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PANRE > Cardiology-Panre > Flashcards

Cardiology-Panre Flashcards

1
Q

What diameter is AAA defined?

A

> or equal to 3 cm

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2
Q

When is surgery required for AAA?

A

> or equal to 5.5 cm, increase diameter, or change >.5 cm in 6 mos or >1 cm in 1 yr , symptomatic

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3
Q

What are the symptoms of AAA?

A

usually asymptomatic, severe abdominal pain/hip/backpain, pulsatile abdominal mass, syncope, **beare of that a kidney stone can present just like a AAA including hematuria

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4
Q

What is the best imagining in stable puts for AAA?

A

CT angiography CTA or magnetic resonance angiography MRA; o CT and MRA may be used to assess abdominal aortic aneurysm, CT/MRA is preferred for thoracic aneurysm

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5
Q

At what age is triple AAA screening recommended? what imaging?

A

65-75 1 time for mlaes who have every smoked ; ultrasound

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6
Q

AAA is typically located below what arteries?

A

renal (90%)-infrarenal arteries

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7
Q

RF for AAA?

A

Smoking (strongest), atherosclerosis, ht., older age, male gender, family hx and marfan (other conditions that predisposes to abnormal aortic dilation)

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8
Q

AAA affects which layers of the vessels?

A

All three-intima, media and adventitia

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9
Q

What is Aortic Dissection?

A

Involves inner lining of the aorta only one layer –intima (there are 3 layers)

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10
Q

Which imaging modality is used to for preop evaluation for triple AAA?

A

CT angiogram

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11
Q

Classic presentation of Aortic Dissection?

A

severe tearing sensation begins and stays 10/10 pain

o Radiates to back, pain is most severe at onset

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12
Q

If all three layers of vessel tears in Aortic dissection does the person lives?

A

Yes for 1 minute

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13
Q

Gold standard imaging for Aortic Dissection is ?

A

aortic angiography

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14
Q

Gold standard imaging for Aortic Dissection is ?

A

aortic angiography

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15
Q

Aortic Dissection is most common in males or females? Age ?

A

Males 2X , 40-80 years old

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16
Q

Which cardiac enzyme is the most specific and sensitive?

A

Troponin

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17
Q

Which cardiac enzyme appears first?

A

myoglobin (elevates 1-4 hours)

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18
Q

Which cardiac enzyme begins to rise at 4-8 hours, peaks 12-24 hours and lasts for 7-10 days

A

Troponin

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19
Q

which cardiac enzyme Appears at 4-6 hours, peaks at 12-24 hours and lasts for 3-4 days

A

CKMB

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20
Q

Most common cause of NSTEMI?

A

Acute thrombus in an atherosclerotic coronary artery

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21
Q

NSTEMI EKG?

A

ST-segment depression,

T-wave inversion, or both

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22
Q

What is NSTEMI?

A

A subendocardial myocardial necrosis without ST-segment
elevation or pathological Q waves; caused by myocardial ischemia with evidence of
myocardial injury or necrosis

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23
Q

What are Framingham non-modifiable RF for NSTEMI (coronary dz)

A

FAM-Family hx, increase age, male(sex)

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24
Q

Modifiable RF for NSTEMI (Coronary dz)

A

Tobacco use, hyperlipidemia, diabetes mellitus (DM), HTN,

obesity, stress, sedentary lifestyle

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25
Q

Typical Presentation of NSTEMI?

A

Prodrome of fatigue, chest discomfort or malaise several days prior; Intense pressure/squeezing, unremitting
retrosternal chest pain, radiation to neck, shoulders, jaw &/or left arm
■ Some patients have burning, stabbing or even sharp, needle-like
pain;

May present w/ sudden cardiac death

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26
Q

Atypical presentation of NSTEMI

A

MC-Women, DM, Older pt; shortness of breath (SOB), lightheadedness or
syncope, nausea/vomiting (N/V), diaphoresis, palpitations or
‘indigestion’

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27
Q

NSTEMI dx?

A

ECG-Depressed ST &/or with T wave inversion; Troponin I or troponin T and CK will be elevated); Angiography -delayed 24-48 hours unless complications present

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28
Q

TX of NSTEMI?

A

Beta Blockers + NTG + aspirin and clopidogrel + heparin + ACEI + statins + reperfusion; Reperfusion via percutaneous coronary intervention (not thrombolysis)
Less time-sensitive than in STEMI: IV oxygen (if pulse-oximetry if <90%)
Think MONA B CASHPAD

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29
Q

STEMI

A

A TRANSMURAL MYOCARDIAL NECROSIS with ST-segment elevation

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30
Q

STEMI are similar to NSTEMI except

A

Chest pain is usually sudden onset

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31
Q

Dx of STEMI?

