Cardiology 2 Flashcards
Recall
Diseases presenting with high output HF (8)
Thyrotoxicosis
Obesity
Anemia
Beri beri
Myeloproliferative disorder
Chronic lung disease
Arteriovenous shunt
Cirrhosis
Most common cause of high output HF
obesity
Target resting heart rate range in chronic HF on GDMT
<70-75bpm
Abdominojugular test mechanism
Increase in right atrial pressure during 10 s of firm midabdominal compression followed by an abrupt drop on pressure release, suggests elevated left-sided filling pressures
Pathophysiologic link between sleep apnea and heart failure
Decreased preload
Increased afterload
Intermittent hypoxia
Sympathetic activation
Preferred drugcombination as a disease-modifying approach in HFrEF if unable to tolerate RAAS-based therapy
Hydralazine + nitrates
Contraindication of ARNI for HF
With prior history of angioedema
Note: If transitioning from ACEi, give ARNI with 36 hour gap to limit risk of overlap
Antiarrhythmic drug therapy preferred for atrial arrhythmias in HF
Amiodarone and Dofetilide
Appropriate candidates for ICD prophylactic therapy
NYHA II or III and LVEF < 35% irrespective of etiology
Single most important associated of extent of dyssynchrony
Widened QRS interval, particularly in the presence of a left bundle branch blck pattern
ECG findings in px that would benefit from CRT placement
QRS width of >149ms and a left bundle branch block pattern
MRA should be withdrawn how many weeks before measuring PA/PRA in work up for secondary hypertension
4-6 weeks
Two most common causes of sporadic primary aldosteronism
Aldosterone producing adenoma and bilateral adrenal hyperplacia
Tumor is most often unilateral, measures <3cm
BP lowering strategy in hypertensive urgency
By 25% of the initial value over 24h
IF with encephalopathy: reduce MAP by no more than 25% within MINUTES or 2 hours to a BP range of 160/100-110
Drug choice: IV nitroprusside; labetalol, nicardipine
Definition of SEVERE LV outflow obstruction in AS
mean systolic pressure gradient >40mmHg with a normal cardiac output or
aortic orifice area <1cm2
Moderate AS: valve area 1-1.5cm2
Mild AS: valve area 1.5-2cm2
Cardinal symptoms of AS
exertional dyspnea, angina pectoris, syncope
Murmur of AS
Low pitched, rough, rasping
Loudest at the base of the heart
Most commonly in 2nd right ICS
Tramitted along the carotid arteries, occasionally downward and to the apex
Ejection (mid) sIystolic murmur that commences shortly after the S1, increases in intensity to reach a peak toward the middle of ejection, and ends just before aortic valve closure
Indications for surgical treatment in AS
Severe AS (<1cm2 area or 0.6cm2/2 body surface area) who are symptomatic
Exhibit LV systolic dysfunction (EF<50%)
AS due to BAV disease and aneurysmal root or ascending aorta (max dimension >5.5cm)
Operation for aneurysm disease recommended
At small aortic diameters (4.5-5cm) with family history of an aortic catastrophe or
Rapid aneurysm growth (>0.5cm/year)
Murmur of aortic regurgitation
High-pitched, blowing, decrescendo diastolic murmur, heard best in the third intercostal space along the left sternal border
In isolated AR - mid systolic ejection murmur frequently audible (base of the heart and transmitted along the carotids)
Murmur in severe AR described a soft, low pitched, rumbling mid to late diastolic
Produced by diastolic displacement of the ANTERIOR leaflet of the mitral valve by the AR streatm
Austin Flint murmur
Characteristic echo finding in AR
Rapid, high-frequency diastolic fluttering of the anterior mitral leaflet produced by the impact of the regurgitant jet
Hemodynamic hallmark of MS
Abnormally elevated left atrioventricular pressure gradient
Definition of severe MS
<1.5cm2 orifice area
very severe: <1cm2
Murmur of MS
Opening snap os the mitral valve most readily audible in expiration at or just medial to the cardiac apex
Followed by low pitched rumbling diastolic murmur heard best at the apex
Eponym for a functional TR murmur that is due to pulmonary hypertension in MS
(pansystolic murmur produced by a functional TR that may be audible at the left sternal border, louder during inspiration and diminishes during forced expiration)
Carvallo’s sign
High pitched diastolic descresndo blowing murmur along the left sternal border that results from dilation of the PULMONARY valve ring (occurs in px with MITRAL valve disease and severe pulmonary hypertension)
Graham Steel murmur
MR associated with HOCM is dependent on:
systolic ANTERIOR motion of the ANTERIOR mitral valve into a narrowed LV outflow tract
