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BiB Midterm 2 > Lecture Week 5 > Flashcards

Lecture Week 5 Flashcards

1
Q

What is a Swan-Ganz Cather and how is it used? What are the points of entry?

A

A catheter is used to measure cardiac chamber and pulmonary artery pressures.

Right internal jugular vein (RIJ) or femoral vein.

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2
Q

What data can be obtained from using a Swan-Ganz Catheter? (3)

A

Chamber pressures (minus LV and Aorta)
Cardiac Output
Systemic and Pulmonary Vascular Resistance

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3
Q

How does the Pulmonary Capillary Wedge Pressure (PWCP) work to estimate left atrial pressure?

A

It works by inflating the balloon behind the catheter in order to pick up blood flow from the left atrium. Done under the assumption that there are no cardiac abnormalities.

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4
Q

What is a transducer? What does it do?

A

The transducer is a fluid system (a part of the swan-ganz catheter) that converts the movement of fluid into pressure waveforms.

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5
Q

A transducer should be level with the____.

A

patient.

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6
Q

What are the three “waves” of the right atrial waveform and what do they mean?

A

a-wave: pressure generation during atrial systole

c-wave: AV valve movement (toward RA) during isovolumetric contraction.

v-wave: pressure generation during venous filling or atrial diastole

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7
Q

What are the three “descents” of the right atrial waveform and what do they mean?

A

x-descent: pressure decay resulting from atrial relaxation.

x’-descent: downward movement AV junction during ventricular ejection. (AV moves down because of less pressure pushing it up against RA)

y- descent: pressure decay resulting from atrial volume unloading (ventricular filling)

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8
Q

What vein is RA pressure reflected in? What right atrial waveforms can be observed in this vein?

A

The Jugular Vein

a-wave - atrial contraction
v-wave - atrial filling

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9
Q

Why can’t the c-wave be observed in the jugular vein?

A

c-wave is the pressure of ventricle pushing the AV wall toward the right atrium during isovolumetric contraction, so you won’t see that pressure go up to the jugular vein. (normal circumstance)

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10
Q

What is diastasis mean in regard to ventricular pressure?

A

The end of passive filling of blood into ventricle, right before the “atrial kick.”

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11
Q

What does PCWP measure directly?

A

The pressure of the pulmonary artery.

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12
Q

What is a pigtail catheter used for?

A

Used to measure aortic valve and left ventricle pressure.

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13
Q

Define Stroke Volume. How is it calculated?

A

The amount of blood that leaves the heart after ejection.

SV = LV EDV - LV ESV

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14
Q

The Law of LaPlace, which refers to preload/afterload as “wall stress” tells us that…

A

The preload is proportional to
[Ventricular Diastolic Pressure x Radius (EDV)] / Wall thickness (h)

The afterload is proportional to
[Ventricular Systolic Pressure (P) x Radius (EDV)] / Wall thickness (h)

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15
Q

What is the idea behind the Fick principle in relation to Cardiac Output (CO)? What is the Fick equation?

A

The Fick principle allows us to determine CO based on oxygen saturation.

CO = (oxygen consumption) / [(theoretical oxygen carrying capacity) (Pt’s Hgb level) (10) (Aortic O2 % Sat - Pulmonary O2 % Sat)]

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16
Q

What is the ejection fraction? How is it calculated?

A

The proportion of EDV pumped out of heart during ejection.

EF = (SV/ LV EDV)x100%

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17
Q

______ volume and _____ output can be conserved despite a low ejection fraction. Why?

A

stroke, cardiac

A low EF means that you will have a higher EDV which will allow for SV to increase despite low EF.
ex:
EDV= 100mL and EF =50%, SV=50mL
EDV= 200mL and EF=25%, SV=50mL

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18
Q

What are the two equations for MABP?

A 
MABP = 1/3 (Systolic - Diastolic) + Diastolic
MABP = CO x TPR
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19
Q

What are the equations for Systemic Vascular Resistance (SVR) & Pulmonary Vascular Resistance (PVR)?

A

SVR = (Mean Aortic pressure - Right Atrial pressure) / CO

PVR = (Mean Pulamonary artery pressure - PCWP) / CO

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20
Q

Normal (right atrial) RA pressure value?

A

2-6 mmHg

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21
Q

Normal Pulmonary Capillary Wedge Pressure (PCWP) value?

