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CV II - Unit III > Dow & Darrow > Flashcards

Dow & Darrow Flashcards

1
Q

what are some buzz words you may hear while taking a Hx about an infant

A

infant who presents w/ diaphoresis & tacypnea w/ feeding (cyanosis while feeding?)

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2
Q

What must you remember when looking at a kiddo’s BP?

A

kiddo BP norms are different based on age, gender & height

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3
Q

What is an abnormal heart sound in a kid?

A

wide & fixed split S2 is abnormal

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4
Q

characteristics of an innocent murmor in kiddo?

A

a low-pitched (non-turbulent, not high velocity)

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5
Q

characteristics of a suspicious murmor in kiddo?

A

High-pitched
Harsh
S1 coincident (holosystolic)
Diastolic murmor

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6
Q

are physiologic murmors more common in kids or adults?

A

more common in kids

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7
Q

What may appear abnormal in the EKG of a newborn?

A

normally are RV dominant, so light look like RV hypertrophy. Manifested by a right-axis deviation
several interval lengths vary with age

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8
Q

4 syndromes with which congenital heart defects are assx?

A

Down: endocardial cushion defect, VSD
Turner: coarc, AS, ASD
Noonan: PS, ASD, AVSD (partial), coarc, HCM
FAS: VSD, PDA, ASD, TOF
** she only had the names in red, not the details **

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9
Q

Is cyanotic congenital disease always obvious @ birth?

A

No! May be OK until PVR decreases, PDA closes, etc

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10
Q

How does transposition of the great vessels present?

A

TGV is associated with severe cyanosis in the first hours after birth (in other words, TGV is the mostly likely diagnosis in a severely cyanotic neonate who is just a few hours old)

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11
Q

How does coarctation of the aorta present w/in the 1st yr of life?

A

rather dramatic! (HF, circulatory collapse, death)

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12
Q

M.C. etiology of myocarditis, how to test for it, and Tx?

A

Viral, test for with PCR. Tx = IV IGs

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13
Q

Inheritance pattern of Hypertrophic Cardiomegaly (HCM)

A

auto dom

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14
Q

Discuss Kawasaki (diagnosing and complication)

A 
High fever for FIVE days 
            \+
4+ of the following:
   1. conjunctival injection,
   2. strawberry tongue
   3. Cervical lymphadenopathy
   4. Swelling of hands and feet 
(the others she didn't have in red)
15-25% develop aneurysm of the coronary arteries
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15
Q

When evaluating a kid (before puberty) with HTN, what makes you think of secondary causes?

A

The younger the child, and the higher the HTN - the more likely it is secondary to an identifiable cause (such as renal disease)

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16
Q

M.C. etiology of CP in kids?

A

noncardiac (MSK especially is very common)

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17
Q

When should you refer a kid w/ CP?

A

Exertional CP
Exertional Syncope
Significant FHx of arrhythmias, sudden death or genetic disorders

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18
Q

When should you refer a kid that you see during a sports physical?

A

FHX SCD
Murmors (think HCM)
Marfan’s Stigmata
Other PE findings which are consistent w/ cardiac disease (eg clubbing, etc)

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19
Q

What sis a fast/easy/cheap lab you should you get for a kiddo who c/o CP + lung complaints/findings

A

CXR

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20
Q

impotence + buttocks claudication

A

think aorto-iliac occlusion

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21
Q

What does P2Y12 signaling modulate?

A

modulates thrombin generation = ADP feedback loop

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22
Q

pain in both calves with walking 2-4 blocks, decreased A/B Index

A

blockage of the superficial femoral aa

(if it was in the profunduc (provides collaterals) it would present after 1-2 blocks

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23
Q

What is Osler’s Sign? What finding would be falsely abnormal?

A

Pseudohypertension because of calcified vessels. A/B Index would be falsely high d/t calcified vessels

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24
Q

How do you differentiate lumbar spinal stenosis (LSS) from PVD? What makes it better or worse?

A

Pain is relieved when the Pt flexes the spine (shopping cart, sitting, squatting, lumbar flexion).

Neurogenic claudication pain is excascerbated by standing erect and downhill ambulation.

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25
Q

How do you differentiate neuropathy d/t PVD from neuropathy d/t diabetes? How do you Dx Tibial or pedal artery occlusion?

A

Relief from dangling separates it from diabetes
MRA to Dx
Vein bypass to distal tibial or pedal arteries.

26
Q

Irregular rate & rhythm + sudden pain, paleness, weakness and numbness of LE

A

A-Fib, threw a clot

27
Q

Name the 6 P’s of arterial occlusion

What is an indication for immediate surgery?

