Cardiac Adult 2.0 Flashcards
(94 cards)
1
Q
Crawford Extent 1
A
Type I involves most of the descending thoracic aorta from:
- the origin of the left subclavian to
- the suprarenal abdominal aorta.
2
Q
which crawford classificaition is the antatomically most extensitve
A
Type II
3
Q
Crawford Extent II
A
is the most extensive,
extending from (1) the subclavian (above the 6th ICS) to the (2) aortoiliac bifurcation.
4
Q
Crawford extent III
A
Type III involves the distal thoracic aorta to the aortoiliac bifurcation
5
Q
Crawford Extent IV
A
TAAAs are limited to the abdominal aorta below the diaphragm.
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
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.
8
Q
how does brain temperature compare to nasalpharyngal temperature
A
brain temperature is often 2-3oC less than nasopharyngeal temperature.
9
Q
Management of CSF leak following drain removal
A
Initial management:
- bed rest with limited elevation of the head of the bed to <30 degrees,
- intravenous hydration,
- 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.
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)
*
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
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.
*
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.
- Antigen testing has close to 100% sensitivity but specificity is less than 30%.
- functional assay such as the serotonin release assay, which is 95% sensitive and specific.
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%.
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.
16
Q
Type 2 HIT … how long does it take the platelets to recover?
A
10-14 days after withdraw of heparin
17
Q
What is the primairy goal of treating type 2 HIT
A
preventing thrombosis
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
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.
- ECG:
- 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.
20
Q
How is typical (type 1) atrial flutter best treated
A
.
Typical flutter is currently managed by catheter ablation at the cavotricuspid isthmus.
21
Q
Rapid atrial pacing
used for?
how is it done?
A
- Unlike AF – it responds to rapid atrial pacing
- 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%)..
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
23
Q
Next best treatment with bilatteral lung nodule
both shown to be nonsmall cell
A
Mediastinoscpy to evaluate the potential for hematogenous spread
24
Q
NCCN guidelines for genetic test that should be performed on all patients with adenocarcinoma
A
Anaplastic lymphoa kinase
25
NCCN Reccomendations for differentiate **adenocarcinoa** from **squamous cell** on _IHC_
Two stains
TTF-1: positive in adenoca, negaive scc
p63: positive in scc, and negative in adeno
26
Thoracic aortic aneurysms
overall 5 year survival
40%
27
Overall 5 year survival for a thoracoabdominal aneurysm
20%
28
average growth rate of a thoracic anneurysm
0.4 cm per year
29
comparison of aneurysm rupture risk:
6.0-6.9 cm vs 4.0-4.9cm
1. Aneurysm 6.0 – 6.9 has a 4 -fold risk of rupture compared to a 4.0 – 4.9 cm aneurysm
30
median size of ascending aneurysm rupture
5.9cm
31
median size of descending anurysm rupture
6.9 cm
32
Annual risk of rupture for 5.0 -5.9cm anurysm
5-6%
33
Annual risk of rupture for aneurysm \> 6.0cm
10-15%
34
Ascending aneurysm
## Footnote
A generally accepted threshold for aortic replacement in otherwise “normal” patients is:
5.0cm
35
Svennson criteria for aortic surgery based on size
area / to height
(pi x r2 (cm)) / height (m) \> 10
36
size to replace aorta with concominant elective avr
\> 4.0cm
37
indications for surgery on aortic arch aneurysm
1. symptomatic
2. \> 5.5 cm
3. potential source of emboli in pt with hx of embolic disease
38
indiciations for surgery in decending aortic disease
1. symptomatic
2. asymptomatic \> 6.5 cm
3. doccumented progressive enlargement
4. chronic type B dissection
39
Operative mortality for Ascending aortic aneurysm repair
* _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
Operative mortality for elective arch repair
_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
Operative mortality for descending aortic aneurysm repair
_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
5 year survival for ascending aneurysm repair
* **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
5 year survival for aortic arch repair
_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
5 year survival for descending aortic aneurysm repair
_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
Mode of death for aortic aneurysm
Rupture 40-70%
Dissection
Cerebral embolism
Visceral Embolism
46
Three most important variable to identify patients at increased risk of blood loss or transfusion needs :
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
Acquired LV pseudoaneurysm
tx for acute pseudoaneurysm
urgent surgical repair
48
Acquired LV pseudoaneurysm
chronic and symptomatic
elective surgical repair
49
Acquired LV pseudoaneurysm
tx if asymptomatic
1. if \> 3cm in diamter or expanding
* elective repair
2. if \< 3cm and not expanding
1. surveilance
50
**Coronary Artery Dissection**
Epidemiology:
**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
**Coronary Artery Dissection**
*Risk factors*
**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
Coronary artery disssection
Risk of recurance
20%
53
**Transmyocardial Laser Revascularization**
Indication:
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
Transmyocardial Revascularization
Contraindications
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
Transmyocardial Laser Revascularization
Outcomes
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
Ranolazine
inhibitor of late sodium channels,
one of several novel "metabolic modulators"
* enhance cardiac glucose metabolism to improve exercise tolerance and decrease angina.
