DIT review - Cardiology 3

Question 1

In the cardiac cycle graph, show were mitral and aortic valve opening and closing occur

Answer 1

Question 2

What causes S1 and S2 heart sound

Answer 2

S1 = closing of mitral valve

S2 = closing of aortic valve

Question 3

What causes S3 heart sound

Answer 3

• S3 = rapid flow of blood from the atria to the ventricles
  
  • Occurs right after mitral valve opens
  • Normal in children but not heard in adults
  • Presence of S3 in adults indicates volume overload (e.g. congestive heart failure, advanced mitral or tricuspid regurgitation) or dilated ventricles
  • Causes of S3 heart sound:
    
    • Dilated cardiomyopathy, congestive heart failure, mitral regurgitation, L-to-R shunting

Question 4

What causes S4 heart sound

Answer 4

• S4 = atrial contraction
  
  • Not present in normal adults
  • Caused by atrium contracting against a stiffened ventricle
  • Causes of S4:
    
    • Hypertrophic cardiomyopathy, aortic stenosis, chronic HTN with LV hypertrophy, post-MI

Question 5

Label the jugular venous tracing graph

Answer 5

• A wave = atrial contraction
• C wave = ventricular contraction
• V wave = atrial filling against closed tricuspid valve

Question 7

Describe what normal heart sound splitting is

Answer 7

• Inspiration = decreased intrathoracic pressure = increased venous return = increased RV filling = increased RV stroke volume = increased RV ejections time = delayed closure of pulmonic valve

Question 8

Describe wide splitting

Answer 8

• Splitting occurs both in inspiration and expiration (but still more on inspiration)
• Due to conditions that delay RV emptying (e.g. Pulmonic stenosis, R bundle branch block)

Question 9

Describe fixed splitting

Answer 9

• Occurs during right heart overload (e.g. atrial septal defect)
• ASD = L-to-R shunt = increased RA and RV volumes = increased flow through pulmonic valve such that, regardless of breath, pulmonic closure is delayed

Question 10

Describe paradoxical splitting

Answer 10

• Due to conditions that delay aortic valve closure (e.g aortic stenosis, left bundle branch block)
• Normal order of valve closure is reversed so that P2 occurs before delayed A2
• On inspiration, P2 closes later and moves closer to A2, thereby “paradoxically” eliminated the split

Question 11

What valves associate to what auscultation locations on the chest?

Answer 11

Question 12

What murmurs are increased by inspiration?

Answer 12

• This decreases intrathoracic pressure, thus increased venous return to the heart
• Increased intensity of R heart sounds (e.g. Tricuspid murmur)

Question 13

What murmur are increased by hand grip?

Answer 13

• This increases SVR, this increasing afterload
• Increased intensity of mitral regurgitation, aortic regurgitation, and VSD

Question 14

What murmurs are increased by Valsalva maneuver?

Answer 14

• This increases intrathoracic pressure, thus decreasing preload (opposite of inspiration)
• Decreases the intensity of most murmurs EXCEPT increases intensity of hypertrophic cardiomyopathy

Question 15

Holosystolic, high-pitched “blowing” murmur best heard at apex

Answer 15

Mitral regurgitation

Question 16

Causes of mitral regurgitaton

Answer 16

• Rheumatic heart disease, endocarditis, ischemic heart disease, LV dilation, mitral valve prolapse

Question 17

What maneuver enhances mitral regurg vs. tricuspid regurg

Answer 17

Mitral regurg enhanced by increased afterload (e.g. hand grop or squatting)

Tricuspid regurg enhanced by inspiration

Question 18

High-pitched “blowing” early diastolic decrescendo murmur

Answer 18

Aortic/pulmonic regurgitation

Question 19

Common presentation of aortic regurgitation

Answer 19

• Wide pulse pressure with head bobbing – bounding pulses

Question 20

Causes of aortic regurgitation

Answer 20

• Aortic root dilation (e.g. syphilis or Marfan)
• Bicuspid aortic valve
• Endocarditis
• Rheumatic fever

Question 21

Holosystolic, harsh-sounding murmur loudest at tricuspid area

Answer 21

Tricuspid regurg or VSD

Differentiate due to clinical picture:

Tricuspid regurg = IV drug user

VSD = murmur present at birth

Question 22

Late systolic cresecendo murmur, preceded by a mid-systolic click

Answer 22

Mitral valve prolapse

Question 23

Delayed, rumbling mid-to-late diastolic murmur following an opening snap

Answer 23

Mitral/tricuspid stenosis

Question 24

Continuous, machine-like murmur (heard through systole and diastole)

Answer 24

Patent ductus arteriosus

Question 25

• Crescendo/decrescendo systolic ejection murmur
  
  • Ejection click may be present

Answer 25

Aortic stenosis

Question 26

Complications/presentation of aortic stenosis

Answer 26

SAD:

Syncope, angina, dyspnea

Question 27

Causes of aortic stenosis

Answer 27

• Bicuspid aortic valve in younger patients, senile (degenerative) calcification in older patients, chronic rheumatic valve disease, unicuspid aortic valve, syphilis

Question 28

Describe electrolytes responsible for each phase in cardiac myocyte fast action potential (Phase 4, 0, 1, 2, 3)

Answer 28

• Stage 4 (baseline negative state)
  
  • Only “leaky” potassium channels open (K+ leaking out of cell - inward rectifier current)
• Stage 0
  
  • Voltage gated Na+ channels open (after threshold -70 is reached by Na+ and Ca+ leaking through gap junctions)
  • Na enters very quickly à fast depolarization
• Stage 1
  
  • Initial repolarization – Na+ channels close and voltage gated K+ channels open (K+ leaves cell), causing repolarization
• Stage 2
  
  • Plateau – Ca2+ channels open (Ca enters cells) – L-type channels
  • Ca2+ and K+ channels pull voltage in opposite directions, so reach sort of plateau
  • This is the phase that causes myocyte contraction (due to Ca2+ triggering more Ca2+ release from sarcoplasmic reticulum)
• Stage 3
  
  • Rapid repolarization – Ca2+ channels close, so only K+ channels open
  • But eventually the voltage gated K+ channels will close, leaving only open the “leaky” potassium channels, so there is membrane stabilization

Question 29

Describe electrolytes responsible for each phase of pacemaker slow action potential (Phase 4, 0, 3)

Answer 29

• Stage 4
  
  • Na+ channels (If – funny current) are open (Na+ enters cells) and allow depolarization (voltage gated K+ channels are closed)
  • The rate of stage 4 depolarization is what sets the heart rate
• Stage 0
  
  • Threshold reached where voltage gated Ca2+ channels open causing more rapid depolarization at threshold (-40)
  • Ca2+ enters pretty quickly, but not as quickly as Na+ in stage 0 of myocytes à slow action potential
• Stage 3
  
  • At threshold +10, voltage gated Ca2+ channels close and voltage gated K+ channels open (potassium leaves cell), causing repolarization (at -60, the voltage-gated K+ channels will close and Na+ channels will reopen)
  • At certain threshold, K+ channels close, so Na+ is only channel open and cycle restarts