Flashcards in Heart Deck (15):
acute decompensated heart failure.
- dyspnea, orthopnea, elevated jugular venous pressure, lower extremity edema, and lung crackles
- tx: Loop diuretics (furosemide, torsemide, bumetanide) act by inhibiting the Na-K-2Cl symporter in the luminal membranes of the thick ascending limb of the loop of Henle
——-blocks Na+ and Cl- reabsorption from the tubular lumen, decreasing the medullary concentration gradient
——impairs the kidney's ability to concentrate urine, causing increased excretion of Na+, Cl-, and H2O.
——adverse effects of loop diuretics include hypokalemia, volume depletion, and ototoxicity.
- complication of endocarditis
- local destruction and dilation of an arterial wall due to infection.
- patient's heavy smoking history, progressive exertional dyspnea, and physical examination findings are suggestive of chronic obstructive pulmonary disease (COPD) caused by chronic bronchitis/emphysema.
- his right ventricular dilation and elevated central venous pressure are indicative of cor pulmonale secondary to COPD.
- increased central venous pressure predisposes him to developing noninflammatory edema- This condition is characterized by excess accumulation of transudative fluid in the interstitial tissues
- have elevated levels of aldosterone in response to decreased cardiac output and renal hypoperfusion
Right heart failure increases central venous pressure (CVP), which leads to a rise in capillary hydrostatic pressure, net plasma filtration, and interstitial fluid pressure.
- As the interstitial fluid pressure increases, so does lymphatic drainage, which can compensate for moderate CVP elevations and prevent the development of clinically apparent edema.
- Large CVP elevations can overwhelm lymphatic reabsorptive capacity, leading to the development of overt edema.
- causes blood to back up in the systemic venous circulation due to decreased cardiac output.
- This increases pressure within the liver
orthostatic (postural) hypotension
- drop in blood pressure on standing from the supine position (>20 mm Hg systolic and/or >10 mm Hg diastolic).
- Standing causes pooling of a significant amount of blood (500-1000 mL) into the veins below the heart.
- This initiates the following sequence of events in otherwise healthy individuals:
1. Decreased venous return to the heart
2. Decreased ventricular filling and subsequent drop in cardiac output
3. Drop in blood pressure that evokes compensatory baroreceptor reflex
4. Increased sympathetic tone that increases peripheral vascular resistance (α1-adrenoreceptors) as well as heart rate and myocardial contractility (β1-adrenoreceptors)
left ventricular (LV) volume overload/failure
Cardiac auscultation in this patient reveals a low-frequency sound occurring after S2, known as the third heart sound (S3)
- Although the S3 can be normal in young individuals and pregnant patients, its presence in those age >40 is typically a sign
- In early diastole, the ventricles relax and the atrioventricular valves open, allowing blood to rush in and fill the ventricles
- an S3 develops with forceful rapid passive filling that exceeds the expansion capacity of the ventricle leading to sudden deceleration of the entering blood column and reverberation of the ventricular walls
Aortic valve sclerosis
midsystolic ejection murmur
- Progression to severe aortic stenosis may eventually produce an S3 indicative of LV
accumulation of large quantities of pericardial fluid prevents the expansion of the ventricular free walls.
- During inspiration, venous blood return increases and the intraventricular septum bulges into the left ventricle to allow the right ventricle to accommodate the increased blood volume.
- resultant decrease in LV filling volume causes pulsus paradoxus (>10 mm Hg decrease in systolic blood pressure during inspiration).
- cause dynamic LV outflow obstruction, producing a crescendo-decrescendo ejection systolic murmur.
- outflow obstruction can also cause systolic anterior motion of the mitral valve, resulting in mitral regurgitation (holosystolic murmur).
Elevated pulmonary arterial pressure (pulmonary hypertension)
present with exertional dyspnea and fatigue and eventual right ventricular failure (elevated jugular venous pressure, peripheral edema).
- most commonly presents as dyspnea and exercise intolerance in women aged 20-40
- px’s positive FH is s/o the familial form of PAH which is most often caused by inactivating mutations involving the pro-apoptotic BMPR2 gene.
- the increase in endothelial and smooth muscle cell prolif leads to vascular remodeling, elevated pulmo vascular resistance and progressive pulmo hypertension
auscultation will show increased intensity of the pulmonic closure sound (P2), and affected patients typically lack nocturnal dyspnea due to intact LV function.
- causes specific morphologic findings in the branches of the pulmonary artery, including increased arteriolar smooth muscle thickness (medial hypertrophy), intimal fibrosis, and significant luminal narrowing.
In the setting of severe hypertension, lesions can progress to form interlacing tufts of small vascular channels called plexiform lesions.
- lung transplant is the definitive tx but vasodilators are effective for improving sx
carotid sinus hypersensitivity,
multiple episodes of lightheadedness while buttoning a tight shirt collar
- triggered by pressure on the carotid sinus by a tight shirt collar.
- carotid sinus baroreceptors are important in blood pressure control and use arterial wall stretch as an indicator of systemic blood pressure.
- carotid sinus is a dilation of the internal carotid artery located just above the bifurcation of the common carotid artery.
- The carotid sinus reflex has an afferent limb that arises from the baroreceptors in the carotid sinus and travels to the medullary centers via the Hering nerve, a branch of the glossopharyngeal nerve (CN IX).
efferent limb of the carotid sinus carries parasympathetic impulses via the vagus nerve (CN X).
- Carotid sinus pressure or massage stimulates the baroreceptors and increases the firing rate from the carotid sinus, leading to an increase in parasympathetic output and withdrawal of sympathetic output to the heart and peripheral vasculature.
- The result is decreased blood pressure (via peripheral vasodilation) and decreased cardiac output (decreased contractility/stroke volume and heart rate).
In sensitive individuals, this response can cause severe bradycardia, hypotension, and sometimes syncope.
Acute rheumatic fever (ARF)
- immune-mediated complication of an untreated group A streptococcal pharyngeal infection
- most serious manifestation of ARF is pancarditis, which can cause nonspecific fever, fatigue, and anorexia as well as altered vital signs (tachycardia, tachypnea, hypotension)
- Endocardial involvement resulting in valvular dysfunction (specifically acute mitral valve regurgitation) is the most likely cause of the patient's new holosystolic murmur.
- This patient's myocardial biopsy shows interstitial fibrosis with central lymphocytes and macrophages as well as scattered multinucleated giant cells
This interstitial myocardial granuloma, or Aschoff body (encircled), is pathognomonic for ARF-related myocarditis.
Plump macrophages with abundant cytoplasm and central, slender chromatin ribbons called Anitschkow (or caterpillar) cells are also often present.
Over subsequent years, Aschoff bodies are replaced by fibrous scar tissue, leading to chronic mitral valve stenosis and regurgitation.
results from an autoimmune reaction to a medication, is characterized by an interstitial infiltrate of eosinophils. Many classes of drugs, including diuretics (eg, furosemide, hydrochlorothiazide) and antibiotics (eg, ampicillin, azithromycin), can cause this hypersensitivity
hypertrophic cardiomyopathy (HCM).
- genetic mutation involving sarcomere genes
- leads to left ventricular hypertrophy and, in turn, both systolic and diastolic dysfunction.
- involves disorganized, hypertrophied myocytes.