Cardiovascular Flashcards
What is the most likely diagnosis?
Abdominal aortic aneurysm (AAA).
What are the major branches of the aorta below the diaphragm?
Blood flow to the major organs is of special concern with an AAA. The inferior phrenic arteries, celiac trunk, middle suprarenal arteries, renal arteries, superior mesenteric artery, testicular arteries, inferior mesenteric artery, lumbar arteries, and the common iliac arteries are located below the diaphragm.
What is the three-layer composition of muscular arteries?
An increased risk of AAA is associated with defects in the genes coding for which proteins?
Once the aortic wall is disrupted in AAA, how does coagulation proceed?
What are the risk factors for AAA?
What are the treatment options for AAA?
What is the most likely diagnosis?
Aortic stenosis.
What factors increase the risk of Aortic stenosis?
What type of murmur is caused by Aortic Stenosis?
How is Aortic Stenosis associated with congestive heart failure (CHF)?
What complications are associated with Aortic Stenosis?
What is the appropriate treatment for Aortic Stenosis?
What is the most likely diagnosis?
What risk factors increase a person’s likelihood of developing Stable angina?
What is the pathophysiology of stable angina?
Endothelial injury resulting from various factors, including hyperlipidemia, smoking, and hypertension, can lead to monocytic and lipid infiltrates into the subendothelium (fatty streaks), release of growth factors leading to smooth muscle cell proliferation into the intima (proliferative plaque), and subsequent development of foam cells and complex atheromas with calcification and ischemia of the intima.
Which arteries are most commonly affected in stable angina?
Atherosclerosis preferentially affects the branching points of arteries or areas of turbulent blood flow including the proximal coronary arteries, popliteal arteries, renal arteries, carotid arteries, and arteries of the circle of Willis.
What complications are commonly associated with stable angina?
In addition to angina, other complications of atherosclerotic injury include aneurysms, myocardial infarction, stroke, ischemia, and ischemic bowel disease.
What are the 3 major forms of angina?
1. Stable angina: Chest pain with exertion; responds to nitroglycerin.
2. Unstable angina: Chest pain at rest secondary to thrombus in a branch. May not completely respond to
nitroglycerin; antithrombic agents and heparin may also be required.
3. Prinzmetal angina: Chest pain at rest, secondary to coronary artery spasm. Treatment includes calcium
channel blockers.
What is the likely diagnosis?
Atrial fibrillation.
What clinical and electrocardiographic abnormalities are commonly associated with AF?
Lightheadedness, palpitations, anxiety, pallor, and diaphoresis are commonly associated with atrial fibrillation. Likewise, as in this patient, heart rate is elevated and borderline hypotension is possible. Electrocardiogram (ECG) shows an absence of P waves, irregular R-R intervals, and tachycardia, as in this patient. Irregularly irregular uncoordinated atrial contractions can lead to tachycardia and stasis of blood in the left atrium; the development of clot within the heart often ensues.
What is the appropriate treatment for AF?
How do heparin and warfarin work together to treat AF?
Given intravenously, heparin activates antithrombin III. Its effectiveness is determined by partial thromboplastin time (which reflects activity of the intrinsic pathway). Given orally, warfarin impairs the synthesis of vitamin K–dependent clotting factors (II, VII, IX, and X). It is monitored by prothrombin time (extrinsic pathway).
Why does paradoxical coagulation sometimes occur after starting warfarin therapy?
Warfarin also inhibits the synthesis of protein C and protein S. Because proteins C and S inhibit factors Va and VIIIa, a deficiency in these proteins promotes coagulation.
What is the most likely diagnosis?
Cardiac myxoma of the left atrium. Most myxomas arise from the mural endocardium and measure 1–15 cm.
What is the epidemiology of Cardiac myxoma?
Primary tumors of the heart are rare. Myxomas account for approximately 50% of benign tumors in the heart. The majority (75%) are located in the left atrium, although all chambers can be affected. The typical age of onset is 30–60 years. Familial occurrences have been reported in approximately 5% of cases via autosomal dominant transmission. These are associated with a younger age of presentation and higher rates of recurrence.
What are 3 complications of left atrial myxomas?
Complications from left atrial myxomas can be categorized as follows:
1. Embolization occurs in 40%–50% of cases with tumor fragments lodging in distal organs (eg, brain, heart, or extremities).
2. Infection is rare but may lead to further complications with embolization.
3. Obstruction of the mitral or pulmonary venous orifices may occur, resulting in pulmonary hypertension
and right heart failure.
How can the results of the cardiac examination be explained?
