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SESATS > Cardiac Adult 2.0 > Flashcards

Cardiac Adult 2.0 Flashcards

1
Q

Crawford Extent 1

A

Type I involves most of the descending thoracic aorta from:

  1. the origin of the left subclavian to
  2. the suprarenal abdominal aorta.
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2
Q

which crawford classificaition is the antatomically most extensitve

A

Type II

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3
Q

Crawford Extent II

A

is the most extensive,

extending from (1) the subclavian (above the 6th ICS) to the (2) aortoiliac bifurcation.

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4
Q

Crawford extent III

A

Type III involves the distal thoracic aorta to the aortoiliac bifurcation

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5
Q

Crawford Extent IV

A

TAAAs are limited to the abdominal aorta below the diaphragm.

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6
Q

Crawford Extent V

A

Safi’s group modified this scheme by adding Extent V:

which extends from the distal thoracic aorta including the celiac and superior mesenteric origins but not the renal arteries

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7
Q

early mortality rate of Type A dissection

A

The mortality rate of patients with aortic dissection is 1%-2% per hour for the first 24-48 hours, and initial therapy should begin when the diagnosis is suspected.

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8
Q

how does brain temperature compare to nasalpharyngal temperature

A

brain temperature is often 2-3oC less than nasopharyngeal temperature.

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9
Q

Management of CSF leak following drain removal

A

Initial management:

  1. bed rest with limited elevation of the head of the bed to <30 degrees,
  2. intravenous hydration,
  3. a caffeine infusion.
  • An epidural blood patch to seal the hole in the dura may be needed if these conservative measures fail.
    • lateral position
    • 5-10 mL of blood is drawn by venipuncture
    • then slowly injected into the epidural space.
    • The patient is kept supine for 60 minutes afterward.
  • Activity and posture are not restricted if the headache resolves.
  • Formal suture repair of the dura is rarely required.
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10
Q

What are the subtypes of heparin induced thombocytopenia ?

A

There are 2 types of heparin associated thrombocytopenia:

  • non-immune (HIT Type 1)
  • immune heparin induced thrombocytopenia (HIT Type 2)
    *
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11
Q

HIT type 1

typical timing and laboratory results

A
  • HIT Type 1 is associated with:
    • mild thrombocytopenia within 2-3 days after starting heparin treatment.
    • Platelet counts less than 100 K/mm3 are rare
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12
Q

Timing and laboraory values relaed to the the diagnosis of type 2 HIT

A
  • immune heparin induced thrombocytopenia (HIT Type 2)
    • The timeline of HIT Type 2 is broader (4-14 days) unless there has been previous heparin exposure,
    • thrombocytopenia is usually moderate to severe (commonly <100).
    • the counts recover within days after discontinuation of heparin.

*

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13
Q
  • immune heparin induced thrombocytopenia (HIT Type 2)

how is the diagnosis confirmed

A
  • immune heparin induced thrombocytopenia (HIT Type 2)
  • Diagnosis:
    • Testing for HIT type 2 is confirmed by antigen and functional testing.
    • A high percentage of postoperative cardiac surgery patients have postoperative thrombocytopenia and positive antigen tests.
      1. Antigen testing has close to 100% sensitivity but specificity is less than 30%.
      2. functional assay such as the serotonin release assay, which is 95% sensitive and specific.
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14
Q

immune heparin induced thrombocytopenia (HIT Type 2)

senstivity and specificity of antigen testing ?

A

Antigen testing has close to 100% sensitivity but specificity is less than 30%.

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15
Q

immune heparin induced thrombocytopenia (HIT Type 2)

sensitivity and specificity of the functional assay ?

A

immune heparin induced thrombocytopenia (HIT Type 2)

Confirmatory testing is done by a functional assay such as the serotonin release assay,

which is 95% sensitive and specific.

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16
Q

Type 2 HIT … how long does it take the platelets to recover?

