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Ventricular Hypertrophy LVH

The potential presence of LVH is identified by an increase in the QRS voltage (Fig. 5.10), this is due to the increased muscle mass of the hypertrophied left ventricle (Fig. 5.11). There are many different scoring systems and criteria identified in the texts for detecting LVH (e.g. Romhilt-Estes scoring system, Sokolow-Lyon criteria, Cornell criteria, etc.). For the purpose of this introductory text, only two methods are shown, one using the limb leads and the other using the chest leads. [Pg.70]

The S wave in lead Vi is added to the R wave in Vg. If the sum is greater than or equal to 35 mm then the voltage criteria for LVH is met. The other method that can be used involves the limb leads 1 and aVL. If a QRS complex exceeds 20 mm (4 large boxes) then the voltage criteria for LVH can be seen using just the Umb leads. [Pg.70]

S wave in Vi +R wave in Vg 35 mm in height Accompanied left atrial abnormality [Pg.71]

In severe cases associated ST segment depression and T wave inversion, strain pattern . [Pg.71]

When recording findings on the ECG it is good practice to write something like voltage criteria for LVH met instead of LVH becanse only a cardiac echo can truly diagnose LVH. [Pg.71]


The progenitor cells of the kidney produce 90% of the hormone erythropoietin (EPO), which stimulates red blood cell (RBC) production. Reduction in nephron mass decreases renal production of EPO, which is the primary cause of anemia in patients with CKD. The development of anemia of CKD results in decreased oxygen delivery and utilization, leading to increased cardiac output and left ventricular hypertrophy (LVH), which increase the cardiovascular risk and mortality in patients with CKD. [Pg.382]

Administration of one of the jS-blockers and an ACE-I is mandatory for all patients with a recent MI, regardless of the ejection fraction (EE). If the LVEE is reduced in patients without a history of MI, yS-blockers and/or ACE-I should be administrated as long as the patients do not have heart failure symptoms. If an ACE-I is contraindicated, it has to be substituted by an ARB, if the patient is post-MI with low EE, but no manifest HF. This may also be true without a history of MI. ACE-I and ARB are beneficiary for those with hypertension and left ventricular hypertrophy (LVH), without HF symptoms. [Pg.595]

Examine the patient fundi, bruits, left ventricular hypertrophy (LVH), large kidneys, radial-femoral (R-F) pulse lag, edema ... [Pg.175]

The incidence of cardiovascular disease is sevenfold to tenfold greater in patients with CKD than in non-CKD age-and seX matched controls. By the time patients develop the need for RRT there is an approximately 17 times greater risk of cardiovascular death or nonfatal myocardial infarction than age-matched and sex-matched individuals without kidney disease.The spectrum of cardiovascular disease studied in CKD includes (1) angina, (2) congestive heart failure, (3) myocardial infarction, (4) peripheral vascular disease, (5) stroke, and (6) transient ischemic attack. Structural heart disease, such as left ventricular hypertrophy (LVH) and valvular heart disease, is a very common sequela to CKD. Up to 75% of patients commencing dialysis have echocardiographic evidence of The risk factors for... [Pg.1695]

Several disorders can impair ventricular function and play a role in the development of DHF. DHF is seen often in patients with hypertension, coronary artery disease (CAD), valvular heart disease, and hypertrophic cardiomyopathies. Hypertension is the most common underlying cardiovascular disorder in patients with DHF. There are several proposed mechanisms by which hypertension may impair diastolic function. Hypertension can alter diastolic function through its effects on (1) wall tension, (2) myocardial hypertrophy and fibrosis, and (3) small vessel structure and function, and (4) by predisposing to epicardial CAD. An association between impaired LV filling and subnormal high-energy phosphate metabolism has been shown in hypertensive patients, even in the absence of left ventricular hypertrophy (LVH). ... [Pg.358]