Splitting of S1 is accentuated as the tumor is extruded from the mitral orifice. P2 can also be louder if the tumor obstructs the mitral orifice or pulmonary venous return. The third heart sound is produced by the tumor “plopping” within the atrium during diastole.
What pathology does the ECG in Figure 5-5 depict?
Second-degree atrioventricular (AV) block type I, also known as Mobitz type I block or Wenckebach block. Progressive lengthening of the PR interval from one beat to the next is seen until finally a beat is dropped (a P wave is not followed by a QRS complex).
What is the pathophysiology of Mobitz type I block (Wenckebach block)?
Second-degree AV block type I occurs secondary to impaired conduction at the level of the AV node, such that atrial impulses fail to reach the ventricles. Given the location of the patient’s prior MI, it is possible that it may have compromised the conductive ability of his AV node. An MI involving the right coronary artery may disrupt blood supply to the sinoatrial [SA] node and atrioventricular [AV] node. By contrast, involvement of the left anterior descending coronary artery causes infarction of the His-Purkinje system.
How is Heart Block classified?
What is the appropriate treatment for Mobitz type I block (Wenckebach block)?
Often, no treatment is necessary in asymptomatic patients with a second-degree Mobitz type I block. In symptomatic patients, atropine or isoproterenol may be used, or a pacemaker may be required.
What is the most likely diagnosis?
Coarctation of the aorta occurs two to five times more often in males than in females.
In Coarctation of the aorta, which part of the aorta is typically affected?
What is the characteristic finding on physical examination in patient’s with coarctation of the aorta?
Auscultation over the chest and/or back may reveal a midsystolic ejection murmur. A continuous murmur over the chest may also be heard in older individuals who have developed collateral circulation. Weak, delayed pulses in the lower extremities are also characteristic of coarctation.
What chromosomal abnormality is associated with Coarctation of the aorta?
Coarctation of the aorta is associated with Turner syndrome (45,XO).
What findings on physical examination, ECG, and x-ray of the chest often develop over time in patients with Coarctation of the aorta?
What is the most likely diagnosis?
This constellation of clinical findings, including cardiac manifestations, a “blueberry muffin” rash, and the maternal history strongly suggest congenital rubella syndrome (CRS). Rubella virus (RV) is an RNA virus of the Togaviridae family, and it is associated with an 85% risk of congenital defects if acquired in the first 12 weeks of pregnancy. Other infections acquired in utero that can present with rash and ocular findings can be recalled with the ToRCHeS acronym: Toxoplasmosis, other infections, Rubella, Cytomegalovirus infection, Herpes simplex, and Syphilis.
What laboratory test in the neonate can help confirm this diagnosis?
Congenital Rubella Syndrome (CRS)
What laboratory test in the neonate can help confirm the diagnosis of congenital rubella syndrome?
Viral culture of nasal secretions or monthly serology testing for anti-rubella IgM antibody with rising titers can establish a laboratory CRS diagnosis.
What cardiac anomalies are associated with the murmur seen in this patient?
What other symptoms are common in patients with congenital rubella syndrome (CRS)?
Primary rubella infection early in pregnancy results in defective organogenesis. The classic permanent abnormalities include cataracts, retinopathy, heart defects, and sensorineural deafness. Transient abnormalities include meningoencephalitis, thrombocytopenia with or without purpura, and bony radiolucencies. Since CRS is a persistent infection, more abnormalities, such as developmental difficulties and progressive panencephalitis, can occur.
What is the appropriate treatment for congenital rubella syndrome (CRS)?
Since no therapy currently exists for CRS, the focus is on prevention through vaccination. Rubella vaccine contains live, attenuated rubella virus and therefore is contraindicated in pregnant women. Rubella has been eliminated in the United States and Scandinavia but persists elsewhere because of inadequate vaccination programs.
Which area of the heart is affected by this obstruction?
The LAD runs along the anterior interventricular (IV) groove and supplies the anterior right and left ventricles as well as the anterior IV septum. The LAD is the most common coronary artery to become occluded.
From what vessel does the LAD originate?
The left main artery bifurcates, in most people, to the LAD and the circumflex artery (Figure 5-9).
What are the branches of the right coronary artery (RCA), and what territories do they supply?
The RCA first travels in the atrioventricular (AV) groove then wraps around the inferior border of the heart to the posterior IV groove. In 80% of people, the SA nodal artery is the first branch of the RCA. Other branches of the RCA include the right marginal, posterior descending (in 80% of people) and AV nodal arteries.
During which part of the contraction cycle do coronary arteries fill?
