DARROW: shock, blood vessels, lympathic disorders, and pericarditis Flashcards

1
Q

Hypovolemic shock

A

↓ CO and PCWP, ↑ SVR
o Hemorrhage induced
o Fluid loss
o Poor intake

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2
Q

Cardiogenic shock

A

↓ CI (cardiac index), ↑ PCWP and SVR
o Cardiomyopathies
o Arrhythmias
o Mechanical (valvular)
o Extracardiac/obstruction – blocking blood flow
• Tension pneumothorax, PE, cardiac tamponade

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3
Q

Distributive shock

A

↑ CI, ↓ PCWP and SVR
o AKA warm shock → vasodilatory
• Sepsis, toxic shock syndrome, anaphylaxis, SIRS, toxin reactions, spinal cord injury
o May have normal to high central venous O2 saturation due to redistribution of fow
o Increase CO because vascular resistance has dropped

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4
Q

BP that indicates shock

A

SBP

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5
Q

blood lactate that indicates shock

A

> 1.0 mmol/L

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6
Q

treatment of hypovolemic shock

A

give them fluids!
o 0.9% saline: 1-2 liters wide open- continue based on BP, skin, urine, and mentation
o PRBCs

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7
Q

treatment for cardiogenic shock

A
  • Low BP- dobutamine
  • Normal or high BP- IV nitroglycerin or nitroprusside with IV loop diuretic/furesomide
  • Post MI- antiplatelets, norepinephrine
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8
Q

Beck’s triad for Cardiac Tamponade

A
  1. Distended neck veins
  2. Distant heart sounds
  3. Distressed BP (hypotension)
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9
Q

Temp for SIRS

A

> 38.3C (101F) or

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10
Q

HR for SIRS

A

> 90 bpm

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11
Q

RR for SIRS

A

> 20

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12
Q

WBC for SIRS

A

12000 with bandemia

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13
Q

septic shock treatment

A
  1. Fluids: maintain CVP at 8-12 mm Hg
  2. Vasopressors: need to maintain MAP at > 65 mm Hg and cardiac index at 2-4 L/min
    a. Use norepinephrine 5-20 mcg/min- mainly alpha agonist/vasopressor
    b. If norepi fails, give epinephrine- beta agonist
    c. Can also consider vasopressin- potentiates norepinephrine
  3. Maintain central venous O2 saturation of > 70%
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14
Q

What is Osler’s sign?

A

• Pseudohypertension because of calcified vessels

o It is falsely high because you have to pump the cuff way up to get the reading

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15
Q

What is the most potent predictor of stent thrombosis?

A

clacification

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16
Q

Absolute indication for femoral-popliteal bypass

A

resting pain and non-healing ulceration

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17
Q

6 P’s of acute arterial occlusion

A
  1. Pain
  2. Pallor
  3. Paralysis
  4. Paresthesias
  5. Pulslessness
  6. Poikilothermia
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18
Q

When can you see aortic dissection?

A

Marfans, pregnancy, bicuspid aortic valve, and coarctation

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19
Q

causes of mediastinal widening

A
•	Artifact- patient rotated
•	Mediastinal mass: 4 T’s
o	T and B cell lymphoma, teratoma, thyroid, thymus
•	Vessels- aortic aneurysm
•	Anthrax
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20
Q

venous ulcers

A
  • History of trauma, pregnancy and varicose veins
  • Medial malleolus
  • Superficial, irregular margins
  • Ruddy, beefy, fibrinous, granulation
  • Edema
  • Dermatitis
  • Lipodermatosclerosis- indurated
  • Hyperpigmentation- hemosiderin
  • Moderate to heavy exudate
  • Cap refilling
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21
Q

arterial ulcers

A
  • History of smoking, rest pain, claudication
  • Site of pressure
  • Deep, “punched out” with sharp borders
  • Bed pale grey or yellow
  • Dry necrotic base with eschar
  • Lateral
  • Pale, hair loss, cold feet, atrophic skin, no pulses
  • Cap filling > 4-5 sec
  • Elevation pallor
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22
Q

neuropathic ulcer

A
  • History of numbness
  • Common DM
  • Pressure site
  • Variable depth
  • Surround callus
  • Cap refill normal
  • ABI- normal
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23
Q

Phlegmasia cerulean dolens

A

• Inflammatory, blue, and painful
o Due to primary venous insufficiency with secondary arterial insufficiency