A

5-15 mmHg

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22
Q

Normal ejection fraction value? (%)

A

55%-65%

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23
Q

Why is stroke volume (SV) preserved despite a lower EF?

A

You have more blood in the ventricle (more preload).

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24
Q

What is the equation for flow (Q)?

A

Q = (P1-P2) / R

Flow = (pressure difference at 2 points) / Resistance

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25
Q

What is the Bowditch (Treppe) effect?

A

Autoregulation method in which myocardial tension (and therefore force generation) increases with increasing heart rate (HR).

26
Q

How are ventricular muscle fibers arranged? Why is this important?

A

Ventricular muscle fibers are arranged in counter-wound sheets that change orientation based on where they are in the ventricle.
This is important because it allows a more effective contraction (“twisting and squeezing” more blood out)

27
Q

What are eccentric and concentric hypertrophy?

A

Eccentric - sarcomeres are arranged in series

Concentric - sarcomeres are arranged in parallel

28
Q

What are the 3 General Components of Cardiac Remodeling?

A
  1. Myocte Hypertrophy
  2. Myocyte Loss
  3. Fibrosis
29
Q

What are the three stages of myocarditis? How long does each occur?

A

Acute myocarditis: 0 to 4 days
Subacute myocarditis: 4 to 14 days
Chronic myocarditis: 14 days +

30
Q

What are the three stages of myocarditis? What is happening during each stage?

A

Acute myocarditis - Viral mediated myocarditis

Subacute myocarditis - Immune-mediated myocarditis (inflammation due to immune cells reacting)

Chronic myocarditis - Cardiac remodeling (dilation), Fibrosis, & Heart Failure

31
Q

What stage of myocarditis is it best to do a biopsy?

A

Subacute myocarditis. In chronic myocarditis phase, you will see nonspecific findings (ie. fibrosis)

32
Q

What are the 4 criteria of myocarditis diagnosis?

A

Compatible Symptoms
Positive pathological exam findings
Regional delayed contrast enhancement on MRI
Myocardial defect or damage without CAD

33
Q

List and describe the 4 common ways to treat myocarditis.

A

Immunosuppressant - To lower immune-mediated myocarditis ( generally ineffective, especially during viremia/acute myocarditis)

Anti-viral - Give within 24 hours of onset (not practical)

Supportive care - managing symptoms (ie. shock)

Neurohormonal Antagonists - Treats symptoms; Blocks sympathetic nervous & aldosterone (decrease water retention) systems.

34
Q

What are some of the main functions of the pericardium?

A

Anchors the heart in place
Controls diastolic filling from getting excessive
Barrier for infection

35
Q

What’s the most common cause of pericarditis?

A

Viral infection (ie. coxsackie or adenovirus)

36
Q

What are the pathologic appearances of pericardial effusion/pericarditis? What do they indicate? (5)

A

Serous - Non-inflammatory fluid in the pericardium. Usually secondary to heart failure, cirrhosis, hypoalbuminemia

Purulent - Pus in pericardium; bacterial infection

Fibrinous - Fibrin deposition; typically seen in all types of infection; specific to uremia

Caseous - Cheese-like; Tuberculosis

Hemorrhagic - Blood in pericardium; trauma, aortic dissection, coagulopathy

37
Q

What is Dressler (aka Post myocardial infarct) Syndrome?

A

Pericarditis occurring about 2-10 weeks after a myocardial infarct without an infective cause.

38
Q

What disease state is associated with “Pulsus Paradoxus?” Explain how this leads to poor cardiac function.

A

Cardiac Tamponade (Pericardial Effusion)

On inhalation venous return to the heart increases which creates more pressure in the right ventricle. Due to excess fluid in the pericardium RV cannot expand outward to the pleural space. instead the septal wall pushes into the LV which decreases LV filling, lowers CO, and decreases BP.

39
Q

What disease is associated with “Ewart’s Sign?” What does this mean?

A

Cardiac Tamponade (Pericardial Effusion)

Dullness of sound in the left lower lung because pericardial effusion pushes into it.

40
Q

What is the major cause of restrictive pericarditis in the US? What about third world countries?

A

US - Open heart surgery

3rd World - Tuberculosis

41
Q

Restrictive Pericarditis is a problem in ___ to ___ diastole.