The coronary arteries have maximal blood flow during diastole and minimal flow during systole. This is due to their location above the cusps of the aortic valve, which obstructs flow into the coronary arteries when the valve opens during systole.
What biomarkers indicate myocardial injury?
Creatine kinase (CK) is an enzyme that is found in muscle tissue throughout the body and may become elevated from damage to muscle cells. Elevated CK levels are not specific to myocardial infarction (MI) and may be seem in rhabdomyolysis, myocarditis, and myositis. CK-MB is an isoenzyme of CK that is expressed in higher levels in cardiac muscle and is thus more specific for myocardial necrosis. Cardiac troponin I and T are sensitive and specific markers of damage to the heart.
What is the timing of biomarker release after myocardial injury?
CK levels rise within 4–8 hours, peak at 12–24 hours, and return to baseline by 4 days. The CK-MB isoenzyme curve peaks slightly earlier and is cleared within 48 hours. Troponin I and T may be detected as early as 2 hours after MI but usually rise by 6 hours, peak at 12 hours, and return to baseline by 7–10 days, making the test useful to identify patients with delayed presentations of MI.
What is the most likely diagnosis?
Left heart failure (LHF) is evidenced by orthopnea, paroxysmal nocturnal dyspnea, dyspnea on exertion, and mild edema.
What are the common causes of Left heart failure (LHF) ?
Hypertension, myocardial infarction, valvular heart disease, myocarditis, and cardiomyopathies are associated with the development of LHF.
What symptoms help differentiate right heart failure from left heart failure?
Right heart failure is characterized by compromised venous return. This can manifest as ascites, significant edema of the lower extremities, jugular venous distention, and hepatosplenomegaly secondary to liver and spleen congestion.
This patient is at risk for which other conditions?
LHF is the most common cause of right heart failure. In addition, her history of smoking increases her risk for chronic lung disease. This can lead to cor pulmonale, characterized by right ventricular hypertrophy and failure due to pulmonary congestion in patients with lung disease or pulmonary hypertension. Emphysema is commonly associated with cor pulmonale.
What are the likely findings on gross pathology?
Hemosiderin-laden macrophages in the lung are commonly seen in LHF. If LHF leads to right heart failure, patients may develop chronic passive liver venous congestion (called nutmeg liver). Congestion in the central region of the hepatic lobule causes deposition of red/brown pigment from blood cells and can lead to centrilobular necrosis.
What is the most likely diagnosis?
Deep venous thrombosis (DVT) is most common in the lower extremities. Hospitalized patients are at high risk for DVT and the associated complications of pulmonary embolism. Risk of DVT is higher in surgical patients than medical patients and is particularly high for patients who have had hip or knee surgery.
How is VTE diagnosed?
The level of D-dimer, a fibrin degradation product, is often elevated in DVT. Assays for D-dimer are highly sensitive and have a low false-negative rate in symptomatic patients. A negative D-dimer test therefore may exclude DVT in low-risk patients. In DVT-prevalent populations (eg, surgical patients), additional tests may be used to diagnose or confirm DVT, especially deep venous ultrasonogram with examination for the flow abnormalities (that would be present with a thrombus). Other tests include MRI and venography.
In what conditions other than DVT is D-dimer elevated?
D-dimer may be elevated in a number of inflammatory conditions including liver disease, autoimmune disease, malignancy, surgery, and in elderly patients. D-dimer therefore has a low specificity for DVT.
What is the most likely diagnosis?
Dilated cardiomyopathy (DCM) is defined as a left ventricular (LV) EF < 40% and a ventricular chamber with increased diastolic and systolic volumes. In this patient, it is likely of ischemic etiology. DCM is a major cause of congestive heart failure in young people. Males and African Americans are at an increased risk for DCM.
What is the pathogenesis of Dilated cardiomyopathy (DCM)?
After an MI, it is hypothesized that the reduced peripheral (particularly renal) perfusion leads to fluid retention in an attempt to increase cardiac output. This ultimately results in cardiac remodeling. Figure 5-10 shows the relationship between renin- angiotensin and autonomic nervous system activation and cardiac myocyte cell death.
What is the most likely diagnosis?
Acute endocarditis caused by Staphylococcus aureus. The man’s new heart murmur suggests a possible valvular lesion as the source of infection. In this case, a Gram stain that demonstrates gram-positive organisms in clusters suggests staphylococci.
What is the most likely diagnosis?
Hypertrophic cardiomyopathy (HCM) is suggested by the patient’s age, symptoms, family history of sudden death (a common presentation in young people with HCM), murmur, and ECG findings. It is characterized by the overgrowth of myocardium with myocardial disarray.
How should the ECG findings in Figure 5-11 be interpreted?
