Cardiology-Panre Flashcards
1
Q
What diameter is AAA defined?
A
> or equal to 3 cm
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
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
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
5
Q
At what age is triple AAA screening recommended? what imaging?
A
65-75 1 time for mlaes who have every smoked ; ultrasound
6
Q
AAA is typically located below what arteries?
A
renal (90%)-infrarenal arteries
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)
8
Q
AAA affects which layers of the vessels?
A
All three-intima, media and adventitia
9
Q
What is Aortic Dissection?
A
Involves inner lining of the aorta only one layer –intima (there are 3 layers)
10
Q
Which imaging modality is used to for preop evaluation for triple AAA?
A
CT angiogram
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
12
Q
If all three layers of vessel tears in Aortic dissection does the person lives?
A
Yes for 1 minute
13
Q
Gold standard imaging for Aortic Dissection is ?
A
aortic angiography
14
Q
Gold standard imaging for Aortic Dissection is ?
A
aortic angiography
15
Q
Aortic Dissection is most common in males or females? Age ?
A
Males 2X , 40-80 years old
16
Q
Which cardiac enzyme is the most specific and sensitive?
A
Troponin
17
Q
Which cardiac enzyme appears first?
A
myoglobin (elevates 1-4 hours)
18
Q
Which cardiac enzyme begins to rise at 4-8 hours, peaks 12-24 hours and lasts for 7-10 days
A
Troponin
19
Q
which cardiac enzyme Appears at 4-6 hours, peaks at 12-24 hours and lasts for 3-4 days
A
CKMB
20
Q
Most common cause of NSTEMI?
A
Acute thrombus in an atherosclerotic coronary artery
21
Q
NSTEMI EKG?
A
ST-segment depression,
T-wave inversion, or both
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
23
Q
What are Framingham non-modifiable RF for NSTEMI (coronary dz)
A
FAM-Family hx, increase age, male(sex)
24
Q
Modifiable RF for NSTEMI (Coronary dz)
A
Tobacco use, hyperlipidemia, diabetes mellitus (DM), HTN,
obesity, stress, sedentary lifestyle
25
Typical Presentation of NSTEMI?
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
26
Atypical presentation of NSTEMI
MC-Women, DM, Older pt; shortness of breath (SOB), lightheadedness or
syncope, nausea/vomiting (N/V), diaphoresis, palpitations or
‘indigestion’
27
NSTEMI dx?
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
28
TX of NSTEMI?
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
29
STEMI
A TRANSMURAL MYOCARDIAL NECROSIS with ST-segment elevation
30
STEMI are similar to NSTEMI except
Chest pain is usually sudden onset
31
Dx of STEMI?
Urgent coronary angiography with PCI
| ■ Fibrinolytics if timely PCI is not available
32
True LBBB + chest pain =; Posterior MI=
MI(STEMI) until proven otherwise : STEMI
33
Who develops pathological q waves?
STEMI pt's who do not received rapid reperfusion therapy
34
TX for STEMI
MONA B CASH PAD; urgent cardiac cath within 90 mins to ballon
35
MONA B CASHPAD?
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
36
What is Acute pericarditis?
Inflammation of the pericardiac sac -cavity btw the thin membrane surrounding the heart =narrowing space
37
If acute pericarditis is not treated can lead?
pleural effusion(when pericardial space is fill with extra fluid causes extra pressure in heart muscles=cardiac dysfunction
38
Acute pericarditis-MC
1. Viral (coxsac virus ) 2. Autoimmune/inflammatory dx, post-MI, cancer (CA), drugs (eg. procainamide, hydralazine), radiation-tx
39
S/S of Acute pericarditis
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
40
Acute pericarditis dx?
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
41
When is pericardial friction rub heard best?
A pericardial friction rub is heard best with patient upright and leaning forward
42
acute pericarditis tx?
Treat underlying cause. viral/idiopathic:
○ NSAIDs & colchicine
○ Corticosteroids are controversial → in general, avoid this for examination
purposes
○ Pericardiocentesis for large effusions
43
what is Dressler's syndrome
Pericarditis after an acute MI
44
Most common form of infective endocarditis
Can be right-sided and/or left-sided (most common) → in part, determines
sx complex
45
Rf of endocarditis?
Invasive medical procedures, age >60 yo, male, injection drug use,
poor dentition, congenital heart defects, valvular dz, prior endocarditis &
intracardiac devices
46
CM of endocarditis?
