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DOC terminating SVT
Adenosine
side effects of adenosine
HA, flushing, SOB, chest pain, nausea
tx of Wolff-parkinson-white
radiofrequency catheter ablation

medical - procainamide, quinidine
drugs to avoid with Wolff-Parkinson-White
drugs active on the AV node (e.g., digoxin, verapamil, β-blockers) because
they may accelerate conduction through the accessory pathway. Type IA or IC

antiarrhythmics are better choices
what does the EKG look like with VTach
Wide & bizarre QRS complexes
does PSVT respond to vagal maneuvers or adenosine
yes
does VT respond to vagal maneuvers or adenosine
no
EKG findings on PSVT
Narrow QRS complexes with P waves
which may or may not be discernible,
depending on the rate.
tx for stable sustained VT pts
IV amiodarone, IV procainamide,
or IV sotalol
tx non-sustained VT in pt with underlying heart disease, a recent MI, evidence of left ventricular dysfunction, or is symptomatic
order an electrophysiologic study: If it
shows inducible, sustained VT,
ICD placement is appropriate
EKG Inferior leads
2, 3, avF
define  Cardiac arrest:
Sudden
loss of cardiac output;
potentially reversible if
circulation and oxygen
delivery are promptly
restored.
define  Sudden cardiac death:

Unexpected death within
1 hour of symptom onset
secondary to a cardiac
cause.
Where do narrow and wide complex tacchycardias originate and which is worse?
Narrow complex tachycardias originate above ventricles.

Wide complex tachycardias originate within ventricles and are more ominous because they are more likely to progress to VFib.
what is needed to convert VFib?
Drugs cannot convert VFib by themselves. Defibrillation is key, along with CPR & Epi.

Defibrillation generally does not work for asystole. Perform CPR & administer Epi.
Which antiarrhythmic agent is most effective in VFib?
IV amiodarone
DOC for sinus bradycardia?
Atropine

It can elevate the sinus rate by blocking vagal stimulation to the SA node
define sick sinus syndrome
persistent spontaneous sinus bradycardia
Pts usually elderly
first degree AV block
PR interval is prolonged (>0.20 second)
QRS complex follows each P wave
Delay is usually in the AV node.
Benign condition that does not require tx
Second degree AV block 

Mobitz type I (Wenckebach)
progressive prolongation of PR interval until a P wave fails to
conduct
b. Site of block is usually within the AV node
c. Benign condition that does not require tx
Second degree AV block 

Mobitz type II
P wave fails to conduct suddenly, without a preceding PR interval prolongation;
therefore, the QRS drops suddenly
b. Often progresses to complete heart block
c. Site of block is within the His-Purkinje system
d. Pacemaker implantation is necessary
Third degree (complete) AV block
Absence of conduction of atrial impulses to the ventricles; no correspondence
between P waves & QRS complexes
2. A ventricular pacemaker (escape rhythm) maintains a ventricular rate of 25-40 bpm
a. Characterized by AV dissociation
b. Pacemaker implantation is necessary.
most dilated cardiomyopathies are idopathic, what are other causes?
a. CAD (with prior MI) is a common cause
b. Toxic: Alcohol, doxorubicin, Adriamycin
c. Metabolic: Thiamine or selenium deficiency, hypophosphatemia, uremia
d. Infectious: Viral, Chagas disease, Lyme disease, HIV
e. Thyroid disease: Hyperthyroidism or hypothyroidism
f. Peripartum cardiomyopathy
g. Collagen vascular disease: SLE, scleroderma
h. Prolonged, uncontrolled tachycardia
i. Catecholamine induced: Pheochromocytoma, cocaine
j. Familial/genetic
anticoagulate a pt with dilated cardiomyopathy?
Anticoagulation should be considered because pts are at increased risk of embolization
HOCM systolic ejection murmur increase of decrease with: sustained hand grip?
Decreases due to increased SVR
leads to decreased gradient across
aortic valve
HOCM systolic ejection murmur increase of decrease with: valsalva and standing
Intensity increases due to decreased
LV size and thus increases the
outflow obstruction
HOCM systolic ejection murmur increase of decrease with:
squatting, lying down, or straight leg raise
Decreases due to decreased
outflow obstruction
HOCM symptomatic pts DOC and why
B-blockers because they reduce symptoms by improving diastolic filling (as HR decreases, duration in diastole increases), and also reduce myocardial contractility and thus oxygen consumption

