A 65-year old man is admitted to your ward with worsening dyspnea over the last two days. He has noticed increased swelling of his legs, and has had episodes of waking up short of breath for the past two nights. He has a history of congestive heart failure, and is taking furosemide 40mg PO daily at home. Physical exam demonstrates normal heart sounds, crackles at the base of both lungs, and pitting edema at both ankles up to his knees.
- What clinical syndrome is this patient demonstrating?
This patient is demonstrating Acute Decompensated Heart Failure. This is a syndrome characterized by dyspnea in the setting of an acute increase in left-sided heart filling pressures, which may lead to pulmonary edema as a result. Heart failure is caused by functional or structural cardiovascular dysfunction, leading to inadequate systemic perfusion. It can be classified into two categories, each with different possible etiologies:
- Heart failure with reduced ejection fraction
- Systolic dysfunction
- Main causes include: coronary artery disease, idiopathic dilated cardiomyopathy, hypertension
- Heart failure with preserved ejection fraction
- Diastolic dysfunction
- Main cause: hypertension
- Heart failure with reduced ejection fraction
- What initial steps would you take in the management of this condition?
Goals of initial management for an acute exacerbation of CHF include symptom management, treating pulmonary edema, and prevention of further volume overload:
- O2 supplement
- Loop diuretic (furosemide)
- Salt restriction <3g/d
- Fluid restriction to ~1.5L/d
- Position sitting up
- What change, if any, would you make to the patient’s home medication?
Change furosemide 40mg PO to 40mg IV for greater efficacy. As the patient went into acute decompensated heart failure despite diuretic use at home, an increase in the patient’s diuretic dose is required. The efficacy of furosemide IV is 2x that of furosemide PO. Treating this patient with furosemide 40mg IV (equivalent to 80mg PO) would be an appropriate start point for this patient. If this patient was diuretic-naïve, you could start at a lower dose of furosemide 20mg IV.
- Felker GM et al. Diuretic strategies in patients with acute decompensated heart failure. N Engl J Med. 2011, 364: 797-805.
- Heart Failure Society of America, Lindenfeld J et al. HFSA 2010 Comprehensive Heart Failure Practice Guideline. J Card Fail. 2010, 16:e1.
- Ware LB and Matthay MA. Clinical practice. Acute pulmonary edema. N Engl J Med. 2005, 353: 2788-96.
- Yancy CW et al. 2013 ACC/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013, 62: 147-239. Epub 2013 Jun 5.
You are called to the ward because of a patient with sudden onset chest pain.
- Outline your initial steps.
An initial approach for this patient involves obtaining the following:
- History – onset, location, provoking/relieving factors, quality, radiation, severity, past history of similar pain, associated symptoms (diaphoresis, nausea, breathlessness, vomiting, hemoptysis, relationship of pain to food (r/o GERD or other esophageal etiologies), melena/hematochezia.Be sure to ask closed-ended, targeted questions, as a patient with acute chest pain will not tolerate a lot of talking.
- Past Medical History – similar symptoms, ACS, GERD
- Acquire data from patient chart – reason for admission, medications, past medical history
- Physical exam – vitals (HR, BP, RR, O2 sat, Temp), cardiac exam, respiratory exam
- What investigations would you order?
Investigations to order at this time:
- CBC, lytes
- ECG, Troponin, CK
- Chest xray
- CT Pulmonary Embolism if suspect PE
- Assuming your tests suggest an acute coronary syndrome (but no STEMI), what is your initial management at this time?
Put the patient on a monitor or telemetry
O2 supplementation (if O2 sat<94% or respiratory distress)In the event of ACS:
- Aspirin 81mg 2tab PO chew
- Metoprolol 25mg PO (if BP is elevated)
- Nitroglycerine 0.4mg spray SL (if BP will support)
An elderly patient is admitted with a serum [Na+] of 120mmol/L. She is alert and oriented and appears well.
- What specific initial laboratory tests would you order to further delineate the cause of her hyponatremia?
Hyponatremia is defined as a low serum sodium concentration and reflects an excess of free water as opposed to a loss of sodium.
Specific laboratory tests to order at this time include:
- Serum Osmolality – helps differentiate between hypotonic/isotonic/hypertonic hyponatremia
- Urine Na+ (UNa)
- Urine Osmolality (UOsm)
Hypotonic hyponatremia can be further divided into hypovolemic/isovolemic/hypervolemic. A clinical assessment of the patient’s volume status will assess this.
- What treatment options would you consider if…
- Your physical exam demonstrated she was euvolemic?
- Your physical exam demonstrated she was hypervolemic?
- Your physical exam demonstrated she was hypovolemic?
