2A. S3/b2 Pathology Chf

Front 1

4 things to look for in a Chest xray

Back 1

1. Air under the diaphragm
2. Look for cracked ribs
3.Look for the 4 bumps
4. Look at the costophrenic andgle should be 30 degrees

Front 2

4 bumps on the left side of the chest xray

Back 2

1. Aorta(clavicle)
2. pulmonary artery
3. Left atrium
4. Left ventricle

Front 3

Problem with the siluhoutte = problem with the lungs

Back 3

Ratrium = fluid in R middle lobe; Latrium = problem with the left lingula

Front 4

Xray of enlarged aortic knob?

Back 4

Calcification as a sign of atherosclerosis

Front 5

Eisenmenger's Syndrome

Back 5

1. Starts as a VSD, L to R shunt
2. increases flow in the pulmonary vasculature
3. Causes pulmonary hypertension
4. Shunt gets reversed R to L 5. Patient becomes Cyanotic

Front 6

Mitral Stenosis can cause?

Back 6

L Atrial enlargement

Front 7

Couer en Sabot?

Back 7

Heart of the boot 1. RV(mediastinum) enlargement is pushing LV up 2. Caused by a tetrology of Falot

Front 8

What is a tetrology of Falot?(4)

Back 8

1. Pulmonary Stenosis
2. R-V hypertrophy
3. Overriding Aorta
4. V-SD

PROVe

Front 9

Common Vasoconstrictors(6) VCU

Back 9

1. Angiotensin 2
2. Catecholamine
3. Thromboxane(Platelets)
4. Leukotrienes
5. Endothelin
6. Alpha Adrenergic

LET CAA Play

Front 10

Common Vasodialators(4)

Back 10

1. Prostaglandins(prostacyclin) 2. Kinins
3. NO/EDRF
4. Beta 2 adrenergic

PKNB

Front 11

Describe a Tamponade(4)

Back 11

1. Fluid in pericardial space
2. less blood enters the ventricles
3. Decrease SV
4. Obstructive shock

Front 12

Hypertrophic Cardiac Myocyte, how does it grow?(4)

Back 12

1. Sarcomeres growth by Proto-oncogenes
2. Increase size of cells not number
3. Increase Ca influx(contraction)
4. Decrease Beta receptors

Front 13

Newborn hypertrophy(4)

Back 13

1. Lungs are shut
2. RV has a R to L shunt
3. At birth the lungs open
4. RV doesn't work as hard and atrophies

Front 14

Concentric Hypertrophy

Back 14

1. Tissue overgrowth without overall enlargement, sarcomeres added in parallel 2. Walls of the organ are thickened
3. Capacity or volume is diminished
4. CHF here will have normal EF because all that comes in is squeezed out

Front 15

Eccentric hypertrophy(3)

Back 15

1. Hypertrophic growth in series
2. Overall size and Volume are enlarged
3. CHF here will have a decreased EF because the weaker muscle can't squeeze out the increased volume

Front 16

Bicuspid Aortic Valve(4)

Back 16

1. Most common Valve abnormality
2. 2 cusps instead of normal 3 3. Diastole pressure is normal, systole pressure is low(longer time)
4. one out of 75 people, Problems manifest later in life 50-60

Front 17

What does the silhouette of concentric hypertrophy look like?

Back 17

looks normal

Front 18

What is heart failure?

Back 18

when the heart is not able to supply enough flow to meet the bodies needs

Front 19

What are the physiological effects of CHF?(5) energy wise

Back 19

Decreased
1. FA and glucose metabolism
2. ATP generation
3. O2 consumption
4. Phosphocreatine
5. CPK

Front 20

What causes High Output CHF?(6)

Back 20

1. Anemia
2. Thyrotoxicosis
3. Ateriovenous fistulas
4. Paget's Dz
5. Beri-Beri Dz
6. Pregnancy

Front 21

Why does High Output CHF occur?

Back 21

Increased volume return to the heart, overloads it and causes excess strain on the pump and it will fail.

Front 22

How does the RAS work against the failing heart?

Back 22

It promotes VasoC and increased fluid retention. Overloading the pump a little more in order to get O2.

Front 23

How do the V1 and V2 ADH receptors work?

Back 23

V1 = VasoC

V2 = Antidiuretic

Front 24

What neuro hormonal actions occur in myocardial failure(5)?

Back 24

increased; NE, RAS, ADH, ANP and BNP

Decrease B1 receptors(VasoC), and Ca mobilization(inotropic)

Front 25

Tx for decreased Ventricular performance?

