Cardiothoracic Flashcards
Suspect this in a baby with stridor and episodes of respiratory distress with “crowing” respiration, during which the baby assumes a hyperextended position. They also have some difficulty swallowing.
Vascular rings exerting pressure on the tracheobronchial tree and esophagus. (Ps If only the respiratory symptoms are present, one should think of tracheomalacia.)
How is a morphological cardiac anomaly best diagnosed?
Echocardiogram
What PE characteristics will be observable when the heart has a left-to-right shunt?
Presence of a murmur, overloading of the pulmonary circulation, and long term damage to pulmonary vasculature
Suspect this in a patient with a minor, low-pressure, low-volume shunt. Patients typically grow into late infancy before it is recognized. A faint pulmonary flow systolic murmur and fixed split second heart sound are characteristic. A history of frequent colds is elicited.
Atrial septal defect
What will happen with Small, restrictive ventricular septal defects low in the muscular septum
Will produce a heart murmur, but otherwise few symptoms. They are likely to close spontaneously within the first 2 or 3 years of life.
Suspect this in a patient who in the first few months has a “failure to thrive,” a loud pansystolic murmur best heard at the left sternal border, and increased pulmonary vascular markings on chest x-ray.
Ventricular septal defect
Suspect this in a pt who becomes symptomatic in the first few days of life. There are bounding peripheral pulses and a continuous “machinery-like” heart murmur.
Patent ductus arteriosus
What can you use to achieve closure of a patent ductus arteriosus, provided the baby is premature and hasn’t gone into CHF.
Indomethacin
How do you fix a baby with a PDA who is full term, in CHF, or failed to close with indomethacin?
Surgical division (or embolization with coils)
What PE characteristics will you see in a right-to-left shunt?
Murmur, diminished vascular markings in the lung, and cyanosis
Although this heart anomaly is crippling, it often allows children to grow up into infancy. It is also the most common cyanotic anomaly, and thus any exam question in which a 5- or 6-year-old is cyanotic is bound to be this.
Tetralogy of Fallot
Suspect this in a 5 or 6 year old who is small for their age, have a bluish hue in the lips and tips of their fingers, clubbing, and spells of cyanosis relieved by squatting. There is a systolic ejection murmur in the left third intercostal space, a small heart, diminished pulmonary vascular markings on chest x-ray, and EKG signs of right ventricular hypertrophy.
Tetralogy of Fallot
Suspect this diagnosis in a 1- or 2-day-old child with cyanosis who is in deep trouble.
Transposition of the great vessels
How are babies with transposition of the great vessels kept alive for as long as they are?
Atrial septal defect, ventricular septal defect, or patent ductus (or a combination). But they die very soon if not corrected.
This heart condition produces angina and exertional syncopal episodes. There is a harsh midsystolic heart murmur best heard at the right second intercostal space and along the left sternal border.
Aortic stenosis
This heart condition produces wide pulse pressure and a blowing, high-pitched, diastolic heart murmur best heard at the second intercostal space and along the left lower sternal border, with the patient in full expiration.
Chronic aortic insufficiency
In what kind of patient might you see acute aortic insufficiency?
Young drug addicts, due to endocarditis
Suspect this in young drug addicts who suddenly develop congestive heart failure and a new, loud diastolic murmur at the right second intercostal space.
Acute aortic insufficiency s/p endocarditis
This heart condition produces dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, cough, and hemoptysis. There is a low-pitched, rumbling diastolic apical heart murmur. As it progresses, patients become thin and cachectic and develop atrial fibrillation.
Mitral stenosis
What history is associated with mitral stenosis?
Rheumatic fever, many years before presentation
Suspect this in a pt with exertional dyspnea, orthopnea, and atrial fibrillation. There is an apical, high-pitched, holosystolic heart murmur that radiates to the axilla and back.
Mitral regurgitation
When is surgical intervention for coronary disease indicated?
If one or more vessels have 70% (or greater) stenosis and there is a good distal vessel. Preferably, the patient should still have good ventricular function (you cannot resuscitate dead myocardium). The general rule is the simpler the problem, the more it is amenable to angioplasty and stent; whereas more complex situations do better with surgery.
Suspect this in a pt w/ dyspnea on exertion, hepatomegaly, and ascites, and shows a classic “square root sign” and equalization of pressures (right atrial, right ventricular diastolic, pulmonary artery diastolic, pulmonary capillary wedge, and left ventricular diastolic) on cardiac catheterization.
Chronic constrictive pericarditis
What are the chances that a coin lesion found on x-ray is malignant in a pt over 50?
