Acute Cardiac Failure Case File

Acute Cardiac Failure Case File

Eugene C. Toy, MD, Manuel Suarez, MD, FACCP, Terrence H. Liu, MD, MPH

Case 16

A 56-year-old man with long-standing ischemic cardiomyopathy (ischemic heart disease [IHD]) was admitted to the intensive care unit (ICU) 24 hours previously. He had hypotension, dyspnea, and respiratory distress. His condition deteriorated following 48 hours of overeating and drinking beer during the Super Bowl Sunday weekend. He has been given intravenous (IV)  furosemide without improvement.  IV angiotensin-converting enzyme (ACE) inhibitor and IV β-blocker (BB) have also  been administered. To improve his respiratory  distress, noninvasive  ventilation (NIV) has been initiated. Early today, he developed worsening chest pain, shortness of breath, and has become acutely lethargic. On physical examination, his temperature is 99°F, heart rate is 130 beats/minute, blood pressure is 90/50 mm Hg, and respiratory  rate is 25 breaths/minute. His jugular venous pressure is elevated while sitting at 45 degrees upright. Lung rales are noted two-thirds up from the bases. The heart rhythm is regular with normal S1 and S2 heart sounds; the presence of a new S3 heart sound is noted. A new 4/6 holosystolic murmur is now heard best at the apex of the point of maximum impulse (PMI) and radiates to the axilla. There is bilateral peripheral edema to the thighs, and his extremities are cool. His central  venous pressure (CVP) is 22 mm Hg (normal, 0-5 mm Hg) with a venous O2 saturation (O2sat) of 60% versus 98% on arterial O2 saturation. The laboratory reported his hemoglobin as 13 g/dL.

⯈ What is the most likely diagnosis? 

⯈ What complications should be anticipated in this patient? 

⯈ What treatment modalities should be initiated?

ANSWER TO CASE 16:

Acute Cardiac Failure

Summary: This is a 56-year-old man with acute decompensating heart failure (ADHF) with cardiogenic shock (CS) . The central venous line (CVP) pressure is markedly increased and the cardiac output (CO) is decreased as evidenced by the cool extremities and low SVO2 saturation. Distention of the jugular vein is the most sensitive clinical sign for ADHF. This patient has a history of CHF aggravated initially by fluid and sodium overload. He deteriorated when he suffered a myocardial infarction (MI) , complicated b y papillary muscle dysfunction, and acute mitral insufficiency. There is a decreased CO with hypotension and evidence of organ hypoperfusion based on his mental status change and cool extremities, all are compatible with shock.

• Most likely diagnosis: Severe CHF with acute decompensated heart failure and cardiogenic shock.
• Likely complications: Fluid and sodium overload, MI, papillary muscle dysfunction or rupture, cardiac arrhythmias, pulmonary embolism.
• Treatment modalities to initiate: Noninvasive ventilation (NIV) or endotracheal intubation (ETI) and mechanical ventilation (MV), IV ACE inhibitors, IV nitroglycerin, β-blockers, furosemide, and anticoagulation are all indicated. An aortic balloon pump (IABP) should be considered to bridge the patient to a PCI or CABG to reverse the papillary muscle dysfunction. IV nitroprusside and dobutamine are added for improvement of CO by afterload reduction and positive inotropic effect.

ANALYSIS

Objectives

1. To understand how to diagnose acute cardiac failure.
2. To understand which drugs are effective in treating cardiac failure.
3. To understand the underlying causes for acute and chronic cardiac failure.

Considerations

This 56-year-old man with a long-standing IHD was admitted to the ICU 24 hours previously with cardiogenic shock, now has an acute change in mental status and new-onset chest pain. This is indicative of worsening cardiogenic shock. He requires an intra-aortic balloon pump (IABP) to improve CO, BP, and flow to the coronary arteries. Vasopressors are also needed to improve the hemodynamic status. The new holosystolic murmur indicates mitral valve papillary muscle rupture or dysfunction leading to mitral regurgitation. Mechanical ventilation may be required to decrease the work of breathing and respiratory failure. A definitive procedure such as CABG or PTCA will be required since all other measures are simply temporary. This patient's condition is an emergency, and requires urgent intervention.

Approach To:

Acute Heart Failure

DEFINITIONS

CONGESTIVE HEART FAILURE (CHF): It is defined as the inability of the heart to supply sufficient substrate to meet the needs of the body.

