inability of the heart to pump blood effectively. It is caused by impaired contractile function (e.g., MI), increased afterload (e.g., hypertension), cardiomyopathy, and mechanical abnormalities (e.g., valvular heart disease).
high filling pressures due to stiff or noncompliant ventricles and results in venous engorgement in both the pulmonary and systemic vascular systems. The diagnosis of diastolic failure is made based on the presence of pulmonary congestion, pulmonary hypertension, ventricular hypertrophy, and a normal EF
First thing triggered when CO drops Least effective compensatory mechanism SNS is activated Catecholamines (epinephrine & norepinephrine) released Increases HR, contractility & CO rises Overtime makes heart need more O2 and increases workload of failing heart Vasoconstriction increases preload; increase in venous return to already overloaded heart worsens ventricular performance
How do neurohormonal responses in the kidneys compensate for HF?
When CO falls blood to kidneys drops Juxtaglomerular apparatus senses drop Renin released Renin converts Angiotensin I into Angiotensin II Angiotensin II causes adrenal cortex to release aldosterone Aldosterone = Na + water retention Na + water retention = increased BP
How do neurohormonal responses in the pituitary gland compensate for HF?
Low CO = decrease in cerebral perfusion pressure Posterior pituitary secrets ADH (vasopressin) ADH = increased water reabsorption in renal tubles = water retention = increase in blood volume
a potent vasoconstrictor produced by the vascular endothelial cells. It is stimulated by ADH, catecholamines, and angiotensin II. Endothelin results in further arterial vasoconstriction and an increase in cardiac contractility and hypertrophy. Can contribute to HF.
It occurs when pressure in the heart chambers (usually the left ventricle) is elevated over time. The muscle fibers of the heart stretch in response to the volume of blood in the heart at the end of diastole.
The degree of stretch is directly related to the force of the contraction (systole) (this is the Frank-Starling law). This increased contraction initially leads to increased CO and maintenance of arterial BP and perfusion.
Dilation starts as an adaptive mechanism to cope with increasing blood volume. Eventually this mechanism becomes inadequate because the elastic elements of the muscle fibers are overstretched and can no longer contract effectively, thereby decreasing the CO
How does natriuretic peptides try to counterbalance the HF compensatory mechanisms?
Natriuretic peptides (atrial natriuretic peptide [ANP] and b-type natriuretic peptide [BNP]) are hormones produced by the heart muscle that promote venous and arterial vasodilation (thus reducing afterload and preload).
Kick start diuresis by increasing glomerular filtration rates (pee = DEC volume) & blocking RAAS (angiotensin I & II cascade). Inhibit development of hypertropy & may be an antiinflammatory
How are ANP and BNP released?
ANP is stored within granules in the atria & ventricles. Minor cardiac muscle stretch can cause a release of this peptide into the circulation.
In contrast, only small amounts of BNP are stored within granules in the ventricles. The release of BNP is triggered by increased pressure, especially in the left ventricle.
respiratory rate and a decrease in partial pressure of oxygen in arterial blood (PaO2)
s/s of pulmonary edema:
pt usually anxious, pale, and possibly cyanotic. The skin is clammy and cold from vasoconstriction caused by stimulation of the SNS. The patient has severe dyspnea, as evidenced by the use of accessory muscles of respiration, a respiratory rate greater than 30 breaths per minute, and orthopnea. Wheezing, coughin, blood-tinged sputum. Crackles, wheezes, rhonchi. HR rapid.
Caused by pulmonary pressures d/t interstitial and alveolar edema
Paroxysmal nocturnal dyspnea (PND) occurs when
the patient is asleep. It is caused by the reabsorption of fluid from dependent body areas when the patient is recumbent. The patient awakens in a panic, has feelings of suffocation, and has a strong desire to seek relief by sitting up. May have a dry, hacking cough that doesn't go away.
