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Section 7 Cardiology > sect 7 cardiology > Flashcards

sect 7 cardiology Flashcards

1
Q

What make CP more likely to be cardiac? Less likely?

A

Increased probability of ACS with radiating CP, diaphoresis/nv/sob, lasting 2 or more hours, or angina is 2-20 minutes, described as pressure
Sharp brief pain, positional, palpation reproduces, and inframammary location less likely

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2
Q

Who presents with atypical presentations?

A
  • Women (fatigue, nausea, painless)
  • Elderly
  • Diabetics
  • Alterend mental status
  • Non white minorities
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3
Q

List angina equivalents?

A
  • Dyspnea at rest or exertion
  • Shoulder/arm/jaw discomfort
  • Nausea
  • Light headedness
  • Generalized weakness
  • Acute changes in mental status
  • Diaphoresis
  • Epigastric discomfort in those > 50 yo
  • Palpitations
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4
Q

Discuss the use of high sensitivity troponin?

A

High sensitivity Troponin I and T may be detectable as early as 2 hours after AMI but not relieably elevated in all pts until 6-12 hrs.

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5
Q

When do troponin levels peak and how long do they stay elevated? CK -MB?

A

Levels reach peak at 12 hours and stay elevated for 7-10 days
CK MB elevates within 4-8 hrs of Coronary occlusion, peaks between 12 and 24 hours, and returns to normal between 3-4 days.

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6
Q

List different ways to dx MI?

A

vsMI: troponin elevation with one of: ischemic sx, new ST T waves changes, LBB, new Q waves, or imaging evidence of a new loss of viale myocardium or new regional wall abnormality

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7
Q

Discuss Troponin T vs I in renal failure?

A

Troponin T (15%) more likely to be elevated in dialysis c/t I (

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8
Q

Which other conditions can troponin elevate in?

A
  • Cardiac contusion
  • Cardioinvasive procedures
  • Acute or chronic CHF
  • Aortic dissection
  • Aortic valve rupture
  • Hypertrophic cardiomyopahty
  • Arrythmias
  • Apical balloon sndomre
  • Rhabdo
  • Severe pulmonary htn
  • Acute neuro disease (stroke, SAH)
  • Infliltrative myocardial disease
  • Drug toxicity
  • Resp failure
  • Sepsis
  • Burns
  • Extreme exhaustion
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9
Q

List the blood supply of the heart?

A
  • Anterior and septal LAD
  • Anterior wall/lateral wall- circumflex
  • Right side of heart RCA
  • AV conduction RCA and septal branch LAD
  • Posteriomedial papillary usually RCA
  • Coronary blood flow is determined by diastolic duration and peripheral vascular resistance
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10
Q

What are high likelihood signs and sx for ACS?

A
  • Ches or left arm discomfort
  • Prior or known CAD
  • Transient mitral regurg murmur, hypotension, diaphoresis, pulomary edema or rales
  • ECG-new ST seg elevation > 1mm or T wave inversion in multiple precordial leads
  • Elevated Trop I, T or MB fraction
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11
Q

A new systolic murmur with ACS is bad. What might it represent?

A

Papillary muscle rupture, flail leaflet of mitral valve- regurg, or ventricular septal defect

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12
Q

What is sgarbossa criteria?

A
  • ST segment elevation 1mm or greater concordant with QRS
  • ST segment elevation discordant > 5mm discordant
  • ST segment depression 1 mm or more in leads v1, v2, v3
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13
Q

List other causes of ST elevation?

A
  • LBBB
  • Paced rhythm
  • BER
  • Pericarditis
  • Myocarditis
  • Hypothermia
  • Hypertrophic cardiomyopathy
  • Left ventricular aneurism
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14
Q

List other causes of ST depression?

A 
ST depression other causes; 
•	Hypokalemia 
•	Digoxin effect 
•	Cor pulomonale or right heart strain 
•	Early replorization 
•	LVH
•	Ventriclur paced rhythm 
•	LBBB
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15
Q

What are causes of T wave inversion?