CARDIOGENIC SHOCK (CS): It is end-stage CHF and is a largely irreversible condition and as such is more often fatal than not.

PULMONARY EDEMA: Accumulation of fluid in the pulmonary air spaces and the interstitial spaces of the lungs, which inhibits oxygen and carbon dioxide diffusion, leading to impaired gas exchange and respiratory failure.

CLINICAL APPROACH

The main cause of CHF is an ischemic cardiac event. Acute MI is the most common cause of CHF and may necessitate emergent revascularization with thrombolytic therapy (rTpa), percutaneous coronary intervention (PCI), or coronary artery bypass graft surgery (CABG). Other causes of CHF include anemia, hyperthyroidism, arrhythmia, and NSAIDs. Worsening CHF is a side effect of oral hypoglycemic drugs in the thiazolidinedione class (also known as glitazones), making these drugs contraindicated in patients with CHF (see Table 16-1). ADHD, pulmonary edema, and CHF are all multifactorial syndromes that result from CO impairment. In systolic heart failure, the heart cannot contract adequately, leading to fluid retention. Both the kidneys and vascular baroreceptors sense the decrease in CO inducing an increase in the renin-angiotensin-aldosterone system and the sympathetic system. This increase ultimately leads to irreversible cardiac dilatation (remodeling) and further fluid overload by a decreasing CO.

DIAGNOSIS

Symptoms of acute decompensated heart failure (ADHF) include dyspnea, fatigue, orthopnea, dyspnea on exertion, and paroxysmal nocturnal dyspnea. CHF can present atypically in patients with nonspecific complaints such as insomnia, nocturia, irritability, anorexia, fatigue, and depression. β-Type natriuretic peptide (BNP) is released by the atria when it becomes acutely dilated, a reflection of increased preload. An elevated BNP level in the absence of renal failure is suggestive of CHF and is used to diagnose CHF and to follow the effectiveness of treatment. An increase in BNP induces diuresis and helps decrease fluid levels. A BNP value of < 100 pg/mL is useful in ruling out CHF. It is important to distinguish between the 2 types of CHF, diastolic versus systolic, since the treatment differs. This can be done via transesophageal echocardiogram (TEE) or transthoracic echocardiograms (TE).

The functional capacity in CHF can serve as a guideline for a stepwise strategy of treatment. A common classification scheme for CHF is that of the New York Heart

Association (NYHA) (Table 16-2). CHF often presents with signs of both left and right heart failure. The most common cause of right heart failure is left heart failure. Right heart failure presents with elevated JVD, dependent edema, and ascites but with an absence of pulmonary congestion typical of left heart failure. When evaluating ADHF, one should first obtain a resting 12-lead ECG in all patients. An old ECG is extremely helpful for comparison with the current findings to determine progression of the disease and its time of onset.

A chest x-ray (CXR) often reveals signs of fluid overload and pump failure in the form of pulmonary edema accompanied by cardiomegaly, vascular congestion, Kerley B lines (dilated lymphatics), blunting of costophrenic angles, cephalization of the pulmonary vasculatures, and pleural effusions are common in ADHF/CHF. TE is used to determine the etiology of ADHF. TE evaluations assist in determining whether systolic dysfunction (ejection fraction [EF] <40%) or diastolic dysfunction (normal EF) exists. Significant valvular disease can also be revealed by TE determinations. Left ventricular remodeling with increased left ventricular end diastolic volume and decreased contractility accompanies systolic dysfunction. Coronary artery disease (CAD) , the main underlying cause of ADHF in two-thirds of all patients, must be aggressively treated. Patients with post-Ml often show evidence of ventricular remodeling.

Diastolic Dysfunction

Patients with diastolic dysfunction have EF values >40% and have normal left ventricular end diastolic volumes. Left ventricular hypertrophy (LVH) is frequently present with an increased stiffness in the ventricles and a decreased compliance of the ventricular wall. Diastolic heart failure is common especially in elderly patients with the previously described findings, which can be documented by TE/TEE and ECG studies.

