Heart failure and circulatory shock Flashcards
Heart failure?
complex syndrome resulting from any functional or structural disorder of the heart that results in or increases the risk of developing manifestations of low cardiac output and/or pulmonary or systemic congestion
Cardiac reserve?
ability to increase cardiac output during increased physical activity
Cardiac output=?
heart rate x stroke volume
reflects how much blood it pumps with each beat
Preload?
the volume or loading conditions of the ventricle at the end of diastole, just before onset of systole
determined by venous return to the heart
End diastolic volume?
max volume of blood filling the ventricle is present at the end of diastole
As end diastolic volume or preload increases what happens to stroke volume?
increases (frank starling)
Afterload?
the force that the contracting heart muscle must generate to eject blood from the filled heart
systemic (peripheral) vascular resistance and ventricular wall tension
Excessive afterload may?
lead to increased wall tension and impair ventricular ejection
because the ventricular pressure must increase to overcome the increased peripheral vascular resistance
ATP provides energy for what during muscle contraction/ relaxation?
cross bridge formation and cross bridge detachment
When an AP passes over the cardiac muscle fiber?
impulse spreads to interior of muscle fiber along transverse T tubules
T tubule action potential in tune act to cause Ca2+ release from the sarcoplasmic reticulum
Ca2+ promote chemical rxns for the sliding of actin and myosin filaments to shorten muscle
Ca2+ also dissufes through voltage gated L type Ca2+ channels (without contraction weaker)
Open L type Ca2+ channels?
second messenger cAMP from the beta adrenergic receptor
2 pumps that if controlled can increase inotropy?
Na/Ca exchange pump and the ATPase dependent Ca pump
Digitalis and cardiac glycosides are inotropic agents that exert their effects by inhibit K-ATPase pump, lead to increase in Ca through Na/Ca exchange pump
Systolic dysfunction?
decrease in myocardial contractility, ejection fraction of less than 40%
Diastolic dysfuntion?
heart contacts normally, relaxation is abnormal
cardiac output, esp during exercise is comprimised by the abnormal filling of the ventricle
Right sided heart failure?
impairs the ability to move deoxy blood from systemic circulation into pulmonary circulation
Left ventricular dysfunction?
impairs movement of blood from low pressure pulmonary circulation into high pressure arterial side of systemic circulation
High output failure?
excessive need for cardiac output, rare function of the heart may be supranormal but inadequate owing to excessive metabolic needs
Low output failure?
impair the pumping ability of the heart
Relationship between contractility/inotropy, cardiac output, and end diastolic volume
An increase of inotropy will increase cardiac output at any EDV
How can an increase in SNS become maladaptive?
lead to tachycardia, vasoconstriction, and cardiac arrhythmias
leads to increased myocardial oxygen demand and leads to cardiac ischemia
prolonged, leads to desenitization of beta adrenergic receptors
How can the adaptations by Frank starling become maladaptive?
in heart failure, decrease CO and renal blood flow leads to Na and water retention, leads to increase VR and end diastolic volume
resultant increase in CO, but this may lead to an increase in ventricular wall tension and an increase in myocardial oxygen consumption (diuretics can help)
Renin-Angiotensin-Aldosterone-Mechanism can become maladaptive in heart failure?
leads to Na and water retention
generalized excess vasoconstriction (Ang II)
reabsorption of sodium and increase in water retention (aldosterone)
vasoconstrictor and inhibitor of water excretion (ADH)
ventricular dilation and increased wall tension
increased 02 demand leads to decrease in inotropy and exacerbate heart failure
Ang II and aldosterone inflammatory and reparative process?
in addition, RAAS will cause fibroblast and collagen deposits, result in ventricular hypertrophy and myocardial wall fibrosis, decreasing compliance
Natriuretic peptides?
Atrial natriuretic peptide (ANP) and brain natriueretic peptide (BNP)
released in response to atrial strecth, pressure, or fluid overload
promote rapid and transient natriuresis and diuresis through and increase in the FRG and inhibit tubular sodium and water reabsorption
Do you see pulmonary edema more in new-onset acute heart failure syndrome or chronic?
new onset, stronger sympathetic response with enchanced pulmonary vascular permeability causing rapid and dramatic symptoms of pulmonary edema
chronic tolerate higher pulmonary vascular pressures
Signs and symptoms of heart failure?
shortness of breath, fatigue, limited exercise tolerance, fluid retention and edema, cachexia and malnutiriton, and cyanosis
diaphoresis and tachycardia
Major manifestation of left sided heart failure?
dyspnea
Respiratory manifestations of heart failure?
dyspnea, orthopnea, Cheyne-Stokes respiration, Acute pulmonary edema,, cachexia and malnutrition, cyanosis
fatigue/weakness/metnal confusion presentation?
not present in the morning but appears and progresses as activity increases during the day
fluid retention and edema presentation?
peripheral ciruclation with right sided heart failure
pulmonary circulation with left sided heart failure
Central cyanosis?
caused by conditions that impair oxygenation of the arterial blood such as pulmonary edema, left side heart failure, or right to left cardiac shuntin
peripheral cyanosis?
caused by conditions such as low output failure that result in delivery of poorly oxygenated blood to the peripheral tissues, or by conditions such as peripheral vasoconstriction that cause excessive removal of oxygen from the blood
Arrhythmia associatied with heart failure?
Atrial fibrilation
Cause systolic dysfunction?
impair contractility performance of the heart, produce a volume overload, or generate a pressure overload
ischemic heart disease, cardiomyopathy, valvular insufficiency, anemia, hypertension and valvular stenosis
cause diastolic dysfunction?
impede expansion of the ventricle, increase wall thickness and reduce chamber size, and those that delay diastolic relaxation
pericardial effusion, constricitive pericarditis, myocardial hypertrophy, hypertophic cardiomyopathy, aging, ischemic heart disease
cause right sided heart failure?
conditions that impede blood flow into the lungs or compromise the pumping effectiveness of the right ventricle, pulmonary hypertension
left ventricular failure is most common
cause left sided heart failure?
hypertension and acute myocardial infarction
Cause high output failure?
severe anemai, thyrotoxicosis, conditions that cause arteriovenous shunting and Paget disease
Cause low output failure?
ischemic heart disease and cardiomyopathy
