Acute Heart Failure - Lohr/Gaglianello Flashcards
In a sentence, what is heart failure?
Does heart failure always mean impaired ejection?
Heart failure is a failure of the heart to pump blood.
This can be due to impaired filling or ejection.
What is the outlook for heart failure?
How many cases are there–how widespread is it?
Bad. 5-year mortality exceeds 50%.
Millions of cases (“550k/year), most common diagnosis for those aged 65+, largest expense for medicare.
Distinguish between the intrinsic and extrinsic factors that contribute to CO (& thereby heart failure).
Intrinsics: Contractility, Heart Rate.
Extrinsics: Preload, Afterload.
What effect does tachycardia have on stroke volume?
On cardiac output?
Increased heart rate decreases diastolic filling time, which means that stroke volume is reduced.
Cardiac output increases initially, then peaks and falls. Recall that CO = HR x SV.
How is CVP influenced by heart contractility?
By blood volume?
What should CVP ideally be?
CVP increases as heart contractility declines in heart failure.
Increased blood volume increases CVP.
CVP should ideally be 0-2mm Hg (*according to lecturer. According to outside sources, 2-6mm Hg).
Explain how ventricular dilation contributes to heart failure.
How does compensation change this process?
Ventricular dilation increases wall stress via Laplace’s Law. This increases myocardial oxygen demand & ischemia, weakening the heart further.
Compensation increases the thickness of the wall, reducing the stress.
Explain how each of the following factors can exacerbate heart failure:
Increased sodium intake
Uncontrolled hypertension
Acute MI
Hyperthyroidism
Increased Na >> Increased fluid retention >> Increased preload.
Hypertension >> Increased afterload.
Acute MI >> Loss of myocyte function >> Decreased contractility.
Hyperthyroidism >> Increased heart rate*
What are some important components of a heart failure patient’s history?
Changes to medication
Diet (observe salt intake)
Weight changes
Angina
Exercise tolerance
Orthopnea/PND
What findings are seen on physical exam in a patient with acute heart failure?
Murmurs (mitral regurg, crescendo-decrescendo, S3 gallop, P2 knock)
Jugular distension, lower extremity edema, painful hepatomegaly.
Tachypnea, inspiratory crackles.
Decreased pulses & cold, clammy skin.
Hypotension (predictive of increased mortality)
What is the signifiance of jugular venous distention?
How does this relate to CVP?
Jugular venous distention is a sign of right-sided heart failure–systemic congestion.
CVP can be estimated as JVP + 5.
Describe the lab findings in a patient with acute heart failure.
Elevated natriuretic peptides.
Elevated troponins.
Basic metabolic panel (BUN/Creatinine) suggesting renal dysfunction (indicative of mortality)
CBC: Possible anemia
CXR: Pulmonary edema
Venous oxygen saturation: <70%
What metrics can be measured by echocardiography in acute heart failure?
Hemodynamic parameters such as RAP, CO, LAP, EF. The cause of failure may be identified (wall/valve), and risk can be estimated.
A swan-ganz catheter is also called a PAC. Where is its sensor placed?
When is its use indicated?
In the pulmonary artery.
When there is uncertainty about hemodynamic parameters, to evaluate difficult cases (refractory, possible shock, decompensation), and to evaluate for VAD/transplant.
Describe the class of heart failure (dry/wet, warm/cold) each of the following patients best fits under.
Paroxysmal nocturnal dyspnea with hypotension despite use of an ACE-inhibitor
Mentally obtunded but otherwise normal
Lower limb edema with warm extremities
Cold & Wet
Cold & Dry
Warm & Wet
What does pulmonary wedge pressure estimate?
If PAWP is elevated, what can be said about the stroke volume of the left ventricle?
Wedge pressure estimates LVEDP.
Higher wedge pressure = elevated LVEDP. Stroke volume is probably elevated, but is certainly inadequate.
Is increased systemic vascular resistance a sign of “cold” or “wet” heart failure?
Is increased central venous pressure a sign of “cold” or “wet” heart failure?
Is decreased cardiac output a sign of “cold” or “wet” heart failure?
Increased SVR >> Cold
Increased CVP >> Wet
Decreased CO >> Cold
What hemodynamic parameters define heart failure as “wet” and/or “cold”?
What hemodynamic parameters are the goals of treatment?
Wet: PCWP > 18 or RAP > 8
Cold: CI < 2.2
Keep CI above 2.2, PCWP above 16 (18?), and RAP above 8. Try to reduce SVR below 1200.
