Class I: normal Rx: chronic HF therapy
Class II Rx: diuretics,
vasodilators
Class III:
Hypovolemic shock Rx: volume repletion
Class IV:
Cardiogenic shock Normal BP: vasodilators low BP: inotropes, pressors Normal
or high
Low CI 2.2 Cardiac index (tissue perfusion)
Low High
PCWP 18
Pulmonary capillary wedge pressure
Pulmonary edema
HF, heart failure; Rx, therapy; CI, cardiac index; BP, blood pressure; PCWP, pulmonary capillary wedge pressure.
T R E A T M E N T
Most patients with ADHF present with volume overload and pulmonary congestion.
The mainstays of therapy are diuretics and vasodilators, reserved for those patients with adequate cardiac output to maintain sufficient blood pressure (systolic blood pressure
>85 to 90 mm Hg) and end-organ perfusion (Algorithm 22.2, Forrester Class II) prior to their initiation. These therapies are considered Class I recommendations and reduce the work that must be performed by the failing heart by reducing both preload and afterload while providing symptomatic relief. Initial therapy with intravenous (IV) diuretics has a relatively rapid effect, with reductions in right atrial pressure, PCWP, and PVR within 5 to 30 minutes. For patients requiring high doses of furosemide, a continuous drip may be more effective than boluses>1 mg/kg. Guidelines for prac- tical diuretic use are shown in Table 22.2, and include adding thiazide diuretics for refractory cases. In selected patients with ADHF (such as MI with pulmonary edema), vasodilator therapy with IV nitroglycerin should be considered the first-line agent (Table 22.3). Nitroglycerin IV is a balanced arterial and venous vasodilator when given in appropriate doses, effectively reducing both preload and afterload without impairing tissue perfusion. At low doses, IV nitroglycerin induces venodilation (with- out significant coronary artery dilation), and may not effectively unload the failing heart. Therefore, IV nitroglycerin should be titrated aggressively (with careful blood pressure monitoring) in patients suffering from ADHF in the setting of myocardial ischemia. In other patients with pulmonary congestion in the setting of ADHF, the combination of IV nitroglycerin and IV loop diuretics provides rapid symptomatic relief and has been found to be more effective than high-dose diuretics alone.
Nesiritide is recombinant BNP that, like nitroglycerin, is a balanced arterial and venous vasodilator, but also promotes natriuresis in combination with loop diuretics.
Cardiac Disorders rAcute Decompensated Heart Failure 1 6 7
TABLE 22.2 Diuretics for Acute Decompensated Heart Failure Severity of
volume overload Diuretic Dose Comments
Mild to moderate Furosemide 20–40 mg PO or IV Follow Na+and K+
Severe Furosemide 40–120 mg IV, or IV
drip at 2–20 mg/hr
Up to every 6 hr for bolus dosing Refractory to loop
diuretics
Add metolazone 30 min prior to each furosemide dose
2.5–5 mg PO Most helpful when CrCl<30 mL/min
Refractory to combination of loop and thiazide diuretics
Consider inotrope (dobutamine) if renal perfusion is inadequate.
Consider renal replacement therapy if renal failure (HD or CVVHDF).
PO, by mouth; IV, intravenously; CrCl, creatinine clearance; HD, hemodialysis CVVHDF, continuous venovenous hemodiafiltration.
Nesiritide decreases PCWP promptly and improves dyspnea in patients with ADHF.
Nesiritide can be initiated most safely without a bolus at 0.01μg/kg/min, with titration to a maximum dose of 0.03μg/kg/min.
ACEIs and ARBs have an important role in the management of chronic HF, but their role in the setting of ADHF is less clear. Chronic ACEI or ARB therapy promotes afterload reduction, but may require dosage reduction or discontinuation in patients with ADHF to facilitate diuresis without impairment of renal function. Cautious initiation of ACEI or ARB therapy in the intensive care unit setting may be helpful with careful monitoring of renal function and electrolytes. The short-acting ACEI captopril (starting dose 6.25 to 12.5 mg every 6 to 8 hours) may be carefully titrated with each dose until a prespecified goal is met (systolic blood pressure<100 mm Hg, reduced SVR, or 300-mg daily dose). For patients with chronic HF, ACEIs or ARBs should be initiated approximately 48 hours after stabilization of an ADHF episode, most likely after transfer out of the critical care setting (Class I recommendation, level of evidence A).