A

Urgent coronary angiography with PCI

■ Fibrinolytics if timely PCI is not available

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32
Q

True LBBB + chest pain =; Posterior MI=

A

MI(STEMI) until proven otherwise : STEMI

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33
Q

Who develops pathological q waves?

A

STEMI pt’s who do not received rapid reperfusion therapy

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34
Q

TX for STEMI

A

MONA B CASH PAD; urgent cardiac cath within 90 mins to ballon

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35
Q

MONA B CASHPAD?

A

M-morphine(vasodilator decreases anxiety)
O. oxygen (NC>NRB>CPAP>intubate)
N. Nitro SL>paste or IV drip
A. Aspirin 325 mg
B. Blockers
C. Calcium channel blockers (cardizem for a fib rate only)
A> ACE inhibitors (prevents remodeling)
S. statin (short tem antiinflammatory/platelet)
H. heparin for STEMI or Lovenox for NSTEMI
P. plavix (load 300 mg then 75 mg daily)
A. amiodarone
D. Dopamine /Dobutamine/Diuretics

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36
Q

What is Acute pericarditis?

A

Inflammation of the pericardiac sac -cavity btw the thin membrane surrounding the heart =narrowing space

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37
Q

If acute pericarditis is not treated can lead?

A

pleural effusion(when pericardial space is fill with extra fluid causes extra pressure in heart muscles=cardiac dysfunction

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38
Q

Acute pericarditis-MC

A
  1. Viral (coxsac virus ) 2. Autoimmune/inflammatory dx, post-MI, cancer (CA), drugs (eg. procainamide, hydralazine), radiation-tx
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39
Q

S/S of Acute pericarditis

A

low-grade fever, tachycardia, dull or sharp substernal
chest pain (± radiation) MADE WORSE by coughing, breathing or swallowing
food, and MADE BETTER BY sitting up & leaning forward. Pre-cordial rub

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40
Q

Acute pericarditis dx?

A

Clinical
○ ECG: classic finding is ST segment elevation (concave upwards) & PR
segment depression in most leads; large effusion may be associated with ↓
QRS voltage & electrical alternans
○ Echocardiography: presence of effusion
○ CXR: may show enlarged cardiac silhouette

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41
Q

When is pericardial friction rub heard best?

A

A pericardial friction rub is heard best with patient upright and leaning forward

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42
Q

acute pericarditis tx?

A

Treat underlying cause. viral/idiopathic:
○ NSAIDs & colchicine
○ Corticosteroids are controversial → in general, avoid this for examination
purposes
○ Pericardiocentesis for large effusions

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43
Q

what is Dressler’s syndrome

A

Pericarditis after an acute MI

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44
Q

Most common form of infective endocarditis

A

Can be right-sided and/or left-sided (most common) → in part, determines
sx complex

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45
Q

Rf of endocarditis?

A

Invasive medical procedures, age >60 yo, male, injection drug use,
poor dentition, congenital heart defects, valvular dz, prior endocarditis &
intracardiac devices

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46
Q

CM of endocarditis?

A

ever initially, appear
toxic & have a murmur early in course of dz, night sweats, chills, fatigability, malaise
& weight loss
■ Roth spots: Hemorrhagic retinal lesions with central white spots
■ Petechiae
■ Osler nodes: Painful, red nodules on digit tips
■ Janeway lesions: Nontender hemorrhagic macules on palms/soles
■ Splinter hemorrhages under nails; Central nervous system (CNS) effects (eg. embolic stroke)

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47
Q

Dx of Endocarditis?

A

transthoracic

echocardiography diagnositc; Clinical criteria (eg. revised Duke criteria), blood cultures

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48
Q

Modified Duke Criteria for Diagnosis of Infectious Endocarditis

A

Definite: 2 major criteria, or 1 major and 3 minor criteria, or 5 minor criteria

Possible: 1 major and 1 minor criteria, or 3 minor criteria

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49
Q

Major Criteria for Duke?

A

Positive blood culture: isolation of typical microorganism for IE from 2 separate blood cultures or persistently positive blood culture
Single positive blood culture for C. burnetii or antiphase-1 IgG antibody titer >1:800
Positive echocardiogram: presence of vegetation, abscess, or new partial dehiscence of prosthetic valve; must be performed rapidly if IE is suspected
New valvular regurgitation (change in preexisting murmur not sufficient)

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50
Q

Minor criteria for duke?

A

Predisposing factor in history
○ Fever >38.0°C (100.4°F)
○ Vascular phenomena (emboli, pulmonary infarction)
○ Immunological phenomena (glomerulonephritis, Osler nodes, Roth spots)
○ Positive blood culture not meeting definite criteria for major criteria

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51
Q

TX for native pts for endocarditis (no valve replacement)

A

PCN/nafcillin/vancomycin (gram +) PLUS gentamicin (gram -)

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52
Q

TX for valve replacement for endocarditis? if tx fails?