What is the classic murmur associated with Hypertrophic cardiomyopathy?
What additional symptoms would indicate an emergent situation?
Blood pressure goals in most patients are < 140/90 mm Hg; the goal is lower in patients with diabetes or other comorbid conditions. Hypertensive urgency is characterized by severely elevated blood pressure (systolic > 180 mm Hg or diastolic > 110 mm Hg) without evidence of end-organ damage. Hypertensive emergencies are characterized by severely elevated blood pressure with signs of end-organ damage including mental status changes, stroke, myocardial infarction, and renal failure.
What is the primary treatment for this condition?
Lifestyle modification is attempted before pharmacologic therapy is undertaken. This includes moderate dietary sodium restriction, weight reduction in obese patients, avoidance of smoking and excess alcohol intake, increased fruit and vegetable intake, and regular aerobic exercise.
What is the initial pharmacologic therapy of choice for hypertension?
The initial pharmacologic therapy of choice is a thiazide diuretic, which inhibits sodium chloride reabsorption in the distal tubule, thereby promoting diuresis. Compared to other classes of diuretics, these drugs are equally effective and less expensive. Chlorthalidone has the longest half-life and the best evidence to support its use. Hydrochlorothiazide is also frequently used.
What is the most likely diagnosis?
Kawasaki disease (mucocutaneous lymph node syndrome). Commonly presents with fever lasting > 5 days, erythematous rash (Figure 5-12), edema in the conjunctivae, lips, and mouth (“strawberry tongue”), palmar and solar erythema, cervical lymphadenitis, and mucositis.
What is the most likely diagnosis?
Mitral valve prolapse (MVP), a condition found in 0.6%–2.4% of the population, is the most common valvular heart disease. Most cases are asymptomatic and discovered incidentally. However, left atrial enlargement may occur, resulting in occasional benign supraventricular arrhythmia that the patient perceives as palpitations. Men and women are affected equally. MVP is defined by the echocardiographic measurement of the superior displacement of one or both mitral leaflets into the left atrium (LA).
What is the most likely diagnosis?
Chest pain that occurs at rest is commonly seen in unstable angina, subendocardial infarction, and transmural infarction. However, only unstable angina presents without damage to the myocardium, and hence does not produce a troponin leak. In this condition, the flow of a coronary vessel is limited to the extent that it cannot meet the metabolic demand of the heart, but it does not cause death of myocardial tissue. Rest and dilation of the coronary vessels (nitroglycerin) improve the pain. Given his history of coronary heart disease, unstable angina is most likely.
How can ECG studies differentiate between ischemia, subendocardial infarction, and transmural infarction?
Inverted T waves and pathologic Q waves occur once the infarction progresses (Figure 5-13A). In the event of a subendocardial infarction, the subtotal occlusion of the feeding artery allows the epicardial side of the myocardium to remain viable while the endocardial side is starved of nutrients. Subendocardial infarctions appear as inverted T waves without ST-segment changes on ECG. Stable and unstable angina pectoris lead to ST-segment depression in at least two contiguous leads (Figure 5-13B). Transmural infarction features ST-segment elevation > 1 mm in at least two contiguous leads.
What is the most likely diagnosis?
Acute myocardial infarction (AMI) most often results from a thrombotic event in a coronary artery due to plaque rupture. Myocardial tissue dies (infarction) if perfusion is not reestablished.
What complications are associated with an acute MI?
What is the most likely diagnosis?
Pericarditis often presents with diffuse ST-segment elevation, positional chest pain, and friction rub. The latter is due to inflammation of the pericardium, resulting in decreased production of lubrication. The typical friction rub has three phases (atrial contraction, ventricular contraction, and ventricular relaxation).
What is the most likely diagnosis?
The patient’s severe gastrointestinal symptoms that are out of proportion to the physical signs elicited suggest mesenteric ischemia. Given the sudden onset, this is most likely a thrombotic event. Ischemia affecting the small bowel initially presents with severe pain; peritoneal signs develop later. Ischemia of the large bowel is less painful and typically presents with hematochezia.
What composes the arterial supply of the intestines?
The superior mesenteric artery (SMA) supplies part of the duodenum and part of the head of the pancreas (the territory of inferior pancreaticoduodenal artery), jejunum, ileum, ascending colon, and proximal two-thirds of the transverse colon. The inferior mesenteric artery (IMA) supplies the hindgut, which includes the distal third of the transverse colon, the descending colon, the sigmoid colon, and the rectum. This is schematically shown in Figure 5-15.
What is the most likely diagnosis?