A 
•	Seizures 
•	PE 
•	Spontaneous pneumo 
•	Myocardial contusion 
•	LVH 
•	LBBB
•	RBBB 
ischemia
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16
Q

What is the timeline for fibrinolysis? PCI?

A
  • PCI within 90 minutes
  • Fibrinolysis within 30 minutes
  • In pts presenting within 3 hours of CP it is up to instituition
  • PCI is better with longer sx: better in establishing flow, reducing reocclusion, non fatal reinfarction, and intracranial hemorhagae
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17
Q

What is the tx for NSTEMI/UA?

A
  • UA: need antiplatlets, antithrombins, B blockers, nitrates
  • GIIbIIIa antagonists for those with UA/Nstemi undergoing PCI
  • 02 for sats
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18
Q

When should one give fibrinolytics?

A

• For patients with STEMI if time to tx is

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19
Q

What are the complications of fibrinolytics?

A
  • Complications: TPA has more ICH than streptokinase , 0.5-1% of pts
  • 40-50% of pts do not achieve complete restoration of blood flow
  • Always give pts full dose anticoagulants after for 48 hrs as thrombin is exposed
  • Streptokinase allergic reactions in 5%, and avoid re treatment due to antibodies
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20
Q

When would one do rescue PCI in pts given fibrinolytics?

A
  • Rescue PCI recommended in; cardiogenic shock
  • Pts with severe heart failure or pulmonnary edema,
  • Ventricular arryhtmias that are hemodynamically unstable
  • Failure of fibrinolytics with moderate or large area of myocardium at risk
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21
Q

What are the high likelihood features of UA for death/non fatal MI?

A

crescendo decrescendo pain, prolonged ongoing rest pain > 20 min, pulmonary edema, new or worsening murmur, hypotension, brady, tacky, age > 75, angina at rest with transient ST segment changes > 0.5mm, BBB, new vtach, elevated cardiac markers

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22
Q

List the CI to fibrinolytic therapy?

A

Any prior ICH
known structural cerebral vascular lesion
known intracranial neoplasm
ischemic stroke within 3 monte
active internal bleeding
suspected aortic dissection or pericarditis
Other relative…..

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23
Q

In NSTEMI/UA, when should one consider early PCI? (within 48 hrs)

A
  • Recurrent angina/ischemia with or without sx of CHF
  • Elevated cardiac troponins
  • New ST seg depression
  • High risk findings on NST
  • Depressed left ventricular function
  • Hemodynamic instability
  • Sustained vtach
  • PRev CABG or PCI within last 6 months
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24
Q

Discuss the use of antiplatlets in ACS?

A

• ASA: preferable 325 mg, inhibition of thromboxane 2 lasts 8-12 days. Hold if active peptic ulcer disease and give plavix.
• Plavix: Adenosine diphosphate receptor antagonist: In pts undergoing PCI 600 mg is better at preventing post procedure MI. Withhold 5 days before CABG
• GIIBIIA inhibitor: IV infusion act on platlet activation , no role in STEMI
Ticagrelor- Cleaner drug c/t plavix, found in PLATO to be superior to to plavix with no increased risk of bleeding
CI: bradycardia (this can induce bradycardia), thrombolytic within 24hrs, CYP p450 inducers/enhancers

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25
Q

Discuss the use of anti thrombins?

A

• Antithrombins:
o UFH: recommended in combo with asa. DC after 48 hrs to reduce risk of HIT.
o LMWH: more reliable anticoag effect. Enoxaparin with ASA and fibrinolysis for STEMI pts has improved outcome (vs UFH)- but not first line for pts receiving PCI for STEMI. For pts receiving CABG LMWH should be held and UFH used in the 12-24 hrs proceeding surgery.
o Fondaparinux: xa inhibitor. Good for NSTEMI.