A

prosthetic valve: ADD rifampin (never rifampin alone)
● Valve replacement if:
○ Antibiotics fail
○ Valve abscess develops
○ Fungal infection
○ Valve dysfunction produces hemodynamic instability

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53
Q

What is the abx prophylaxis for high risk pts undergoing high risk procedures?

A

1-2 hours before procedure
○ Amoxicillin 2g PO/IV/IM OR Ceftriaxone 1g IV/IM
○ PCN allergy: Azithromycin 500mg PO OR Clindamycin 600mg IV/IM
○ Vancomycin/Clindamycin if concern for MRSA

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54
Q

What is Acute endocarditits?

A

Develops abruptly & progresses rapidly over days
■ #1 cause is Staph aureus
■ #1 valve is mitral
■ In IV drug users, Tricuspid valve is most common

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55
Q

What is subacute endocarditits?

A

Develops insidiously & progresses slowly over weeks to months;
■ Leading cause is viridans group streptococci
■ Infection usually develops on abnormal valves

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56
Q

What is the MC sites of Aortic Dissection?

A

Proxima ascending aorta (within 5 cm of aortic valve) & descending thoracic aorta (just distal to origin of left subclavian artery?

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57
Q

Type A of Aortic Dissection-Location, therapy, disposition

A

Proximal/ascending aorta, Surgical, OR for repair

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58
Q

Type B of Aortic Dissection-Location, therapy, disposition

A

Distal, Medical, ICU for BP mgmt (B blocker gtt)

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59
Q

TX of Aortic Dissection?

A

Aggressive blood pressure (BP) control (systolic BP (SBP) < 120 mmHg)
■ β-blockers given 1 st (eg. esmolol)
■ Nitroprusside should not be given without β-blocker or
Ca ++ -channel blocker 2° reflex sympathetic activation
○ Serial imaging to monitor disease progression
○ Surgery depending upon location & extent of dissection

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60
Q

Complications of Aortic Dissection?

A

Compromise in blood flow to arteries that branch off of the aorta,
aortic valve dilation ; regurgitation, HF ; aortic rupture; high mortality rate

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61
Q

Causes/RF of Aortic Stenosis?

A

Bicuspid aortic valve (<70 yo), idiopathic degenerative sclerosis with
Ca ++ (>70 yo) & rheumatic fever

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62
Q

Aortic stenosis presents with what symptoms?

A

Classic triad of syncope, angina & exertional dyspnea

○ Also HF, dysrhythmias, sudden death

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63
Q

Aortic stenosis mumur is located? Radiation? Type of murmur? Increases with what type of maneuver? Decrease?

A

Location: Right second intercostal space (aortic area) ; Radiation: to the neck and to the APEX; Crescendo-decrescendo systolic ejection murmur; ↑ with leg-raising & squatting d/t ↑ LV volume & contractility; with Valsalva d/t ↓ LV volume & isometric handgrip d/t ↑ afterload

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64
Q

Treatment -AS

A

Tx in adults: Asymptomatic → usually ∅ tx; symptomatic → valve replacement

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65
Q

Arterial Embolism CM? Arterial Thrombotic dz?

A

Remember the “six P’s” (You must know these!): Pain, Paralysis, Pallor, Paresthesia, Polar (some say Poikilothermia—temp same as ambient), and Pulselessness; clot forms in situ instead of originating from heart/aorta
○ Example: SMA (superior mesenteric artery) thrombus - classic presentation is older patient
that presents with acute abdominal pain that is out of proportion to exam (i.e. physical
exam is not as concerning as the patient’s pain would infer)

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66
Q

MC cause of Arterial Embolism/thrombus?

A

Atrial fibrillation & mitral stenosis?

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67
Q

Arterial Embolism most originate where?

A

Heart , originate in the left heart

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68
Q

What are more effected with arterial embolism upper or lower extremities?

A

Lower extremities are more common than upper extremities

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69
Q

Arterial embolism /thrombus tx?

A

anticoagulate with IV heparin (bolus followed by constant infusion)

If not limb threatening then call the vascular surgeon for angioplasty, graft or endarterectomy

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70
Q

Dx of Arterial embolism? Gold std?

A

Angiography is considered the gold standard for diagnosis

ECG (looking for MI, AFib)
Echocardiogram (+/- ) looking for clot, MI, valve vegetation

71
Q

Arterial embolism?

A

occurs when a mass of tissue or a foreign substance travels
through the arterial tree eventually lodging in a distal artery where it obstructs
blood flow
○ This is an acute process where patients develop sudden & severe Sx

72
Q

Arterial thrombosis? Common areas affected/

A

rupture of an atherosclerotic plaque
leading to platelet aggregation & fibrin deposition, Sx onset may be less dramatic & less severe; coronary arteries, arteries of the head &
neck, lower limbs & bowel

73
Q

What is Atrial Fibrillation?

