Cardio. NBME 10 and 11, mehl. Cardio bullets (HF, MI) Flashcards
NBME 10. 20Q. Pneumonia + ischemic cardiomyopathy + Temp 38.8°C, pulse 100/min, RR 22/min, BP128/74 mm Hg. SpO2 88%. Crackles are heard in the middle lobe of the right lung. There is no edema of the lower extremities. A chest x-ray shows a right middle lobe infiltrate. His ejection fraction is 30%. Which of the following is the most appropriate intravenous fluid maintenance therapy?
No intravenous fluids are indicated
In patients with heart failure, cirrhosis, and end-stage renal disease, physicians are often reluctant to provide adequate fluid resuscitation because of concerns about volume overload. In this patient who is presenting without hypotension, no intravenous fluids are indicated at this time. His volume-depleting and blood pressure- lowering medications should be held, and he should be admitted to the hospital for antibiotics and monitoring.
NBME 10. 20Q. Pneumonia + HrEF. When fluids would be indicated?
Is distributive shock present: tachy, low BP, tachypnea, leukocytosis/leukopenia.
Risk for mortality is greater for patients who do not receive adequate fluid resuscitation if evidence of hypoperfusion is present, such as hypotension, altered mental status, or abnormal laboratory chemistry values indicating organ dysfunction.
NBME 10. 20Q. Pneumonia + HrEF –> lets say progress to shock. Fluids?
If the patient develops hypotension or presents with evidence of impaired perfusion, initial fluid resuscitation in the setting of sepsis can be accomplished with a variety of crystalloid and colloid solutions.
Isotonic crystalloid solutions such as 0.9% saline (Choice D) or lactated Ringer solution are preferred because of their low cost, high availability, and demonstrated efficacy
NBME 10. 20Q. Hypotonic solutions such as 5% dextrose in 0.45% saline (Choice A) can be used to Tx what?
hypernatremia
NBME 10. 21Q. 64y/o + SOB+ nausea+ vomiting+ BP 90/50 + HR 64 + RR 22. EKG: II, III, aVF ST elevation. Dx? What drug is contraindicated?
Dx = right ventricular myocardial infarction (RVMI).
Contraindicated: nitroglycerin
NBME 10. 21Q.
Why Cardiac rhythm disturbances are common in RVMI?
result of impaired perfusion to the sinoatrial and atrioventricular nodes.
NBME 10. 21Q. Patients with RVMI become exceptionally preload-dependent because of the impaired function of the right ventricle.
!!! NBME 10. 21Q. RVMI = management?
I/V fluids to maintain adequate cardiac output and avoidance of preload- lowering medications such as nitrates and opioid analgesics, which are commonly used to treat angina.
Coronary reperfusion with percutaneous coronary intervention (PCI), or fibrinolytics if PCI is unavailable, should be performed as soon as possible.
Negalima nitroglycerin + morfin. Kitas gydymas = kaip left MI
!!! NBME 10. 21Q. RVMI (cia tas pats Mx ir left MI)
Early anticoagulation with heparin (Choice A), dual antiplatelet therapy, and statin therapy such as with simvastatin (Choice D) improve morbidity and mortality.
Reperfusion, particularly via PCI, is indicated as soon as possible.
Fibrinolytics such as streptokinase (Choice E) may be used in settings where timely PCI is not available.
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!!! NBME 10. 21Q. RVMI and fluids?
Optimization of right ventricular preload with intravenous fluids, such as 0.9% saline, is also particularly important in the management of RVMI to maintain adequate cardiac output.
!!! NBME 10. 21Q. RVMI = 2 contraindicated?
Nitrates and opioids since the right ventricle is highly preload- dependent.
NBME 10. 43Q. 77y/o palpitations for the past month + 2DM + Her pulse is 120/min and irregularly irregular, and blood pressure is 135/78 mm Hg. Crackles are heard at the lung bases. A grade 2/6 systolic murmur is heard best at the lower left sternal border. Leg edema. Afib ventricular rate: between 90/min and 140/min. EF 40 proc.
Lab: Ht 37 proc.; leu 4,7k; urea nitrogen 27; creat 1,4. next step in management?
Measurement of serum thyroid-stimulating hormone concentration
NBME 10. 43Q. afib. CP? 2 in general
Can be asymptomatic
Symptoms with rapid ventricular response include palpitations, fatigue, shortness of breath, light-headedness, angina, and presyncope or syncope.
NBME 10. 43Q. Afib, what confirms the diagnosis?