TABLE 22.3 Vasodilators (all have potential for causing hypotension) Indication Vasodilator Dose (μg/min) Comments
ADHF Nitroglycerin 10–200 Headache,
tachyphylaxis
ADHF Nesiritide 0.01–0.03 Use bolus dosing with
caution
Hypertensive crisis Nitroprusside 0.5–5 Isocyanate toxicity ADHF, acute decompensated heart failure.
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Other medical therapies such as beta-blockers and calcium channel blockers have a limited role in the management of patients with ADHF. Beta-blockade is a mainstay of treatment for acute MI as well as for chronic HF, but patients presenting with MI and ADHF involving hypotension, or more than mild-to-moderate pulmonary congestion, have not been included in most of the relevant clinical trials. As such, IV metoprolol and other agents should be used with caution in this setting. Patients receiving chronic beta-blocker therapy may require a dose reduction, but beta-blockers should not be abruptly discontinued to avoid adverse events related to elevated catecholamine levels in patients with ADHF. Milrinone should be considered for these patients if they require inotropic support as it acts downstream from the beta-adrenergic receptor. Calcium channel blockers (including diltiazem, verapamil, and amlodipine) are contraindicated in patients with ADHF, secondary to their negative inotropic effects.
For patients in cardiogenic shock with hypotension and evidence of inadequate tissue perfusion (Algorithm 22.2, Forrester Group IV), dobutamine and milrinone are the inotropic agents of choice. Dobutamine is predominantly a beta-1 and beta-2 adrenergic receptor agonist, which augments both inotropy and chronotropy. There is frequently a reflex decrease in sympathetic tone that leads to lowered SVR, further augmenting cardiac output. In patients receiving chronic beta-blocker therapy or in patients in whom tachycardia is problematic, milrinone is an effective alternative to dobutamine. Milrinone is a type-III phosphodiesterase inhibitor with characteristics of both an inotrope and peripheral vasodilator. It has the disadvantage of renal clear- ance, and must be used with caution in patients with acute or chronic renal failure.
The peripheral vasodilation of milrinone may also cause hypotension, particularly if it is given inappropriately in the setting of volume depletion (Algorithm 22.2, For- rester Class III). Dobutamine and milrinone increase myocardial oxygen demand and should be reserved for cases of documented or suspected cardiogenic shock and sys- temic hypoperfusion. They do not have a role for mild episodes of ADHF. The use of vasopressors (e.g., dopamine or norepinephrine) may also be necessary in urgent situations to maintain blood pressure while the patient is being stabilized, but they should be weaned quickly as they increase afterload, and may further reduce end-organ perfusion. Table 22.4 shows typical dosing of inotropic agents and vasopressors.
For patients who cannot be adequately stabilized with medical therapy, consider- ation should be given to mechanical support, particularly if the patient is a candidate for advanced HF therapies such as cardiac transplantation or mechanical circulatory support with a left ventricular assist device (LVAD). Acute dialysis, especially contin- uous venovenous hemodialysis, can be used for volume control of diuretic-refractory
TABLE 22.4 Inotropic Agents and Vasopressors Dose
Drug Class (μg/kg/min) Comments
Dobutamine Inotrope 2.5–10 First line for ADHF Milrinone Inotrope/vasodilator 0.25–0.75 Useful with beta-blockade Dopamine Inotrope/vasopressor 5–50 Relatively weak agonist Epinephrine Inotrope/vasopressor 0.05–0.5 If refractory to dobutamine Norepinephrine Vasopressor 0.05–1 More appropriate for sepsis ADHF, acute decompensated heart failure.