A

10-14 days after withdraw of heparin

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17
Q

What is the primairy goal of treating type 2 HIT

A

preventing thrombosis

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18
Q

Type II HIT

when should coumadin be started?

for how long ?

A

coumadin should be strated when platelets > 150

the patient should remain on coumadin for 6 months

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19
Q

what is typical atrial flutter ?

A

Typical flutter (Type I) accounts for over 90% of atrial flutter cases and involves the IVC and tricuspid isthmus in the re-entry circuit.

  1. ECG:
    1. the flutter waves are upright in V1, and inverted in II, III, and aVF, indicating an “anti-clockwise” re-entry circuit, which is the most common direction.
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20
Q

How is typical (type 1) atrial flutter best treated

A

.

Typical flutter is currently managed by catheter ablation at the cavotricuspid isthmus.

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21
Q

Rapid atrial pacing

used for?

how is it done?

A
  1. Unlike AF – it responds to rapid atrial pacing
    1. Rapid external atrial pacing is frequently initiated at a rate slightly slower than the ventricular rate for 10-15 seconds. The endpoints are either conversion to sinus rhythm (approx 50%) or to atrial fibrillation (25%)..
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22
Q

Surgery as a role in small cell lung cancer

A

Small cell is usally responsive to chemotherapy

if residual tissue need to consider surgery as the cancer may be mixe in etiology

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23
Q

Next best treatment with bilatteral lung nodule

both shown to be nonsmall cell

A

Mediastinoscpy to evaluate the potential for hematogenous spread

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24
Q

NCCN guidelines for genetic test that should be performed on all patients with adenocarcinoma

A

Anaplastic lymphoa kinase

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25
Q

NCCN Reccomendations for differentiate adenocarcinoa from squamous cell on IHC

A

Two stains

TTF-1: positive in adenoca, negaive scc

p63: positive in scc, and negative in adeno

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26
Q

Thoracic aortic aneurysms

overall 5 year survival

A

40%

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27
Q

Overall 5 year survival for a thoracoabdominal aneurysm

A

20%

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28
Q

average growth rate of a thoracic anneurysm

A

0.4 cm per year

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29
Q

comparison of aneurysm rupture risk:

6.0-6.9 cm vs 4.0-4.9cm

A
  1. Aneurysm 6.0 – 6.9 has a 4 -fold risk of rupture compared to a 4.0 – 4.9 cm aneurysm
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30
Q

median size of ascending aneurysm rupture

A

5.9cm

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31
Q

median size of descending anurysm rupture

A

6.9 cm

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32
Q

Annual risk of rupture for 5.0 -5.9cm anurysm

A

5-6%

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33
Q

Annual risk of rupture for aneurysm > 6.0cm

A

10-15%

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34
Q

Ascending aneurysm

A generally accepted threshold for aortic replacement in otherwise “normal” patients is:

A

5.0cm

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35
Q

Svennson criteria for aortic surgery based on size

A

area / to height

(pi x r2 (cm)) / height (m) > 10

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36
Q

size to replace aorta with concominant elective avr

A

> 4.0cm

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37
Q

indications for surgery on aortic arch aneurysm

A
  1. symptomatic
  2. > 5.5 cm
  3. potential source of emboli in pt with hx of embolic disease
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38
Q

indiciations for surgery in decending aortic disease

A
  1. symptomatic
  2. asymptomatic > 6.5 cm
  3. doccumented progressive enlargement
  4. chronic type B dissection
39
Q

Operative mortality for Ascending aortic aneurysm repair

A
  • Location: Ascending
  • Operative Mortality: 1-5%
  • 5- year Survival: 85%