ECG with an irregular RR interval and absent P wave
NBME 10. 43Q. Afib. Physical examination will demonstrate what?
Irregularly irregular pulse and occasionally may show signs of heart failure or a heart murmur.
patients can fall while walking.
NBME 10. 43Q.
Risk factors for the development of atrial fibrillation include hypertension, coronary artery disease, structural heart or valvular disease, pulmonary embolism, lung disorders such as OSA or COPD, stimulant abuse, and hyperthyroidism.
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NBME 10. 43Q. Afib complications? 3
Tachycardia-induced heart failure, hemodynamic instability, and left atrial appendage thrombus formation with subsequent embolic strokes.
NBME 10. 43Q. Patients with a new diagnosis of atrial fibrillation should receive evaluation for what?
Evaluation for potentially reversible causes with measurement of serum thyroid-stimulating hormone concentration and screening for high-risk amounts of alcohol intake
NBME 10. 43Q. afib Tx?
Treatment includes heart rate control with β-adrenergicblockers or nondihydropyridine CCB, such as metoprolol or diltiazem, and anticoagulation for patients at an increased risk for stroke, which can be assessed by using a validated tool such as the CHA DS -VASc score.
NBME 10. 43Q. afib access risk for stroke?
Can be assessed by using a validated tool such as the CHA DS -VASc score.
NBME 10. 43Q. kiti ats. Tilt test used to Dx what?
evaluation of presyncope, syncope, and unexplained falls to identify a vasovagal or orthostatic cause. Patients typically report symptoms with changes in position.
NBME 10. 43Q. kiti ats. 24-Hour ambulatory ECG monitoring, for what?
can be useful for evaluation of reported palpitations, presyncope, syncope, and unexplained falls in a patient with an unrevealing office examination.
for this patient: is not required with an established diagnosis of atrial fibrillation observed on ECG in the office.
NBME 10. 43Q. kiti ats. Electrophysiologic studies (Choice D) may be considered when?
later in the patient’s management if her atrial fibrillation is refractory to medical management and/or catheter ablation is considered.
NBME 10. 43Q. kiti ats. cardiac pacemaker, indications?
Sinus node dysfunction, symptomatic bradycardia, and high-grade atrioventricular block.
NBME 10. 43Q. Afib. Patients should initially be evaluated for hemodynamic stability and potential need for hospitalization, symptoms of heart failure, potential underlying causes (including structural heart disease, electrolyte disturbances, hyperthyroidism, and chronic alcohol or stimulant use)
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NBME 10. 65Q. Typical MI Dx. Chest pain + low BP, tachy, crackles, ST depression and LBBB. Q was what Dx?
MI
NBME 10. 65Q. Use of NSAIDs, even for short durations, is associated with an increased risk for acute myocardial infarction.
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NBME 10. 65Q. typical MI.
Significant left ventricular dysfunction may result in cardiogenic pulmonary edema with shortness of breath, tachypnea, hypoxemia, audible rales, and S3 or S4 gallop.
NBME 10. 65Q. typical MI, Tx?
Antiplatelet agents (eg, aspirin, clopidogrel) plus anticoagulants (eg, heparin), pain control, and revascularization through angioplasty, thrombolysis, or coronary artery bypass grafting.
For patients who cannot receive percutaneous coronary intervention in a timely manner, thrombolytics are indicated. Thrombolytics such as tissue plasminogen activator function by catalyzing the formation of plasmin from plasminogen. Plasmin is a serine protease that cleaves fibrin clots.
NBME 10 143Q. Typical decompensated HF case. no need to revise. The major causes of new-onset decompensated heart failure include ?
acute coronary syndrome, myocarditis, acute or progressive valvulopathy, toxin- and stress- induced cardiomyopathy, and hypertensive crisis.
NBME 10 143Q. Typical decompensated HF case. CP –> what work up need to do?
Routine laboratory testing, cardiac biomarkers, ECG, chest x-ray, and echocardiography
NBME 10 143Q. Typical decompensated HF case. In case was murmur 2/6 harsh, late-peaking, systolic murmur heard best at the upper right sternal border. WHAT PATHOLOGY?
Have been worsening over the past year is concerning for progressive aortic stenosis, which is best evaluated with echocardiography.
NBME 10 143Q. Typical decompensated HF case + aorta stenosis murmur. Next step in determing Dx?
ECHOCARDIOGRAPHY (To detect stenosis)
NBME 11 64Q. typical decompensated HF presentation. What is decreased?
Stroke volume index
NBME 11 64Q. typical decompensated HF presentation.
