Clinical considerations for heart failure Flashcards
Impact Left sided heart failure?
Diastolic (preserved EF) -impaired relaxation -pericadial disease Systolic (reduced EF) -impaired contractility -increased afterload Valvular
Impact Right sided heart failure?
Cardiac
Pulmonary
-Pulmonary Parenchymal disease
-Pulmonary Vascular disease
Impair contractility?
Myocardial infarction
Transient myocardial ischemia
Dilated cardiomyopathy
Increase afterload?
Aortic stenosis
Uncontrolled Hypertension
Impair relaxation?
left ventricular hypertrophy
hypertrophic cardiomyopathy
restrictive cardiomyopathy
transient myocardial ischemia
Cause Valvular failure?
mitral stenosis
aortic reguritation
Chronic mitral reguritation
Cause preicardial disease?
pericardial constriction
pericardial tamponade
Cause cardiac disease?
left sided heart failure
pulmonic valve stenosis
right ventricular infarct
Cause pulmonary parenchymal disease?
COPD intersitial lung disease respiratory distress syndrome chronic lung infection bronchiectasis
Cause Pulmonary vascular disease?
pulmonary embolism
Primary Pulmonary Hypertension
Etiology Heart Failure?
Any insult that causes altered structure or function of the heart -Coronary artery disease -Hypertension Rheumatic heart disease (Africa/Asia) Chagas disease (south america)
Prognosis Heart Failure?
30-40% patients dies within one year of onset
60-70% die within 5 years
Adaptive measures to acute injury/ chronic insidious insult?
Short term- bring heart back to normal cardiac output
long term- lead to further heart failure
Basic Heart Failure?
myocardial dysfunction which leads to inadequate tissue perfusion
Generally Heart failure is what kind of output?
Low output failure
high output is possible, when heart is unable to meet increased metabolic demands despite increased cardiac output (Thyrotoxicosis, severe anemia, sepsis)
Angiotensin II and Aldosterone cause?
Increased cytokine production
Inflammatory cell adhesion and chemotaxis
Activation of macrophages at sites of injury and repair
Stimulates growth of fibroblasts and synthesis of collagen fiber
Endothelins cause?
Vasoconstriction
Induce vascular smooth muscle proliferation
Myocyte hypertrophy
Short term adaptive mechanisms?
Increase CO by increasing heart rate, preload, and contractility
Maintain adequate perfusion to critical organs by volume expansion and selective vasoconstriction
Facilitate repair
Long term adaptive mechanisms?
- High catecholamine state can provoke dysrhythmias, increased oxygen demand (increase HR and increase afterload)
- Hypertrophy meant to enhance CO can further exacerbate HF by increasing preload and afterload and/or decrease diastolic filling
- Chronic activation of RAAS can lead to total body volume overload and increased preload
- Myocardium can become infiltrated with fibroblasts, impairing both contractility and diastolic filling
Things that cause symptoms and signs of clinical presentation?
decrease oxygen delivery/ gas exchange
Activation of RAAS
Altered cardiac structure
passive hepatic congestion
NYHA Functional Class?
Relies on patient report of symptoms and can underestimate the limitation in exercise capacity
Functional Classes?
1- not limited
2- slight limit
3- everyday activity
4- can be symptomatic at rest
AHA/ACC Objective Stages?
Emphasizes development and progression of disease
Objective Stages?
A- only at risk
B- no symptoms
C- symptoms now/ past
D- End stage