Presentation on theme: "Congestive Heart Failure and Cardiomyopathy Mark Bromley PGY-1."— Presentation transcript:
Congestive Heart Failure and Cardiomyopathy Mark Bromley PGY-1
Case 1 A 63-year-old male presents with breathlessness x 3 days. ?Approach, ?Hx PMHx: MI 3 years ago 4-vessel CABG asymptomatic since surgery with no complaints of CP HPI: Over the last 3 months, the patient notes onset of shortness of breath while unloading groceries, and walking stairs. –2 weeks ago, he was unable to complete his daily one-mile walk at the high school track. He noted swelling in his feet and ankles. –4 days ago he woke at 2 am short of breath and had to sleep in his recliner the rest of the night. He has been unable to lay flat in bed at night since then and has slept on 3 pillows. –Yesterday, he became breathless walking from one room to another –He presents today with extreme shortness of breath –He denies chest pain
BP 108/52 P 140, irreg. R 30 and labored Temp 99°F Ht: 5'8" Wt: 210. General: Breathless, moderately obese male in acute distress sitting upright complaining "I am going to die. Please help me." Chest: Scattered rhonchi throughout, rales bilateral one third lower bases. Cough is productive and frothy. CVS: Tachycardia and irreg. Grade 3/6 systolic murmur at LSB, S3 gallop noted. JVP to jawsystolic murmur Abd: Liver palpable three centimeters below right costal margin. HJR. Extremities: 4+ pitting edema of lower extremities to the knees. Pulses intact.
Importance Increasing burden Aging population Improved survival (Hypertension/CAD) Nationwide, heart failure affects more than 400 000 Canadians 1 (10% of those >75) >50 000 new cases are diagnosed /yr 1
Bad Disease Mortality 1 year – 10-20% 6 year – 60-80% ED visits 20% new diagnosis 80% repeat visit (decompensation)
Definition CHF –Inability of the heart to maintain adequate vital organ perfusion at normal filling pressures Decreased exercise capacity Associated neurohumoral-endocrine changes, initially compensatory but ultimately maladaptive Pulmonary Edema –A condition associated with increased loss of fluid from the pulmonary capillaries into the pulmonary interstitium and alveoli
The heart is a pump that works together with the lungs. It pumps blood in 2 ways 1.It pumps blood from the heart to the lungs to pick up oxygen. The oxygenated blood returns to the heart 2.It then pumps blood out into the circulatory system of blood vessels that carry blood through the body
In HF the pumping action of the heart becomes less and less efficient/powerful The heart does not pump blood as well as it should When this happens, blood does not move efficiently through the circulatory system It starts to back up, increasing the pressure in the blood vessels, forcing fluid from the blood vessels into body tissues.
Classification of Heart Failure Low Output Cardiac output is low, but demand for blood flow is normal The heart is unable to meet this demand and fails Dx: IHD, HTN, dilated cardiomyopathy, valvular and pericardial dz High Output High-output heart failure Cardiac output is normal or a little bit high Demand for blood flow is abnormally high (hyperthyroidism, anemia, severe infections) The heart is unable to deliver the increased amount of blood and fails Dx: hyperthyroidism, anemia, pregnancy, AV fistulas, beriberi, & Paget’s Rx: ↓volume overload and correct the underlying disorder
Classification of Heart Failure Acute MI, Acute Valve Dysfunction largely systolic sudden reduction in cardiac output often results in systemic hypotension without peripheral edema Chronic Cardiomyopathy arterial pressure tends to be well maintained until very late in the course there is often accumulation of peripheral edema
Classification of Heart Failure Right Sided (right ventricle) (pulmonic stenosis or pulmonary hypertension) When the right side of the heart starts to fail, fluid collects in the feet and lower legs As the heart failure becomes worse, the legs swell and eventually the abdomen collects fluid (ascites, hepatic congestion) Weight gain accompanies the fluid retention and is an excellent measure of how much fluid is being retained. Left Sided (left ventricle) left ventricle is mechanically overloaded (aortic stenosis) or weakened (post MI) When the left side of the heart starts to fail, fluid collects in the lungs (Orthopnea/PND) Breathing becomes more difficult, and the patient may feel short of breath, particularly with activity or lying down This extra fluid in the lungs makes it more difficult for the airways to expand on inhalation ↓O 2 diffusion
Classification of Heart Failure Systolic –The heart has difficulty contracting and pumping out enough blood weakness, fatigue and decreased ability to exercise ↓Ejection fraction = (stroke volume)/(end diastolic volume) –A normal ejection fraction is greater than 50% –Systolic heart failure has a ↓EF < 50%. Diastolic –The heart is unable to fill properly during diastole –↑ filling pressure –This impedes blood filling into the heart → backup into the lungs → CHF symptoms –↑ in patients > 75 years; women; HTN –Ejection fraction is normal
Classification of Heart Failure Directional Heart Failure Backwards heart failure –The ventricle is not pumping out all the blood that comes into it. ↑ ventricular filling pressure and systemic or pulmonary edema –In fact, the heart can only meet the needs of the body if the ventricular filling pressure is high Forward heart failure –The heart is not pumping out enough blood to meet the needs of the body –↓ blood reaches the kidneys, they conserve salt and water, which contributes to excess fluid retention and edema –Forward failure also decreases the blood flow to various organs, causing weakness and fatigue
“First, strike for the jugular and let the rest go!” Oliver W. Holmes Jr.