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)
47
Dx of Endocarditis?
transthoracic
| echocardiography diagnositc; Clinical criteria (eg. revised Duke criteria), blood cultures
48
Modified Duke Criteria for Diagnosis of Infectious Endocarditis
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
49
Major Criteria for Duke?
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)
50
Minor criteria for duke?
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
51
TX for native pts for endocarditis (no valve replacement)
PCN/nafcillin/vancomycin (gram +) PLUS gentamicin (gram -)
52
TX for valve replacement for endocarditis? if tx fails?
prosthetic valve: ADD rifampin (never rifampin alone)
● Valve replacement if:
○ Antibiotics fail
○ Valve abscess develops
○ Fungal infection
○ Valve dysfunction produces hemodynamic instability
53
What is the abx prophylaxis for high risk pts undergoing high risk procedures?
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
54
What is Acute endocarditits?
Develops abruptly & progresses rapidly over days
■ #1 cause is Staph aureus
■ #1 valve is mitral
■ In IV drug users, Tricuspid valve is most common
55
What is subacute endocarditits?
Develops insidiously & progresses slowly over weeks to months;
■ Leading cause is viridans group streptococci
■ Infection usually develops on abnormal valves
56
What is the MC sites of Aortic Dissection?
Proxima ascending aorta (within 5 cm of aortic valve) & descending thoracic aorta (just distal to origin of left subclavian artery?
57
Type A of Aortic Dissection-Location, therapy, disposition
Proximal/ascending aorta, Surgical, OR for repair
58
Type B of Aortic Dissection-Location, therapy, disposition
Distal, Medical, ICU for BP mgmt (B blocker gtt)
59
TX of Aortic Dissection?
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
60
Complications of Aortic Dissection?
Compromise in blood flow to arteries that branch off of the aorta,
aortic valve dilation ; regurgitation, HF ; aortic rupture; high mortality rate
61
Causes/RF of Aortic Stenosis?
Bicuspid aortic valve (<70 yo), idiopathic degenerative sclerosis with
Ca ++ (>70 yo) & rheumatic fever
62
Aortic stenosis presents with what symptoms?
Classic triad of syncope, angina & exertional dyspnea
| ○ Also HF, dysrhythmias, sudden death
63
Aortic stenosis mumur is located? Radiation? Type of murmur? Increases with what type of maneuver? Decrease?
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
64
Treatment -AS
Tx in adults: Asymptomatic → usually ∅ tx; symptomatic → valve replacement
65
Arterial Embolism CM? Arterial Thrombotic dz?
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)
66
MC cause of Arterial Embolism/thrombus?
Atrial fibrillation & mitral stenosis?
67
Arterial Embolism most originate where?
Heart , originate in the left heart
68
What are more effected with arterial embolism upper or lower extremities?
Lower extremities are more common than upper extremities
69
Arterial embolism /thrombus tx?
anticoagulate with IV heparin (bolus followed by constant infusion)
If not limb threatening then call the vascular surgeon for angioplasty, graft or endarterectomy
70
Dx of Arterial embolism? Gold std?
Angiography is considered the gold standard for diagnosis
ECG (looking for MI, AFib)
Echocardiogram (+/- ) looking for clot, MI, valve vegetation
71
Arterial embolism?
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
Arterial thrombosis? Common areas affected/
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
What is Atrial Fibrillation?
lose SA node signa to Av node results in atria spasms = sporaic waves, leads to Signaling AV node erractically;
74
Most common chronic tachydysrhythmia?
A fib
75
A-Fib rhythm ?
Rapid, irregularly irregular atrial rhythm
76
A-fibrillation rate?
>110 (a fib with rapid ventricular response), 70-110 controlled fib, rate <60 a fib with slow ventricular response
77
A-fibrillation P waves? EKG findings
No p waves ; ,
| irregular R-R intervals, usually narrow complex QRS
78
no clear P waves,
| irregular R-R intervals, usually narrow complex QRS
A-fibrillation?
79
A-fibrillation causes? (think pirates)
```
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
A-fib tx ? (generalized)
Rate control, sometimes rhythm control, prevention of thromboembolism
81
Rate control for A fib?
(<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
Rhythm control for A fib?
Anticoagulation + synchronized cardioversion (esp. HF or
hemodynamic compromise)
■ Antiarrhythmic drugs: Class Ia (eg. disopyramide), class Ic (eg.
flecainide) or class III (eg. amiodarone);
83
A-fib stable <48 hours?