Back 25

Digoxin excites the myocardium

Front 26

Tx for sympathetic stimulation

Back 26

Beta blockers

Front 27

Tx for RAS(3)

Back 27

ACE-I, ARB, sprinolactone

Front 28

ANP and BNP effects(4)

Back 28

1. decrease resistance

2.decrease CVP

3. increase in natriuresis.

4. Decrease CO and BV

Front 29

Metalloproteinase actions(2)

Back 29

1. Causes increased collagen degradation(remodelling)

2. Myocyte slippage occurs

Front 30

Inhibit Metalloproteinase what happens?(4)

Back 30

1. Decreased collagen degradation

2. Fibrosis

3. Increase stiffness of tissue

4. Increase myocardial thickness

Front 31

Alcoholic Cardiomyopathy 4 signs

Back 31

1. Lots of collagen
2. Less contraction
3. Myocardial fibrosis
4. less muscle density

Front 32

Causes of mitral valve prolapse(5)

Back 32

1. Myxomatosis
2. Endocarditis
3. SLE/Marfans
4. Trauma
5. Cardiac fibrosis

Front 33

Cardiogenic shock vs. CHF

Back 33

1. When LV performance is no longer able to meet systemic needs ...Acute

2. Left or right heart CHF possible, chronic condition of decreased perfusion over time

Front 34

What is a Schwan-Ganz Catheter?

Back 34

1. Measures pul. venous pressure at the capillaries

2. measurement of LA pressure which is increased in shock

3. A sign of impending edema

Front 35

Etiology of CHF(7)

Back 35

1. Hypertension
2. CAD
3. Myocardial Dz
4. Valvular Dz
5. Pericardial Dz
6. Congential Heart Dz
7. High output Dz

Front 36

What are the CHF precipatating factors?(6)

Back 36

1. Inappropriate Tx or non compliance
2. Ischemic cardiomyopathy
3. Arrythmia
4. Hypertension sustained
5. ROH cardiomyopathy, pregnancy or myocarditis
6. High output

Front 37

Framingham criteria for CHF(6)

Back 37

1. Supine Dyspnea
2. Kussumal Sign
3. Rales
4. CVP>16torr - normal 5
5. Hepatojugular reflux
6. CXR - cardiomegaly, air space, edema, kerley B lines

Front 38

Kussmaul Sign?

Back 38

1. Deep breath and RA fills
2. Jugular should not be distended
3. If it is there is pressure back up

Front 39

CHF Systolic characteristics?(4)

Back 39

1. Impaired muscle shortening
2. Reduced ejection fraction
3. Infarction
4. Myocarditis, vavular Dz or shunts

Front 40

CHF Diastolic(3) causes what?

Back 40

1. Impaired compliance
2. Concentric hypertrophy
3. Systemic hypertension and aortic stenosis

Front 41

Why no cardiomegaly in diastolic heart failure?

Back 41

Because it is usually due to increased volume, causing concentric hypertrophy.

Front 42

What is a secondary pulmonary lobule?(3)

Back 42

1. 3-5 terminal bronchioles and septa
2. Veins and lymphatics are in the septa
3. Arteries are in the center with the bronchioles

Front 43

On a CXR what are the primary colors?

Back 43

1. Air = black
2. Blood/fluid = white
3. Connective Tissue = white

Front 44

Significance of septa in the lungs?

Back 44

1. They are one continuous piece of tissue
2. The veins are in them at points
3. Venous swelling(edema) will cause the septa to swell

Front 45

Radiographic signs of CHF(6)

Back 45

1. Cepahlization of blood flow in the lungs
2. Widening of vascular pedicle
3. Kerley B lines
4. Hilar Haze
5. Pleural effusions
6. Airspace edema

Front 46

What is the vascular pedicle?

Back 46

The combination of Aorta and IVC in a CXR

Front 47

Location of the secondary lobules?

Back 47

They are at the edges of the lungs where gas exchange takes place

Front 48

What are Kerley B lines?

Back 48

1. Stair stepped lines on the outer edges of a lung CXR
2. Widening of the lobular septi
3. Visible in the lower lobes

Front 49

What is the hilar haze?

Back 49

1. Hilar lymph nodes around pulmonary arteries
2. Lymphatics pick up the excess fluid from venous swelling first
3. Drain back to pulmonary trunk and create the haze

Front 50

Interlobular pleural effusion is when, what?(3)

Back 50

1. After hilar haze
2. Fluid leaks out
3. Costophrenic angle is widened as the lung swells

Front 51

What is the Batwing?(2)

Back 51

1. Late pulmonary edema due to CHF
2. The edema has made it into the alveoli

Front 52

Emphysema and CHF

Back 52

1. Blebs have no BV
2. Therefore those areas will become opaque on a CXR easier
3. No Hstatic pressure to prevent the edema