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26
Q

Discuss medications used for limiting infarcts size?

A
  • Nitrates: Dilates coronary arteries, reduces preload and afterload, and inhibits platlet aggregation. IV nitrates in ACS should be titrated to 10 % decr in BP for normotensive pts, and 30 % reduction in hypertensive to see true mortality benefits. Caution in RV infarct. Avoid if PDEI in last 24 hrs for sildenafil or 48 hrs of tadalafil.
  • B blockers: Antharrythm, anti ischemic, antihypertensive. Start within 24 hrs if no: signs of CHF, low CO, increased risk cardiogenic shock (age >70, SBP 110, and longer duration of stemi sx ac dx) or standard relative CI to B blockers: (pr interval > 0.24, 3rd degree heart block, active asthma, reactive airways disease).
  • Ace-I; decree LV dysfunction and left ventricular dilatation . CI include: hypotension, angioedema, renal failure, bilat renal artery stenosis.
  • Mg: no benefit
  • CCB: only for rapid ventricular response with no CHF/lv dysfunction
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27
Q

Which medications have been shown to have mortality reduction in ACS?

A
  • Asa
  • Plavix
  • G3b2AI-
  • Fibrinolytics
  • Pci
  • Enoxaparin
  • UFH
  • Nitrates
  • Ace-I
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28
Q

List the complications of ACS?

A

• Dysryhtmias (72% -100% of the time) : Top three: Vtach non sustained, accelerated idioventricular rhytm, Sinus bradycardia, sinus tachycardia , Atrial fibrillation (usually in first 24hrs and transient often secondary to hypok, hypomg, hypoxia, CLD, sinus node or left circumflex ischemia)
o Sinus brady does not alter mortality in AMI
o Don’t treat ventricular escape rhytms or idovent rhytms,
• Heart failure:
o 15-20%
• Mechanical complications
o Rupture of papillary muscles, interventricular septum, and ventricular free wall l/t dyspnea, cp, decompensation
o Free wall ruputure usually 1-5 days after AMO
o Intervent: often new holosystolic murmur
o Papillary muscle rupt more common with inferior MI- also new holosystolic murmur
• Pericariditis:
o 10-20 %
o More common in transmural MI
o 2-4 days after
o Dressler syndrome: 2-10 weeks after AMI: CP, fever, pleuropericarditis (tx ASA 650 mg Q4- hrs)
• Right ventricular infarction
o l/t shock , need adequate preload AVOID NITRATES – give 1-2 L NS, if still no increase in CO then add dobutamine
o May need pacing
• Other:
o LV thrombus formation
o Arterial embolization
o Venous thrombosis
o PE
o Postinfarction angina
o Infarct extension
o Stent stenosis- bare metal more likely in short term, drug eluting stents more likely to present with late stent thrombosis after cessation of daily plavix 9-12 months later

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29
Q

What is the management of a cocaine induced MI?

A
  • Tx Nitrates, ASA, and benzos
  • CI beta blockers
  • PCI is best mgmnt
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30
Q

List other disorders associated with MIs?

A
  • GI bleed
  • CVA (3.2 RR increase of death ct normal troponin)
  • Sepsis/infection
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31
Q

Which pre test probability of ACS means no further WU required?

A

• Pretest probability of ACS

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32
Q

What is the role for CT coronary angiography?

A

• CT coronary angiography: - picks up lesions >50%, if + follow with angio – high sens and sp (91%-100% and 52-100%) for picking up sign cathetrization defined lesions. + is >50%

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33
Q

List the causes of syncope?

A

• Cardiac
o 1. Structural cardiopulmonary lesions
• Valvular disease (ie AS will see pain, dyspnea on exertion, and syncope)
• Cardiomyopathy
• Pulmonary htn
• Pe
• Mi
o 2. Dysrrhythmias
• Neural reflex mediated
o Vasovagal (can include carotid body stim- bradycardia or hypotension)
• Consider carotid hypersensitivity in all older pts with recurrent syncope and negative cardiac evals
o Situation (cough, micturation, defecation, swallow, neuralgia)
• Orthostatic (sx within first 3 minutes usually, but sometime delayed)
o BP taken after 5 minutes supine, then standing at 1 and 3 minutes
o A decrease >20 sbp or

34
Q

What are the worrisome ECG findings in syncope?