If the patient does not demonstrate any symptoms of acute hyponatremia (confusion, lethargy, seizure, nausea), and there is no record of a recent sodium concentration, assume that this patient’s hyponatremia is chronic. The main tenets of managing hyponatremia are:
- Fluid restrict <1.5L/day
- Furosemide (if hypervolemic)
- IV NS (if hypovolemic)
Monitor the patient’s serum sodium closely to avoid overly rapid correction, which could lead to osmotic demyelinating syndrome (central pontine myelinolysis). Limit correction of [Na+] to<8mmol/day.
If administering IV NS to correct hypovolemic hyponatremia, use the following formula to determine how much IV NS to administer to avoid raising the serum [Na+] above 8mmol/day:
- A sign of overly rapid correction may be free water diuresis (high output of dilute urine).
- Monitor urine output to ensure it does not exceed 200cc/2hrs
- Measure UOsm to ensure it is not <100mOsm/L
- How would your management change if this patient presented with new onset confusion, lethargy, a single episode of seizure, and a serum [Na+] 115mmol/L?
This patient is experiencing acute symptomatic hyponatremia. This is a medical emergency, and is likely the result of cerebral edema. This requires rapid correction of her serum sodium with hypertonic saline (3% NS). Ensure the following while treating:
- Raise the serum [Na+] by 1-2mmol/L/hour for the first 4-6hrs (can use the formula above to calculate)
- Never give more than 100cc/hr
- Do not increase serum [Na+] by more than 8mmol/L/day to avoid osmotic demyelinating symdrome
- Monitor urine output and Uosm for free water diuresis at least every 4 hours (may require a monitored setting)
- Call nephrology if you have any concerns
If overly rapid correction occurs, can give IV D5W and/or DDAVP 1-2ug IV (patient must be NPO for 8 hours after giving DDAVP to ensure no free water ingestion, aka “locking”)
Adrogué HJ and Madias NE. Hyponatremia. NEJM. 342:1581-1589.
A patient on your ward has a serum [K+] of 6.4.
- Outline the steps you would take to manage her hyperkalemia.
Management of hyperkalemia involves:
- Ensure the value is not spurious – check pre-existing K+ values if available to compare. Repeat electrolytes if there is time (i.e. no ECG changes)
- ECG – check for changes that reflect hyperkalemic effects on the myocardium
- Tented and peaked T waves
- Flattening/absent P waves
- Widening of the QRS
- Sine waves
- Calcium gluconate 1g IV – administer if ECG changes are present to protect the myocardium and avoid cardiac dysregulation.
- Insulin 10U IV with dextrose 12.5-25g – insulin promotes the shifting of potassium into cells, thereby lowering serum [K+]. Glucose administration is to protect against hypoglycaemia with insulin. Accucheck for blood glucose first.
- Salbutamol 10mg nebulized – β2-agonists can be used as an alternative to insulin to shift K+ intracellularly. It can also be used with insulin in cases of severe hyperkalemia.
- Repeat electrolytes in 1-2 hours to ensure there is a change in K+ with treatment
- Search for an underlying cause of hyperkalemia:
- Renal failure
- Urinary obstruction
- Exogenous intake (supplements/diet)
Elliot ME, Ronksley PE, Clase CM, Ahmed SB and Hemmelgarn BR. Management of patients with acute hyperkalemia. CMAJ. 182:1631-1635.
Nyirenda M, Tang JI, Padfield PL and Seckl JR. Hyperkalaemia. BMJ. 2009, 339:1019-1024.
What are the criteria for Systemic Inflammatory Response Syndrome (SIRS)?
SIRS is a system-wide inflammatory response to an inciting agent. The criteria for diagnosing SIRS are the presence of 2 or more of the following:
- Temperature >38.5oC or <35.0oC
- Heart rate >90 beats/min
- Respiratory rate >20 breaths per minute (or arterial CO2 tension <32mmhg, or need for mechanical ventilation)
- WBC >12 000/mm3 or <4000/mm3 or >10% band forms
What is the definition of Sepsis? Severe Sepsis?
Sepsis is SIRS caused by a documented infection. Any presentation of SIRS from an unknown etiology should be worked up for an infectious cause to rule out sepsis.
Severe sepsis is sepsis with hypotension (SBP<90, MAP <70)
What is your initial workup and management for a patient with suspected sepsis?
- CBC, Lytes, Cr, BUN, AST, ALT, ALP
- Serum Lactate (a marker for tissue hypoperfusion)
- Serum glucose (may be elevated in sepsis)
- Urine dip, Urine C&S
- Lumbar puncture (consider if suspect meningitis)
- Blood cultures x2 (blood cultures x3 with a new murmur for suspected infectious endocarditis)
- IV NS to maintain BP and prevent shock
- Empiric IV broad-spectrum antibiotics (differnet hospitals may have different protocols). Switch to narrow-spectrum antibiotics once a specific pathogen has been identified
- Treat hyperglycemia (if present) with insulin
- Annane D, Bellissant E and Cavaillon JM. Septic shock. Lancet. 2005, 365:63-78.
- Dellinger R.P. et al. Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2012. Intensive Care Med. 2013; 39:165-228.