A

lose SA node signa to Av node results in atria spasms = sporaic waves, leads to Signaling AV node erractically;

74
Q

Most common chronic tachydysrhythmia?

A

A fib

75
Q

A-Fib rhythm ?

A

Rapid, irregularly irregular atrial rhythm

76
Q

A-fibrillation rate?

A

> 110 (a fib with rapid ventricular response), 70-110 controlled fib, rate <60 a fib with slow ventricular response

77
Q

A-fibrillation P waves? EKG findings

A

No p waves ; ,

irregular R-R intervals, usually narrow complex QRS

78
Q

no clear P waves,

irregular R-R intervals, usually narrow complex QRS

A

A-fibrillation?

79
Q

A-fibrillation causes? (think pirates)

A 
P-pulmonary (PE, COPD, pneumonia)
I-Iatrogenic (cocaine, amphetamines)
R-Rheumatic heart(MR/MS structural change in atrium)
A-Atherosclerotic : MI/CAD
Thyroid: hyperthyroid
Endocaritis, electrolye imbalances
S-sick sinus syndrome, sepsis
80
Q

A-fib tx ? (generalized)

A

Rate control, sometimes rhythm control, prevention of thromboembolism

81
Q

Rate control for A fib?

A

(<100 bpm): Nondihydropyridine Ca ++ -channel blockers (eg.
diltiazem), β-blockers (eg. esmolol)
■ AV nodal blockers should not be used in patients with
Wolff-Parkinson-White (WPW) syndrome (wide QRS) → could lead
to ventricular fibrillation

82
Q

Rhythm control for A fib?

A

Anticoagulation + synchronized cardioversion (esp. HF or
hemodynamic compromise)
■ Antiarrhythmic drugs: Class Ia (eg. disopyramide), class Ic (eg.
flecainide) or class III (eg. amiodarone);

83
Q

A-fib stable <48 hours?

A

Dilitazem/Esmolol (rate control); pharmacological cardioversion digoxin/amiodarone; sedation & synchronized cardioversion; Stable Rhythm pt-may be used in younger puts with lone A fib-DCC (direct current synchronized cardioversion)-preferred over pharmacologic rhythm control. DCC can be done if 1. Afib <48 hrs 2. After 3-4 weeks of anticoagulation & TEE shows no atrial thrombi

84
Q

A fib unstable>48 hours

A

Dilitazem/Esmolol (rate control), Heparin IV until TEE confirms thrombus; consider pharm cardio version; considered sedation & synchronized cardioversion

85
Q

Unstable pt with rapid ventricular rate of A-fib?

A

Synchronized cardioversion

86
Q

A-fib risk stratification ?

A

CHA DS 2 -VASc score ≥2 = high risk

87
Q

What is CHADS2VAS

A

C: Congestive HF or left ventricular (LV) systolic dysfunction
■ H: HTN (BP>140/90 mmHg or on meds)
■ A 2 : Age ≥75 yo
■ D: DM
■ S 2 : Stroke, transient ischemic attack (TIA), thromboembolism
V: Vascular dz
■ A: Age 65-74 yo
■ Sc: Sex category
ADD SCORE-0-1=ASA/+ OR- PLAVIX; >OR = WARFARIN OR COUMADIN

88
Q

If you have a valvular dz + atrial fibrillation what do you use warfarin or direct thrombolytics ?

A

Warfarin, direct thrombolytics can not be used in valvular dz

89
Q

Complications of Afib?

A

Formation of atrial thrombi → significant risk of embolic stroke

90
Q

Regular, sawtooth pattern, atrial rate 250-350 BPM, narrow QRS complex

A

Atrial flutter

91
Q

Atrial flutter occurs in?

A

Occasionally occurs in COPD, congestive heart failure, atrial septal defect, coronary artery disease

92
Q

Atrial flutter?

A

Rapid, regular rhythm where the atria depolarize at a rate of 250-350 bpm → since
AV node cannot conduct at this rate, ~½ of these impulses get through often
leading to a 2:1 block

93
Q

Atrial flutter symptoms?

A

Palpitations, dyspnea, weakness, presyncope, exercise intolerance

94
Q

Atrial flutter tx?

A

Similar to Afib; Rate control, rhythm control & prevent thromboembolism
○ Rate control is more difficult than with A Fib → initial episodes usually
require anticoagulation + synchronized cardioversion
■ Drug options: Nondihydropyridine Ca ++ -channel blockers,
β-blockers
○ Rhythm control: Class Ia & Ic antiarrhythmics
○ Long-term oral anticoagulation is required for patients with chronic or
recurrent atrial flutter

95
Q

AF risk factors?

