Heart failure and circulatory shock

Question 1

Heart failure?

Answer 1

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

Question 2

Cardiac reserve?

Answer 2

ability to increase cardiac output during increased physical activity

Question 3

Cardiac output=?

Answer 3

heart rate x stroke volume

reflects how much blood it pumps with each beat

Question 4

Preload?

Answer 4

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

Question 5

End diastolic volume?

Answer 5

max volume of blood filling the ventricle is present at the end of diastole

Question 6

As end diastolic volume or preload increases what happens to stroke volume?

Answer 6

increases (frank starling)

Question 7

Afterload?

Answer 7

the force that the contracting heart muscle must generate to eject blood from the filled heart

systemic (peripheral) vascular resistance and ventricular wall tension

Question 8

Excessive afterload may?

Answer 8

lead to increased wall tension and impair ventricular ejection

because the ventricular pressure must increase to overcome the increased peripheral vascular resistance

Question 9

ATP provides energy for what during muscle contraction/ relaxation?

Answer 9

cross bridge formation and cross bridge detachment

Question 10

When an AP passes over the cardiac muscle fiber?

Answer 10

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)

Question 11

Open L type Ca2+ channels?

Answer 11

second messenger cAMP from the beta adrenergic receptor

Question 12

2 pumps that if controlled can increase inotropy?

Answer 12

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

Question 13

Systolic dysfunction?

Answer 13

decrease in myocardial contractility, ejection fraction of less than 40%

Question 14

Diastolic dysfuntion?

Answer 14

heart contacts normally, relaxation is abnormal

cardiac output, esp during exercise is comprimised by the abnormal filling of the ventricle

Question 15

Right sided heart failure?

Answer 15

impairs the ability to move deoxy blood from systemic circulation into pulmonary circulation

Question 16

Left ventricular dysfunction?

Answer 16

impairs movement of blood from low pressure pulmonary circulation into high pressure arterial side of systemic circulation

Question 17

High output failure?

Answer 17

excessive need for cardiac output, rare
function of the heart may be supranormal but inadequate owing to excessive metabolic needs

Question 18

Low output failure?

Answer 18

impair the pumping ability of the heart

Question 19

Relationship between contractility/inotropy, cardiac output, and end diastolic volume

Answer 19

An increase of inotropy will increase cardiac output at any EDV

Question 20

How can an increase in SNS become maladaptive?

Answer 20

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

Question 21

How can the adaptations by Frank starling become maladaptive?

Answer 21

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)

Question 22

Renin-Angiotensin-Aldosterone-Mechanism can become maladaptive in heart failure?

Answer 22

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

Question 23

Ang II and aldosterone inflammatory and reparative process?

Answer 23

in addition, RAAS will cause fibroblast and collagen deposits, result in ventricular hypertrophy and myocardial wall fibrosis, decreasing compliance

Question 24

Natriuretic peptides?

Answer 24

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

Question 25

Do you see pulmonary edema more in new-onset acute heart failure syndrome or chronic?

Answer 25

new onset, stronger sympathetic response with enchanced pulmonary vascular permeability causing rapid and dramatic symptoms of pulmonary edema

chronic tolerate higher pulmonary vascular pressures

Question 26

Signs and symptoms of heart failure?

Answer 26

shortness of breath, fatigue, limited exercise tolerance, fluid retention and edema, cachexia and malnutiriton, and cyanosis

diaphoresis and tachycardia

Question 27

Major manifestation of left sided heart failure?

Answer 27

dyspnea

Question 28

Respiratory manifestations of heart failure?

Answer 28

dyspnea, orthopnea, Cheyne-Stokes respiration, Acute pulmonary edema,, cachexia and malnutrition, cyanosis

Question 29

fatigue/weakness/metnal confusion presentation?

Answer 29

not present in the morning but appears and progresses as activity increases during the day

Question 30

fluid retention and edema presentation?

Answer 30

peripheral ciruclation with right sided heart failure

pulmonary circulation with left sided heart failure

Question 31

Central cyanosis?

Answer 31

caused by conditions that impair oxygenation of the arterial blood such as pulmonary edema, left side heart failure, or right to left cardiac shuntin

Question 32

peripheral cyanosis?

Answer 32

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

Question 33

Arrhythmia associatied with heart failure?

Answer 33

Atrial fibrilation

Question 34

Cause systolic dysfunction?

Answer 34

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

Question 35

cause diastolic dysfunction?

Answer 35

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

Question 36

cause right sided heart failure?

Answer 36

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

Question 37

cause left sided heart failure?

Answer 37

hypertension and acute myocardial infarction

Question 38

Cause high output failure?

Answer 38

severe anemai, thyrotoxicosis, conditions that cause arteriovenous shunting and Paget disease

Question 39

Cause low output failure?

Answer 39

ischemic heart disease and cardiomyopathy