TREATMENT

Nonpharmacological Therapy of CHF

When the CHF is compensated, limiting dietary sodium to < 2 g/d and limiting fluids to 2 qt/d have decreased hospital readmissions for CHF. Mild exercise, specifically aerobic exercise, is known to improve hemodynamic values in patients with CHF. Exercise also eases the activities of daily living (ADL) and the quality of life (QOL) . Identifying sleep disturbances and nighttime hypoxia is also an important step in the management of CHF. Accurately diagnosing and treating obstructive sleep apnea (OSA) can be life saving for these patients. Treatment of OSA will decrease BP, increase the capacity of exercise, decrease hospital admissions and improve QOL. The delivery of positive pressure decreases preload by delivering PEEP. Patients with NYHA class III or class IV (Table 16-2) with a QRS > 120 msec should be considered for biventricular pacing. If the EF is <35%, an implantable cardioversion device (ICD) is indicated. Cardiac resynchronization therapy via the pacer and ICD improve the QOL and decrease mortality. Cardiac transplantation improves survival, functional status, and the QOL in patients with NYHA of class III or class IV. Patients on maximal therapy but still displaying ADHF should be considered as subjects for transplantation if <65 years old. Contraindications for transplantation include end organ damage from diabetes, vascular disease, cancer, cerebrovascular accident (CVA) , lack of psychological support, or active psychiatric illness.

Drug therapy: CHF patients with systolic dysfunction have improved survival on angiotensin-converting enzyme inhibitors, β-blockers and for some patient groups, aldosterone antagonists. Digitalis used cautiously will decrease hospital readmission for CHF. In black patients with hypertension and CHF, adding the combination of hydralazine and nitrates to standard therapy increases survival

rates. Table 16-3 outlines the various pharmacological interventions that should be considered in patients with CHF. In patients with rare forms of CHF, efforts to treat diastolic dysfunction are designed to increase the cardiac output; these interventions include treating the hypertension, maintaining NSR, and treating any form of ischemia.

Management of right ventricular failure: Definitive therapy for an acutely decompensated

right ventricular failure (RVF) requires primary treatment of the underlying condition in addition to hemodynamic support. Patients with right ventricular failure can be very resilient and they can recover substantially if the underlying causes are successfully treated. Treatment options include percutaneous coronary intervention for RV infarction. Thrombolytic therapy should be applied if catheterization is not available. Open surgical embolectomy may be required for massive pulmonary emboli (PE) with heart failure due to acute pump failure.

Oxygen: Oxygen should be administered to all CHF patients whether the patient is hypoxic or not. This decreases the anxiety which usually accompanies CHF The minimal FIO2 is one that achieves an O2sat of 92% or greater. NIV and MV may be needed to assist the ventilatory and oxygenation requirements. The application of PEEP should also be considered.

Noninvasive ventilation (NIV): NIV is a perfect treatment modality for ADHF It decreases the work in breathing, improves oxygenation and ventilation, and decreases preload. NIV may be helpful in pre-oxygenating patients with hypoxemic respiratory failure before ETI. NIV is increasing in ICUs throughout Europe and the United States. Closely monitor for mask tolerance and leaks, alterations in the respiratory rate, the use of accessory muscles, and their synchrony with the ventilator. Within 1 to 2 hours of admission, determine the success or failure of NIV use. (see NIV Chapter 12).

Surgical treatment: Coronary artery bypass graft (CABG) surgery is the removal of an autologous vein and using it to replace the blocked coronary artery in the heart. When the valve responsible for CHF requires modification due to excess valve tissue, valve repair is considered. In some cases, annuloplasty is required to replace the ring around the valve . If repair of the valve is not possible, it should be replaced with an artificial heart valve . The last level in the treatment of CHF is replacement of the heart. When severe heart failure is present and medication or other procedures are not effective, the diseased heart needs to be replaced or augmented. Unfortunately, the number of patients that qualify for heart replacement outnumber the supply of available donors.

Pacemaker: Pacemakers function by sending electric pulses to the heart forcing it to beat at a rate that is considered normal or required by the patient. Pacemakers with sensory capacity can adjust their output rate depending on the cardiac demand of the patient. These devices are used to treat patients with arrhythmias or rhythm problems such as symptomatic bradycardia and tachycardia.

CARDIOGENIC SHOCK

Management of CS should focus on the augmentation of oxygen delivery and BP to maximize tissue perfusion. Delay in the diagnosis or therapy of CS increases mortality. The management of CS can be accomplished by pharmacological and mechanical means, or by revascularization.