A 
Hemodynamic stress
Atrial ischemia
Inflammation
Noncardiovascular respiratory causes
Alcohol and drug use
Endocrine disorders
Neurologic disorders
Genetic factors
Advancing age
96
Q

AF occurs more in men or women?

A

Men

97
Q

irregularly, irregular rhythm with a varying PR interval and various P wave morphologies (Three or more foci).

A

Multifocal atrial tachycardia

98
Q

What is the difference btw A-fib and atrial flutter?

A

Atrial flutter and atrial fibrillation are both abnormal heart rhythms. … In atrial fibrillation, the atria beat irregularly. In atrial flutter, the atria beat regularly, but faster than usual and more often than the ventricles, so you may have four atrial beats to every one ventricular beat

99
Q

unstable AF tx?

A

Direct current synchoronized cardioversion

100
Q

Stable AF tx?

A

Vagal , B blockeror calcium channel blocker

101
Q

Definitive management of AF?

A

radio frequency ablation

102
Q

NOAC-Non-vitamin K antagonist oral anticoagulants (NOAC) preferred? benefits? Examples?

A

Preferred over warfarin (if no CI), has similar or lower rates of bleeding with LOWER risk of ischemic stroke, no need to check INR
EX: Dabigatran (direct thrombin inhibitor-binds and inhibits thrombin, Rivaroxaban, Apixaban, Edoxaban-Factor Xa inhibitors

103
Q

When is Warfarin preferred (in AFib)? What is INR goal

A

Preferred in pots with severe CKD, CI to NOAC (HIV pts on PI based therapy, on CP450 anti epileptic medications such as carbamazepine , phenytoin, puts on already warfarin, mechanical heart valves. cost issues. Warfarin usually bridged with heparin, until warfarin is therapeutic, INR goal2-3

104
Q

What is the fastest way to rapidly lower the patient’s INR in a bleeding pt on coumadin?

A

Fresh frozen plasma is the most rapid way to lower the patient’s INR.

105
Q

Antidote for overdose of warfarin (coumadin) but no bleeding

A

Protamine sulfate or Vitamin K

106
Q

.

Left BBB is associated with more than RBB?

A

Left bundle branch block is associated with a structural heart disorder more often than is RBBB. LBBB usually precludes use of ECG for diagnosis of MI

107
Q

Left BBB ECG findings?

A 
New LBBB + Chest Pain = MI until proven otherwise!
Wide QRS > 0.12 sec
R and R’ (upward bunny ears) in V4-V6
Deep S in V1 and V2
ST elevations in V1-V3
108
Q

Right BBB ECG findings?

A

Almost always benign but can be associated with pulmonary embolism and ASD
Wide QRS > 0.12 sec
R and R’ (upward bunny ears) in V1-V3
Wide S wave in V6

109
Q

If the QRS complex is widened and downwardly deflected in lead V1 it is?

A

LBBB

110
Q

If the QRS complex is widened and upward deflected in lead V1 it is?

A

RBBB

111
Q

The ECG criteria for a left bundle branch block (LBBB) include:

A
  1. QRS duration of > 120 milliseconds.
  2. Absence of Q wave in leads I, V5, and V6.
  3. Monomorphic R wave in I, V5, and V6.
  4. ST and T wave displacement opposite to the major deflection of the QRS complex.
112
Q

The ECG criteria for a right bundle branch block include

A
  1. QRS duration of > 120 milliseconds
  2. rsR’ “bunny ear” pattern in the anterior precordial leads (leads V1-V3)
  3. Slurred S waves in leads I, aVL and frequently V5 and V6 (lateral leads)
113
Q

General etiology for BBB? LBBB? RBBB?

A

Aging, HTN, CAD, cardiomyopathies, myocarditis, valvular heart
dz; Acute MI; Congenital heart dz ; cor pulmonale, pulmonary embolism

114
Q

What is cardiac tamponade? Causes/etiology?

A

Excessive fluid Fluid filled in pericardial space, leads to increase pressure on heart results in r. Side of heart collapse(right side of heart collapse as its weaker than the left). In other words, decreases function of ventricular filing which decreases CO; Penetrating or blunt chest trauma, pericarditis, iatrogenic (invasive heart procedures & post surgery), MALIGNANCY.

115
Q

S/S of Cardiac tamponade

A

Acute- Cardiogenic shock; Chronic -Beck’s triad-Muffle heart sounds, increase JVP, systemic hypotension; Pulsus paradoxes (exaggerated >10 mmhg decrease in systolic blood pressure with inspiration & decreases pulses with inspiration); Dyspnea, fatigue, tachycardia, chest fullness

116
Q

Dx of Cardiac tamponade?

