Patho Exam 3 Heart Failure Flashcards
signs of acute cardiogenic pulmonary edema (deadly)
impaired gas exchange
severe dyspnea and anxiety
bolt upright posture
bubbly crackles and pink frothy sputum
cyanosis
three types of dysrhythmias
abnormal rates of sinus rhythm
abnormal sites of impulse initiation
disturbances in conduction pathways
NYHA class C
Objective evidence of moderately severe cardiovascular disease. Marked limitation in activity due to symptoms, even during less-than-ordinary activity. Comfortable only at rest.
FACES tool for diagnosing HF
fatigue
activity limitation
congestion
edema
shortness of breath
normal QRS interval
.06-.1 sec
signs of pulmonary congestion
cough, rales/crackles, hypoxemia, S3 gallop, and high left atrial pressure
normal PR interval
.12-.2 sec
NYHA class 2
Slight limitation of physical activity. Comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea (shortness of breath).
cor pulmonale
right ventricular hypertrophy
Commonly used criteria for determining heart failure
dyspnea, pulmonary rales, cardiomegaly, pulmonary edema, S3 heart sounds, and tachycardia.
NYHA class 4
Unable to carry on any physical activity without discomfort. Symptoms of heart failure at rest. If any physical activity is undertaken, discomfort increases.
Diastolic dysfunction happens mostly in
the elderly, women, and those without history of MI.
NYHA class 3
Marked limitation of physical activity. Comfortable at rest. Less than ordinary activity causes fatigue, palpitation, or dyspnea.
How does sympathetic activation affect the heart?
Increased HR, contractility, and preload (from fluid retention)
ventricular tachycardia
sustained for 30 seconds, with or without a pulse, 100-220 bpm
What causes reentry?
continued depolarization after the main impulse has ceased due to slow or long pathway of the electrical conduction in the heart. Caused by gap junction issues, myocardial ischemia, excessive Epi/NE, and electrolyte imbalances.
Which cells are stimulated by the SNS to start the RAAS system?
juxtaglomerular cells release renin
How does SNS become problematic in HF?
Increased afterload due to HTN decreased stroke volume and increases cardiac workload. Causes cardiac remodeling which is less functional
ventricular fibrillation
low electrical activity of the heart, no effective heart contraction or pulse. rapid uncoordinated cardiac rhythm.
What causes triggered activity?
digoxin toxicity, excessive Epi/NE, and increased intracellular free calcium (genetic issues)
NYHA class B
Objective evidence of minimal cardiovascular disease. Mild symptoms and slight limitation during ordinary activity. Comfortable at rest.
causes of impaired contractility
loss of cardiac muscle cells, B1-receptor down regulation, reduced ATP production (due to ischemia), and altered CA2+ regulation.
treatment for sinus bradycardia
if due to low CO, sympathomimetic or parasympatholytic drugs
signs of left-sided heart failure
dyspnea, orthopnea, crackles, cough, pulmonary edema, and hypoxemia
How does SNS become problematic in HF?
Increased afterload due to HTN decreased stroke volume and increases cardiac workload
cause of eccentric hypertrophy (elongated muscle fibers)
excessive preload
what causes abnormal automaticity
failure to repolarize to resting membrane potential or abnormal plasma membrane leakiness to sodium or calcium ions at rest. Action potentials are set off too frequently. Hypokalemia is a cause.
What causes cardiac hypertrophy?
chronic elavation of myocardial wall tension from increased diastolic blood volume (high preload) or high systolic pressures needed to overcome high afterload
treatment for sinus tachycardia
sympatholytic agents or calcium channel blockers
signs of right-sided heart failure
systemic venous congestion, jugular vein distension, hepatomegaly, splenomegaly, and peripheral edmea
sick sinus syndrome
alternating periods of tachy and brady sinus rhythms
normal HR
60-100 bpm
What are the three main compensatory mechanisms activated in heart failure?
SNS activation, increased preload, and myocardial hypertrophy.
NYHA class A
No objective evidence of cardiovascular disease. No symptoms and no limitation in ordinary physical activity.
lack of abdomen sounds
ileus
HEAD right sided heart failure
hepatomegaly
edema
ascites
distended jugular vein
How is the sympathetic nervous system activated?
when baroreceptors detect low blood pressure due to dimished stroke volume
Heart failure risk factors
Coronary artery disease, hypertension, and cardiomyopathies.
CHOP left sided heart failure
cough, hemoptysosis, orthopnea, pulmonary congestion
cause of concentric hypertrophy (muscle fibers grow in diameter and thicken the ventricle wall)
high afterload
NYHA class 1
No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea (shortness of breath).