Patent ductus arteriosus (PDA) is indicated by the characteristic continuous “machine-like” murmur and physical examination.
What is the most likely diagnosis?
This patient has polyarteritis nodosa with palpable purpura and other common symptoms such as weight loss, inflammatory markers, and evidence of vasculitis in her retina.
What other small to medium vasculitides could this patient have?
Churg-Strauss syndrome is a variant of polyarteritis nodosa characterized by eosinophilia and asthma. Autoantibodies mostly target blood vessels in the lungs, but in the late stage other organ systems can become involved (including the skin). Wegener granulomatosis features ANCAs that damage blood vessels in the upper respiratory tract and kidney. However, it can also involve joints, skin, and the gastrointestinal tract.
What is the most likely diagnosis?
This patient has rheumatic heart disease. Mitral stenosis (fish-mouth buttonhole deformity) is often seen in patients with previous rheumatic fever infection. This disease primarily affects the mitral and aortic valves; involvement of tricuspid and pulmonary valves is rare. This condition is not commonly seen in the United States.
What is the most likely diagnosis?
Biopsy of the temporal artery reveals temporal arteritis. An elevated erythrocyte sedimentation rate and elevated C-reactive protein levels are nonspecific markers associated with temporal arteritis.
What is the most likely diagnosis?
Tetralogy of Fallot (TOF) (cyanotic congenital heart disease known as “blue baby syndrome”) presents as dyspnea on exertion, such as feeding or crying. Exertion results in systemic vasodilation, which lowers left-sided resistance, thereby increasing the right-to-left shunting of blood. Bypass of oxygen exchange in the lungs causes hypoxia and cyanosis. Squatting significantly increases systemic (left-sided) resistance, reducing the amount of blood shunted and alleviates symptoms.
Which developmental defect is responsible forTetralogy of Fallot?
In TOF, the infundibular septum (the portion of the septum adjacent to the outflow tracts) is anteriorly and superiorly displaced during development, leaving a hole in the ventricular septum (Figure 5-17). This displacement also causes pulmonary stenosis by blocking flow to the pulmonary artery; the result is increased pressure on the right side of the heart and right ventricular hypertrophy.
What is the most likely diagnosis for this condition?
Truncus arteriosus (TA) accounts for 1% of congenital cardiac malformations. It is also associated with DiGeorge syndrome, as is the case in this patient.
What is the characteristic anatomy in Truncus arteriosus (TA)?
The TA is the embryologic precursor that normally separates into the aorta and pulmonary artery by formation of the spiral septum. Persistent TA is caused by failure of the spiral septum to develop and thereby failure of aorta and pulmonary artery to septate. Normally, neural crest cells that are present in the TA grow in a spiral formation, separating the two outflow tracts and forming the intertwined aorta and pulmonary artery. If this septum fails to form, a single outflow tract persists (Figure 5-19A). A ventricular septal defect (VSD) is always present; lack of a VSD in the setting of TA is incompatible with life and results in stillbirth. Instead of separate aortic and pulmonary valves, there is one truncal valve with two to six leaflets (leading to the characteristic absence of S2 splitting). Surgical repair of these defects is required for survival (Figure 5-19B).
What are the reasons for this patient’s symptoms?
The clinical presentation depends on the amount of pulmonary flow. High pulmonary flow ultimately increases arterial oxygen saturation, reducing risk of cyanosis. However, this patient likely has low pulmonary flow; this results in central cyanosis and earlier presentation with congestive heart failure, which is indicated by the tachycardia and respiratory distress.
What is the most likely diagnosis?
Wolff-Parkinson-White (WPW) syndrome (also known as preexcitation syndrome).
What is the most likely diagnosis?
Wegener granulomatosis. Necrotizing granulomatous vasculitis of small and medium-sized vessels leads to manifestations in the kidney and lungs (Figure 5-21).
What laboratory test can help establish a diagnosis of Wegener granulomatosis?
The presence of C-ANCA is associated with Wegener granulomatosis, which must be differentiated from Goodpasture syndrome, an autoimmune disorder that also presents with hemoptysis and renal disease (Table 5-2). Instead of C-ANCA antibodies, Goodpasture syndrome features anti–glomerular basement membrane antibodies (anti-GBM).
What other findings are common in patients with Wegener granulomatosis?
Perforation of the nasal septum (the so-called “saddle-nose” deformity; Figure 5-22), chronic sinusitis, mastoiditis, cough, hemoptysis, hematuria, and RBC casts are common findings in patients with Wegener granulomatosis. See Table 5-2 for the distinguishing features of Wegener granulomatosis and Goodpasture syndrome.