Etiology Dysrhythmia –Tachy ↓Diastolic filling time +/- atrial kick ↓CO ↓Coronary perfusion ↑ Myocardial O 2 demand –Brady ↓HR ↓CO = SV x ↓HR
Infection ↑ systemic met demands Pulm infection = ↓O 2 Tachycardia Anemia Isovolumic hemodilution ↑CO meet O 2 demands ↓Coronary O 2 delivery
Pregnancy ↑ demand for CO Acute Myocarditis ↓ contactility Acute valvular dysfunction 2 o to MI ↑preload or ↑↑afterload
PE ↓O2 supply ↑ Pulmonary Hypertension Pharmacologic ↓ inotropic effects ↑ Na / H 2 O retention
Etiology Decompensation/Causes of exacerbation FAILURE: Forgot medication Arrhythmia/ Anemia Ischemia/ Infarction/ Infection (Pneumonia) Lifestyle: taken too much salt Up-regulation of CO: pregnancy, hyperthyroidism Renal failure Embolism: pulmonary Inappropriate treatment Failure to seek care 25% 20% 10%
Case 1 Management A 63-year-old male presents with breathlessness x 3 days. ?Approach, ?Hx PMHx: MI 3 years ago 4-vessel CABG asymptomatic since surgery with no complaints of CP HPI: Over the last 3 months, the patient notes onset of shortness of breath while unloading groceries, and walking stairs. –2 weeks ago, he was unable to complete his daily one-mile walk at the high school track. He noted swelling in his feet and ankles. –4 days ago he woke at 2 am short of breath and had to sleep in his recliner the rest of the night. He has been unable to lay flat in bed at night since then and has slept on 3 pillows. –Yesterday, he became breathless walking from one room to another –He presents today with extreme shortness of breath –He denies chest pain
Management Treat the maladaptation ↑ Vascular resistance ↑ Sympathetic tone ↑ Total blood volume ? LMNOP
Airway/Breathing Non-rebreather facemask delivering 100% O 2 Once initial therapy has begun, oxygen supplementation can be titrated in order to keep the patient comfortable and arterial oxygen saturation above 90 percent.
NIPPV If respiratory distress and/or hypoxia persist, consider non-invasive PPV –↓ preload, ↓ afterload, and ↑ left ventricular performance –Meta-analysis of 15 clinical trials: ↓mortality and ↓intubation with NPPV compared to conventional therapy –Patients who fail/do not tolerate/have contraindications to NPPV should be intubated –Positive end-expiratory pressure is often useful for improving oxygenation
Multi-centre RCT 130 pts Cardiogenic Pulmonary Edema Emergency Department Medical therapy+O2 (65 pts) non-invasive pressure support ventilation (65 pts) Primary outcome – need for intubation
Loop Diuretics ↑Na & H 2 O excretion Useful in volume overload Rapid onset –Mild vasodilator ↑1/2 life in CHF …be careful Depletion of K + and Mg ++
Loop Diuretics Dosing – not well established High dose Lasix and low dose Nitro has worse outcomes than low dose Lasix and high dose Nitro
Nesiritide Recombinant BNP ↓ Aldosterone ↓ Endothelin ↑ Na & H 2 O excretion – no reflex tachy Good for Nitro contraindications
VMAC Randomized, Double Blind 489 inpatients IV Nisiritide vs IV Nitrates vs Placebo PCWP and Dyspnea –Improvement in PCWP – 2mm HG @ 6h –No change in Dyspnea Problems: ↓Nitro dosing Prolonged Hypotension Not ED patients Industry sponsored
Vosodilator Therapy: Nesiritide Efficacy Phase –432 patients –In the efficacy phase, 127 patients underwent hemodynamic monitoring with a pulmonary artery catheter –A six hour infusion of nesiritide (0.015 and 0.03 µg/kg per min) decreased pulmonary capillary wedge pressure –(6 and 10 mmHg versus an ↑ of 2 mmHg for placebo) –Improved the clinical status in a greater number of patients (60% and 67% versus 14%) Comparative phase –305 patients –Randomly assigned to nesiritide or standard vasoactive agents for seven days without hemodynamic monitoring –Compared to standard treatment with a single vasoactive agent (dobutamine, milrinone, nitroglycerin, or nitroprusside) –nesiritide produced a similar significant improvement in clinical status and reduction in dyspnea and fatigue that persisted during the entire infusion period. –Asymptomatic, dose-related hypotension was the most common side effect
Death within 30 days tended to occur more often among patients randomized to nesiritide therapy –35 [7.2%] of 485 vs 15 [4.0%] of 377 patients RR from meta-analysis: 1.74 –(95% confidence interval [CI], 0.97-3.12; P =.059) Hazard ratio after adjusting for study, 1.80 –(95% CI, 0.98-3.31; P =.057)
