Cardiology Flashcards
Recall
Indications for permanent pacemaker insertion in sinus node dysfunction (5 items)
- Symptoms that are directly attributable to SND
- Symptomatic sinus bradycardia because of essential medication therapy for which there is no alternative treatment
- Tachy-brady syndrome and symptoms attributable to bradycardia
- Symptomatic chronotropic incompetence
- In patients with symptoms that are possibly attributable to SND, a trial of oral theophylline may be considered to increase heart rate and determine if permanent pacing may be beneficial
Class IIB recommendation if symptoms are likely/uncertain to correlate with bradycardia in sinus node dysfunction
Oral theophylline
Indications for permanent pacemaker implantation in AV block (regardless of symptoms)
Aquired Mobitz Type II, high grade AV block, third degree AV block that is not reversible or physiologic
Adjunct pharmacologic treatment for block in the AV node
Atropine or Isoproterenol
Indication for pacing in Mobitz I
Symptomatic (Class IIA)
Asymptomatic but with with neuromuscular disease associated with progressive conduction tissue disorder (Class I)
Regular atrial tachycardia with defined P wave; may be sustained, nonsustained, paroxysmal, or incessant; frequent sites of origin occur along the valve annuli of left or right atrium, pulmonary veins, coronary sinus musculature, superior vena cava
Focal atrial tachycardia (AT)
Commonly seen as sawtooth flutter waves at rates typically faster than 200 beats/min, macroreentry reflected as organized atrial activity on an electrocardiogram (ECG)
Atrial flutter and macroreentrant atrial tachycardia
The most common sustained cardiac arrhythmia in older adults; chaotic rapid atrial electrical activity with variable ventricular rate
Atrial fibrillation
Multiple discrete P waves often seen in patients with pulmonary disease during acute exacerbations of pulmonary insufficiency
Multifocal atrial tachycardia
Regular tachycardia with P waves visible at the end of the QRS complex or not visible at all; the most common paroxysmal sustained tachycardia in healthy young adults; more common in women
AV nodal reentry tachycardia (AVNRT)
ECG changes stage 1 in acute pericarditis
Widespread elevation of the ST segments, often with upward concavity, involving two or three standard limb leads and V2–V6, with reciprocal depressions only in aVR and occasionally V1
Depression of the PR segment below the TP segment, reflecting atrial involvement, an early change that may occur prior to ST segment elevation
ECG changes stage 2 in acute pericarditis (several days after stage 1)
ST segments return to normal
ECG changes stage 3 in acute pericarditis
T waves become inverted
ECG changes stage 4 in acute pericarditis
ECG returns to normal
Medical treatment for acute percarditis
Bed rest and anti inflammatory
Aspirin 2-4 g/day or
Ibuprofen 600-800mg/ TID or
Indomethacin 25-50mg/tab with Omeprazole 20mg/d
(over 1-2 weeks then tapered)
Colchicine 0.5mg qd (<70kg) or 0.5mg BID if >70kg x 3 months
If NSAIDS/colchicine not tolerated- prednisone 1mg/kg/day 2-4 days then tapered
JVP characteristics in cardiac tamponade
Prominent x, absent y
Which pericardial pathology presents with Kussmaul’s sign?
Constrictive pericarditis (also right ventricular MI, and to a lesser extent restrictive cardiomyopathy)
Pulsus paradoxus definition
Greater than 10mmHg inspiratory decline in SYSTOLIC arterial pressure
Present in cardiac tamponade
JVP characteristics in constrictive pericarditis
Prominent x AND y descent
Ventricular filling is impeded throughout the diastolic cycle (which percardial pathology)
Cardiac tamponade
vs chronic constrictive pericarditis - during early diastole ventricular filling is unimpeded and is reduce abruptly
Only definitive treatment for constrictive pericarditis
Pericardial resection
Pattern of congestive symptoms in DCM
Left before right, except right prominent in young adults
EF in DCM
usually <30%
vs restrictive: 40-50%
hypertrophic: >60%
Best known defective protein associated with DCM
Dystrophin
Most commonly recognized genetic cause of DCM
Truncating mutation of titin encoded by TTN
Most common toxin implicated in DCM
Alcohol
Most common drugs implicated in toxic cardiomyopathy
Chemotherapy agents
Threshold of serum iron and transferrin saturation to diagnose cardiac siderosis from hemochromatosis DCM
Men >60%
Women >45-50%
Most common restrictive cardiomyopathy
Amyloidosis
Proteasome inhibitor used for tx of AL amyloidosis
Bortezomib
First line agents used in hypertrophic cardiomyopathy
B blockers and L type CCB (e.g. verapamil) to slow heart rate, enhance diastolic filling, and decrease contractility
Preferred anti arrhythmic agents in hypertrophic cardiomyopathy
Disopyramide and amiodarone
Avoid cardiac glycosides (increases contractility and worsens obstruction)
Major determinants of myocardial oxygen demand (MVO2)
Heart rate, myocardial contractility, myocardial wall tension (stress)
Major determinant of coronary resistance
R2 prearteriolar vessels and R3 arteriolar and intramyocardial capillary vessels
Positive stress test (Ischemic ST segment repsonse)