A

Echocardiogram (best choice of test)

117
Q

Tx of cardiac tamponade

A

removing fluid of heart=pericardiocentesis or pericardiotomy sx drainage

118
Q

What is cardiogenic shock?

A

Heart stops working= impaired contractibility which results decrease blood towards body (decrease CO) to maintain adequate perfusion to body (not enough o2 to tissues)

119
Q

Causes of Cardiogenic shock?

A
  1. MI, Cardiac tamponade (Cardiomyopathic), PE, 2. dysrhythmic(heart block 3 degree) and 3. mechanical -acute aortic regu, MV papillary muscle chordae tendineae rupture
120
Q

s/s of Cardiogenic shock?

A

Depends of etiology. 1.MI-substernal chest pain, n/v etc 2. Dysrhythmic -palpitations, syncope, presyncope 3. Mechanical-Sob & tachypnea
Signs: cold pale mottled extremities with decrease peripheral pulses, hypotension, decrease urine output and altered CNS

121
Q

How is Cardiogenic shock dx?

A

Clinical, echocardiography

122
Q

How is Cardiogenic shock tx?

A

Tx underlying cause Give pressers – dobutamine, norepinephrine and ultimately a balloon pump

Supplemental 02 by face mask or by intubation
Structural disorders (eg, valvular dysfunction, septal rupture) are repaired surgically
Judicious use of diuretics (monitor renal functio)
123
Q

What is Coronary artery dz?

A

Blood flow is block/obstruct through coronary arteries mc by subintimal deposition of atheromas in large & medium size vessel, less common from artery spasm

124
Q

What dz fall under CAD? Acute coronary dz includes what?

A

Angina’s (stable, unstable, Prinzmetal variant angina), NSTEMI, STEMI & sudden death; Unstable, NSTEMI, STEMI

125
Q

What is the prevention of CAD

A

Stop smoking, exercise, lose weight, healthy balance diet, statins, low sodium diet, control dm /htn/hld.

126
Q

What is angina pectoris ?

A

Known as stable angina, partial obstruction of blood flow in coronary arteries, pain is relieved by rest & nitroglycerin & <30 mins,

127
Q

Describes stable angina pattern?

A

Stable angina is a regular pattern of chest discomfort that occurs predictably
& reproducibly following physical or emotional stress

128
Q

MC cause of stable angina?

A

Coronary artery artherosclerosis

129
Q

What are the rf of stable angina?

A

Smoking, obesity, htn, dm, hld, sedentary, poor diet

130
Q

s/s of angina pectoris

A

vague, achy discomfort to severe intense crushing/squeezing chest pain, last no more than a few mins, improves with rest and nitroglycerin. Trigger by stress, exertion, eating cold etc.

131
Q

dx of angina pectoris

A

Normal EKG( no chest pain); During anginal pain-ST depressions and T inversions; Normal troponin

132
Q

Tx for angina pectoris ; Tx for persistent angina pectoris or positive stress exam?

A

aspirin, nitrates, β-blockers, Ca channel blockers, ACE inhibitors, statins, and coronary angioplasty or coronary artery bypass graft surgery;PCI with coronary artery bypass grafting

133
Q

What a DVT?

A

Blood clot in deep vein of an extremitiy such as leg, calf, thigh , pelvis

134
Q

What is the MC cause of PE?

A

DVT

135
Q

s/s of DVT?

A

Asymetrical pain/ tenderness along deep vein, Asymetrical leg swelling >3 cm circumference, Asymetrical pitting edema, HOMAN’S SIGN + (edema, erythema, warmth)

136
Q

RF? Etiology?

A

Age, Smoking, Cancer, OCP used, Pregnancy/POst partum , hyper coagulability dz, immobilization, obesity, sx less or equal 3 most, trauma, prior DVT ; impaired venous return, endothelial injury, hyper coagulability

137
Q

How to dx a DVT?

A

Venous doppler u/s -s first line imaging test; Venography “ gold standard”; D-dimer - a negative D-dimer will rule out DVT in low risk patients

138
Q

What is Virchow’s triad?

A
  1. Venous stasis (car rides/plane flight >4 hrs etc) 2. endothelia damage-lower leg injury 3. hyper coagulability: malignancy, pregnancy, oops
139
Q

How is DVT treated? Prevention? Anticoagulation? Other methods?

A

Prevention for at-risk patients: Early mobilization, leg elevation, pneumatic
compression devices, elastic stockings; Anticoagulation: Unfractionated or LMW heparin, warfarin (oral factor Xa
& direct thrombin inhibitors is still evolving) for 3-6 mos; some patients
require lifelong tx
○ Inferior vena cava filter: Patients with recurrent DVT

140
Q

Types of anticoagulation therapy for dvt?