A 
Pain 
Pallor
Paralysis
Paresthesias *Means nn are hypoxic (this is the most worrisome one) --> immediate surgery
Pulselessness
Poikilothermia (irregular temperature)
28
Q

Name the 6 D’s of Vertebro-basilar (VB) TIA? Why do we see these Sxs?

A 
diabetic
dizziness
diploplia
dysphagia
dysarthria
dysmetria
Also have ataxia, though not a "D"

The basilar aa feed the brainstem, so loose those basic functions (swallowing, vision, talking, dizziness, etc)

29
Q

What are the PE findings for mesenteric occlusion? How to you manage it?

A

Not much tenderness to abd palpation. Tx = bypass surgery to avoid having necrotic bowel

30
Q

Amaurosis fugax + One-sided numbness + post-prandial abd pain + CT angiogram shows Portal vein thrombosis

A

Amaurosis fugax = sudden loss of vision on one side)
One-sided numbness = carotid (???)
post-prandial abd pain (mesenteric ischemia)
Dx = Clotting of both arterial and venous system

31
Q

Red vs White Clots

A

Arterial clot = lots of plts –> white

Venous clot = lots of fibrin, which catches passing RBCs –> red

32
Q

Marfanoid Pt + diastolic decrescendo murmor at the base + systolic murmor at the apex. Why do you worry about an IWMI?

A

diastolic decrescendo murmor at the base = aortic regurg
systolic murmor at the apex = mitral regurg

Marfanoid Pts often have dilation of aortic root, which pulls aortic valve apart –> aortic regurg. The problem is, this can turn into an aortic dissection, and if it expands down to where the RCA comes off (right next to the aortic root) –> IWMI

33
Q

Name 2 things assx w/ dissecting aortic aneurysm

A

HTN & paraplegia

If aneurysm dissects more distally, can interrupt aa going to the spinal cord –> paraplegia)

34
Q

Things that cause mediastinal widening

A
  1. artifact from Pt being rotated
  2. Mediastinal mass - can be d/t 4 T’s
    a. T-cell lymphoma
    b. Teratoma
    c. Thyroid
    d. Thymus
  3. Vessels - eg aortic aneurysm
  4. Anthrax
35
Q

What is vircHow’S Triad

A

remember the H, S & T in the name
Hypercoagulability
Stasis
Trauma

36
Q

May-Thurner Syndrome

A

May account for 30% of venous events in the US q yr

Occurs because the R iliac artery passes over/compresses the L iliac vein–> venous clots occur more on the L

37
Q

Characteristics of ARTERIAL ulcers

A 
Claudication
Site of Pressure
Sharp Borders
Bed Pale Grey or Yellow
Hair Loss
Cold Feet
No Pulses
38
Q

Characteristics of VENOUS ulcers

A 
Hx trauma
medial malleolus
irregular margins
beefy
edema
induration
hyperpigmentation (d/t hemosiderin)
moderate - heavy exudate
39
Q

What is Phlegmasia Cerulean Dolens

A

Condition in which venous insufficiency –> leg swells –> blocks aa –> ischemic limb

You can tell the PRIMARY PROBLEM IS VENOUS b/c of the color (would be pale if primary problem was arterial)

40
Q

What are the Sxs of, and the M.C.C. of vena cava syndrome?

A

Sx = flushed facies + dilated neck vv

Most common causes =

  1. Non-small cell carcinoma of the lung,
  2. next is small cell,
  3. followed by lymphoma
41
Q

when should you be worried about a popliteal aneurysm? Tx

A

If it is:
1. Palpable AND
2. Loss of sensation in Feet
If these two exist, then they need to go to surgery

42
Q

What is lymphedema?

A

partial agenesis of lymphatics (think mut of VEG-F)

43
Q

How to differentiate adipose dolorosa from lymphedema?

A

They look similar, but adipose dolorosa DOES NOT involve the feet

44
Q

What are the 3 different kinds of shock? What is the primary problem, and secondary rxn for each?

A
  1. Hypovolemic (low volume)
    PP = ↓ CO & PCWP, response is to ↑ SVR
  2. Cardiogenic (Problem w/ pump)
    PP = ↓ CI (cardiac index), response is to ↑ PCWP & SVR.
    ***Can be subdivided into Extracardiac vs Obstructive etiology)
  3. Distributive/Septic/Warm (Can’t distribute)
    PP = ↑ CO, response is to ↓ PCWP & PVR
45
Q

3 Clinical Markers of shock

A
  1. SBP 1
46
Q

What is the big problem in hypovolemic shock? What is your Tx?

