tricupsid area.

Front 75

What enhances murmur of VSD?

Back 75

Handgrip (bc of increased afterload)

Front 76

What is the most common valvular lesion?

Back 76

MVP

Front 77

What does MVP sound like and where is it best heard?

Back 77

Late systolic crescendo murmur with midsystolic click (click due to sudden tensing of chordae tendineae). Best heard over apex

Front 78

When is MVP loudest?

Back 78

S2

Front 79

What is the prognosis for MVP?

Back 79

Usually benign, but can predispose to infective endocarditis

Front 80

What can cause MVP?

Back 80

Myxomatous degeneration, rheumatic fever, or chordae rupture

Front 81

What enhances murmur of MVP?

Back 81

Decreased venous return (standing or valsalva)

Front 82

What does the murmur of AR sound like?

Back 82

Immediate high-pitched "blowing" diastolic decrescendo murmur

Front 83

What murmur do you see wide pulse pressure?

Back 83

AR if chornic

Front 84

What murmur can you have bounding pulses and head bobbing?

Back 84

AR

Front 85

What can cause AR?

Back 85

Aortic root dilation, bicuspid AV, endocarditis, rheumatic fever.

Front 86

What increases and decreases sound of AR murmur?

Back 86

Increased with hand grip, decreased with vasodilators

Front 87

What does the murmur of MS sound like?

Back 87

Follows opening snap (OS due to halt in leaflet motion in diastole after rapid opening due ot fusion at leaflit tips).

Delayed rumbling late diastolic murmur.

Front 88

What is often the cause of MS?

Back 88

Rehumatic fever

Front 89

What can chronic MS lead to?

Back 89

LA dilation

Front 90

What increases murmur of MS?

Back 90

Maneuvers that increase LA return (ex: expiration)

Front 91

What does the murmur of PDA sound like? Where is it best heard? When is it the loudest?

Back 91

Continuous machine-like murmur.
Loudest at S2.
Best heard at L infraclavicular area.

Front 92

What is often the cause of PDA?

Back 92

Congenital rubella or prematurity

Front 93

What occurs in Phase 0 of the ventricular action potential?

Back 93

Rapid upstroke - voltage gated Na channels open

Front 94

What occurs in Phase 1 of the ventricular action potential?

Back 94

Initial repolarization - inactivation of voltage-gated Na channels and voltage-gated K channels begin to open

Front 95

What occurs in Phase 2 of the ventricular action potential?

Back 95

Plateau - Ca inflex through voltage-gated Ca channels balances K efflux. Ca influx triggers Ca release from sarcoplasmic reticulum and myocyte contraction

Front 96

What occurs in Phase 3 of the ventricular action potential?

Back 96

Rapid depolarization - massive K efflux due to opening of voltage-gated slow K channels and closure of voltage-gated Ca channels

Front 97

What occurs in Phase 4 of the ventricular action potential?

Back 97

Resting potential - high K permeability through K channels

Front 98

What are the 3 main differences between cardiac and skeletal muscle (hint: 1. Ca 2. spontaneous depolarization 3. coupling)

Back 98

1. Cardiac muscle action potential has a plateua, which is due to Ca influx and K efflux; myocyte contraction occurs due to Ca-induced Ca release from the SR

2. Cardiac nodal cells spontaneously depolarize during diastole resulting in automaticity due to If channels ("funny current" channels responsible fo ra slow, mixed Na/K inward current)

3. Cardiac myocytes are electrically coupled to each other by gap junctions

Front 99

How is phase 0 of pacemaker (SA, AV nodes) action potential different from that of ventricular action potential?

Back 99

Upstroke - opening of voltage-gated Ca channels. Fast voltage-gate Na channels are permanently inactivated bc of the less negative resting voltage of these cells. Results in a slow conduction velocity that is used by the AV node to prolong transmission from the atria to ventricles

Front 100

How is phase 2 of pacemaker (SA, AV nodes) action potential different from that of ventricular action potential?

Back 100

Plateau is absent

Front 101

How is phase 3 of pacemaker (SA, AV nodes) action potential different from that of ventricular action potential?