Pharmacologic therapy: The initial treatment for patients with CS focuses on the restoration of normal hemodynamics, oxygenation, and reestablishment of a normal heart rhythm. In patients without significant pulmonary edema, a fluid challenge before vasopressor therapy is advised to improve splanchnic blood flow. If pulmonary edema is present or there is a lack of response to the fluid challenge, pharmacologic therapy should be initiated. The initial therapy should include medications that have both a positive inotropic and vasopressor effect. Cardiogenic shock requires both rapid diagnosis and appropriate therapy. ICU patients often have multiple-organ failure, and differentiating CS from other forms of shock can be difficult. Drugs considered for use as first-line treatments include norepinephrine, dopamine, dobutamine, epinephrine, and phenylephrine. In patients with heart failure, an increased mortality has been described in those given adrenergic inotropic agents. The improved hemodynamics resulting from the use of these agents comes at the cost of increased myocardial consumption of oxygen.

Using vasopressin instead of epinephrine resulted in similar hemodynamic effects via a direct effect on vasopressin receptors. Vasopressin has been recommended as the drug of first choice to be given during cardiac arrest, supplanting epinephrine. Therapy with phosphodiesterase inhibitors (eg, milrinone) may be considered, particularly in cases with right ventricular dysfunction, although the hemodynamically unstable patient often poorly tolerates the resultant decrease in SVR. Levosimendan, an investigational calcium sensitizer that also promotes coronary vasodilation, continues to show promise as a novel treatment for CS. The maintenance of normal physiologic parameters (eg, MAP, cardiac index) should be the goal of therapy with any drug intended to correct CS, although high-dose vasopressor treatment has been associated with poorer patient survival.

Mechanical therapy: In patients who are unresponsive to pharmacologic therapy, mechanical augmentation of blood flow may be of benefit. The placement of an IABP in patients with CS decreases the 6-month mortality. IABP counterpulsation devices can be put in place at the bedside to improve diastolic pressure, simultaneously reducing left ventricular afterload without increasing myocardial oxygen demand. The incidence of major complications (eg, arterial injury and perforation, limb ischemia, visceral ischemia) associated with IABP insertion is 3 % . IABP is contraindicated in patients with severe aortic insufficiency, severe peripheral vascular disease, and aortic aneurysm or dissection. In these conditions the placement of a ventricular assist device (VAD) may be considered.

Other potentially useful procedures include extracorporeal membrane oxygenation (ECMO) and placement of an artificial heart. These have varying degrees of success. Newer percutaneous VADs are a more feasible choice in smaller medical- surgical centers. Patients with LVAD demonstrated significant improvement in hemodynamics, renal function, and in the clearance of serum lactate compared to the use of IABP There are a limited number of centers that have access to such technology. Experiences in the placement of LVAD devices and in hemodynamic management are necessary to achieve an optimal benefit for patients. The use of IABP was independently associated with survival in the centers most experienced in its use. These devices are intended to serve as a bridge to cardiac transplantation, and resources must be available to continue this, often lengthy, workup.

Revascularization therapy: Because AMI is frequently the cause of CS, reestablishing blood flow to the affected myocardial area is critically important and decreases mortality. Reestablishing coronary arterial flow by the administration of thrombolytic agents works, but the preferred modality of revascularization remains either PCI or CABG. Thrombolytic therapy for CS after STEMI is only for patients in whom definitive therapy is contraindicated or unavailable. Fibrinolytic agents may still be considered in those situations in which PCI is not attainable for >90 minutes or patients within 3 hours of their MI, and free of contraindications. Early revascularization reduces mortality by 22% in patients with CS and by 16% in those who developed CS subsequent to admission. Early revascularization therapy is recommended for patients < 75 years with complications of ACS. Revascularization in NSTEMI did result in a significant decrease in mortality. Therefore it is not as important to revascularize NSTEMI patients. Both acute hemodialysis and ultrafiltration are used to remove the overload of fluid, especially in renal compromised patients.

Prevention

Long-standing hypertension is associated with both systolic and diastolic ventricular dysfunction leading to CHF. Hypertension is an independent risk factor for CAD. Controlling hypertension markedly lowers the mortality and the risk for developing CHF. Diabetics suffer from increased cardiac events, independent of CAD and hypertension. Diabetes is also associated with LVH and arterial vessel wall stiffening. Aggressive BP control and lipid control with statins have beneficial effects in diabetic patients beyond those seen in the general population. Patients with CHF should avoid exposure to cardiotoxins such as alcohol, smoking, and illicit drugs. Smoking markedly increases the risk of CAD. Cocaine use has both direct and indirect cardiac effects that increase the risk for CHF and sudden cardiac death.