A 
•	ECG in everyone 
o	Brugada
o	Prolonged QT
o	Ischemia
o	Dysrrhytmias
o	Hypertrophic cardiomyopathy 
Arrythmogenic right ventricle 
WPW
35
Q

What is the dispo for syncope?

A

• Admit those with cardiac and neurologic cause
• Those with vasovagal, orthostatic, and medication related syncope have no increased risk of cardiovascular mortality and do not need admission
Other reasons to admit include:
o CHF
o Abnormal ECG
o Hematocrit 45-65)
o Fam hx sudden cardiac death

36
Q

List the different types of heart failure?

A

• Hypertensive HF
o Signs and sx of hf with relatively preserved ef, sx onset within 48 hrs, and typical CHF cxr, bp > 140/90
• Pulmonary edema
o Resp distress, 02 satus reduced from baseline, verified by cxr
• Cardiogenic shock
o Evience of tissue hypoperfusion sbp

37
Q

What are the CXR findings of CHF?

A

cephalization, interstial edema, alveolar edema, look for other causes SOB
• Kerley b lines, redistribution, cardiomegaly, interstial edema, enlarge pulmonary artery, pleural effusion, prominent superior vena cava,

38
Q

What does nitroglycerin do in the tx of CHF?

A

• Decr preload, afterload, coronary vasodilation

39
Q

Apart from diuretics and nitrates what are the key tx in CHF?

A
  • Ace-I, bb, and spirinolactone long term
  • Can try hydralazine/isosorbide dinitrae if can’t tolerate acei or arbs
  • Digoxin if other tx failus
  • Avoid CCB, NSAIDS antiarrythmics,
40
Q

What is the classic triad for AS?

A

o Classic triad: dyspne, chest pain, and syncope (most often in setting of exertion)

41
Q

What are the target INRs for valve replacements?

A

• Mechanical mitral valves require INR or 2.5-3.5, whereas bileaflet aorta mech valves require INR of 2-3.

42
Q

List the key features of myocarditis?

A

a. FEVER, tachycardia, myalgias, CP
b. ECG Non specific st-t wave changes, often with pericarditis
c. Common cause of dilated cardiomyopathy
d. Common infections agents
i. Viral: coxsackie, nfluenza, parainfluenxa, ebv, ebv, HIV
ii. Bacterial: Cornybaaterium diphteria, N. mening, mycoplasma, beta hemolytic strep (rheum fever), lyme disease
e. Often hear pericardial friction rub
f. May have elevated cardiac enzymes
g. Tx: supportive for idiopathic and viral, abx for bacterial, admission if in CHF

43
Q

What are the key features of hypertrophic cardiomyopathy?

A
  • Dyspnea on exertion
  • Chest pain
  • Palpitations
  • Syncope
  • Prominent j wave
  • Pulses bisferiens
  • Systolic murmur, increases with valsalva, decr with squatting
  • ECG-LVH, larges septal Q waves
  • Lv/and or RV hypertrophy
  • Murmur best heard at lower left sternal border at apex- made louder with interventions that decr LV filling and pressure in LV outflow tract (ie squatting, hand grip, squatting)
  • Tx: echo, syncope with exercise and murmur equals admit, (can lt scd)
44
Q

List the causes of pericarditis?

A

• Idiopathic
• Malignant (leukemia, lymphoma, metastatic breast and lung, melanoma)
• Infectious
o Viral (coxsackie, HIV, echo)
o Bacterial (staph, strep, mycobacterium tb)
o Fungal (histoplasma capsulatum)
• Uremic
• Systemic disease (RA, SLE, polyarteritis nodosum, dermatomyositis)
• Radiation induced
• Post mi (dressler syndrome)
• Myxedema

45
Q

List the ECG changes associated with pericarditis?