Chronic severe MR is progressive due to
enlargement of LA places tension on POSTERIOR mitral valve leaflet
Murmur of MR
Most characteristic of chronic severe MR: systolic murmur at least grade III/IV, holosystolic, decrescendo and ceases in mid to late systole
Prominent at the apex and radiates to axilla
Wide but physiologic splitting of S2
Low pitched S3 after closure of aortic valve
Short rumbling mid-diastolic murmur
S4 often audible in patients with ACUTE severe MR
Severe PS defined by
Peak systolic gradient across the pulmonic valve of > 64mmHg (jet velocity >4m/s)
Moderate PS: 36-64mmHg (jet velocity 3-4m/s)
Mild PS <36mmHg (jet velocity <3m/s)
Hallmark of PR (PE)
High pitched decresendo diastolic murmur (Graham Steel) heard along the left sternal border - louder on inspiration
Common causes of HF with preserved EF
Aging, obesity, hypertension
Conditions that result to concentric hypertrophy (consequence of pressure overload)
Hypertension and AS
vs eccentric hypertrophy d/t volume overload - MR and AR
Microbial etiologies of nosocomial PVE (within 2 months of valve surgery)
S. aureus, CoNS, facultative gram-negative bacilli, diphtheroids, and fungi
Lifestyle Modifications to Manage Hypertension
- Weight reduction: BMI <25 kg/m2
- Dietary salt reduction: <6 g NaCl/d
- Moderation of alcohol consumption: ≤2 drinks/d in men and ≤1 drink/d in women
- Adapt DASH-type dietary plan: Diet rich in fruits, vegetables, and low-fat dairy products with reduced content of saturated and total fat. Diet is also rich in potassium, calcium, and magnesium.
- Physical activity: Regular aerobic activity, e.g., brisk walking for 30 min/d
Initial goal of therapy in malignant hypertension
reduce mean arterial blood pressure by no more than 25% within minutes to 2 h or to a blood pressure in the range of 160/100–110 mmHg
Most common gas exchange abnormalities in Pulmonary Embolism
arterial hypoxemia and an increased alveolar-arterial O2 tension gradient
Chest radiographic findings in pulmonary embolism
- focal oligemia (Westermark’s sign)
- peripheral wedge-shaped density usually located at the pleural base (Hampton’s hump)
- enlarged right descending pulmonary artery (Palla’s sign).
Most frequent cited ECG abnormality in pulmonary embolism
sinus tachycardia; S1Q3T3 sign: an S wave in lead I, a Q wave in lead III, and an inverted T wave in lead III
Effective anticoagulation strategies in venous thromboembolism
- waning strategy: parenteral anticoagulation with unfractionated heparin (UFH), low-molecular-weight heparin (LMWH), or fondaparinux “bridged” to warfarin
- parenteral therapy, switched after 5 days to a novel oral anticoagulant such as dabigatran (a direct thrombin inhibitor) or edoxaban (an anti-Xa agent)
- oral anticoagulation monotherapy with rivaroxaban or apixaban (both are anti-Xa agents) with a 3-week or 1-week load- ing dose, respectively, followed by a maintenance dose
***For patients with VTE in the setting of suspected or proven heparin-induced thrombocytopenia, one can choose between two parenteral direct thrombin inhibitors: argatroban and bivalirudin
Best-known indirect sign of PE on transthoracic echocardiography
McConnell’s sign: hypokinesis of the RV free wall with normal or hyperkinetic motion of the RV apex
Non cardiac causes of elevated BNP levels
advanced age, female sex, CKD
Condition that will give FALSELY LOW NT-pro BNP
Obesity
Treatment for patients unable to tolerate RAAS-based therapy in HFrEF
Hydralazine + Nitrates
Subset of patients with HFrEF that will benefit most from cardiac resynchronization therapy? (CRT)
Most benefit in mildly symptomatic HFrEF patients accrues from applying this therapy in those with a QRS width of >149 ms and a left bundle branch block pattern.
**Cardiac Resynchronization in Heart Failure Study (CARE-HF) trial was the first study to demonstrate a reduction in all- cause mortality with CRT placement in patients with HFrEF on opti- mal therapy with continued moderate-to-severe residual symptoms of NYHA class III or IV HF.
First line agents in reducing severity of obstruction in HOCM
Beta blockers and calcium channel blockers
Risk factors for postpartum cardiomyopathy
increased maternal age
increased parity
twin pregnancy
malnutrition
use of tocolytic therapy for premature labor
preeclampsia or toxemia of pregnancy
Preferred anti arrythmic agents for HCOM
Disopyramide and Amiodarone
Medication that should be avoided in HCOM
Digitalis glycosides
Maneuvers that intensify murmur of mitral valve prolapse?
