AACN: ECCO 4.0: Caring for Patients with Cardiovascular
Disorders: Part 3 - ICU: Assessing and Managing Patients
with Cardiomyopathies Questions with Verified Answers.
Terms in this set (20)
ef < 40% in the presence of
increased left ventricular end diastolic
dilated cardiomyopathy
volume. can affect one or all 4
chambers, and does not involve
myocardial hypertrophy.
1. weakened contractility
pathophysiology of dilated
2. decreased cardiac output and backward pressure
cardiomyopathy
3. pulmonary and systemic congestion
-triggerend by low CO
SNS activation (compensatory -release epinephrine and norepinephrine to: increase HR,
mechanism) increase myocardial contractility and peripheral
vasoconstriction (increases afterload)
RAAS activation as leads to an increase in preload and afterload. initally the
compensatory mechanism increased prelad can augment stroke volume and cardiac
output.
Renin is released by kidneys in response to decreased blood
RAAS (renin-angiotensin- volume; causes angiotensinogen to split & produce
aldosterone system) angiotensin I; lungs convert angiotensin I to angiotensin II;
angiotensin II stimulates adrenal gland to release aldosterone
& causes an increase in peripheral vasoconstriction
1. HS: S3/S4 heart sound,
systolic murmur LS: crackles
assessing cardiomyopathy in a
patient or diminished, tachypnea
2. ecg lbbb, and other dysrhythmias \
3. cxr reveal p. congestion and p. effusion
Disorders: Part 3 - ICU: Assessing and Managing Patients
with Cardiomyopathies Questions with Verified Answers.
Terms in this set (20)
ef < 40% in the presence of
increased left ventricular end diastolic
dilated cardiomyopathy
volume. can affect one or all 4
chambers, and does not involve
myocardial hypertrophy.
1. weakened contractility
pathophysiology of dilated
2. decreased cardiac output and backward pressure
cardiomyopathy
3. pulmonary and systemic congestion
-triggerend by low CO
SNS activation (compensatory -release epinephrine and norepinephrine to: increase HR,
mechanism) increase myocardial contractility and peripheral
vasoconstriction (increases afterload)
RAAS activation as leads to an increase in preload and afterload. initally the
compensatory mechanism increased prelad can augment stroke volume and cardiac
output.
Renin is released by kidneys in response to decreased blood
RAAS (renin-angiotensin- volume; causes angiotensinogen to split & produce
aldosterone system) angiotensin I; lungs convert angiotensin I to angiotensin II;
angiotensin II stimulates adrenal gland to release aldosterone
& causes an increase in peripheral vasoconstriction
1. HS: S3/S4 heart sound,
systolic murmur LS: crackles
assessing cardiomyopathy in a
patient or diminished, tachypnea
2. ecg lbbb, and other dysrhythmias \
3. cxr reveal p. congestion and p. effusion