Cardiac Disorders rAcute Decompensated Heart Failure 1 6 9
patients with renal failure. Intra-aortic balloon pump placement can provide mechan- ical afterload reduction, and augmented diastolic pressure to improve coronary artery filling in low-output states. Several temporary VADs have recently become available to provide less invasive mechanical circulatory support in the short term. The Tandem- Heart is a left atrial to femoral artery bypass system capable of providing up to 4 L/min of flow. It consists of an inflow cannula placed into the left atrium from femoral vein via trans-septal puncture, a continuous flow centrifugal (extracorporeal) pump, and an outflow cannula to the femoral artery. The Impella is an all-arterial percutaneous LVAD that utilizes a contained microaxial pump placed retrogradely across the aortic valve via the femoral artery. The catheter removes blood from the left ventricular cavity and pumps it into the ascending aorta. Two different sizes are available, capable of providing 2.5 and 5 L/min of flow, respectively. Finally, the CentriMag is a surgically implanted, temporary LVAD, which can be used to bridge severely decompensated HF patients to definitive therapy with LVAD or heart transplant. Pursuing more advanced mechanical therapy (e.g., LVAD support) or cardiac transplantation is an increasingly viable option for patients without irreversible end-organ damage who are at centers with the appropriate resources; thus early involvement of heart-failure and cardiac surgery specialists should be considered in such patients to facilitate institution of appropriate advanced therapy.
S U G G E S T E D R E A D I N G S
Cuffe MS, Califf RM, Adams KF Jr, et al. Short-term intravenous milrinone for acute exacerbation of chronic heart failure: a randomized controlled trial.JAMA.2002;287:1541–1547.
This RCT highlights the dangers of routine inotrope use in ADHF and demonstrates that inotropic agents should be reserved for those patients with evidence of clinically significant hypoperfusion.
Dickstein K, Cohen-Solal A, Filippatos G, et al. ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2008: the Task Force for the diagnosis and treatment of acute and chronic heart failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM).Eur J Heart Fail.2008;10:933–989 The 2005 ESC guidelines were the first to address the diagnosis and treatment of ADHF in a systematic fashion. The 2008 update cited here remains an excellent overview of the topic and the supporting scientific literature.
Heart Failure Society of America. Executive summary: HFSA (Heart Failure Society of America) 2010 comprehensive heart failure practice guideline.J Card Fail.2010;16:475–539.
While the ESC guidelines are dedicated specifically to ADHF, the 2010 HFSA guidelines represent a consensus-driven approach to establish best practices for diagnosis and treatment of HF, in general, including ADHF.
Hunt S, Abraham W, Chin M, et al. 2009 Focused update incorporated into the ACC/AHA 2005 guidelines for the diagnosis and management of heart failure in adults. A report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines developed in collaboration with the International Society for Heart and Lung Transplantation.J Am Coll Cardiol.2009;53:e1–e90.
The ACC/AHA practice guidelines regarding chronic heart failure provide a broad review of the data substantiating state-of-the art therapies for management of the heart failure patient.
New to the 2009 update is a section (4.5) ‘The Hospitalized Patient’ which provides recommendations for evaluation and management of acute decompensated heart failure.
Lloyd-Jones D, Adams R, Brown T, et al. Heart disease and stroke statistics–2010 update: a report from the American Heart Association.Circulation.2010;121:e46–e215.
This AHA update details the extensive cardiovascular disease burden in the United States.
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McCullough PA, Nowak RM, McCord J, et al. B-type natriuretic peptide and clinical judg- ment in emergency diagnosis of heart failure: analysis from Breathing Not Properly (BNP) Multinational Study.Circulation.2002;106:416–422.
This study is the most widely recognized trial validating the utility of serum BNP measurement for differentiating heart failure from other entities with similar presentations.
Publication Committee for the VI. Intravenous nesiritide vs nitroglycerin for treatment of decom- pensated congestive heart failure: a randomized controlled trial. [erratum appears inJAMA.
2002;288:577].JAMA.2002;287:1531–1540.
This trial demonstrates the utility of nesiritide for improving the hemodynamics of patients with ADHF.
Sarkar K, Kini A. Percutaneous left ventricular support devices.Cardiol Clin.2010;28:169–184.
This review describes available percutaneous mechanical support devices. The authors also provide details of placement technique, complications, contraindications, and hemodynamics of each device.