A

CVP

47
Q

What is the big problem in cardiogenic shock? What is your Tx?

A

CI is 18
Tx depends on etiology, but we will either use a ionotropic agent (eg dobutamine, a B1 agonist) OR a vassopressor (eg NE or dopamine, alpha 1 agonist)

48
Q

What is the big problem in septic shock? Characteristic of it? What is the Tx?

A

Bacteria are releasing PAMPs, which bind our PRRs –> release inflammatory cytokines & chemokines. Body responds, but it can go crazy

Characteristic = warm extremities d/t response VD

Tx = Fluids to maintain CVP @ 8-12 mmHg
Vassopressors (eg NE, E or Vassopressin) to
maintain MAP > 65 and CI @ 2-4 L/min
Maintain CV02 > 70% - use PRBC or ionotropic
agents

49
Q

What is SIRS?

What is the usual acid base imbalance at this stage?

A

Systemic Inflammatory Response Syndrome = dysregulation of inflammation (considered same category as sepsis)

They are usually breathing fast –> resp alkalosis (PCO2 38.3 (101) OR 90
RR > 20
WBC > 12,000 OR

50
Q

When can we call it ‘sepsis’?

A

Diagnosis of SIRS + Found bacteria

51
Q

When can we call it ‘severe sepsis’?

A

Diagnosis of SIRS + Found bacteria + AT LEAST 1 End organ damage

52
Q

When can we call it ‘septic shock’?

A

Diagnosis of SIRS + Found bacteria + AT LEAST 1 End organ damage + we cannot maintain MAP > 60 even with fluid resuscitation

53
Q

Recent hiking in New England + rub @ LSB

A

Think lyme’s disease (has 3 phases) –> pericarditis

54
Q

Classic Triad of Lyme Disease. Which are seen in the 3 phases

A 
The classic triad of EARLY
	1. acute neurologic abnormalities 
	2. Heart block 
	3. Myopericarditis
LATE -- > oligoarthritis
55
Q

Discuss Cardiac Tamponade - what kind of shock does it cause, what triad and other findings are we looking for?
** on test **

A

BECK, you PAY for the CT (Cardiac Tamponade)

Beck’s triad 
   1. Neck v distention
   2. Low BP
   3. Muffled heart sounds
PAY
   1. Pulsus paradoxus (↓ LV ejection when inspiring (???)     
   2. Electrical Alterans (alternating QRS complex sizes)
   3. Slowed Y descent

This causes obstructive (a subtype of cardiogenic) shock

Tx = paracentesis

56
Q

Discuss Constrictive Pericarditis ** on test **

A

He described this as a “a steel trap around the heart”(???)

√CPK (square root sign, CP, Kussmal)

“Square root” sign on heart cath (rapid ventricular filling followed by a plateau phase during the rest of diastole) related to the rigid pericardium impairing mid and late diastolic filling resulting in decreased and equal diastolic filling pressures in all the cardiac chambers

Kussmaul sign = Jugular engorges (doubles in size) w/ inspiration

Also have Diastolic pericardial knock (auscultation - like an S3) and “septal bounce” (ECHO) due to rapid early filling in diastole. Also shows decreased mitral inflow.

57
Q

what do a, x, v & y mean on jugular venous tracing

What is y abnormal?

A 
a = atrial contraction
x = atrial relaxation
v = atrial filling
y = atrial emptying 
   slowed descent in CT
   much sharper and shorter in Constrictive Pericarditis (this is called a "M or W configuration" d/t it's shape)
58
Q

What is restrictive heart disease (RC)? How does one differentiate CP from RC?
** on test **

A

RC = decreased ventricular filling orLV diastolic dysfunction

Restrictive Cardiomyopathy (RC)
LV end diastolic pressure is 5+ mmHg > than RV
Pulmonary pressure is high
BNP is elevated

Constrictive Pericarditis (CP)
   Usually effects BOTH sides

Both
Cause equilibration during diastole & limited filling on the L side

59
Q

acute vs chronic pericarditis. What position aggravates pain, EKG causes, and MCC?

A

Supine -> worse, sitting up and leaning forward -> better
Acute –> ST segment elevation in all leads, “signs of an inflamed atrium” (???)
Chronic –> T-wave changes
MCC = viral

60
Q

Characteristics of pericarditis

A

troponin elevations, heart block, wall motion abnormalities, and CHF

CV II - Unit III (4 decks)

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