HF causes atrial and ventricular stretching Organized spread of electricity no longer occurs Patients with HF and an EF less than 35% have a high risk of fatal dysrhythmias. Nearly one half will experience SCD, usually due to ventricular tachycardia or ventricular fibrillation
Normally in ICU ECG, O2 sats, hemodynamic continuous I&Os every hour
Ultrafiltration (UF) is used on pts:
with volume overload. It can rapidly remove extracellular and intravascular fluid volume.8 When UF is performed, volume is removed similar to hemodialysis but without hemodynamic instability. The ideal patients for UF are those with significant pulmonary or systemic volume overload who are hemodynamically stable.
The intraaortic balloon pump (IABP) is a device that
increases coronary blood flow to the heart muscle and decreases the heart's workload through a process called counterpulsation. The IABP is placed in the aorta and can be useful in hemodynamically unstable patients because it decreases SVR, PAWP, and PAP leading to improved CO
By decreasing venous return to the LV (excreting of edematous fluid) and thereby reducing preload, the overfilled LV may contract more efficiently and improve CO. This increases left ventricular function, decreases pulmonary vascular pressures, and improves gas exchange
reduces circulating volume by decreasing preload and also increases coronary artery circulation by dilating the coronary arteries. Therefore nitroglycerin reduces preload, slightly reduces afterload (in high doses), and increases myocardial oxygen supply
How does morphine sulfate help the HF & pulmonary edema pt?
It dilates both the pulmonary and systemic blood vessels, a goal in decreasing pulmonary pressures and improving the gas exchange. IV morphine decreases oxygen demands, which may be increased as a result of anxiety and subsequent increased musculoskeletal and respiratory activity
The main goals in the treatment of chronic HF are to
treat the underlying cause and contributing factors, maximize CO, provide treatment to alleviate symptoms, improve ventricular function, improve quality of life, preserve target organ function, and improve mortality and morbidity risks
Biventricular pacing or cardiac resynchronization therapy (CRT):
CRT coordinates right and left ventricle contractility through biventricular pacing. The ability to have normal simultaneous electrical conduction (synchrony) within the right and left ventricles increases left ventricular function and CO
CO is dependent on afterload in chronic HF, the reduction in SVR seen with the use of ACE inhibitors produces a significant increase in CO. Though the use of ACE inhibitors may decrease BP, tissue perfusion is maintained or increased
When is a pt prescribed Angiotensin II receptor blockers?
When they can't tolerated ACE inhibitors
How do aldosterone antagonists inhibitors help the chronic HF pt?
block the harmful neurohormonal effects of aldosterone on the heart blood vessels. They are also potassium-sparing diuretics that promote sodium and water excretion while retaining potassium. These effects occur because these agents bind to receptors at the distal renal tube
Spironolactone (Aldactone) can cause what side effect in men?
Gynecomastia (male boobs)
How does nitrates help the chronic HF pt?
vasodilation by acting directly on the smooth muscle of the vessel wall. Nitrates can be used in combination with hydralazine (Apresoline) for chronic HF management in patients who cannot tolerate ACE inhibitors or ARBs
directly block the negative effects of the SNS on the failing heart, such as increased HR. Because β-blockers can reduce myocardial contractility, care must be taken to start gradually, increasing the dosage slowly every 2 weeks as tolerated by the patient
Are fluid restrictions ever implemented in HF cases?
Yes. But only in moderate to severe cases with renal insufficiency.
Usually sodium is limited to 2.5 g; OR 500 - 1000 mg in severe cases
Can sleep apnea cause HF?
a patient with sleep-disordered breathing may not regularly use his or her continuous positive airway pressure device at night causing poorly controlled hypertension and ultimately an exacerbation of HF
SCD Acute rejection (within first year major cause of death) Infection (within first year major cause of death) Lymphoma Cardiac vasculopathy (accelerated CAD)
How is heart transplant rejections caught?
endomyocardial biopsy (EMB) is obtained on a weekly basis for the first month, monthly for the following 6 months, and yearly thereafter. In this procedure, a catheter is inserted into the jugular vein and moved into the right ventricle where a small amt tissue is taken