23 Approach to Hypertensive Emergencies
Derrick R. Fansler and Daniel H. Cooper
Hypertensive emergencies have become a less frequent cause for admission to the inten- sive care unit (ICU) with the widespread availability of antihypertensive medications in the current medical era. Only 1% of patients with hypertension will present with a hypertensive emergency during their lifetime. Unfortunately, severe hypertension is still very common, so distinguishing a true hypertensive emergency from hypertensive urgency is key to guiding therapy. Therefore, the following terms are worth defining.
rHypertensive crisis:A generic term for severe elevations in blood pressure that have the potential to cause target organ (heart, vasculature, kidneys, eyes, brain) damage.
This includes bothhypertensive emergencyandhypertensive urgency.
rHypertensive urgency:A severe elevation in blood pressurewithoutevidence of acute and ongoing target organ damage (TOD).
rHypertensive emergency:A severe elevation in blood pressurewithevidence of acute, ongoing TOD.
rHypertensive encephalopathy:A specific hypertensive emergency characterized by irritability, headaches, and mental status changes caused by significant and often, rapid elevations in blood pressure.
rAccelerated-malignant hypertension:A specific hypertensive emergency characterized by fundoscopic findings of papilledema and/or acute retinal hemorrhages and exudates.
Timely differentiation between hypertensive emergencies and urgencies is imper- ative so that patients with severely elevated blood pressure can be triaged to the appro- priate level of care and monitoring (i.e., outpatient follow-up vs. inpatient ward vs.
ICU) with the appropriate antihypertensive agents initiated (parenteral vs. oral) and the establishment of blood pressure lowering goals at the appropriate time interval (minutes-to-hours vs. days-to-weeks). In the absence of acute, progressive end-organ damage, elevated blood pressure alone does not require immediate, emergent ther- apy. The above definitions intentionally are devoid of any absolute blood pressure numbers because the level at which individuals develop TOD can vary depending on clinical substrate and the rapidity with which the blood pressure rises. For exam- ple, a patient with long-standing poorly controlled hypertension may tolerate a blood pressure in excess of 230/120 mm Hg without evidence of acute end-organ damage,
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Aortic Dissection • Minimize shear stress. Decrease dP/dt. • Goal: MAP 60–75 mmHg HR 60-70 bpm • Beta Blocker +/- SNP • See chapter 21 for detailed discussion. Preeclampsia/Ecclampsia • Definitive Tx: Delivery • Hydralazine, labetalol, or methyldopa + IV MgSO • See chapter 68 for detailed discussion
Subarachnoid Hemorr
hage • Nimodipine • See chapter 54 for detailed discussion.
Cerebrovascular Accident • “Permissive HTN” to protect ischemic penumbra. • Controversial • See chapter 52 for detailed discussion. Intracerebral Hemorrhage • Controversial • SNP: Treat BP if MAP > 130 or SBP >220 mm Hg • See chapter 55 for detailed discussion.
•Hypertensive Emergency Initiate syndrome specific management Cardiac • Unstable Angina • Myocardial Ischemia • Myocardial Infarction • LV Failure w/ acute pulmonary edema History: • CP, SOB/DOE, orthopnea, PND, diaphoresis • Cardiac RF: DM, HTN, ↑chol,↑age, smoking, etc. • Dietary indiscretion • Med Compliance • Meds: ASA, nitrates • Hx of CAD, CHF Physical Exam: •↑HR,↑RR,↑SaO •↑JVP, S3, S4, displaced PMI • Crackles/Rales, • Peripheral Edema Diagnostic Studies: •↑Cardiac enzymes,↑BNP • ECG: dynamic ST/T wave changes, Q waves. • CXR: cardiomegaly, bilateral infiltrates c/w pulmonary edema. Management Pearls: • NTG gtt titrated to symptom relief. • Add β blocker for all except acute LV failure (hold until compensated/euvolemic). • Add loop diuretics if pulmonary edema present. • ACE-I should be initiated unless contraindicated. • See chapters on AMI (19) and CHF(22) for further discussion Renal • Acute Renal Failure • Acute Glomerulonephritis • Scleroderma Renal Crisis • Renal Artery Stenosis • Renal Transplant Rejection History: • Hematuria • Decreased urine output • Recent URI • Hx of CRI, renal transplant • Meds: ACE-I, NSAIDs, cyclosporin, steroids, diuretics Physical Exam: • Skin findings of scleroderma • Abdominal Bruits • Gross hematuria Diagnostic Studies: •↑Serum creatinine • U/A: RBCs, protein, casts Management Pearls: • HTN may be result or cause of acute renal impairment. • Previous creatinine vital to document acute change that warrants emergent treatment. • Nicardipine or Fenoldapam • Fenoldapam, in comparison to SNP, improves natriuresis, diuresis and CrCl. • SNP: Caution given renal impairment (cyanide toxicity). • Goals: ↓MAP by 10-20% within mins-1 hour, then another 10% over next 5 hours. • Hemodialysis if necessary. • Scleroderma renal crisis: Must include ACE-I.