A

• ECGS 4 stages (occur over several weeks)
o 1) Diffuse ST seg elevation, esp in 1, V5, V6, ST amplitude: t wave amplitude >0.25 often with pr depression
o 2) Returns to isoelectric line, T wave amplitude decreases
o 3) QRS isoelect, T wave inversion esp in 1, V5, V6
o 4) Normalization of T wave
o IF large pericardial effusion may have electrical alternans and low voltage QRS

46
Q

What are potential CXR findings of pericarditis?

A

• CXR- may have enlarged pericardial silouhette or fat pad sign on lateral view

47
Q

What are some ancillary studies for pericarditis?

A

• Ancillary studies include: CBC, BUN, CR, ASOT, Blood cultures, Serologic rhem studies if systemic sx, CRP. Viral studies, TSH)

48
Q

What is the tx for pericarditis?

A

• Tx: depends on cause, most pts are idiopathic or viral and sx respond to NSAIDS for 1-3 weeks.

49
Q

How does one differ BER from ST elev in pericarditis?

A

ratio of ST amplitude to T wave amplitude from pr segment ending, if > 0.25 acute pericarditis is likely,

50
Q

Which cancers are most associated with PE/DVT risk?

A
  • Adenocarcimona from anywhere
  • Next is blood cancers- non Hodgkin lymphoma, AML, ALL, mm
  • Solid organ mets
51
Q

What defines a massive PE?

A 
•	Massive: sbp  15 minutes or  40% reduction in baseline sbp
o	Cardiac arrest
o	Arterial hypotension
o	Reps failure 
o	Right heart starin on echo 
o	Elevated levels of trop t or I 
•	Submassive normal or near normal bp
OR
Massive PE: sbp
52
Q

What are the CXR findings of PE?

A

Presence of clear lung lungs and absence of pulmonary edema actually helps point more towards PE. May see: Cardiomegale, bi bisalar atalectasis, infiltrate, pleural effusion, westermark sign, hamptons hump

53
Q

Ecg findings of PE?

A
  • Sinus tachy
  • When pressure increased in RV will see t wave inversion V1-v4
  • S1Q3T3
  • Imcomplete RBB
54
Q

List the potential for a false positive d dimer?

A
  • Age > 70
  • Pregnancy
  • Active malignancy or mets
  • Surgical procedures in prev week
  • Liver disease
  • RA
  • Infections
  • Trauma
55
Q

List potential false negatives for D dimer?

A
  • Warafarin
  • Sx lasting > 5 days
  • Presence of small clots
  • Isolated small pulm infarction
  • Isolated cell vein thrombosis
56
Q

What is the significance of leg size difference in DVT?

A

A difference of > 2cm at 10cm below tibial tubercle is predictive of DVT

57
Q

What are the indications for thrombolysis in DVT? PE?

A
  • In DVT: if phlegmasia cerulea dolens (swollen/painful/ischemic limb) then thrombolyse
  • IN PE: pts in cardiac arrest, hypotension and massive PE, respiratory failure (severe hypoexemia with 02), right heart strain
58
Q

What are the key features of dx/tx of DVT/PE in pregnancy?

A

• US +- VQ scan for dx
• Lmwh or heparin for tx
• Can use PERC rule in pregnancy and increased D dimer cut offs (increase with trimester) together to rule out D dimer
States VQ preferred bc studied in pregnant pop, less breast rad to mom, and acceptable level of rad to fetus

59
Q

What is the age adjusted D dimer?

A

D dimer- may need to look at age adjusted cut off (10x age) (for pts >50)
Age adjusted D dimer

60
Q

Discuss the differences of VQ scan and CTPE for dx of PE?