Placebo-Controlled, Randomized, Double-Blind Study of Intravenous Enalaprilat Efficacy and Safety in Acute Cardiogenic Pulmonary Edema The purpose of this study was to evaluate the efficacy and safety of a single IV 2-hour infusion of enalaprilat (1 mg) placebo-controlled, randomized, double-blind study –20 CHF patients (NYHA class III or IV) Compared with placebo, enalaprilat –↓ pulmonary capillary wedge pressure (-37% versus -10%, P=.001), –↓ diastolic and mean systemic blood pressures (-21% vs 0%, P=.009, and -18% vs -1%, P=.026) –↓ diastolic and mean pulmonary blood pressures (-21% vs -8%, P=.040; -18% vs -9%, P=.046) –↓ brachial and renal resistances (-44% versus -14%, P=.017, and -22% versus -2%, P=.014) –↑ brachial and renal blood flows (+77% versus +8%, P=.036, and +12% versus 0%, P=.043) –↑ arterial oxygen tension (+2% versus -16%, P=.041) –↑ arterial oxygen saturation (+1% versus -2%, P=.045) Enalaprilat did not affect CO or carotid or hepatosplanchnic hemodynamics Excluded those already on ACE I
BNP Why do we need another diagnostic test? –Diagnostic uncertainty How uncertain are we? How uncertain should we be? –ER docs are rarely wrong when they rate the probability of HF as very high or very low 2 –ER docs are uncertain of the diagnosis in the in-betweeners (30%) 2
Breathing Not Properly - Analysis BNP brings us closer to the “gold standard” Low Prob -EP 17% had CHF 90% would have been corrected by BNP High Prob -EP 4% did not have CHF 80% would have been corrected by BNP Uncertain -EP BNP correctly classified 74% Misclassified 7%
BNP Levels < 100 pg/ml may prompt clinician to focus on alternative diagnosis (COPD) Reasonable neg pred value Prognostic Value ?Variation with Age/Gender/Kidney fxn
Prospective, Randomized, Controlled Single blind 452 Pts with dyspnea Diagnostic Strategy (BNP) vrs Standard Assessment Told EP if 500 CHF likely, 100-500 indeterminate End Points: Time to D/C & Total Cost Safety: Similar Conclusion: BNP improved evaluation thereby improving time to D/C and cost – no change in safety
Case Previously well 10 year old girl presents with 2 weeks of progressive right sided ABD pain. General malaise. Mild fatigue on exertion. Parents report mild lethargy, pallor and decreased PO intake over same period. Shallow rapid breathing, worse when reclining at night. –37.8 o C 123 24 94/54 –Pale irritable –HEENT: MMM. No adenopathy –CVS: regular S1S2, no murmer, PPPx4, no edema –CHEST: AE=AE slight decrease at bases –ABD: palpable liver edge below umbilicus EKG: sinus tach, LAD, flattened T-waves, decreased voltages.
Dilated Cardiomyopathy Most common CM –30% idiopathic –Hereditary X-linked (dystrophin gene) –Booze –Heavy Metal –Drugs –Infectious Viral Chagas –Post partum –Collagen vascular disease –Glycogen storage disease –Thiamine, PO4, zinc deficiency –Amyloidosis –Neuromuscular disorders
Dilated Cardiomyopathy Biopsy helpful for etiology Rx same as other CHF MDC (Metoprolol in Dilated CM) – 34% reduction in Death Multicenter Myocarditis Treatment Trial – no benefit of corticosteroids and azathioprine for Rx of biopsy-proven inflammation in dilated CM
HCM Inappropriate hypertrophy w/o stimulus Usually asymmetric 4% mortality per year (sudden death)
Diagnosis Chest x-ray –Absence of cardiomegaly, normal cardiac silhouette –CHF Electrocardiogram –LBBB common, RBBB possible –Low voltage –Nonspecific ST-T changes –Various arrhythmias –Chamber enlargement
Echocardiography –Normal to symmetrically thickened walls –Rapid early-diastolic filling, slow late- diastolic filling –Normal or slightly reduced ventricular volume and systolic function
Cardiac catheterization –Elevated ventricular end-diastolic pressure –Dip and plateau configuration of the diastolic portion of the ventricular pressure pulse –Normal to slightly decreased ejection fraction –Prominent x and y descent
Endomyocardial biopsy –May detect typical eosinophil infiltration in the inflammatory stage –May detect myocardial fibrosis in later-stage cases –Negative findings do not exclude diagnosis
Treat underlying cause if possible Therapy similar for other causes of CHF Consider anticoagulation as prone to stasis –thromboembolism
References 1.Kostuk WJ. Congestive heart failure: what can we offer our patients? CMAJ 2001;165(8):1053-5 2.Schwam E. B-type natriuretic peptide for diagnosis of heart failure in emergency department patients: a critical appraisal. Acad Emerg Med 2004;11:686-91.