Back 101

Inactivation of the Ca channels and increased activation of the K channels -> inc K efflux

Front 102

How is phase 4 of pacemaker (SA, AV nodes) action potential different from that of ventricular action potential?

Back 102

Slow diastolic depolarization - membrane potential spontaneously depolarizes as Na conductance increases (I(f) different from I(Na) in phase 0 of ventricular action potential). Accounts for the automaticity of SA and AV nodes. The slope of phase 4 in the SA node determines heart rate. ACh/adenosine decrease the rate of diastolic depolarization and decrease heart rate, while catechoalmines increase depolarization and increase HR. Sympathetic stimulation increases the chance that I(f) channels are open and thus increase HR

Front 103

What does the P wave represent?

Back 103

Atrial depolarization (atrial repolarization is masked by QRS)

Front 104

What does PR interval represent and what is normal?

Back 104

Conduction delay thru AV node. Normal <200 msec

Front 105

What does the QRS complex represent adn what is normal?

Back 105

Ventricualr depolarization. Normal <120msec

Front 106

What does QT interval represent?

Back 106

Mechanical contraction of the ventricles

Front 107

What does T wave represent?

Back 107

Ventricular repolarization

Front 108

What might T wave inversion indicate?

Back 108

Recent MI

Front 109

What does ST segment represent?

Back 109

Isoelectric, ventricles depolarized

Front 110

What can cause a U wave?

Back 110

Hypokalemia, bradycardia

Front 111

What is the order of speed of conduction from fastest to slowest?

Back 111

Purkinje > atria > ventricles > AV node

Front 112

What is the order of pacemakers from most common to least?

Back 112

SA > AV > bundle of His/Purkinje/ventricles

Front 113

What is the order of the conduction pathway of an action potential?

Back 113

SA node -> atria -> AV node -> common bundle -> bundle branches -> Purkinje fibers -> ventricles

Front 114

What is the "pacemaker" of the heart

Back 114

SA node

Front 115

Does the SA node have a fast or slow phase of upstroke?

Back 115

Slow

Front 116

What is the delay between the SA and AV node?

Back 116

AV node has a 100msec delay - the atrioventricular delay - this allows time for ventricular filling

Front 117

What does ventricular tachycardia look like on EKG and what can it progress to?

Back 117

VT characterized by shifting sinusoidal waveforms on EKG and can progress to Ventricular Fibrillation

Front 118

What can predispose to torsades de pointes?

Back 118

Anything that prolongs WT interval.

Front 119

What is the treatment for torsades de pointes?

Back 119

Magnesium sulfate

Front 120

What are congenital long QT syndromes most often due to?

Back 120

Defects in cardiac Na or K channels.

Front 121

What can congenital long QT syndromes present with besides torsades de pointes? What are the names of these syndromes?

Back 121

Severe congenital sensorineural deafness (Jervell and Lange-Nielsen syndrome)

Front 122

What does Afib look like on EKG?

Back 122

Chaotic and erratic baseline (irregularly irregular) with no discrete P waves in between irregularly spaced QRS complexes.

Front 123

What can Afib lead to?

Back 123

Atrial stasis and stroke

Front 124

What are the treatment options (generally) for Afib?

Back 124

Rate control, anticoagulation, and possible cardioversion

Front 125

What does Atrial Flutter look like on EKG?

Back 125

Rapid succession of identical, back-to-back atrial depolarization waves. The identical appearance accounts for the "sawtooth" appearance of the flutter waves.

Front 126

What meds can be used to convert atrial flutter to seinus rhythm? What drugs can be used for rate control?

Back 126

Convert to sinus rhythm: class IA, IC, or III antiarrhythmics.

Rate control: beta blocker or calcium channel blocker

Front 127

What does ventricular fibrillation look like on EKG? What is the prognosis?

Back 127

Completely erratic rhythm with no identifiable waves. It is fatal without immediate CPR and defibrillation.

Front 128

What is 1st degree AV block? What are the symptoms?