Location: Arch

Operative mortality: 5-10%

5 Year survival: 75%

Location: Descending

oper mortality: 5-10%

5- year survival: 60%

Location: Thoracoabdominal

Operative mortality: 5-10%

5-year survival: 60%

40
Q

Operative mortality for elective arch repair

A

Location: Ascending

Operative Mortality: 1-5%

5- year Survival: 85%

  • Location: Arch
  • Operative mortality: 5-10%
  • 5 Year survival: 75%

Location: Descending

oper mortality: 5-10%

5- year survival: 60%

Location: Thoracoabdominal

Operative mortality: 5-10%

5-year survival: 60%

41
Q

Operative mortality for descending aortic aneurysm repair

A

Location: Ascending

Operative Mortality: 1-5%

5- year Survival: 85%

Location: Arch

Operative mortality: 5-10%

5 Year survival: 75%

  • Location: Descending
  • oper mortality: 5-10%
  • 5- year survival: 60%

Location: Thoracoabdominal

Operative mortality: 5-10%

5-year survival: 60%

42
Q

5 year survival for ascending aneurysm repair

A
  • Location: Ascending
  • Operative Mortality: 1-5%
  • 5- year Survival: 85%

Location: Arch

Operative mortality: 5-10%

5 Year survival: 75%

Location: Descending

oper mortality: 5-10%

5- year survival: 60%

Location: Thoracoabdominal

Operative mortality: 5-10%

5-year survival: 60%

43
Q

5 year survival for aortic arch repair

A

Location: Ascending

Operative Mortality: 1-5%

5- year Survival: 85%

  • Location: Arch
  • Operative mortality: 5-10%
  • 5 Year survival: 75%

Location: Descending

oper mortality: 5-10%

5- year survival: 60%

Location: Thoracoabdominal

Operative mortality: 5-10%

5-year survival: 60%

44
Q

5 year survival for descending aortic aneurysm repair

A

Location: Ascending

Operative Mortality: 1-5%

5- year Survival: 85%

Location: Arch

Operative mortality: 5-10%

5 Year survival: 75%

  • Location: Descending
  • oper mortality: 5-10%
  • 5- year survival: 60%

Location: Thoracoabdominal

Operative mortality: 5-10%

5-year survival: 60%

5-10%

60%

45
Q

Mode of death for aortic aneurysm

A

Rupture 40-70%

Dissection

Cerebral embolism

Visceral Embolism

46
Q

Three most important variable to identify patients at increased risk of blood loss or transfusion needs :

A
  1. Advanced age (> 70 years)
  2. emergent or complex operations
  3. decreased preoperative red blood cell volume
    1. small body size or preoperative anemia or both
47
Q

Acquired LV pseudoaneurysm

tx for acute pseudoaneurysm

A

urgent surgical repair

48
Q

Acquired LV pseudoaneurysm

chronic and symptomatic

A

elective surgical repair

49
Q

Acquired LV pseudoaneurysm

tx if asymptomatic

A
  1. if > 3cm in diamter or expanding
    • elective repair
  2. if < 3cm and not expanding
    1. surveilance
50
Q

Coronary Artery Dissection

Epidemiology:

A

Coronary Artery Dissection

Initially thought to be rare (0.1% of patients undergoing cardiac catheterization), spontaneous coronary artery dissection (SCAD) has been widely reported

more common in women (70%),

  • 25% of all cases are associated with pregnancy.
51
Q

Coronary Artery Dissection

Risk factors

A

more common in women (70%),

  • 25% of all cases are associated with pregnancy. s.

Atherosclerosis - most cases occur in the setting of

Cocaine Abuse

Caffinated energy drinks

Thrombophilia

Sleep depravation

Pathophysiology

52
Q

Coronary artery disssection

Risk of recurance

A

20%

53
Q

Transmyocardial Laser Revascularization

Indication:

A

as sole therapy

  1. patients with refractory class III/IV angina and an ejection fraction greater than 30%.
  2. It is indicated in patients with a region of myocardium with reversible ischemia that is not amenable to PCI or CABG.
54
Q

Transmyocardial Revascularization

Contraindications

A

Transmyocardial Revascularization

Class III evidence suggests that TMLR in acute or evolving myocardial infarction is not useful and may be harmful.