CCB if B-blocker does not work  
rate control drugs for AFib
β-blocker or calcium channel blocker
causes of restrictive cardiomyopathy
1. Amyloidosis
2. Sarcoidosis
3. Hemochromatosis
4. Scleroderma
5. Carcinoid syndrome
6. Chemotherapy or radiation induced
7. Idiopathic
myocarditis causes
viruses (e.g., Coxsackie, parvovirus B19, human HSV-6)

bacteria (e.g., group A strep in rheumatic fever, Lyme disease, mycoplasma)

SLE

medications (e.g., sulfonamides)

can also be idiopathic
myocarditis labs
elevations in cardiac enzyme levels & ESR
define myocarditis
inflammation of the myocardium
define acute pericarditis
inflammation of the pericardial sac
causes of acute pericarditis
a. Idiopathic (probably postviral): Most are presumed to be postviral, preceded by flulike illness, URI or GI symptoms
b. Infectious: Viral (e.g., Coxsackievirus, echovirus, adenovirus, EBV, influenza, HIV, Hep A or B), bacterial (TB), fungal, toxoplasmosis
c. Acute MI (first 24 hours after MI)
d. Uremia
e. Collagen vascular diseases (e.g., SLE, scleroderma, RA, sarcoidosis)
f. Neoplasm—especially Hodgkin lymphoma, breast, & lung cancers
g. Drug-induced lupus syndrome - procainamide, hydralazine
h. After MI: (Dressler syndrome) — usually weeks to months after MI
i. After surgery—postpericardiotomy syndrome
j. Amyloidosis
k. Radiation
l. Trauma
4 cardinal manifestations of acute pericarditis
• Chest pain (pleuritis pain, pain with breathing, positional, made better by leaning forwards)
• Pericardial friction rub
• ECG changes—diffuse ST elevation; PR depression, T wave may invert
• Pericardial effusion (with or without tamponade)
acute pericarditis can develop into.... (2)
pericardial effusion 

cardiac tamponade
tx for acute pericarditis
1) NSAIDs
2) Colchicine is often used
3) glucocorticoids if above fails but try to avoid them
If a pt has clinical signs of cirrhosis
(ascites, hepatomegaly) &
distended neck
veins, perform
tests to r/o?
constrictive pericarditis
right sided MI hits which EKG leads and which tx to give
2, 3, avF

do NOT give nitrates because RV is PREload dependent
orthopnea
dypsnea when laying flat
3 symptoms of HF
dyspnea on exertion
orthopnea
paroxysmal nocturnal dyspnea
describe the 4 class of HF
1 - no symptoms
2 - no symptoms with activities of daily living
3 - symptoms with ALD
4 - symptoms all the time
tx's for the different stages of HF
1 - BB + ACE/ARB
2 - add loop diuretic
3 - add isosorbidedinitrate - hydralazine or spironolactone
4 - inotrope (dobutamine or milrinone) - going to die within a yr

ALSO if they are ischemic - need ASA + statin
Oligoarthritis
2-4 joints
polyarthritis
five or more joints
autoimmune dx's that present with alopecia
SLE
autoimmune dx's that present with dry eyes or mouth
necessary to diagnose Sjogren's syndrome. 

Dry eyes & mouth can also be seen in association with joint pain in RA, SLE, scleroderma, & Hep C.
autoimmune dx's that present with oral ulcers
SLE, Behcet's syndrome, Crohn's disease, and reactive arthritides.
autoimmune dx's that present with painful vaginal ulcers
typical in Behcet's syndrome.
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