Category: Cardiology

Shock

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Shock Differential diagnosis
http://en.wikipedia.org/wiki/Shock_(circulatory)#Differential_diagnosis

Abrupt Onset Shock Previously HealthyDIFFERENTIAL DIAGNOSIS — The abrupt onset of shock in a previously healthy individual has a limited number of causes.

Staphylococcal toxic shock syndrome must be considered, particularly in a female during menstruation, or in either sex in association with recent surgery or any localized staphylococcal abscess. In contrast to GAS TSS, bacteremia is uncommon in staphylococcal TSS and has a much lower mortality than GAS TSS [22]. (See “Staphylococcal toxic shock syndrome”.)
Gram-negative sepsis can mimic GAS TSS but is uncommon in healthy patients outside the hospital setting. Typhoid fever is a notable exception. Although sporadic cases of Salmonella bacteremia occur in association with food-borne illnesses, typhoid fever is often related to natural disasters such as hurricanes, floods, and earthquakes or travel to an endemic country. Renal impairment frequently precedes hypotension in GAS TSS whereas renal failure (also due to acute tubular necrosis) develops after hypotension in gram-negative shock. In addition, the white blood count is generally normal or elevated with a marked left shift in GAS TSS, but is usually normal or low in typhoid fever.
Rocky Mountain spotted fever (RMSF) is another disorder that can mimic the findings in GAS TSS. Both cause shock in otherwise healthy individuals. However, severe headache and rash are present in most patients with RMSF, whereas headache is rare and rash is present in only 10 percent of patients with GAS TSS. The character of the rash is also different; it is most often petechial in RMSF and diffusely erythematous in GAS TSS. (See “Clinical manifestations and diagnosis of Rocky Mountain spotted fever”.)
GAS TSS is usually associated with a normal to elevated WBC with a dramatic left shift whereas this is uncommon in RMSF. In addition, the course of illness is much more rapid in GAS TSS. Despite these general differences, the two disorders may be difficult to distinguish if the rash characteristic of RMSF and a local infection possibly due to GAS are absent.

Acute meningococcemia may be confused with GAS TSS. The rash is petechial and meningitis is common in meningococcemia but is infrequent in GAS TSS. (See “Clinical manifestations of meningococcal infection”.)
Some patients with GAS TSS have respiratory symptoms and develop lobar consolidation and empyema. The respiratory symptoms and hypotension may make it difficult to distinguish these patients from those with overwhelming Streptococcus pneumoniae sepsis. (See “Invasive pneumococcal (Streptococcus pneumoniae) infections and bacteremia”.)
Leptospirosis may mimic severe streptococcal infections but the epidemiology of leptospirosis (eg, infection after exposure to environmental sources, such as animal urine, contaminated water or soil, or infected animal tissue primarily in tropical regions) is specific enough to help rule out this diagnosis. In addition, conjunctival suffusion, when it occurs, is one of the most reliable distinguishing features in leptospirosis since it rarely occurs with any other infectious illness. (See “Microbiology, epidemiology, clinical manifestations, and diagnosis of leptospirosis”.)
Heat stroke has been confused with some cases of GAS TSS largely because of the presence of elevated temperature, dehydration with evidence of renal impairment, confusion, hypotension, and sunburn-type erythema. The history of heat exposure is helpful in distinguishing the two illnesses. (See “Severe hyperthermia (heat stroke) in adults”.)

 

 

 

Atrial Fibrillation with RVR

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Acute rate control — In patients with AF and a rapid ventricular response, acute HR control is usually achieved with intravenous medications. (See ‘Urgency of therapy’ above.)

In such patients, we suggest the following approach:

  • In patients without significant heart failure or hypotension, we suggest intravenous beta blockers or nondihydropyridine calcium channel blockers (Grade 2B). (See ‘Acute control with beta blockers’ above and ‘Acute control with calcium channel blockers’ above.)
  • Intravenous diltiazem, using the regimen described above, is our preferred drug in this setting. (See ‘Acute control with calcium channel blockers’ above.) However, comparative data are limited and intravenous verapamil or intravenous beta blockers such as metoprolol, propranolol, or esmolol are reasonable alternatives (see ‘Comparative efficacy’ above) [46].
  • If it is uncertain whether such therapy will be tolerated by the patient, esmolol may be cautiously administered since its very short half-life permits a therapeutic trial to be performed at reduced risk (see ‘Acute control with beta blockers’ above).
  • In patients who do not adequately respond to initial therapy with either an intravenous beta blocker or intravenous calcium channel blocker, we suggest the addition of intravenous digoxin as the second drug in combination therapy (Grade 2C). (See ‘Digoxin’ above.) Some patients have a greater degree of rate control with a beta blocker than with a calcium channel blocker, and vice versa. Thus, in patients who have an inadequate response to one of these drugs, switching to a drug from the other class is an alternative to adding digoxin.If rate control is achieved, we try to use the second drug as a single agent and to avoid using beta blockers and calcium channel blockers as combination therapy for rate control. However, in selected patients who do not have hypotension or significant left ventricular dysfunction, these classes may be used together, and in some cases all three agents (ie, a beta blocker, a calcium channel blocker, and digoxin) may be necessary to achieve adequate rate control.
  • In patients with advanced HF or significant hypotension, we suggest intravenous digoxin as initial therapy (Grade 2C). (See ‘Digoxin’ above.)
  • In patients who do not respond to or are intolerant of intravenous calcium channel blockers, beta blockers, and/or digoxin, we suggest intravenous amiodarone for acute control of the ventricular rate (Grade 2C). (See ‘Amiodarone’ above.) In such patients, the use of amiodarone for rate control is a short-term strategy (eg, hours to days).

Amiodarone — Amiodarone is commonly used to maintain sinus rhythm in AF patients in whom a rhythm control strategy is chosen. However, amiodarone can also slow the ventricular rate in patients who remain in AF. In one study, for example, intravenous amiodarone (7 mg/kg), flecainide, or placebo was given to 98 patients with recent onset AF (0.5 to 72 hours) [42]. Even when AF did not revert to sinus rhythm, amiodarone promptly slowed the ventricular rate during the eight hour observation period (figure 4). In addition, in critically ill patients, amiodarone may be less likely to cause systemic hypotension than intravenous diltiazem [43].
http://www.uptodate.com/contents/control-of-ventricular-rate-in-atrial-fibrillation-pharmacologic-therapy
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