Back 128

Prolonged PR interval (>200msec). Asymptomatic

Front 129

What is Mobitz type I 2nd degree AV block (Wenckebach)? What are the symptoms?

Back 129

Progressive lengthening of PR interval until a beat is "dropped" (a p-wave not followed by a QRS complex). Usually asymptomatic

Front 130

What is Mobitz type II 2nd degree AV block? How do you treat it?

Back 130

Dropped beats taht are not preceded by a change in the length of the PR interval (as in type I). These abrupt, nonconducted P waves result in a pathologic condition. It is often found as 2:1 block, where there are 2 or more p waves to 1 QRS complex. May progress to 3rd degree block. Often treated with a pacemaker (whereas type I is not).

Front 131

What is 3rd degree AV block? How do you treat it?

Back 131

The atria and ventricles beat independently of each other. Both p waves and QRS complexes are present, although the p-waves bear no relation to the QRS complexes. The atrial rate is faster than the ventricular rate. Usually treated with a pacemaker

Front 132

What infection can result in 3rd degree heart block?

Back 132

Lyme disease

Front 133

What is atrial natruiuretic peptide? What does it do?

Back 133

Released froma trial myocytes in response to inc blood volume and atrial pressure. Causes generalized vascular relaxation and dec Na reabsorption at the medullary collecting tubule. Constricts efferent renal arterioles and dilates afferent arterioles (cGMP mediated), promoting diuresis and contributing to the "escape from aldosterone" mechanism

Front 134

What is the function of the aortic arch receptor? (where does it transmit to, what does it respond to)?

Back 134

Transmits via vagus nerve to solitary nucelus of medulla (responds ONLY to inc in BP)?

Front 135

What is the function of the carotid receptor? (where does it transmit to and what does it respond to)?

Back 135

Transmits via glossopharyngeal nerve to solitary nucleus of medulla (responds to both dec and inc in BP)

Front 136

What do baroreceptors respond to and what is their function? What are they especially important in response to?

Back 136

Hypotension -> dec arterial pressure -> dec stretch -> dec afferent baroreceptor firing -> inc efferent sympathetic firing and dec efferent parasympathetic stimulation -> vasoconstriction, inc HR, inc contractility, inc BP. It is an important response to severe hemorrhage (dec blood volume)

Front 137

What does carotid massage do to baroreceptor firing and HR?

Back 137

Carotid massage -> inc pressure on carotid artery -> inc stretch -> inc affferent baroreceptor firing -> dec HR

Front 138

What is the Cushing reaction?

Back 138

Triad of HTN, bradycardia, and respiratory depression

Front 139

How do baroreceptors contribute to the Cushing reaction?

Back 139

Inc intracranial pressure constricts arterioles -> cerebral ischemia and reflex sympathetic increase in perfusion pressure (HTN) -> inc stretch -> reflex baroreceptor induced-bradycardia

Front 140

What are the peripheral chemoreceptors and what are they stimulated by?

Back 140

Carotid and aortic bodies are stimulated by dec PO2 (<60), inc PCO2, and dec in pH of blood

Front 141

What are the central chemoreceptors stimulated by?

Back 141

Changed in pH and PCO2 of brain interstitial fluid, which in turn are influenced by arterial CO2. Do not directly respond to PO2.

Front 142

Which organ has the largest blood flow (100% of cardiac output)?

Back 142

Lung

Front 143

Which organ has the largest share of systemic cardiac output?

Back 143

Liver

Front 144

Which organ has the highest blood flow per gram of tissue?

Back 144

Kidney

Front 145

Which organ has the largest arteriovenous O2 difference?

Back 145

Heart (O2 extraction is ~80%). Therefore, inc O2 demand is met by inc coronary blood flow, not by inc extraction of O2

Front 146

What is PCWP (pulmonary capillary wedge pressure) an approximation of? What is the change of it in mitral stenosis?

Back 146

LA pressure. In mitral stenosis, PCWP > LV diastolic pressure

Front 147

How do you measure PCWP?

Back 147

Pulmonary artery catheter (Swan-Ganz catheter)

Front 148

What is normal PCWP?

Back 148

<12