CHF Flashcards
What mortality is associated with CHF?
Annual death rate of 18.7%.
Once symptomatic, 2-year mortality is about 35% and over the next 6 years increases to 80% for men and 65% for women.
Annual mortality rates are 5% to 10% in mild- moderate heart failure and 30% to 40% in severe heart failure.
After the development of pulmonary edema, only 50% survive 1 year. After cardiogenic shock, up to 85% die within 1 week.
What assoc. syndromes accompany CHF to the ED?
63% have HTN
55% have IHD
35% have DM
30% have Afib
How do you classify acute CHF?
Break acute CHF down to it’s basics.
Pump dysfunction.
Decreased CO, which causes a compensatory increase in SVR. This increase in SVR further worsens CO.
Alternatively, pathologic neurohormonal and HD responses can cause it. Activation of the RAS, norepi and vasopressin, as well as endothelin release potentiate a water and sodium retention, and increased SVR. This precipitates a worsened cardiac workload and wall stress. This may cause remodelling over time.
Fix acute CHF by addressing the basic problems.
Fix CO: 1) improve contractility, decrease SVR and in some cases decrease preload, using ionodilators if in shock, or beta blockers.
Mediate the neurohormonal response: 1) block the RAS with ACE inhibitors. 2) Beta blockers to block norepi and vasopressins effects on increasing SVR.
What is the main concern and etiology of systolic HF?
Diastolic HF?
Systolic HF is LVEF <40%, and afterload sensitivity.
It is most often the result of IHD/MI and remodelling.
Diastolic HF is LVEF >40%, and preload sensitivity (this makes them sensitive to diuresis and vasodilators)
It is most often due to chronic HTN and LV hypertrophy.
What are the limitations of BNP?
What are the cutoff points?
Levels are usually overestimated in renal failure patients, and underestimated in obesity.
Obesity results in lower BNP levels. BNP cutoff values for diagnosis should be reduced by 50% when BMI exceeds 35.
What are common precipitants of acute HF?
What is the efficacy of checking troponins in acute HF?
As many as 14% of ED patients presenting with an acute heart failure syndrome will have biomarkers positive for myocardial infarction.
Management of acute hypertensive HF?
O2, IV access, monitored bed.
subling nitro until IV nitro can be started
(0.5-0.7mcg/kg/min)
Lasix IV (20mg then 40mg)
CPAP/BiPAP
Nitroprusside if Nitro drip not effective (0.3 mcg/kg/min)
What are important predictors of inpatient mortality of HF, as seen on initial ED bloodwork?
Creatinine > 243 umol/L
Systolic BP < 115
Urea > 15 mmol/L
Distinguish MS from MR.
MS: usually presents with exertional dyspnea, that is often worsened in the setting of some other issue (ie. anemia or A fib)
MR: usually presents with severe dyspnea, hypertension, and pulmonary edema.
How does the management of MS and MR differ?
MS: They need their valve opened, and to be anticoagulated so they don’t throw a clot.
MR: If in cardiogenic shock, they need CV surg. If normotensive, they need afterload reduction. If hypotensive, they need ionotropy + afterload reduciton, and possibly a balloon pump.
Why is Afib in the setting of Ao Stenosis such a recipe for disaster?
Ao Stenosis is a preload dependent disease. Loss of atrial ejection fraction from Afib, will cause a dramatic decrease in preload to the LV, and thus, a dramatic decrease in CO. This will lead to very rapid deterioration.