Other common occurrences that lead to ADHF include myocardial ischemia, arrhythmias, AF, severe hypertension, renal dysfunction, unbalanced diet, and noncompliance with treatment. An elevated heart rate can lead to ADHF; thus, causes of tachycardia such as fever, anemia, hyperthyroidism, and infection should be addressed. In CHF the use of BB is indicated in almost all patients. Tachycardia in CHF decreases LV filling time, leading to a drop in CO. Patients with CHF frequently use concomitant medications such as NSAIDs and thiazolidinediones. Thiazolidinedione use for the control of diabetes is contraindicated in patients with CHF.

Daily weight determination at home is still the best evaluator of overall fluid volume. The actual weight is not important but rather the difference from the last measurements and an increased trend in weight is important. The patient or the doctor may increase or decrease the diuretic therapy. Electrolyte imbalances in CHF are mostly related to its treatment. A blood Na⁺ level <134 mEq/L is an independent risk for mortality and Na⁺ levels must be monitored in patients with CHF.

CLINICAL CASE CORRELATION

• See  also  Case 4  (Hemodynamic Monitoring), Case 5  (Vasoactive Drugs and Pharmacology), Case 14  (Acute Coronary Syndromes), and Case 15 (Cardiac Arrhythmias).

COMPREHENSION QUESTIONS

16.1  A 60-year-old man is evaluated in the ICU for chest discomfort that has been present intermittently for 6 hours. The patient was treated with ASA, a β-blocker, and nitroglycerin. The ECG revealed an inferior wall STEMI. Troponins were elevated. On physical examination, the heart rate was 60 beats/minute with a BP of 78/60 mm Hg. The JVD was elevated to the angle of the j aw. Lung auscultation was clear. A parasternal RV lift was present. A right-sided S3 was heard. Which of the following is the most likely cause for this patient's findings ?

A. Acute cardiac tamponade

B. Aortic dissection

C. Left ventricular free-wall rupture

D. Right ventricular myocardial infarction

E. Atrial rupture

16.2  A 68-year-old woman is in the ICU with palpitations and shortness of breath. She has a history of hypertension and chronic AF. Her medications are furosemide, candesartan, and warfarin. On physical examination, her heart rate is 120 beats/minute with an irregular rhythm, and her BP is 130/80 mm Hg. She has an elevated jugular venous pressure, rales in both lungs, and marked pitting edema of the lower extremities. Echocardiography shows LVH, an ejection fraction of 70%, and no significant valvular disease. After IV diuretics were begun, the patient's symptoms improved. Her heart rate is now 90 beats/minute and the BP is 120/75 mm Hg. Which of the following is the most likely primary mechanism causing her heart failure ?

A. Constrictive pericarditis

B. Diastolic dysfunction

C. Systolic dysfunction

D. Valvular disease

E. Mixed dysfunction

CLINICAL PEARLS

⯈ Jugular venous distention is the most sensitive clinical sign of acute cardiac decompensation. 

⯈ Echocardiography confirms the diagnosis of ADHF and aids in directing its management. 

⯈ In patients with right ventricular MI, echocardiography  demonstrates right ventricular enlargement with reduced systolic function. 

⯈ The use of IABP in severe ADHF serves as a  bridge to surgery or angioplasty. 

⯈ Medications have not lowered morbidity or mortality  in CHF secondary to diastolic dysfunction. 

⯈ In CHF, reversible factors that can cause exacerbations should be identi­fied and treated. A  sodium concentration <134 mEq/L is an independent risk factor for greater mortality in CHF. 

⯈ When ECG changes suggest myocardial ischemia, early revascularization is needed. 

⯈ Vasopressin can be added to dobutamine and norepinephrine for improvement in MAP.

References

Chinnaiyan K M , Alexander D, Maddens M, McCullough PA. Curriculum i n cardiology: integrated diagnosis and management of diastolic heart failure. Am Heart ] . 2007 ; 1 5 3 : 1 89- 200. 

Loscalzo J. Harrison's Pulmonary and Critical Care Medicine. New York, NY: McGraw-Hill; 2010. 

Toy E, Simon B, Takenaka K, Liu T, Rosh A. Case Files Emergency Medicine. 2nd ed. New York, NY: McGraw-Hill, Lange; 2009.

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