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
A fib unstable>48 hours
Dilitazem/Esmolol (rate control), Heparin IV until TEE confirms thrombus; consider pharm cardio version; considered sedation & synchronized cardioversion
85
Unstable pt with rapid ventricular rate of A-fib?
Synchronized cardioversion
86
A-fib risk stratification ?
CHA DS 2 -VASc score ≥2 = high risk
87
What is CHADS2VAS
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
If you have a valvular dz + atrial fibrillation what do you use warfarin or direct thrombolytics ?
Warfarin, direct thrombolytics can not be used in valvular dz
89
Complications of Afib?
Formation of atrial thrombi → significant risk of embolic stroke
90
Regular, sawtooth pattern, atrial rate 250-350 BPM, narrow QRS complex
Atrial flutter
91
Atrial flutter occurs in?
Occasionally occurs in COPD, congestive heart failure, atrial septal defect, coronary artery disease
92
Atrial flutter?
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
Atrial flutter symptoms?
Palpitations, dyspnea, weakness, presyncope, exercise intolerance
94
Atrial flutter tx?
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
AF risk factors?
```
Hemodynamic stress
Atrial ischemia
Inflammation
Noncardiovascular respiratory causes
Alcohol and drug use
Endocrine disorders
Neurologic disorders
Genetic factors
Advancing age
```
96
AF occurs more in men or women?
Men
97
irregularly, irregular rhythm with a varying PR interval and various P wave morphologies (Three or more foci).
Multifocal atrial tachycardia
98
What is the difference btw A-fib and atrial flutter?
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
unstable AF tx?
Direct current synchoronized cardioversion
100
Stable AF tx?
Vagal , B blockeror calcium channel blocker
101
Definitive management of AF?
radio frequency ablation
102
NOAC-Non-vitamin K antagonist oral anticoagulants (NOAC) preferred? benefits? Examples?
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
When is Warfarin preferred (in AFib)? What is INR goal
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
What is the fastest way to rapidly lower the patient's INR in a bleeding pt on coumadin?
Fresh frozen plasma is the most rapid way to lower the patient's INR.
105
Antidote for overdose of warfarin (coumadin) but no bleeding
Protamine sulfate or Vitamin K
106
.
Left BBB is associated with more than RBB?
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
Left BBB ECG findings?
```
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
Right BBB ECG findings?
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
If the QRS complex is widened and downwardly deflected in lead V1 it is?
LBBB
110
If the QRS complex is widened and upward deflected in lead V1 it is?
RBBB
111
The ECG criteria for a left bundle branch block (LBBB) include:
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
The ECG criteria for a right bundle branch block include
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
General etiology for BBB? LBBB? RBBB?
Aging, HTN, CAD, cardiomyopathies, myocarditis, valvular heart
dz; Acute MI; Congenital heart dz ; cor pulmonale, pulmonary embolism
114
What is cardiac tamponade? Causes/etiology?
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
S/S of Cardiac tamponade
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
Dx of Cardiac tamponade?
Echocardiogram (best choice of test)
117
Tx of cardiac tamponade
removing fluid of heart=pericardiocentesis or pericardiotomy sx drainage
118
What is cardiogenic shock?
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
Causes of Cardiogenic shock?
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
s/s of Cardiogenic shock?
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
How is Cardiogenic shock dx?
Clinical, echocardiography
122
How is Cardiogenic shock tx?
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
What is Coronary artery dz?
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
What dz fall under CAD? Acute coronary dz includes what?
Angina's (stable, unstable, Prinzmetal variant angina), NSTEMI, STEMI & sudden death; Unstable, NSTEMI, STEMI
125
What is the prevention of CAD
Stop smoking, exercise, lose weight, healthy balance diet, statins, low sodium diet, control dm /htn/hld.
126
What is angina pectoris ?
Known as stable angina, partial obstruction of blood flow in coronary arteries, pain is relieved by rest & nitroglycerin & <30 mins,
127
Describes stable angina pattern?
Stable angina is a regular pattern of chest discomfort that occurs predictably
& reproducibly following physical or emotional stress
128
MC cause of stable angina?
Coronary artery artherosclerosis
129
What are the rf of stable angina?