A
  1. Unfractionated heparin-Ind prevents further emboli (rather than treating current one), TITRATE TO PTT 1.5-2.5 X NORMAL VALUE
  2. Lowe molecular weight heparin-enoxaprin; no need to monitor PTT, Sq injection last 12 hours so pt d/c home, safe in PREGNANCY. CI:thrombocytopenia , renal failure if Cr < 2.0
  3. Warfain
141
Q

Unfractionated heparin MOA? ; SE?

A

Potentiates antithrombin III, inhibits thrombin & other coagulation factors; Protamine sulfate antidote for heparin toxicity, heparin-induced thrombocytopenia

142
Q

Warfarin MOA? Avoid?

A

inhibits vitmain K dependent coagulation factors of extrinsic pathway: 2,7,9,10; inhibits protein C & S. Coumadin should be overlapped with heparin for at least 5 days, until INR is 2-3. Vitamin K is the antidote for toxicity. Avoid cruciferous vegetables with Vit K (spinach, kale, brussel sprouts, greens( green tea, cranberry juice and etoh)

143
Q

Heart Failure: 4 types

A 
o	Left heart-Left ventricle 
	Systolic -S3
	Diastolic S4
o	Right heart failure-right ventricle 
	Cause pulmonary htn 
o	High output cardiac failure-normal pump 
	Cause: metabolic demand
144
Q

What is Diastolic heart failure?

A

HF with preserved ejection fraction (EF) where LV filling pressure is impaired
→ diastolic dysfunction; EF can be normal or slightly ↓ (usually ≥50%)

145
Q

Contributing/associated conditions of Diastolic heart failure?

A

Primarily seen in elderly patients, HTN,

hypertrophic & restrictive cardiomyopathy

146
Q

Sx/S of Diastolic heart failure?

A

Fatigue, dyspnea, orthopnea, exercise intolerance; JVD, S4, rales, peripheral
edema

147
Q

Dx of Diastolic heart failure? TX?

A

Clinical; echocardiography
○ Tx: Directed at contributing factors (eg. HTN), pulmonary congestion &
peripheral edema (eg. diuretics), cardiac rehabilitation

148
Q

What is Dilated Cardiomyopathy?Causes?

A

Ventricular enlargement & abnormal contractile with one or both ventricle -normal LV wall thickness; Decreases ventricular contraction strength, decrease CO (less blood being pump out)=dilated LV(decrease ejection fraction)-systolic dyfunction=heart failure ; Genetic, myocarditis, drugs/toxins (including etoh, cocaine), Pregnancy (risk of developing during pregnancy 3rd trimester), Drugs-chemotherapy DOXORUBICIN/DANGORUBICIN; wet beriberi, decrease vitamin B1=thiamine

149
Q

Dilated Cardiomyopathy CM? Complications?

A

Symptoms present when compensatory mechanisms can no longer maintain cardiac output
● CHF signs: dyspnea, orthopnea, S3, rales, increased JVD, peripheral edema; Common in males >females ; Stagnant clot→ thrombi
● Atrial and ventricular dysrhythmias
● Increased risk for sudden cardiac arrest

150
Q

Dilated Cardiomyopathy dx?

A

Clinical, increase BNP, ECG (LVH, non specific ST/T changes, LBBB); Transthoracic Echocardiogram (TTE): test of choice; diagnoses systolic/diastolic dysfunction;

151
Q

Dilated Cardiomyopathy Tx?

A

Removed underlying cause; Tx of HF and acute complications; LV assist Device/mechanical pump; Heart transplant in extreme cases

152
Q

What is Restrictive Cardiomyopathy? Etiologies?

A

fibrosis or infiltration of ventricular wall =stiffness & ventricles can not be fill(can not relax); normal or near normal systolic function, non dilated ventricle with normal wall thickness ; Radiation, diabetes mellitus, endomyocardial fibrosis, amyloidosis, sarcoidosis, hemochromatosis, scleroderma

153
Q

What is Restrictive Cardiomyopathy? Etiologies?

A

fibrosis or infiltration of ventricular wall =stiffness & ventricles can not be fill(can not relax); normal or near normal systolic function, non dilated ventricle with normal wall thickness(+/- slightly thick) ; Radiation, diabetes mellitus, endomyocardial fibrosis, amyloidosis, sarcoidosis, hemochromatosis, scleroderma

154
Q

TX of Restrictive Cardiomyopathy

A

Treat the CHF

● Transplant

155
Q

DX of Restrictive Cardiomyopathy

A
  1. The ECG is usually nonspecifically abnormal, showing ST-segment and T-wave abnormalities and sometimes low voltage
  2. Echocardiography shows normal systolic function. Common findings include DILATED BL ATRIA AND Diastolic dysfunction
156
Q

What is Hypertrophic Cardiomyopathy? Causes?