A

V/Q scan rad dose, no iodinated contrast (7-10 x less rad than CTPA)
higher rate of non diagnostic scan
can’t dx other causes for sx (i.e. lung cancer)
Good option if Normal cxr, younger pts, contrast allergy, chronic renal insufficiency, pregnancy
CTPA
fast
avail after hours
confirms alternative dx
diasavd: rad, contrast

61
Q

When would one consider an IVC filter?

A

IVC filter if absolute CI to anticoag, failure to warafarin, can’t tolerate further clot burden in lungs

62
Q

What is a hypertensive emergency?

A 
➢	180/120 with associated end organ damange- brian, heart, aorta, kidneys, or eyes
➢	Acute aortic dissection
➢	Acute pulm edema
➢	Acute MI 
➢	ACS
➢	Acute renal failure
➢	Preeclampsia
➢	Retinopahty 
➢	Enchepalopathy 
➢	SAH
➢	CVA
63
Q

What are the BP goals in hypertensive emergency?

A

See list in binder

64
Q

What agents can you use to decrease BP?

A
  • Metoprolol dose 5 mg q 5-15 minutes up to 15 mg
  • Labetolol: 10-20 mg IV over 2 min, up to 40-80 mg, can gie infusion
  • Nicardipine: Can do infusion and titirate at 15 min intervals, onset of action is 5 min
  • Phentolamine for cocaine related hypertensive emergencies
  • Clonidine: use if pt prev on this and rebounding: 0.2 mg
65
Q

What are the causes of pulmonary hypertension?

A

o Pulmonary arterial hypertension: ass with RV dysfunction
o Pulmonary htn ass with left heart disease Dysfunction starts in Left ventricle l/t pulm venous pressure elevation and then pulm cap pressure elve, possibly progressive to PAH
o Pulm htn ass with resp disease Third group is pulm hyperthemion ass with resp derangement or hypoxemia
o Pulm htn ass with chronic thromboembolism 4th: from chornic pe
o Pulm htn ass with unclear or multifactorial etiologies 5th miscalaneous causes

66
Q

List 3 aortic emergencies?

A 
•	Aortic dissection
o	Penetrating atherosclerotic ulcer
o	Intramural hematoma
•	Aortice aneurismal leakage 
•	Ruptured AAA
67
Q

What are the risk fxs for aortic dissection?

A

More common in males, blacks, elderly (50-70). If women present they are usually older.
Predisposing fxs: htn (most important), atherosclerosis, congenital heart disease, ct syndromes ( turners, ehlos, marfans). Blunt trauma (usually more causes rupture or transection). Vasculitis (ra, giant cell arteritis, takayasu artertitis), instrumentation- post cabg. structural abn- bicuspid valve, coarct, valve replacement. High intensity weight lifting, and cocaine use.

68
Q

List the classification of Aortic dissections?

A

Stanford: Type A- Ascending and Arch (higher mortality, surgical mgmnt), Type B- decending, Below subclavian artery- lower mortality, often medical mgmnt
Debaky- Type 1- ascending arch, possible descending, 11-ascending only, 111- descending only

69
Q

What are some px exam findings of aortic dissection?

A
  • Pulse deficit: weak or absent carotid, brachial, or femoral pulse
  • New aortic recur murmur (more common along right sternal border)
  • Hemothorax
  • > 20 mmHG variation in BP between arms
  • Neuro deficits
  • Horner syndrome (if compression of cervical sympathetic chain)
  • vocal cord paralysis
70
Q

What are X-ray findings of Aortic dissection?

A

• Xray: wide mediastinum, or separation of the intimal calcification from outerr part if aorta, obliterated aortic knob, displacement of trachea to the right. Pleural effusion Pleural cap

71
Q

What are the sens/sp of different imaging for dissection?

A

• Contrast CT Sens 100%, spec 98%, MRI sens 98%, spec 98%, TEE- sens 98%, spec 95% Invest: chest angio

72
Q

Aortic dissection is mostly based on hx/exam. What are the key features?

