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22 Cards in this Set

  • Front
  • Back
-acute onset refers to the sudden appearance of symptoms, acute symptoms have progressed to a point at which immediate or emergency intervention is necessary
-chronic symptoms represent the baseline condition, the limitation the pt lives with on a daily basis
Left sided HF
-refers to failure of the left ventricle to fill or empty properly
-this leads to increased pressures inside the left ventricle and congestion in the pulmonary system
Right sided HF
-failure of the right ventricle to pump adequately
-most common cause of right sided HF is left sided HF
-right sided HF can also result from pulmonary disease and primary pulmonary artery HTN, referred to as cor pulmonale
-acute onset of right sided HF is often caused by pulmonary embolus
Systolic dysfunction
-is usually estimated by ejection fraction, or the percentage of the left ventricular end-diastolic volume that is ejected from the ventricle in one cycle
-if the LVEDV is 100ml and the stroke volume is 60ml, the ejection fraction is 60%
-normal EF is 50-70%
-systolic dysfunction is defined as an EF of less than 40% and is caused by a dec in contractility
-the ventricle is not emptied adequately because of poor pumping and the end result is decreased CO
Diastolic dysfunction
-pumping is normal or even inc, with an EF as high as 80%
-it is caused by impaired relaxation and filling
-if the ventricle is stiff and poorly compliant, relaxation is slow or incomplete
-if the heart rate is fast, diastole is short, or if the patient has a-fib there is no organized atrial contraction
-these mechanisms all reduce filling of the ventricle and contribute to diastolic dysfunction, therefore decreasing CO
Mechanical factors
-CO equals stroke volume multiplied by heart rate
-stroke volume equals preload, contractility, and afterload
-afterload is the resistance to the flow of blood from the heart
-resistance is a function of both the compliance and the diameter of the artery
-a high resistance may decrease stroke volume
-contractility is the force and velocity with which the ventricle contract
-preload is the volume of blood in the ventricle at the end of diastole
-pulmonary artery wedge pressure PAWP is used to estimate left ventricular end diastolic pressure
-left ventricular end diastolic pressure is used to estimate left ventricular end diastolic volume, therefore preload
-in a pt with hear or lung disease, CVP does not reliably reflect left ventricular end diastolic pressure
-in pt with a healthy heart CVP is an adequate estimate of LVEDP because variation is most often related to total body volume that affects the right and left ventricles
Heart rate
-the immediate response to a dec in stroke volume, a dec in arterial oxygen content, or an increase in metabolic demand is an increase in heart rate
-because the ventricle fills during diastole, preload becomes compromised at higher heart rates because of the shortened diastolic filling time
-a dec in preload compromises contractility
-any rhythm that does not include a rhythmic atrial contraction, such as a-fib, junctional rhythms, ventricular rhythms, and ventricular pacing, can compromise filling and therefore stroke volume and CO
Acute exacerbation of CHF
-any factor that inc oxygen demand, and therefore demand for inc CO beyond the ability of the ventricle to function, causes an exacerbation
-similarly, any factor that depresses the function of the already compromised ventricle leads to exacerbation, like drugs that exert a negative inotropic effect such as CCB and BB.
-as the ventricle is called on to work harder, it works less efficiently, and the LVEDP increases, leading to increased pulmonary artery pressures
-the increases PAP, in turn lead to orthopnea, pulmonary edema, elevated venous pressures, liver congestion, lower extremity edema, and paroxysmal nocturnal dyspnea
-pt may also present with lower BPs, more rapid heart rates, and prerenal azotemia
Brain Natriuretic Peptide
-BNP is a naturally occurring substance secreted by the ventricles when overfilled
-because the BNP level is well correlated with LVEDP and PCWP, it makes an excellent marker of HF
-pt with BNP levels greater than 80 show evidence of elevated PCWP, confirming HF decompensation as the source of worsening symptoms
Airway and breathing mgmt
-when the acute onset of HF or the acute exacerbation is accompanied by profound pulmonary edema, such as in MI or flash pulmonary edema, the airway may become compromised
-an indication that normal minute ventilation is not being maintained is inc PaC02 associated with inc work of breathing and respiratory acidosis
-evaluation of crackles along with peripheral edema, liver congestion or ascites, and renal function allows for a better assessment of fluid status than crackles alone
-an adequate diuretic response is about 1L of urine within 2hrs of IV dose
-two indicators are used to determine the adequacy of perfusion

first is function of organ systems:
-inadequate perfusion affects the brain, which leads to confusion and change in level of consciousness
-kidneys failure will lead to inc BUN and creatinine, and subsequent oliguria.
-GI system will be affected by leading to ileus and liver failure