A

Asymetrical muscle growth (thick & heavy) of walls of muscle typically affects LV results increase inter ventricular septum muscle growth, causes less compliant ventricle (can not stretch) leads to less filling and less being pumped out (decrease CO). Overall results diastolic heart failure

157
Q

What is Hypertrophic Cardiomyopathy? Causes?

A

Asymetrical muscle growth (thick & heavy) of walls of muscle typically affects LV results increase inter ventricular septum muscle growth, causes less compliant ventricle (can not stretch) leads to less filling and less being pumped out (decrease CO). Overall results diastolic heart failure.

158
Q

Hypertrophic Cardiomyopathy mumur? explanation? Maneuvers?

A

Crescendo decrecendo murmur -LV outflow tract is obstructed due to the muscle growth of septum pulling anterior of MV towards septum. Squats /handgrip (all blood flow going to heart)-decreases murmur -more blood stretches ventricle out =softer murmur; Stands/valsalva=blood away from heart=less blood, increase obstruction=louder murmur

159
Q

S/s of Hypertrophic Cardiomyopathy?

A

Dyspnea, chest pain, syncope, fatigue, palpitations, ventricular dysythmias, sudden cardiac arrest, symptoms typically occur during physical activity or exertion

160
Q

Dx Hypertrophic Cardiomyopathy

A

Doppler Echocardiography is test of choice-demonstrates septal hypertrophy, normal systolic function, poor diastolic function, some type of degree of mitral regurgitation
Chest xray-normal -hypertrophy is inside the heart, EKG-large QRS, abnormal deep narrow Q’s, LAD

161
Q

Dx Hypertrophic Cardiomyopathy

A

Avoid digoxin/vasodialtion and exertion! Improve diastolic function: beta blockers, calcium channel blockers to slow heart Definitive treatment surgical/nonsurgical ablation of hypertrophied septum +/- dual chamber pacing

162
Q

What is Iliac artery occlusion? Difference from arterial embolism?

A

Atherosclerotic plaques occurring in infrarenal (below renal arteries) aorta & lilac arteries (similar location of AAA)=obstruction of blood flow may result in possible more embolic events to distal arteries; Difference is arterial embolism involves of mass of tissue and /or foreign object

163
Q

MC cause of arterial embolism? other etiologies?

A

atherosclerotic plaque with associated thrombus formation (most common);
others include thrombosis of stent/graft, dissection or direct trauma to artery, embolus
from proximal source

164
Q

complications of arterial occlusion ?

A

limb-/life-threatening

165
Q

Mitral Regurgitation type of murmur? description? PE?

A

Systolic murmur (happens when blood is being pushed out from ventricle); SOFT S1, HIGH-PITCHED, BLOWING
HOLOSYSTOLIC MURMUR BEST heard at the APEX WITH the patient in left lateral
DECUBITUS POSITION & RADIATES TO AXILLA; often takes years to develop sx →
exercise intolerance, dyspnea on exertion & left – then right heart failure; Acute can lead to pulmonary edema

166
Q

Mitral Regurgitation causes?

A

1° (degenerative): Intrinsic lesion of mitral valve apparatus (eg. myxomatous
change [mitral prolapse], rheumatic fever)
● 2° (functional): Left ventricular or left atrial dz (eg. cardiomyopathy, MI)

167
Q

What is Mitral Regurgitation

A

Valvular incompetency leading to retrograde flow of blood from left ventricle
through mitral valve into the left atrium during systole

168
Q

Mitral Regurgitation dx? tx?

A

clinical, echo ; In symptomatic patients, valve repair/replacement

169
Q

Most common valvular disorder in US

A

Mitral Regurgitation

170
Q

Revascularization is indicated when stenosis of the left main coronary artery is greater?

A

50%

171
Q

he most useful noninvasive procedure for diagnosis of ischemic heart disease and evaluation of angina

A

nuclear stress testing

172
Q

Four groups most likely to benefit from statin therapy are identified?

A

atients with any form of clinical atherosclerotic cardiovascular disease (ASCVD)
Patients with primary LDL-C levels of 190 mg per dL or greater
Patients with diabetes mellitus, 40 to 75 years of age, with LDL-C levels of 70 to 189 mg per dL
Patients without diabetes, 40 to 75 years of age, with an estimated 10-year ASCVD risk ≥ 7.5%

173
Q

Should Patients with diabetes mellitus, 40 to 75 years of age, with LDL-C levels of >or equal 70 per dL be treated with Statins?

A

yes

174
Q

An EKG demonstrates a PR interval of 0.16 seconds, a P to QRS relationship of 1:1, a variable heart rate and an R to R interval that is noted to accelerate ad decelerate during the respiratory cycle. What is the diagnosis

A

sinus arrhtymia

PANRE (15 decks)

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