Smoking, obesity, htn, dm, hld, sedentary, poor diet
130
s/s of angina pectoris
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
dx of angina pectoris
Normal EKG( no chest pain); During anginal pain-ST depressions and T inversions; Normal troponin
132
Tx for angina pectoris ; Tx for persistent angina pectoris or positive stress exam?
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
What a DVT?
Blood clot in deep vein of an extremitiy such as leg, calf, thigh , pelvis
134
What is the MC cause of PE?
DVT
135
s/s of DVT?
Asymetrical pain/ tenderness along deep vein, Asymetrical leg swelling >3 cm circumference, Asymetrical pitting edema, HOMAN'S SIGN + (edema, erythema, warmth)
136
RF? Etiology?
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
How to dx a DVT?
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
What is Virchow's triad?
1. Venous stasis (car rides/plane flight >4 hrs etc) 2. endothelia damage-lower leg injury 3. hyper coagulability: malignancy, pregnancy, oops
139
How is DVT treated? Prevention? Anticoagulation? Other methods?
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
Types of anticoagulation therapy for dvt?
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
Unfractionated heparin MOA? ; SE?
Potentiates antithrombin III, inhibits thrombin & other coagulation factors; Protamine sulfate antidote for heparin toxicity, heparin-induced thrombocytopenia
142
Warfarin MOA? Avoid?
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
Heart Failure: 4 types
```
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
What is Diastolic heart failure?
HF with preserved ejection fraction (EF) where LV filling pressure is impaired
→ diastolic dysfunction; EF can be normal or slightly ↓ (usually ≥50%)
145
Contributing/associated conditions of Diastolic heart failure?
Primarily seen in elderly patients, HTN,
| hypertrophic & restrictive cardiomyopathy
146
Sx/S of Diastolic heart failure?
Fatigue, dyspnea, orthopnea, exercise intolerance; JVD, S4, rales, peripheral
edema
147
Dx of Diastolic heart failure? TX?
Clinical; echocardiography
○ Tx: Directed at contributing factors (eg. HTN), pulmonary congestion &
peripheral edema (eg. diuretics), cardiac rehabilitation
148
What is Dilated Cardiomyopathy?Causes?
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
Dilated Cardiomyopathy CM? Complications?
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
Dilated Cardiomyopathy dx?
Clinical, increase BNP, ECG (LVH, non specific ST/T changes, LBBB); Transthoracic Echocardiogram (TTE): test of choice; diagnoses systolic/diastolic dysfunction;
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Dilated Cardiomyopathy Tx?
Removed underlying cause; Tx of HF and acute complications; LV assist Device/mechanical pump; Heart transplant in extreme cases
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What is Restrictive Cardiomyopathy? Etiologies?
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
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What is Restrictive Cardiomyopathy? Etiologies?
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
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TX of Restrictive Cardiomyopathy
Treat the CHF
| ● Transplant
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DX of Restrictive Cardiomyopathy
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
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What is Hypertrophic Cardiomyopathy? Causes?
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
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What is Hypertrophic Cardiomyopathy? Causes?
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.
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Hypertrophic Cardiomyopathy mumur? explanation? Maneuvers?
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
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S/s of Hypertrophic Cardiomyopathy?
Dyspnea, chest pain, syncope, fatigue, palpitations, ventricular dysythmias, sudden cardiac arrest, symptoms typically occur during physical activity or exertion
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Dx Hypertrophic Cardiomyopathy
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
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Dx Hypertrophic Cardiomyopathy
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
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What is Iliac artery occlusion? Difference from arterial embolism?
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
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MC cause of arterial embolism? other etiologies?
atherosclerotic plaque with associated thrombus formation (most common);
others include thrombosis of stent/graft, dissection or direct trauma to artery, embolus
from proximal source
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complications of arterial occlusion ?
limb-/life-threatening
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Mitral Regurgitation type of murmur? description? PE?
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
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Mitral Regurgitation causes?
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)
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What is Mitral Regurgitation
Valvular incompetency leading to retrograde flow of blood from left ventricle
through mitral valve into the left atrium during systole
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Mitral Regurgitation dx? tx?
clinical, echo ; In symptomatic patients, valve repair/replacement
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Most common valvular disorder in US
Mitral Regurgitation
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Revascularization is indicated when stenosis of the left main coronary artery is greater?
50%
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he most useful noninvasive procedure for diagnosis of ischemic heart disease and evaluation of angina
nuclear stress testing
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Four groups most likely to benefit from statin therapy are identified?
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%
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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?
yes
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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
sinus arrhtymia
