Classification of cardiogenic shock according to Inotropic/vasopressor and mechanical circulatory support .(What are Pre-Shock, Mild-shock, profound and severe refractory cardiogenic shock ?)

Diabetes mediated vessels toxicity (How high blood sugar can damage the heart's vessels)

High levels of glucose can also damage extracellularly and increase the production of advanced glycosylation end-products (AGEs) in the circulation and on matrix proteins.

The AGEs directly affect cell function, arterial wall stiffness or gene expression of interacting cells. They are ligands for a number of scavenger receptors and the receptor for AGEs (RAGE). As reviewed by Goldberg and Dansky (2006), two lines

of evidence strongly support the theory that AGEs mediate diabetic complications:

-infusions of soluble RAGE, which is presumed to complex AGEs, reduce and stabilise atherosclerotic lesions, and inhibition of AGE formation reduces lesions; and diets enriched in AGEs promote lesions. Beyond AGEs, other mechanisms also link hyperglycaemia to oxidative stress and vascular dysfunction, as well as adverse effects on vascular smooth-muscle cells (Sundell, 2005) (Figure above).

-Finally, hyperglycaemia, at least at the experimental level, has also been shown to induce MMP expression in both endothelial cells and macrophages (Sundell, 2005).

As discussed above, such changes are likely to render the plaque less stable and more susceptible to rupture and hence luminal thrombosis.

Every 10% increase in hypertension treatment would lead to an additional 14,000 deaths annually prevented

Every 10% increase in treatment of elevated low-density lipoprotein cholesterol or aspirin prophylaxis would lead to 8000 deaths prevented in those aged <80 years, per year. Overall, the models suggest that optimal use of all of these interventions could prevent 50,000-100,000 deaths per year in those aged <80 years and 25,000-40,000 deaths per year in those aged <65 years.

2013 and 2014 review of evidence for possible beneficial effects of diuretics and dopamine in patients with decompensated heart failure(HF) and acute kidney injury ( AKI)

2013: Dictum;
---------////-----------//////---------
1-Diuretics: 
Loop diuretics (furosemide, bumetanide, torsemide, ethacrynic acid) have long been used to “convert” oliguric to nonoliguric AKI. However, it is most likely that oliguric patients who respond to diuretics have a lesser renal injury than those who do not, with an intrinsically more favorable outcome. Moreover there is evidence that “forced” diuresis may exacerbate hypovolemia and renal injury. Once dialysis is required, high dose furosemide does not alter the natural history of AKI.

2- Dopamine:
Dopaminergic agents (dopamine, fenoldopam) potentially confer renal protection by increasing renal blood flow (RBF), diuresis and saliuresis. By activating cyclic AMP they “turn off” the energy-dependent tubular sodium pump and thereby decrease tubular oxygen consumption; increased intratubular urine flow protects against tubular obstruction.In part this may be because there is very wide variability in dopamine pharmacokinetics, i.e. some patients given low dose dopamine may achieve high plasma levels, i.e. in the beta- or alpha-adrenergic range.

Unfortunately, in 2013, there is no compelling evidence that any pharmacologic intervention can definitively prevent or attenuate AKI and alter patient outcome. The current recommendation is that diuretic therapy, low dose dopamine, fenoldopam or atrial natriuretic peptide should NOT be used to prevent or treat AKI. The question is, where do we go from here?

2014 Dictums :
-----////---------////-------
The Heart Failure clinical Research Network , funded by the National Heart,Lung and blood Institute in the USA , addressed the possibility that low dose dopamine or low- dose nesiritide could safely augment the diuresis induced by loop diuretics in patients with decompensated HF. The trial , in 360 patients , showed no evidence that diuresis or decongestion was enhanced by such combined therapy or that renal function was better preserved .
The is that we should continue what we are doing maintain aggressive approach to diuretic therapy , and perhaps concern ourselves less when renal function transiently worsen .

Final Message :
-----///-------////-----
Despite more than thirty years of use as a renal vasodilator , low dose dopamine (2Mic/kg/m) has shown no evidence of benefit in patients with acute oliguric renal failure on the basis of its action on dopaminergic renal receptors . In fact , low -dose dopamine can have deleterious effects on hemodynamics ( decreased splanchnic blood flow ) immune function ( inhibition of T-cell lymphocyte function ) and endocrine function ( inhibition of thyroid _stimulating hormone release from the pituitary ) .
For more information read here ;>>>

Greet van den Berghe’s work shows neuroendocrine dysfunction as well as immunological modulation secondary to prolactin

-Reasons Dopamine is Bad

-Does not benefit the renal system

-Induces Natriuresis and Diuresis

-Shunts blood away from outer medulla, which is the region most prone to ischemic damage

-Possible induction of decreased splanchnic perfusion

-Decreases GI Motility

-Impairs ventilatory response to hypoxemia and hypercapnia

-Effects on anterior pituitary–decreases prolactin secretion.

Settings where in ACE inhibitor therapy may result in worsening renal function

Cyanosis and its causes

What is cardiac cachexia ?