What is Cardiac Index (CI)?
Cardiac index (CI) = Cardiac output (CO) / Body surface area
Which form of acute heart disease is least common?
Cold & Dry
(probably won’t be tested)
A patient presents in acute heart failure with RAP 25, PAWP 30, and SvO2 < 30%.
What class of heart failure is this, and how can you tell?
Cold & Wet. Wet because of the apparent congestion (elevated RAP, PAWP), cold because of the inadequate perfusion (low venous oxygen saturation)
What is the treatment of choice for cold & wet acute heart failure?
To correct the “wet”: Diuretics.
To correct the “cold”: Vasodilator or inotrope, depending on MAP.
(renal impairment means that perfusion may have to be reestablished before diuretics may take effect)
Outline the requirements for inotrope use in acute heart failure
- Advanced systolic heart failure + low output syndrome + hypotension
- Vasodilators either ineffective or contraindicated
- Fluid overloaded and unresponsive to diuretics or with deteriorating renal function
Why are inotropes a ‘double-edged sword’ in the treatment of acute heart failure?
Inotropes increase calcium release, which increases cardiac workload and risk of arrhythmia
Describe the mechanism of action and primary effect(s) of milrinone
PDE inhibitor
Inodilator: increases contractility (inotropic) and decreases afterload (vasodilator) with no significant increase in oxygen consumption
List some side effects of milrinone
- Hypotension
- arrhythmia
- tachycardia
Describe the predominant action and effect(s) of dobutamine
- ß1 agonst, weak ß2 agonist
- increases contractility, mild vasodilator effect
What are the primary side effects of dobutamine?
- arrhythmia
- angina
- hypertension
- tachycardia
Diuretics - do they require increased or decreased dosing in the treatment of heart failure?
increased
What are some key challenges of diuretic therapy in heart failure?
- Threshold - need adequate dose to achieve effect (difficult and time-consuming to find right dose)
- Braking phenomenon: long-term loop diuretic use results in a reduced natriuretic response
- Rebound: infrequent dosing leads to excess sodium retention
- long-term tolerance, resulting in tubular hypertrophy
Compare the relative potency of the following diuretics:
- furosemide
- bumetanide
- torsemide
furosemide > tosemide > bumetanide
List some key side effects of diuretics
- electrolyte abnormalities (hypokalemia, hypomagnesia, hyponatremia)
- hypotension
- gout exacerbation
- hearing loss (rare)
- increased digoxin toxicity
- renal insufficiency
- muscle cramps
Most patients with acute decompensated heart failure fall into what category?
(wet-temperature axis)
The majority of these patients require what primary therapy?
wet-warm
IV diuretics (may also require vasodilators)
List some key caridac effects of vasodilators
- decreased afterload
- increased stroke volume
- LVEDP decreases
- decreased preload
What are some side-effects or limitations of IV nitroglycerin use?
- headache
- hypotension
- prolonged profound hypotension and bradycardia (rare)
- tachyphylaxis
- 20% non-response among patients
What are the dosing goals for IV nitroglycerin?
- SBP > 80
- SVR < 1200
- PCWP <= 16
IV nitroglycerin exerts its therapeutic action though what primary hemodynamic mechanism(s)?
low dose: venodilation -> decreases filling pressure
high dose: arterial vasodilation -> decreases SVR, increases CO
Does nitroprusside influence pre-load or after-load?
both (“balanced”)
decreases filling pressures, SVR, PVR, and increases CI
What are the key dosing goals of nitroprusside?
- SBP > 80 mmHg
- SVR < 1200
- PCWP <=16
What are the major limitations/side effects of nitroprusside therapy?
- cyanide toxicity -> nausea, ‘weirdness’. Develops with high dose (>250 mcg/min for >2 days) or with low hepatic perfusion due to low CO
- accumulation of thiocyanate (with chronic use and impaired renal function)
Which of the following therapies may be useful in ‘wet-warm’ heart failure?
- inotropes
- nesiritide
- endothelin anatgonists
- vasopressin antagonists
None. Use of adjunctive therapies beyond diuretics has not been demonstrated to improve outcomes.
Which therapy is indicated with high vascular resistance and BP?
- SBP >=85mmHg
- SBP < 85mmHg
- vasodilator
- inotrope +/- IABP
DO ACE Inhibitors target pre-load or after-load?
pre-load