Prior to offering TMLR all medical treatment options should be exhausted, including the use of ranolazine and other novel strategies for symptom relief.

55
Q

Transmyocardial Laser Revascularization

Outcomes

A

Numerous studies have demonstrated significant improvement in angina symptoms and quality of life following TMLR.

Hospital readmission is significantly reduced with therapy, but survival at 1-year is not changed.

Limited information on late survival suggests possible benefit.

56
Q

Ranolazine

A

inhibitor of late sodium channels,

one of several novel “metabolic modulators”

  • enhance cardiac glucose metabolism to improve exercise tolerance and decrease angina.
57
Q

argentaffin cells

A

Cells of the GI tract that secrete 5-HT and are the origin of carcinoid tumor

58
Q

percent of carcinoid disese that mets to the liver

A

10%

59
Q

% of patients with carcinoid tumors that present to carcinoid syndrome

A

10%

60
Q

Carcinoid heart disease

  • what percent of patients with carcinoid syndrome
  • what are the effects
A

50% of the people with carcinoid syndrome wiill devellop cardiac involvement

Fibrosis –> tricuspid and pulmonary valve resulting in regurgitatio

61
Q

Laboratory evaluaiton of a patient with suspected carinoid syndrome

A

Serum: 5-HT (level correlates with severity )

Urine: 6-Hydroxyindolacetic acid

62
Q

natural history of carcinoid heart disease

A

Rapdid progression to CHF

Cardiac surgery is the only effective treatment for symptomatic patients

63
Q

Are liver mets a contraindication for surgery for carcinoid heart disease ?

A

No

64
Q

Operative mortality for the treatment of carcinoid heart disease

A
65
Q

symptoms of cardiac Myxoma

A

Constitutional

Obstruction

Embolization

Infection

Arrhythmia

66
Q

Carney Complex inheritience

A

autosomal dominance

67
Q

Left atrial myxoma

Histology

A

Histology

Contain:

a. smooth muscle
b. lymphocytes
c. mast cells

68
Q

Diagnosis of Carney’s Complex

A

Features of Carney Complex include:

recurrent atrial myxomas

hyperpigmentation of the skin (lentiginosis)

non-cardiac benign tumors

ACTH-independent hypercortisolism

other endocrine disorders

and a positive family history of these features.

69
Q

Treatment of antibody mediated rejection of an OHT

A
  1. Targeted specific anti-B cell therapies (e.g., anti-CD20, anti-CD40 antibodies),
  2. Antibody-depletion or reconstitution therapies (e.g., plasmapheresis and administration of polyclonal immunoglobulins),
  3. steroid pulses to suppress T and B lymphocyte and leukocyte function,
  4. Antiproliferative therapies,
  5. Bone marrow irradiation to suppress lymphopoiesis.
70
Q

what CD antibodies can be used against B-cells

A

anti-CD20, anti-CD40 antibodies

71
Q

Sirolimus

A

(rapamycin) blocks the activation of T and B cells by inhibiting the response to interleukin-2 (IL-2)

sirolimus may be useful in the prevention of antibody-mediated rejection of kidneys, few data exist regarding its use in the treatment of this process once it is ongoing, and its role in this regard in cardiac transplantation is completely unknown.

72
Q

Protamine Reactions - How many are there ?

A

I: reaction is characterized by hypotension alone.

IIA: characterized by anaphylaxis;

IIB: anaphylactoid response

IIC: results in non-cardiogenic pulmonary edema.

III: involve hypotension and profound pulmonary hypertension that results in right heart failure.

73
Q

Protamine Reaction

what is a type I protamine reaction ?

A

I: reaction is characterized by hypotension alone.

74
Q

Protamine Reaction

what is a type IIA reaction ?