Flat or downsloping depression of the ST segment >0.1 mV below baseline (i.e., the PR segment) and lasting longer than 0.08 s
Contraindications to exercise stress testing (7)
Rest angina within 48 h
Unstable rhythm
Severe aortic stenosis
Acute myocarditis
Uncontrolled heart failure
Severe pulmonary hypertension
Active infective endocarditis
Signs during noninvasive testing indicating HIGH risk for coronary events
Inability to exercise for 6 minutes (stage II Bruce protocol)
Strongly positive test at low work loads:
- >/= 1mV ST segment depression before completion of Stage II
- >/= 2mV ST segment depression at ANY stage
- ST segment depression that persists >5mins after cessation of exercise
Decline in systolic pressures >10mmHg during exercise
Development of ventricular tachyarrhythmia
Most important signs of LV dysfunction measured during cardiac catheterization
elevated LVEDP and ventricular volume and reduced ejection fraction
Used for chronic angina; inhibits late inward sodium current
Ranolazine
contraindicated in hepatic impairment
Choice of anti coagulant in AF patients post PCI (NSTEMI included)
Shortened DAPT - stop aspirin 4 weeks post PCI and continue p2Y12 inhibitor plus DOAC for 1 year (unless very high risk for ischemic events)
Diagnostic hallmark of Prinzmetal’s variant angina
Coronary angiography finding of transient coronary spasm
Main therapeutic agent in PVA
Nitrates and calcium channel blockers
CK rises within ___ hours and generally returns to normal by ___ hours
rises within 4-8 hours
normal by 48-72hrs
Recommended regimen of tPA (tissue plasminogen activator) for ACS-STE
15mg bolus followed by 50mg IV over the first 30 min followed by 35mg over the next 60 minutes
Recommended dose of Streptokinase for ACS-STE
1.5million units (MU) IV over 1 hour
Recommended dose of rPA (reteplase)for ACS-STE
Double-bolus regimen consisting of a 10-MU bolus given over 2–3 min, followed by a second 10-MU bolus 30 min later
Recommended dose of TNK (tenecteplase) for ACS-STE
TNK is given as a single weight-based intravenous bolus of 0.53 mg/ kg over 10 s
Clear contraindications for fibrinolytic agents (ACS-STE)
History of cerebrovascular hemorrhage at ANY TIME
A nonhemorrhagic stroke or other cerebrovascular event within the PAST YEAR
Marked hypertension (a reliably determined systolic arterial pressure >180 mmHg and/or a diastolic pressure >110 mmHg) at any time during the acute presentation
Suspicion of aortic dissection, Active internal bleeding (excluding menses)
Recommended dose of UFH in ACS-STE
60U/kg bolus (max 4000U) then infusion 12U/kg per hr (max 1000u/h). Target aPTT 1.5 to 2 x the normal value
Risk factors for ASCVD (8)
Male
Smoker
Hypertension ≥140/90 mmHg
BMI 25 kg/m2
Family history of premature coronary heart disease
Proteinuria
Left ventricular hypertrophy
Postmenopausal women
2 most common autosomal dominant genetic mutations involved in VTE
(1) Factor V Leiden, which causes resistance to the endogenous anticoagulant activated protein C (which inactivates clotting factors V and VIII), and
(2) the prothrombin gene mutation, which increases the plasma prothrombin concentration
Most common gas exchange abnormalities in PE
Arterial hypoxemia
Increased alveolar-arterial O2 tension gradient
Pathophysiologic abnormalities in PE (5)
Increased pulmonary vascular resistance
Impaired gas exchange
Alveolar hyperventilation
Increased airway resistance
Decreased pulmonary compliance
Most common ECG abnormality in PE
T wave inversion in leads V1 to V4 (due to RV strain and ischemia)
Acute DVT - compression stockings maintained at
30-40mmHg or 20-30mmHg
replaced every 3 months
UFH dose for DVT/PE
Initial bolus of 80U/kg followed by infusion rate of 18U/kg
3 strategies for anticoagulation in DVT/PE
1) LMWH or fondaparinux bridged to warfarin
2) parenteral x 5 days then NOAC (direct thrombin inhibitor e.g. dabigatran or factor Xa inhibitor e.g. edoxaban)
3) oral rivaroxaban or apixaban with 3 week and 1 week loading dose respectively then maintenance
Choice of anticoagulant in patients with suspected/proven HIT
Argatroban and bivalirudin (direct thrombin inhibitors)
Management of bleeding d/t warfarin
Prothrombin complex concentrate (best)
Less serious bleeding: may give fresh frozen plasma or IV vitamin K
Management of bleeding d/t heparin or LMWH
Protamin sulfate
Management of bleeding d/t Dabigatran
Idarucizumab
Two principal indications for IVC filter insertion
(1) active bleeding that precludes anticoagulation and (2) recurrent venous thrombosis despite intensive anticoagulation
First line vasopressor and inotropic agents in massive PE
NE and dobutamine
Claudication characteristically involves the buttocks, thighs, and calves and may be associated with impotence in males
Leriche’s syndrome
Used to determine whether varicose veins are secondary to deep-venous insufficiency
Brodie-Trendelenburg test
As the patient is lying supine, the leg is elevated and the veins allowed to empty. Then, a tourniquet is placed on the proximal part of the thigh and the patient is asked to stand. Filling of the varicose veins within 30 s indicates that the varicose veins are caused by deep-venous insufficienc
