Sept 25, 2015.  Pulmonary HTN is defined as mean pulmonary artery pressure of > 25 mm Hg (as seen on echo)  Causes of Pulmonary HTN include: PE, COPD,

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Presentation transcript:

Sept 25, 2015

 Pulmonary HTN is defined as mean pulmonary artery pressure of > 25 mm Hg (as seen on echo)  Causes of Pulmonary HTN include: PE, COPD, primary Pulm HTN, CHF, OSA, ILD  As Pulm HTN progresses, it alters the structure of the right ventricle and causes Cor Pulmonale  Pulmonary Heart Disease and Cor Pulmonale are synonymous

 Cor Pulmonale causes chronic right sided diastolic heart failure  It is critical to understand when Cor Pulmonale becomes acute as this condition can be life threatening (e.g. pulmonary embolus) Synonymous terms  Acute Cor Pumonale  Acute pulmonary heart disease  Pulmonary HTN with acute right heart strain (failure)

 There is underlying documented chronic lung disease such as COPD, OSA, ILD  There is an acute exacerbation of shortness of breath and the following findings: Elevated JVP, peripheral edema and ascites EKG with S1Q3 pattern RVH/RV strain on echo Blood work includes an elevation of BNP

 Query when the patient presents with acute on chronic dyspnea in setting of known COPD, OSA or ILD  PMH includes pulmonary HTN (usually dx’ed by echo with elevated pulm arterial pressures)  Lung exam has no wheezing but rather crackles, BNP is elevated and echo shows a normal LV size and function but dilated/hypertrophied RV  It will be a slam dunk if echo shows: “right heart strain” (RV dilatation and RV systolic dysfunction)

 If you see the following terms in the chart: Pulmonary HTN, RVH, RV failure/dysfunction, right heart failure, right heart strain  Any admission for PE with elevated BNP, should be queried about acute cor pulmonale!  Any admission for severe COPD exacerbation without acute respiratory failure (no hypoxemia/hypercapnia) but with elevated BNP, JVD and echo evidence of right heart strain

 Estimated GFR calculated: MDRD formula Cockcroft-Gault formula  Used to calculate renal medication adjustment  Assumes stable creatinine

 National Kidney Foundation Definition: Increased creatinine ≥ 0.3 mg/dL (levels obtained within 48 hours) Increased creatinine ≥ 1.5 x baseline within prior 7 days Urine volume of less than 0.5 cc/kg/h ≥ 6 hrs  Note absolute creatinine has nothing to do with definition of AKI

 Pre-renal acute kidney injury  Intrinsic Renal acute kidney injury ATN  Post renal acute kidney injury

 Higher level severity than AKI  1/3 of all causes of AKI in hospitalized patients  Due to: Hypotention Meds (contrast)  Urine often bland (like with pre-renal AKI)  Fractional Excretion Na+ (FENA) > 2%  Recovery ≥ 3 days (pre-renal AKI ≥ 1 day)

 Strong relationship between heart and kidney  Heart failure actives the renin- angiotensin-aldosterone system and vice versa  Kidneys retain salt and water which exacerbates CHF

 Type 1: acute, primary is acute chf affective kidney pefusion leading to AKI  Type 2: chronic,ongoing chronic cardiac hypoperfusion leads to effentual ckd  Type 3: acute kidney injury causes fluid retention leading to acute chf exacerbation  Type 4: severe ckd/esrd causing ongonig fluid retention worsening cardiac output

 Pinson, ACP Hospitalist, April, 2015  Kings, “Cor Pulmonale”, Uptodate, Feb 2014  Kiernan, “Cardiorenal syndrome”, Uptodate Sept 2015  Pinson, ACP Hospitalist, June 2015