Catecholamine Excess • Pheochromocytoma • Tyramine ingestion with MAO inhibitor • Cocaine, Amphetamines • Rebound HTN History: • HA, sweating, palpitations • Hx of depression/MAOI use with dietary indiscretion. • HTN meds: clonidine, beta blockers, compliance? • Illicit drug use Physical Exam: •↑HR • Hyperhidrosis • Restless, agitated, anxious • Café-au-lait spots, port wine stains, neurofibromas Diagnostic Studies: • Urine/serum toxicology • Serum catecholamines/ urine metanephrines Management Pearls: • Pheo/MAOI/cocaine: α-blocker (phentolamine) +/- β-blocker (after α-blocker started). Also, BZDs useful in cocaine intoxication. • Rebound HTN: Typically from clonidine or β blocker withdrawal. Reinstituting a single dose of withdrawn med usually sufficient to abate crisis. • If above strategies yield little response, alternative therapies can be utilized (i.e. SNP, labetalol).
Accelerated-Malignant HTN • See definition in text. • Symptoms include HA/N/V/vision changes • Fundoscopic: hemorrhages, exudates, papilledema. • May be accompanied by renal, neurologic impairment. Management Pearls: • SNP: Reduce MAP by 20–25% in minutes to 1 hour, then to 160/110 over next 5 hours if tolerated.
Hypertensive Encephalopathy • Autoregulation of CBF fails at critically elevated BP levels leading to cerebral hyperperfusion and edema. • Variable symptoms (agitation/restlessness/fatigue to HA/N/V to overt delirium/ encephalopathy) • Typically, no focal neurologic deficits. • Head CT indicated in all patients with MS changes and/or focal neurologic deficit. Management Pearls: • Reduce MAP no more than 20-25% in minutes to 1 hour, then to 160/110 over next 5 hours if tolerated. • SNP traditionally used. Other viable options: labetalol, fenoldapam, nicardipine • If neurologic status worsens with Tx, reduce infusion and consider other etiologies. Figure23.1.Managementofspecifichypertensiveemergencies.CBF,cerebralbloodflow;BP,bloodpressure;HAheadache;N, nauses;V,vomiting;MS,mentalstatus;MAP,meanarterialpressure;SNP,sodiumnitroprusside;Tx,treatment;HTN,hyper- tension;LV,leftventricle;CP,chestpain;SOB,shortnessofbreath;DOE,dyspneaonexertion;PND,paroxysmalnocturnal dyspnea;RF,riskfactors;DM,diabetesmellitus;chol,cholesterol;ASA,aspirin;CAD,coronaryarterydisease;CHF,congestive heartfailure;HR,heartrate;RR,respiratoryrate;SaO2,saturationarterialoxygen;JVP,jugularvenouspressure;PMI,pointof maximalimpulse;BNP,brainnatriureticpeptide;CXR,chestx-ray;IV,intravenous;NTG,nitroglycerin;gtt,drip(intravenous); ACEI,angiotensin-convertingenzymeinhibitor;AMI,acutemyocardialinfraction;URI,upperrespiratoryinfection;Hx,history; CRI,chronicrenalinsufficiency;NSAIDs,nonsteroidalanti-inflammatorydrugs;CrCl,creatinineclearance;MAOI,monoamine oxidaseinhibitor;pheo,pheochromocytoma;BZDs,benzodiazepines;dP/dt,rateofchangeinpressure;bpm,beatsperminute.
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