80%, more if he’s a smoker
First thing to do w/ a pt who has a coin lesion in the lung on chest x-ray
Look at older chest x-rays. If coin lesion is unchanged, it’s not cancer and you don’t have to do the work up for cancer
After new coin lesion or infiltrate on chest X-ray makes you suspect lung cancer, what two non-intrusive tests should be ordered?
Sputum cytology and CT scan (including chest and liver)
Tx of small cell cancer of the lung
Chemoradiation. Operability and possibility of surgical cure applies only to non-small cell cancer.
Operability of lung cancer is predicated on what factor?
Residual lung function after resection. (Assuming pneumonectomy is required. For lobectomy, function is of an issue. Central lesions require pneumonectomy. Peripheral lesions can be removed with lobectomy.) A minimum FEV1 of 800 mL is needed.
Potential cure by surgical removal of lung cancer depends on what factor?
Extent of metastases. Hilar metastases can be removed with pneumonectomy, but nodal metastases at the carina or mediastinum preclude curative resection.
Risk Factors for Myocardial Infarction (MI)?
Increased age, male, hypertension, hypercholesterolemia, diabetes, smoking, and family history of coronary artery disease
Classic presentation of an MI
Chest pain, diaphoresis, anxiety, tachycardia, tachypnea, and nausea/vomiting are classic findings. If there is a large area of ischemic damage to the heart, the patient may have heart failure presenting with bilateral rales (pulmonary edema), jugular venous distention, new S3 or S4 heart sounds, new murmurs, and hemodynamic instability (i.e., cardiogenic shock).
Three types of acute coronary syndrome
Unstable angina (UA), non-ST segment elevation myocardial infarction (NSTEMI), and ST segment elevation myocardial infarction (STEMI).
This kind of acute coronary syndrome is characterized as a nonocclussive thrombosis caused by reduced myocardial perfusion, but no myonecrosis (death of cardiac myocytes), hence no elevation in cardiac enzymes
Unstable Angina (UA)
This type of acute coronary syndrome is characterized as an occlusive thrombosis that eliminates perfusion to only partial thickness of the myocardial wall and (affects the subendocardial side) and causes myonecrosis leading to elevation in cardiac enzymes and possibly ECG findings suggestive of ischemia (but not ST segment elevation)
NSTEMI
This type of acute coronary syndrome is characterized as Occlusive thrombosis which eliminates perfusion to full thickness of the myocardial wall and causes myonecrosis leading to elevation in cardiac enzymes and characteristic elevation of ST segment on EC
STEMI
Most commonly affected coronary artery in acute coronary syndromes
Left anterior descending (LAD) artery
What Is Suggested by Episodic Chest Pain Unrelated to Exertion in a Young Person?
Prinzmetal angina. Coronary artery vasospasms are responsible for transient decreased perfusion to the heart which causes reversible injury to myocytes. ECG shows ST segment elevation secondary to transmural ischemia, similar to what is seen in unstable angina. However, Prinzmetal angina is not due to coronary artery disease.
Work up for suspected MI
12-lead ECG and a blood test for cardiac enzymes.
What cardiac enzymes should you look for after a suspected MI?
Troponin-1 and CKMB
What Is the Best Cardiac Enzyme to Diagnose a Second MI on Top of a Recent MI?
CKMB, because it subsides quickly, so it will rise again if another MI follows the first by 2-3 days
What coronary artery was affected when you see ECG changes in leads V2, V3, and V4?
Left anterior descending artery
What coronary artery was affected when you see ECG changes in leads aVL, V5, V6?
Circumflex branch
What coronary artery was affected when you see ECG changes in leads II, III, aVF?
Posterior descending artery
What can you do surgically to reperfuse the heart after a STEMI?
Best is clot removal and stenting in a cath lab, called percutaneous coronary intervention (PCI). Must be done within 90 minutes of onset of symptoms. If it’s been longer than 90 minutes, do a coronary artery bypass graft (CABG).
Which artery is best to use for the graft artery in CABG?
The (left) internal mammary artery (greater than 95 % of these arteries are patent at 10 years when attached to the LAD)
Management of Prinzmetal angina
Since the etiology of the chest pain is due to transient coronary vasospasms, calcium channel blockers are typically used to treat the underlying cause while nitroglycerin is used to rapidly decrease the chest pain.
What Is the Significance of an S4?
It is most frequently heard in patients that have left ventricular hypertrophy
Three classic symptoms of aortic stenosis
angina, syncope, and congestive heart failure (CHF)
This physical exam finding is where the amplitude of a peripheral pulse changes from beat to beat associated with changing systolic blood pressure.
Pulsus Alternans. It is most commonly caused by left ventricular failure.