A

Protamine Reaction

IIA: characterized by anaphylaxis;

IIB: anaphylactoid response

75
Q

Protamine Reaction

what is a type IIC?

A

Protamine Reaction

IIA: characterized by anaphylaxis;

IIB: anaphylactoid response

IIC: results in non-cardiogenic pulmonary edema.

III: involve hypotension and profound pulmonary hypertension that results in right heart failure

76
Q

Protamine Reaction

what is a type III reaction?

A

Protamine Reaction

III: involve hypotension and profound pulmonary hypertension that results in right heart failure

77
Q

best indicators of contractitlity

A

CI and LVEDP

78
Q

HEART FAILURE: Neurohormonal effects

A

HEART FAILURE: Neurohormonal effects

Sympathetic activity is increased

Cardiac norpinepherine is depleted

Beta receptors - down regulated

G-protein uncoupling from adenyl cyclase

79
Q

Digitalis (Digoxin)

Mechanism:

A

Inhibitis Na-K-ATPase pump, which activate Na-Ca active transport

Ca= positive inotropic effect

Decreases AV conduction

Parasympathomimetic and anti-cholinergic mechanism

Decreases AV-conduction

Increases refractory periord

Reduces ventricular rate

80
Q

Dobutamine

Mechanism of action

A

Dobutamine

Mechanism of action

Direct beta agonist (inotropy) Beta 1

Small beta 2 -

81
Q

Dobutamine

Half life:

A

Half life: 2 min

82
Q

Dobutamine

Metabolism:

A

Dobutamine

Metabolism:

Hepatic

83
Q

Nesiritide

A
  • B-type natruretic peptide
  • Approved when loop diuretics fail in the absence of hypotension and volume dependent (warm and wet)
  • Approved for acute decompensated heart failure
  • Improves PCWP and dyspneas score
84
Q

Causes of heparin resistance

A

Antithrombin III deficiency

Causes:

  1. recent exposure to heparin
  2. from a protein-losing nephropathy
85
Q

Optimal pressure for retrograde cardioplegia

A

40mmHg (30-50mmHg)

86
Q

Right Ventricle stroke work index

A

RVSWI = (mean PA - CVP) x (CI/HR).

87
Q

Transplulmonary gradient

  1. how is it calculated?
  2. what is the limit for OHT ?
A

transpulmonary gradient:

TPG = MPA-PCWP

For OHT

The recommended upper limit for TPG 15 mmHg

88
Q

pulmonary vascular resistance

How to calculate it ?

what is the upper limit for OHT?

A

pulmonary vascular resistance

PVR = TPG/CO

The recommended upper limit for OHT is 4 Woods units.

89
Q

RVSWI

how to calculate it ?

what level is predictive of needing an RVAD

A

RVSWI = (MPA-CVP) x (CI/HR)

a value >0.3 predicts satisfactory RV function for LVAD support.

90
Q

What CVP/PCWP ratio is predictive of low liklihood of needing an RVAD

A

CVP/PCWP≥0.63,

91
Q

Laboratory diagnosis of hemolysis

A
  1. persistent severe anemia
    1. hemoglobin <10 g/dL
    2. hematocrit < 33%
  2. elevated lactate dehydrogenase:
    1. >440 U/L
  3. reduced serum haptoglobin (<37 mg/dL),
  4. RBC Morphology
  5. schistocytes
  6. fragmented cells
  7. polychromasia
92
Q

Most common pathogen related to HIV pericarditis

A

Mycobacteria

93
Q

Most significant predictor of mortality following pericardial stripping

A

The need for CPB

94
Q

Indication for ICD in HOCM patients

A
  • In high-risk patients, ICD placement is recommended.
    1. High-risk patients include:
    2. extremely thick (>3 cm) interventricular septum
    3. evidence of nonsustained ventricular tachycardia
    4. a family history of sudden death
    5. history of syncope.

SESATS (12 decks)

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