Patients with CKD are at increased risk of cardiovascular disease, independent of the etiology of their kidney disease. While a clearly unique pathogenesis of cardiovascular disease specific to CKD has not been identified, it is known that manifestations of kidney disease are contributory. Risk factors for cardiovascular disease in this population include hemodynamic and metabolic abnormalities, as well as hypertension, dyslipidemia, elevated homocysteine levels, anemia, hyperparathyroidism, malnutrition, and oxidative stress. Hypertension induced by volume expansion and increased systemic vascular resistance increases myocardial work and contributes to development of left ventricular hypertrophy (LVH). Hyperlipidemia may enhance atherogenesis, while some uremic toxins can decrease myocardial contractflity. In addition, uremic toxins can induce pericarditis, a potentially fatal complication. Currently, measures to screen this high-risk population for cardiovascular risk factors are not routine. ... [Pg.823]

Left ventricular hypertrophy (LVH) can lead to heart failure or myocardial infarction. The rhythm strips shown here illustrate key electrocardiogram changes of LVH as they occur in selected leads a large S wave (shaded area below left) in V, and a large R wave (shaded area below right) in V5. If the depth (in mm) of the S wave in V, added to the height (in mm) of the R wave in Vj exceeds 35 mm, then the patient has left ventricular hypertrophy. [Pg.250]

CAD, coronary artery disease LVEF, left ventricular ejection fraction LVH, left ventricular hypertrophy. (Algorithm adapted with permission from Tisdale JE, Moser LR. Tachyarrhythmias. In Mueller BA, Bertch KE, Dunsworth TS, et al. (eds.) Pharmacotherapy Self-Assessment Program, 4th ed. Kansas City American College of Clinical Pharmacy 2001 217-267.)50... [Pg.122]

LVH Left ventricular hypertrophy tion no venereal disease nonvalvular disease... [Pg.1556]

HOCM, Hypertrophic obstructive cardiomyopathy LVH, left ventricular hypertrophy 5 FU, 5 fluorouracil PE, pulmonary embolus PCI, percutaneous coronary mteivention TBSA, total surface body area ... [Pg.1625]

ISA intrinsic sympathomimetic activity LVH left ventricular hypertrophy RAAS renin-angiotensin-aldosterone system SBP systolic blood pressme... [Pg.214]

BNP, brain natriuretic peptide CAD, coronary artery disease CRP, C-reactive protein LVH, left ventricular hypertrophy Lp(a), lipoprotein(a). [Pg.64]

Abbreviations MM, multiple myeloma RV dil, right ventricular dilatation Cath, right heart catheterization CCB, calcium channel blocker dig, digoxin dx, diagnosis LVH/RVH, left ventricular hypertrophy/right ventricular hypertrophy. [Pg.795]

Anemia has both direct and indirect effects on left ventricular function and growth. Cardiac output increases because of a combination of increased cardiac preload and a reduction in afterload. Such changes lead to ventricular remodeling, with initial left ventricular dilation followed by subsequent hypertrophy. In ESRD other factors also contribute to LVH, including hypertension, volume expansion, and the metabolic consequences of uremia, to which maybe added the effects of diabetes. By the time patients with diabetes reach ESRD, they are more likely to have concentric LVH, more likely to have had ischemic heart disease, and more likely to have experienced cardiac failure than nondiabetic subjects. ... [Pg.1697]


See other pages where Ventricular Hypertrophy LVH is mentioned: [Pg.8]    [Pg.57]    [Pg.160]    [Pg.204]    [Pg.1632]    [Pg.25]    [Pg.157]    [Pg.203]    [Pg.107]    [Pg.391]    [Pg.519]    [Pg.193]    [Pg.70]    [Pg.8]    [Pg.57]    [Pg.160]    [Pg.204]    [Pg.1632]    [Pg.25]    [Pg.157]    [Pg.203]    [Pg.107]    [Pg.391]    [Pg.519]    [Pg.193]    [Pg.70]    [Pg.401]    [Pg.606]    [Pg.32]    [Pg.54]    [Pg.71]    [Pg.847]    [Pg.66]    [Pg.7]    [Pg.367]   


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