57
argentaffin cells
Cells of the GI tract that secrete 5-HT and are the origin of carcinoid tumor
58
percent of carcinoid disese that mets to the liver
10%
59
% of patients with carcinoid tumors that present to carcinoid syndrome
10%
60
Carcinoid heart disease
- what percent of patients with carcinoid syndrome
- what are the effects
50% of the people with carcinoid syndrome wiill devellop cardiac involvement
Fibrosis --\> tricuspid and pulmonary valve resulting in regurgitatio
61
Laboratory evaluaiton of a patient with suspected carinoid syndrome
_Serum_: 5-HT (level correlates with severity )
_Urine_: 6-Hydroxyindolacetic acid
62
natural history of carcinoid heart disease
Rapdid progression to CHF
Cardiac surgery is the only effective treatment for symptomatic patients
63
Are liver mets a contraindication for surgery for carcinoid heart disease ?
No
64
Operative mortality for the treatment of carcinoid heart disease
65
symptoms of cardiac Myxoma
Constitutional
Obstruction
Embolization
Infection
Arrhythmia
66
Carney Complex inheritience
autosomal dominance
67
Left atrial myxoma
Histology
Histology
Contain:
a. smooth muscle
b. lymphocytes
c. mast cells
68
Diagnosis of Carney's Complex
**_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
Treatment of antibody mediated rejection of an OHT
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
what CD antibodies can be used against B-cells
anti-CD20, anti-CD40 antibodies
71
Sirolimus
(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
Protamine Reactions - How many are there ?
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
**Protamine Reaction**
## Footnote
what is a type I protamine reaction ?
I: reaction is characterized by hypotension alone.
74
Protamine Reaction
what is a type IIA reaction ?
**Protamine Reaction**
_IIA: characterized by anaphylaxis;_
_IIB: anaphylactoid response_
75
**Protamine Reaction**
what is a type IIC?
**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
**Protamine Reaction**
what is a type III reaction?
Protamine Reaction
III: involve hypotension and profound pulmonary hypertension that results in right heart failure
77
best indicators of contractitlity
CI and LVEDP
78
HEART FAILURE: Neurohormonal effects
HEART FAILURE: Neurohormonal effects
Sympathetic activity is increased
Cardiac norpinepherine is depleted
Beta receptors - down regulated
G-protein uncoupling from adenyl cyclase
79
**Digitalis (Digoxin)**
Mechanism:
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
**_Dobutamine_**
Mechanism of action
Dobutamine
Mechanism of action
Direct beta agonist (inotropy) Beta 1
Small beta 2 -
81
Dobutamine
Half life:
Half life: 2 min
82
Dobutamine
Metabolism:
Dobutamine
Metabolism:
**Hepatic**
83
Nesiritide
* 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
Causes of heparin resistance
**Antithrombin III deficiency**
*Causes*:
1. recent exposure to heparin
2. from a protein-losing nephropathy
85
Optimal pressure for retrograde cardioplegia
40mmHg (30-50mmHg)
86
Right Ventricle stroke work index
RVSWI = (mean PA - CVP) x (CI/HR).
87
**Transplulmonary gradient**
1. how is it calculated?
2. what is the limit for OHT ?
**_transpulmonary gradient:_**
TPG = MPA-PCWP
*For OHT*
The recommended upper limit for TPG 15 mmHg
88
**pulmonary vascular resistance**
How to calculate it ?
what is the upper limit for OHT?
_pulmonary vascular resistance_
PVR = TPG/CO
The recommended upper limit for OHT is 4 Woods units.
89
RVSWI
how to calculate it ?
what level is predictive of needing an RVAD
RVSWI = (MPA-CVP) x (CI/HR)
a value \>0.3 predicts satisfactory RV function for LVAD support.
90
What CVP/PCWP ratio is predictive of low liklihood of needing an RVAD
CVP/PCWP≥0.63,
91
Laboratory diagnosis of hemolysis
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
Most common pathogen related to HIV pericarditis
Mycobacteria
93
Most significant predictor of mortality following pericardial stripping
The need for CPB
94
Indication for ICD in HOCM patients
* 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.