A

mid, late (suit of armor)

42
Q

In Kussmaul’s sign, what do we see? Is this a specific finding?

A

We see on inhalation, an increase in RA pressure (RA cannot expand much) and decrease in PCWP (low blood to Pulm artery). These two pressures normally go together. This LEADS TO JVD!!

Nonspecific finding; can be seen in anything impairing RV compliance.

43
Q

What does a high pitched murmur tell you about the pressure and flow of blood? What about a low pitched murmur?

A

High pitch = High-pressure gradient, high flow velocity

Low pitch = Low-pressure gradient, low flow velocity

44
Q

What are the two types of Systolic Murmurs? The two types of diastolic murmurs?

A

Systolic - Mid systolic ejection & Regurgitant (AV valve) Holosystolic Murmur

Diastolic - Mitral (AV valve) Stenosis & Aortic (or Pulm) Regurgitation

45
Q

Describe the changes in pressure & volume that according to chronic aortic stenosis.

A

1) Ventricular pressure builds up to maintain SV.

2) Rate of LV relaxation decreases (higher resting tension)

46
Q

What are the two common causes of aortic insufficiency?

A 
Cusp Abnormality (ie. Bicuspid, Endocarditis)
Root Dilation (ie. Aortic Dissection or Aneurysm)
47
Q

Explain the pathophysiology of Aortic Insufficiency

A

LV volume is overloaded from regurgitation. This leads to cardiac remodeling (eccentric elongation). Also, matrix metalloproteinases are stimulated to dissolve the cardiac fibrous skeleton to make more space.

48
Q

What type of murmur will you hear in Aortic Insufficiency? Why?

A

Early Diastolic Decrescendo Murmur. Backflow of blood back into LV.

49
Q

Why does aortic insufficiency lead to a bounding pulse/?

A

Systolic pressure increases (Due to higher preload from blood backflow into LV) Diastolic pressure (aorta) decreases (Due to blood backflow into LV). This creates a very large difference in pulse pressure –> Bounding Pulse.

50
Q

What is the treatment for aortic stenosis and regurgitation?

A

Surgical - Aortic Valve Replacement after symptoms and hypertrophy starts to develop.

51
Q

What pitch murmur would mitral valve (& tricuspid valve) stenosis have? Why?

A

Low pitch murmur. Obstructed blood flow would occur during diastole (low velocity and pressure)

52
Q

What left atrial abnormalities can occur due to mitral stenosis?

A

Enlargement
Thrombus formation with potential embolism
Atrial Fibrillation

53
Q

What is done to treat mitral valve stenosis? How does it work?

A

Mitral Valvuloplasty.

Blow up catheter balloon inside of the mitral valve to open it up (used to be done with finger)

54
Q

What type of valve disorder is most likely to lead to systemic venous congestion?

A

Tricuspid Stenosis. More blood backed up into the venous system since less of it can get into RV.

55
Q

What are the common causes of mitral valve regurgitation? (4)

A

Flail Mitral Valve
Mitral Valve Prolapse
Papillary Muscle Rupture
Rheumatic Heart DIsese

56
Q

What genetic mutations are found in Dilated Cardiomyopathy (DCM) vs Hypertrophic Cardiomyopathy (HCM)?

A

DCM- DDMT: Dystrophin, Desmin, Mitochondrial proteins, Titin

HCM - MYOSIN heavy chain proteins

57
Q

What are the three findings of Beck’s Triad? What disease does this indicate?

A

Quiet heart sounds on auscultation
Hypotension
Jugular Venous Distension (JVD)

Cardiac Tamponade (Pericardial effusion)

58
Q

Which valve is most commonly affected by Rheumatic Heart Disease?

A

The mitral valve. Possible to occur in the aortic valve also.

59
Q

What does a systolic “click” heard on auscultation of the heart indicate? Why?

A

Mitral Valve Prolapse.
The extra tissue added to the mitral valve makes it very floppy so during systole the flaps are pushed way up until abruptly stopped by the chordae tendineae, which creates the “click.” (Think about parachute)

60
Q

A child presents with fever and heart murmur. What should you suspect? Why?

A

Acute Infective Endocarditis. Children generally do not have murmurs due to other causes.

BiB Midterm 2 (6 decks)

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