Most common cause is cancer

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24
Q

Most common cause of vena cava syndrome

A

non small cell lung cancer

followed by small cell and lymphoma

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25
What position causes pain to be aggravated in a pericarditis patient?
Supine
26
What position relives pain in a pericarditis patient?
Sitting up and leaning forward
27
Changes seen in EKG that represents pericarditis
- ST segment elevation in all leads | - PR segment increased indicating atrium inflammation
28
Clinical presentation of pericarditis
* Myocardial involvement * Troponin elevations * Heart block * Wall motion abnormalities * CHF
29
Early disseminated Lyme disease
• Triad of acute neurologic abnormalities 1. Meningitis 2. Cranial neuropathy- B/l Bell’s palsy a. Other causes of b/l cranial nerve palsies: TB, sarcoid, and trauma 3. Motor or sensory radiculoneuropathy • Cardiac involvement with heart block and myopericarditis
30
Late Lyme disease
oligoarthritis
31
Treatment for pericarditis
* NSAIDs * Colchicine * Azathioprine * IVIGs * IL-1 antagonists (anakinra)
32
Pulsus paradoxus
Greater than 10 mm Hg drop in systolic pressure decreased LV ejection during inspiration due to the high CVP o Leads to increased RV filling with septal motion toward the LV • Limits LV filling and LVEF o Inflow across the mitral valve will decrease by 25%
33
Please Dr. BECK, you PAY for the CT
* Beck’s triad * Pulsus paradoxus * Electrical alterans * Slowed Y descent * Cardiac tamponade
34
kussmaul sign
in constrictive pericarditis, the jugular engorges with inspiration. usually should decrease in inspiration. indicates blood not going into the right atrium
35
Sharp y
seen in constrictive pericarditis • Tricupsid opens and blood rushes to get in o Y is much sharper and shorter o Blood slams into the ventricle due to so much pressure but then meets a steel wall and stops • Get a sharp descent and then plateau
36
Slow y descent
seen in cardiac tamponade • Cardiac tamponade does not allow blood to come in because there is a bag of water around the heart. There is resistance for blood to leave the atrium • Results in delayed filling → slow y descent
37
a wave
atrial contraction
38
x wave
atrial relaxation
39
v wave
atrial filling
40
y wave
atrial emptying
41
diastolic pericardial knock
o Auscultation- like an S3 and “septal bounce” (ECHO) due to rapid early filling in diastole. Also shows decreased mitral inflow seen in constrictive pericarditis
42
square root sign
o On heart cath- rapid ventricular filling followed by a plateau phase during the rest of diastole o Related to the rigid pericardium imparing mid and late diastolic filling resulting in decreased and equal diastolic filling pressures in all the cardiac chambers seen in constrictive pericarditis
43
Causes of constrictive pericarditis
* TB * Post radiation * Cardiac surgery * Viruses * Trauma
44
how to distinguish between constrictive pericarditis and restrictive cardiomyopathy
* The LV end diastolic pressure is unequal to the RV diastolic pressure – restrictive cardiomyopathy * Pressures are equal in constrictive pericarditis –square root sign * Also, pulmonary pressure is high in restrictive cardiomyopathy and low in constrictive pericarditis
45
Etiologies of ischemic heart disease (5)
``` Atherosclerosis Anemia Hyperthyroidism Stress Variant angina ```
46
Metabolic syndrome (6)
``` Obesity HTN High TGL Hyperglycemia Low HDL Insulin resistance ``` 2 fold increase in CAD
47
Conditional risk factors of IHD (6)
``` hrCRP homocysteine lipoprotein(a) LDL particle size antioxidancts omega 3 ```
48
Drugs used for pharmacological stress tests
Dobutamine- increase cardiac stress and oxygen demand | Adenosine/Dipyridamole- vasodilation
49
Diagnostic testing for IHD
1. cardiac enzymes: troponin, CPK, LDH 2. stress test 3. Pharacological stress test 4. Image augmentation- echocardiography 5. Angiography: gold standard 6. CT determined coronary artery calcium score
50
Unstable angina definition
- New onset - Occurs at rest - Crescendo
51
Aortic dissection
- Tearing chest pain - WIDENED MEDIASTINUM Can look like an inferior wall MI because the dissection can go into the right coronary artery
52
Pericarditis
recent viral illness pleuritic chest pain pulses paradoxus
53
Pulmonary embolism
inactivity pleuritic chest pain NEW ONSET OF ATRIAL FIB
54
CHF
SOB | ORTHOPNEA
55
thrombolytic therapy vs rapid revascularization in the cath lab
90 MIN if you can't get them to a cath lab in less than 90 min, give them thrombolytic therapy. Make sure they are having an MI!
56
Early MI complications (3)
1. Thrombolytics 2. Inferior wall MI- bradycardia and AV block 3. Anterior wall MI- pump failure
57
Later MI complications
1. VSD 2. Cardiogenic shock 3. Papillary muscle rupture causing MR 4. Free wall rupture- fatal 5. Left ventricular thrombus
58
ACS mortality intervention
1. Beta blockers 2. Aspirin 3. Ace inhibitor 4. Statins 5. Manage hyperglycemia Percutaneous intervention- not shown to improve overall survival Coronary artery bypass grafting- only in pts with left main disease
59
Drugs for acute angina
- Oxygen - Aspirin - Nitroglycerine - Morphine if nitro doesn't work
60
Carvallo's sign
pansystolic murmur that is louder during inspiration indicating tricuspid insufficiency (differentiates from mitral insufficiency)
61
Stokes-Adams attack
sudden/transient syncopal episode that is characterized by paleness prior and flushing after attack indicates heart block and need for pacemaker
62
Gallaverdin phenomenon
clinical sign of Aortic Stenosis described by a dissociation of noisy and musical portions of the murmur produced, specifically noisy at the URSB and musical at the apex
63
Raised JVP, normal waveform
◦ Bradycardia ◦ Fluid overload ◦ Heart Failure
64
Raised JVP, absent pulsation
superior vena cava syndrome
65
large a wave
increased atrial contraction pressure ◦ tricuspid stenosis ◦ Right heart failure ◦ Pulmonary hypertension
66
cannon a wave
atria contracting against closed tricupsid valve ``` ◦ Atrial flutter ◦ Premature atrial rhythm (or tachycardia) ◦ third degree heart block ◦ Ventricular ectopics ◦ Ventricular tachycardia ```
67
absent a wave
no unifocal atria depolarization atrial fibrillation
68
large v wave
tricupsid regurgitation
69
Austin flint murmur
low-pitched rumbling murmur at apex indicating AR
70
Graham Steel murmur
high-pitched early diastolic murmur at the LSB (2 nd ICS) indicating Pulmonary regurg
71
Trousseau's and Chvostek signs
Indicates hypocalcemia