Second indicator is metabolic acidosis:
-The problem is decreased CO caused by decreased contractility
-The goal of treatment should be to increase cardiac output
-if perfusion is severely inadequate or prolonged past the capacity of the body to buffer the lactic acid produced, the level of sodium bicarb decreases, as does the pH, producing metabolic acidosis
Optimize hemodynamics
-One way to increase CO is to optimize preload
-Increased preload is a problem
-Pt are total body volume-overloaded
-The combination of fluid overload and decreased contractility leads to cardiopulmonary congestion with increased pulmonary artery pressures and overfilling of the heart
-When the heart is overfilled, it becomes stiff and does not empty or fill well
-The result is compromised stroke volume
Increase contractility
-To inc CO, it is necessary to inc contractility and decrease afterload
-All inotropes inc myocardial oxygen consumption
-Dopamine is also an excellent inotrope, it is also a vasoconstrictor, it increases afterload in pt with HF and will decrease stroke volume
-doses of 5-10mcg/kg/min dopamine inc inotropy with significant chronotropy
-at high doses > 10mcg/kg/min alpha effects cause peripheral vasoconstriction
-400mg/250ml D5W, begin 5mcg/kg/min
-smooth muscles of the arteries and veins have mostly alpha1 and alpha2 receptors (A for Arteries & A for Alpha)
-activation of alpha1 and alpha2 receptors in the arteries results in inc contraction by arteriolar smooth muscle and an inc BP
Increase Contractility cont
-Inodilator, are used to stimulate beta receptors located in the heart and blood vessels to increase contractility and cause vasodilation,
-dobutamine is most commonly used, Dobutamine is predominantly a β1-adrenergic agonist
-β1-adrenergic agonist- inc cardiac output, by raising heart rate (positive chronotropic effect) and increasing impulse conduction and increasing contraction thus increasing the volume expelled with each beat (increased ejection fraction).
-heart has mostly beta1 (beta1 - 1 heart)
-Dobutamine also has mild β2 agonist activity, which makes it useful as a vasodilator.
-while Alpha 1 receptors mediate vasoconstriction, Beta 2 receptors induce vasodilation in vascular smooth muscle
-Inodilator, used to stimulate beta receptors located in the blood vessels to cause vasodilation
-Systemic vascular resistance is usually decreased with administration of dobutamine.

-SBP 70-100mmHg with s/s of HF and pulmonary edema
-2-20mcg/kg/min, increase in 5-10mcg, up to 40mcg/kg/min
-mix 250mg in 250ml D5W (1000mcg/ml)
-Sometimes an inodilator alone is not sufficient to decrease after load
-Decreasing and controlling the blood pressure or decreasing the workload of the damaged myocardium requires immediate treatment, and vasodilation with parenteral meds are necessary
-Nitroprusside had the most rapid onset, it provides for rapid, efficient decrease in BP
-IABP has proven very successful in reducing afterload in cardiogenic shock
-Nitroprusside acts on vascular smooth muscle to reduce afterload
-Sodium nitroprusside (SNP) has potent vasodilating effects in arterioles and venules (arterioles more than venules).

-Mix 50mg in 250ml D5W
-Initiate at 0.2mcg/kg/min, titrate 0.1mcg/kg/min
-Titrate at 1mcg/kg/min once 1mcg is reached
-Max dose is 10mcg/kg/min
Nitro gtt
-Is valuable in decreasing preload, It is not a good afterload reducer or antihypertensive
-Nitrates are venodilators, and primary effect is to dec preload
-Nitrates are used in HF to help alleviate the symptoms of orthopnea and dyspnea on exertion
-When pt lie down, the inc venous return leads to inc pulmonary artery pressure because the volume is too great for the weakened left ventricle
-This sudden inc in preload and pulmonary artery pressure causes the sensation of dyspnea
-Sitting up reduces the preload and relieves the symptoms
-Nitrates decrease the preload and mediate the volume of blood presented to the left ventricle
-direct smooth muscle relaxation of the coronary arteries, improves coronary blood flow and increasing myocardial oxygen supply
-dec myocardial oxygen demand by reducing preload

-Nitro gtt 50mg/250ml D5W
-Infuse 10mcg/min inc q 5min by 10mcg/min
-Diltiazem, verapamil, and nifedipine should be avoided in pt with systolic dysfunction
-These drugs exert a strong negative contractility effect
-Calcium ions regulate contraction in smooth and cardiac muscle
-CCB inhibit the movement of Ca ions across myocardial and vascular smooth muscle
-this leads to decreased myocardial contractility and decreased myocardial oxygen demand
-CCB also improve coronary blood flow via direct smooth muscle relaxation
-they also cause peripheral vasodilation from direct smooth muscle relaxation
-Diltiazem administered at initial bolus of 0.25mg/kg IV over 2min
-followed by infusion of 10mg/hr
Atrial dysrhythmias
-approximately 30% of blood flow to the ventricles is the result of atrial contraction, known as atrial kick
-the immediate clinical concern in pt with A-fib is the rate of the ventricular response
-if the ventricular rate is too fast, end diastolic filling time is decreased and CO is compromised
-if the ventricular rate is too slow, CO may again be decreased
-the shortened diastole leads to decreased filling and may cause or aggravate diastolic dysfunction, resulting in dec CO and the symptoms of HF
-pt also are at risk for the formation thrombi and embolic events, such as strokes, MI, and PE
-the goal of therapy is achieve rate control or to convert the rhythm to sinus
-cardioversion is indicated for rhythm control when drug therapy fails or in the setting of hemodynamic compromise
Afib management
-drugs may be selected to slow the conduction of the impulses through the AV node, CCB, digoxin, amiodarone, or BB
-A HR that is too fast or too slow can compromise filling
-When the tachycardia is caused by atrial flutter or atrial fib with RVR, the heart rate is the cause of the problem
-If the pt is unconscious secondary to the heart rhythm, direct cardioversion is indicated
-shock at 120-200j biphasic
-If medication is required to slow the rhythm, Amiodarone is the lease dangerous medication to use in systolic dysfunction
-Amiodarone 150mg IV over 10 min, (possible infusion at 1mg/min
-CCB such and verapamil and diltiazem are powerful negative inotropes (contraction) and may aggravate the low cardiac output state
-Diltiazem administered at initial bolus of 0.25mg/kg IV over 2min
-followed by infusion of 10mg/hr
Aircare protocol
-IF MAP > 60 administer nitro
-IF MAP <60 administer dobutamine
-Consider NPPV or CPAP