The hemodynamic profile of acute decompensated HF is characterized by a decreased stroke volume index caused by severe dysfunction of cardiomyocytes resulting in markedly decreased contractility.
NBME 11 64Q. typical decompensated HF presentation.
Pulmonary artery catheterization: increased CVP and increased PCWP secondary to systolic dysfunction and impaired forward flow of blood.
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NBME 11 64Q. typical decompensated HF presentation.
Systemic vascular resistance is ….?
increased as a physiologic attempt to maintain mean arterial pressure for peripheral perfusion as the cardiac output falls.
NBME 11 64Q. typical decompensated HF presentation. kitas ats. (tarp kurio rinkaus)
Shunt fraction (Qs/Qt) (Choice C) describes the fraction of blood flow that does not participate in gas exchange during a circulatory cycle. The presence of pulmonary edema decreases the effective alveolar surface area that can participate in gas exchange, and the shunt fraction would be expected to increase.
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NBME 11 198Q. flu like illness + S3 + pedal edema. Dx?
Dilated cardiomyopathy (secondary to viral myocarditis).
NBME 11 198Q. flu like illness + S3 + pedal edema. EVALUATION?
x-rays (pulmonary edema) and echocardiography (decreased fraction) can support this diagnosis with cardiomegaly
NBME 11 198Q. flu like illness + S3 + pedal edema. Viruses?
coxsackievirus B, parvovirus B19, human herpes virus-6 (HHV-6), adenovirus, and HIV infections.
NBME 11 198Q. flu like illness + S3 + pedal edema. Mx?
Treatment is generally supportive as most cases remit with time.
Some patients may require diuresis, and depending on severity, mechanical or pharmacologic inotropic support or transplant.
NBME 11 198Q. kiti ats. Restrictive cardiomyopathy 2 causes?
amyloidosis or sarcoidosis
typically have chronic or subacute presentations, not acute heart failure such as with viral myocarditis.
NBME 11 198Q. kiti ats. Hypertrophic cardiomyopathy CP?
Can be asymptomatic, may present with syncope on exertion, or may present with signs of heart failure as in this patient, but typically in a subacute or chronic course. Patients may also have exertional chest pain or arrhythmias.
On examination, a systolic murmur can be heard because of left ventricular outflow tract obstruction.
NBME 10 110Q. A previously healthy 32-year-old man comes to the office because of a 6-month history of palpitations, fatigue, and shortness of breath on exertion. He also has had occasional chest pain after eating large meals. He appears healthy and is not in acute distress. His pulse is 88/min, respirations are 12/min, and blood pressure is 138/86 mm Hg. Carotid pulses are forceful. Cardiac examination shows a left ventricular lift. An S4 gallop and grade 3/6, harsh, systolic crescendo-decrescendo murmur are heard best at the lower left sternal border and apex. Results of Valsalva maneuver (tarp S1 ir S2 su valsalva intensyveja crescendo-decrescendo, nu tipo schema piramides formos) and ECG are shown (left deviation). Which of the following is the most likely diagnosis?
Hypertrophic obstructive cardiomyopathy
kiti ats: aortic sclerosis/stenosis; mitral regurg/stenosis
NBME 10 110Q. HOCM typical CP?
Dyspnea, chest pain, syncope, or sudden cardiac death, often in an exercising young athlete with a potential family history of a similar event.
NBME 10 110Q. HOCM - pulses?
Laterally displaced point of maximal impulse and a systolic murmur loudest in the lower left sternal border because of left ventricular outflow tract obstruction
NBME 10 110Q. HOCM how changes murmur with valsalva?
Becomes louder with the Valsalva maneuver, which decreases left ventricular filling and worsens the outflow tract obstruction.
murmur schema: S1 - systolic crescendo decrescendo - S2
NBME 10 110Q. HOCM. Kiti ats: Aortic sclerosis (thickening of the aortic valve).
Blood flow through a narrowed aortic valve characteristically results in a crescendo-decrescendo systolic murmur best heard at the upper right sternal border that gets softer with Valsalva maneuver.
Sclerosis may or may not progress to clinically significant aortic stenosis (Choice B).
NBME 10 110Q. HOCM. Kiti ats: Mitral regurgitation. murmur?
holosystolic murmur best heard in the left fourth or fifth intercostal space along the midclavicular line with radiation to the left axilla.
NBME 10 110Q. HOCM. Kiti ats: Mitral stenosis. murmur?
opening snap followed by a diastolic rumble, which is loudest over the cardiac apex, and radiates to the axilla.
