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AnatomicPathophysiologic A p p ro a c h t o Hemodynamics: C o m p l e m e n t a r y Ro l e s of Noninvasive and Invasive Diagnostic Modalities
James A. Goldstein, MD*, Amr Abbas, MD
 Hemodynamics  Invasive diagnostic modalities  Noninvasive diagnostic modalities  Cardiovascular system

Symptoms and physical signs reflect distinct pathophysiologic derangements of anatomiccomponents and mechanics, a construct that serves as the foundation for clinical evaluation of the cardiovascular system.1–10 Evaluation of hemodynamic derangements should be based on interrogation of a cardiac anatomic-physiologic approach to circulatory pathophysiology. This article illustrates a pragmatic problem-solving approach to 3 cardinal hemodynamic symptoms and clinical syndromes: (1) rightheart failure (RHF), (2) dyspnea, and (3) low-output hypotension. This treatise focuses primarily on the complementary roles of noninvasive and invasive diagnostic studies in clinical hemodynamic assessment. The anatomicpathophysiologic foundations of this approach based on bedside physical examination have been previously published.1–6

CLINICAL ASSESSMENT BY ANATOMICPATHOPHYSIOLOGIC CORRELATESThe cardiovascular system can be simplistically viewed as a closed fluid system that obeys the

Division of Cardiovascular Medicine, William Beaumont Hospital, Royal Oak, MI, USA * Corresponding author. E-mail address: Cardiol Clin 29 (2011) 173–190 doi:10.1016/j.ccl.2011.01.004 0733-8651/11/$ – see front matter Ó 2011 Elsevier Inc. All rights

rules of hydraulics and physics. Cardiovascular hemodynamic syndromes reflect derangements of cardiac anatomy and physiology and may manifest as either forward or backward syndromes. Forward syndromes may be grouped as hypoperfusion syndromes, manifesting early as fatigue and later as organ failure attributable to inadequate cardiac output (CO); similarly, syncope results fromtransient profound hypoperfusion. Backward syndromes attributable to right heart dysfunction manifest as systemic venous congestion syndromes, including peripheral edema, gastrointestinal-hepatic congestion, and ascites, whereas left heart dysfunction results in pulmonary venous congestion manifest as shortness of breath (dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea). These symptomgroups in isolation are nonspecific. Identical complaints reflecting disparate pathophysiologic processes can occur because of a variety of mechanisms. For example, dyspnea is an expected symptomatic manifestation of pulmonary venous hypertension attributable to a spectrum of left heart derangements, the


Goldstein & Abbas
underlying mechanisms of which vary greatly (eg, mitral stenosis,mitral regurgitation [MR], left ventricular [LV] cardiomyopathy). The treatments and prognoses also vary greatly. Dyspnea is also commonly of pulmonary origin, with circumstances in which the heart may be completely normal or affected only as an innocent bystander (eg, cor pulmonale). Similarly, peripheral edema and ascites reflect systemic venous congestion resulting from a spectrum of RHFmechanisms (eg, tricuspid valve [TV] disease, right ventricular [RV] cardiomyopathies, pericardial disorders). However, edema may also develop under conditions with normal systemic venous pressures, as may occur in patients with cirrhotic liver disease, inferior vena caval compression, and so forth. Thus, for cardiovascular assessment symptoms and signs must be characterized according to the underlyinganatomic-pathophysiologic mechanisms, the next step to delineation of the specific cause. This approach can be applied to individual organ beds, such as the lung: D pulmonary blood pressure 5 CO Â pulmonary vascular resistance (PVR). Alternatively, from a perfusion perspective, the equation is transformed, whereby: CO 5 Dpressure/vascular resistance The key components of blood pressure can be...
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