A

Three key features:
Abrupt onset of thoracic or abdo pain with sharp, tearing, or ripping character (alone 31%)
Mediastinal and/or aortic widening on cxr (39%)
a variation in pulse (absence of proximal extremity or carotid pulse) and or BP (83%)
Can use D dimer however occ false negatives

73
Q

At what size is a AAA dx? What size repaired?

A
  • Considered at > 3cm

* Repear at > 5 cm (size is measured outer wall to outer wall)

74
Q

what is the sense of EDE for AAA?

A
  • If calclified may seen on xray
  • EDE best initially (90 senstivity)
  • CT scan with contrast in stable pts
75
Q

What is critical limb ischemia?

A

Critical limb ischemia is when chronic disease l/t pain at rest, ulceration, or gangrene

76
Q

Once critical limb ischemia is treated on can get reprofusion injury. What is this?

A

myoglobinemia, renal failure, and peripheral muscle infarction
• Supported by myoglobinemia, hyperkalemia, metabolic acidosis, and elevated CK
• 1/3 of deaths from occlusive arterial disease are secondary to metabolic complications upon revascularizaiton

77
Q

List the disorders that can cause acute arterial occlusion?

A

• Thrombus (most common)
• Emobolism (afib then mural thrombus)
o Most common in bifurcation of femoral artery and poplitieal artery
o Upper limb in brachial artery
• Cather complication (including self drug injection into artery)
• Vasculitis (RA, SLE, Polyarteritis nodusum)
• Raynaud (tx: ccb, a blockers, vasodilators)
• Takaysu arteritis
• Beurger disease (thrmoboangitis obliterans)
• HIV arteritis
• Hypothenar hammer syndrome
• Poplitieal artery entrapement
• External iliac artery endofibrosis
• Local arterial trauma
• Shock related arterial ischemia
• Aortic dissection
Upper limb ischemia- much better tolerated with better collateral circulation

78
Q

What are the sx of acute artery occlusions?

A
  • 6 Ps: pain, pallor, paralysis, pulslessness, parethesia, polar
  • Skin changes with complete obstruction- pallor followed by blotchy/mottled/cyanosis, petechiae, blisters
  • Diminished two point discrimination early
79
Q

What are the sx of chronic limb occlusion?

A
  • Chronic- limb claudication (with activity, resolves within 2-5 minutes) vs acute0 pain is not relieved – rest pain aggrevated by elevating foot
  • Vs. Neurogenic claudication- worse with erect posture and responds variably to exercise
80
Q

What will the px exam show of arterial disease?

A
  • Shiny hyperpigmented skin with hair loss and ucleration
  • Thick nails
  • Muscle atrophy
  • Vascular bruits
  • Poor pulses
  • Venous ulcers tend to me medial malleolus, vs arterial which are foot and toes and more painful – consider co existent arterial disease in chronic non healing venous ulcer
  • Do abdo and cvs exam, if other limb affected points more towards thrombotic disease
81
Q

How does one dx occlusive arterial disease?

A 
•	Mostly clinical 
•	ABI: >1.3 = non compressible
o	0.91-1.3 = normal
o	0.4-0.9 = Mild to mod peripheral art disease 
o	0-0.4 severe 
o	Consult if
82
Q

List the tx for occlusive arterial disease?

A

• UFH – Immediate IV tx. 80 units/kg bolus followed by infusion 18 units/kg/h
• ASA – 75-100 mg po first dose
• Dependant position- increases perfusion pressure
• Pain control
• Protect limb from temp extremes
• Surgical options include: catheter directed thrombolysis, percutaneous mechanical thrmobectomy, and revascularization with angioplasty or surgery
• Long term- smoking cessation ,ASA, exercise
Disp: if no acute limb, dc home with fu with vascular surgeon or pcp, daily ASA

Section 7 Cardiology (1 decks)

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