“Biphasic pulse”, refers to two strong systolic pulses with a midsystolic dip. In other words, two pulses during systole.
Pulsus bisferiens. Can be seen in aortic regurgitation with or without aortic stenosis and hypertrophic cardiomyopathy.
Presentation and findings of endocarditis
Fever, valvular regurgitation, Petechiae, Splinter hemorrhages, Osler nodes, Janeway lesions, Roth spots
Aortic sclerosis vs Aortic stenosis
Both are caused by calcification of the aortic valve.
Sclerosis = minimal/no restriction of aortic valve motion (asymptomatic).
Stenosis = significant restriction of aortic valve motion (symptomatic).
Aortic sclerosis may progress to aortic stenosis.
What drives the chest pain on exertion during aortic stenosis?
High myocardial wall tension coupled with left ventricular hypertrophy increases myocardial oxygen demand which is further
compromised by decreased diastolic coronary blood flow.
What drives dyspnea on exertion during aortic stenosis?
The thickened/ischemic left ventricle gets stiffer and requires higher filling pressures to maintain end-diastolic volume. This in turn leads to increased pulmonary venous pressures and sensation of dyspnea.
Workup for aortic stenosis
Labs (electrolytes, coag panels, cardiac biomarkers) and ECG. Chest x-ray also accepted.
Suspect this in a patient with a systolic crescendo-decrescendo murmur loudest at the upper right sternal border and an S4
Aortic stenosis
Definitive treatment for aortic stenosis
Surgical valve replacement
Suspect this in a patient with sudden onset severe tearing chest pain radiating to the upper back. Pt appears tall and thin, w/ long arms, fingers, and hypermobile joints. Early diastolic murmur at the left upper sternal border and muffled heart sounds. ECG demonstrates nonspecific ST segment changes. Troponin and CK-MB are within normal ranges. A chest x-ray demonstrates a widened mediastinum.
Aortic dissection with acute aortic insufficiency, s/p marfan syndrome
Risk factors for aortic dissection
Hypertension (most common), connective tissue disease (e.g., Marfan’s, Ehlers-Danlos), advanced age, atherosclerosis, pregnancy, cocaine use, aortic injury (e.g., trauma, cardiac catheterization), bicuspid aortic valve), and aortic coarctation.
What Is the Significance of Uneven Pulses in the Upper and Lower Extremities in Patients with Aortic Dissection?
Provides a clue as to the location of the dissection. An upper extremity pulse discrepancy suggests a dissection involving the aortic arch; a lower extremity pulse discrepancy suggests involvement of the descending aorta.
What is an aortic dissection?
A progressive separation of the aortic wall that results from a tear in the intima that progresses into the media, essentially splitting the aorta into an inner layer of intima and inner media and an outer layer of outer media and adventitia. This produces two lumens: a true lumen and a false lumen.
Why Are Patients with Marfan’s Syndrome at Increased Risk for Aortic Dissection?
Marfan’s is a connective tissue disease that has an autosomal dominant mode of transmission. Its primary defect involves the misfolding of fibrillin proteins, which can result in cystic medial necrosis of large vessels such as the aorta. The subsequently weakened medial wall is left susceptible to dissection.
Stanford classification of aortic dissections
Stanford type A involves the ascending aorta (more common in Marfan’s). Stanford type B does not involve the ascending aorta, but is distal to where the left subclavian branches off (more common overall).
First imaging for any patient who presents with acute chest pain. What might you see in a pt w/ aortic dissection?
Chest X-ray. Aortic dissection may show a widened mediastinum. F/u w/ a chest CT with intravenous contrast.
What imaging should be ordered for a patient who is hemodynamically unstable with a suspected aortic dissection?
Hemodynamically unstable patients suspected of having a type A aortic dissection should be taken to the OR immediately, without chest CT scan, for surgical intervention. Transesophageal echocardiography (TEE) can be performed in the operating room while the patient is under general anesthesia and if confirmatory, surgery can begin immediately
FIRST step in managing an aortic dissection?
Keep BP low (100-110) with IV beta-blockers, since HTN is what drives pathology.
Management (after beta-blockers) of a pt w/ type-A aortic dissection
Urgent OR for repair w/ median sternotomy.
Management (after beta-blockers) of a pt w/ type-B aortic dissection
Admit to ICU and monitor BP. Surgery is reserved for pts who develop complications (e.g. malperfusion syndrome) or rapidly expanding false lumen.
Contraindications to treating aortic dissection with beta-blockers
Cardiac tamponade and aortic regurgitation; beta-blockers will worsen hypotension and may precipitate cardiac arrest.