Sudden standing and strain phase of valsalva
Chemotherapeutic agent that produces myocardial damage by causing recurrent coronary artery spasm leading to decreased myocardial contractility
5-FU, Cisplatin and other alkylating agents
Test to differentiate true severe AS (with a fixed small valve area) from pseudosevere AS (with a functionally small valve area due to severely LV systolic dysfunction)
low-dose dobutamine stress transthoracic echocardiography
Major determinants of myocardial oxygen demand
heart rate
myocardial contractility
myocardial wall tension
Determinant for adequate supply of oxygen
level of oxygen carrying capacity of blood determined by inspired oxygen, pulmonary function and hemoglobin concentration; level of coronary flow
Contraindications to exercise stress testing
rest angina within 48 h
unstable rhythm
severe aortic stenosis
acute myocarditis
uncontrolled heart failure
severe pulmonary hypertension
active infective endocarditis.
Suggestive of severe IHD during stress test
development of angina and/or severe (>0.2 mV) ST-segment depression at a low workload, i.e., before completion of stage II of the Bruce protocol, and/or ST- segment depression that persists >5 min after the termination of exercise
Clear contraindications to the use of fibrinolytic agents
- 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)
TIMI risk score for NSTE-ACS (7)
- age >65 yrs
- known CAD (>50% stenosis)
- ST deviation >0.5mm on presenting ECG
- increased cardiac markers
- > 2 original episodes in prior 24hrs
- prior angina
- > 3 CAD risk factors.
he case above has 3 of these risk markers and thus has a 13% (high risk) 14-days risk of death, new or recurrent MI or severe recurrent ischemia requiring urgent revascularization.
Relative contraindications to fibrinolytic therapy
- current use of anticoagulants (international normalized ratio ≥2)
- recent (<2 weeks) invasive or surgical procedure
- prolonged (>10 min) cardiopulmonary resuscitation
- known bleeding diathesis
- pregnancy
- hemorrhagic ophthalmic condition (e.g., hemorrhagic diabetic retinopathy)
- active peptic ulcer disease
- history of severe hypertension that is currently adequately controlled
Modified Duke Criteria for the Clinical Diagnosis of Infective Endocarditis
MAJOR:
1. Positive blood culture (two separate blood cultures)
OR
Persistently positive blood culture (blood cultures drawn >12 h apart; or all of 3 or a majority of ≥4 separate blood cultures, with first and last drawn at least 1 h apart
OR
Single positive blood culture for Coxiella burnetii or phase I IgG antibody titer of >1:800
- Evidence of endocardial involvement
MINOR
- Predisposition: predisposing heart conditions or injection drug use
- Fever ≥38.0°C (≥100.4°F)
- Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, Janeway lesions
- Immunologic phenomena: glomerulonephritis, Osler’s nodes, Roth’s spots, rheumatoid factor
- Microbiologic evidence: positive blood culture but not meeting major criterion, as noted previously,d or serologic evidence of active infection with an organism consistent with infective endocarditis
Organisms Causing Major Clinical Forms of Infective Endocarditis (IE)
Native Valve Community-Acquired IE: Streptococci
Native Valve Health Care Associated IE: Staph aureus
Prostatic valve IE <2 months: CONS
Prostatic valve IE 2-12 months: CONS
Prostatic valve IE >12 months: Streptococci
TAPVR PVE: Enterococci –> S. aures –> CONS
CIED IE: CONS
Indications for cardiac surgery in endocarditis
A. Surgery REQUIRED
- Moderate or severe congestive heart failure or shock due to valve dysfunction
- Paravalvular extension of infection with abscess, fistula, or heart block
- Persistent bacteremia without an extracardiac cause despite 7–10 days of optimal antimicrobial therapy
- Lack of effective antimicrobial therapy (e.g., fungal, Brucella, multidrug-resistant gram-negative bacillary endocarditis)
- Partially dehisced unstable prosthetic valve
- Paravalvular extension of infection with abscess, fistula, or heart block
Class I recommendation for permanent pacing in AV blocks
- Complete heart block (acquired)
- Advanced AV block
- Mobitz Type II
- Evidence for infranodal block
- Neuromuscular disease associated with progressive conduction tissue disorder
Class I indications for catheter ablation in symptomatic atrial fibrillation
- Paroxysmal or persistent AF and heart failure with reduced EF
- Persistent AF with FAILED drug therapy
