Heart Failure Pathophysiology

Front 1

Heart Failure (HF)

What?

Back 1

denotes failure of the heart as a pump.

Front 2

Heart Failure (HF)

Involves the interaction b/t 2 factors?

Back 2

1. a decrease in pumping ability w/ consequent decrease in CO & cardiac reserve
2. compensatory mechanisms that act to maintain CO while also contributing to the HF

Front 3

Cardiac Output

Back 3

is the amount of blood ejected into the aorta from the LV during systole-

Front 4

Cardiac Reserve

Back 4

is the ability of the heart to increase CO during increased activity- as much as 5 to 6 x

Front 5

Cardiac Output

is a function of?

Back 5

CO is a function of preload, afterload, and stroke volume-

Front 6

Preload

Back 6

reflects the loading condition of the heart at the end of diastole, that is, the volume of blood stretching the heart muscle at end-diastole-

Front 7

Afterload

Back 7

represents the force that the contracting heart must generate to eject blood from the filled heart - arterial resistance being the main component.

Front 8

Cardiac Contractility

Back 8

mechanical performance. It can increase CO independent of preload & muscle stretch.
+ & - Inotropes have effects here-

Front 9

Compensatory Mechanisms
HF

Frank-Starling Mechanism?

Back 9

^ SV, by ^ in ventricular end-diastolic volume. This ^ filling leads to ^ stretch, leads to ^ force of next contraction.

Front 10

Compensatory Mechanisms
HF
Frank-Starling Mechanism?
negative effects?

Back 10

the resulting elevations in LV end-diastolic volume & pressues is eventually transmitted back to the atria & pulm. circulation, causing pulm. congestion-

Front 11

Compensatory Mechanisms
HF
Sympathetic NS activity?

Back 11

HF leads to ^ SNS activity. causing ^ sympathetic tone, and ^ release of Epi & NorEpi
which cause direct stimulation of HR, contractility, & vascular tone

Front 12

Compensatory Mechanisms
HF
Sympathetic NS activity?
negative effects?

Back 12

^ SNS activity increases peripheral vascular resistance which consequently ^ afterload
Epi & NorEpi may contribute to deadly arrhythmias

Front 13

Compensatory Mechanisms
HF
Renin-Angio-Aldosterone?

Back 13

decreased CO leads to decreased kidney perfusion which leads to release of Renin. Renin begins a cascade of events that lead to Na+ & fluid retention & vasoconstriction

Front 14

Compensatory Mechanisms
HF
Renin-Angio-Aldosterone?
negative effects?

Back 14

^ vascular fluid volume which will ^ preload (can be counter productive), and systemic vasoconstriction that can ^ afterload beyond what the LV can handle

Front 15

Compensatory Mechanisms
HF
Natruretic Peptides?

Back 15

ANP, BNP, CNP
ANP- from atrial cells in response to ^ stretch/pressure
BNP-from ventricle cells in response to ^ stretch/pressure

Front 16

Compensatory Mechanisms
HF
Natruretic Peptides?

Back 16

overall effect of ANP/BNP on the body is to counter increases in BP & blood volume, which can actually lead to ^ CO

Front 17

Compensatory Mechanisms
HF
Endothelins?

Back 17

released from endothelial cells, hormone type subs, potent vasoconstrictors to ^ BP and ^ venous return to heart

Front 18

Compensatory Mechanisms
HF
Endothelins?
negative effects?

Back 18

vasoconstriction. it will lead to ^ afterload which the LV likely can't tolerate very well at that point. may also cause issues with preload-

Front 19

Compensatory Mechanisms
HF
Myocardial hypertrophy/remodeling?

Back 19

is a long-term mechanism to ^ work performance of the heart for the short term. as a response to pressure and volume overload-

Front 20

Compensatory Mechanisms
HF
Symmetric Hypertrophy

Back 20

results in proportionate ^ in muscle length and muscle width as in athletes.

Front 21

Compensatory Mechanisms
HF
Concentric Hypertrophy

Back 21

results in an ^ in muscle/wall thickness d/t pressure overload. as seen in hypertension b/c it takes ^ muscle strength to keep up with ^ afterload

Front 22

Compensatory Mechanisms
HF
Concentric Hypertrophy

Back 22

it can preserve systolic fx for a period of time, but the work being performed by the muscle eventually exceeds its blood supply

Front 23

Compensatory Mechanisms
HF
Eccentric Hypertrophy

Back 23

results in an ^ in muscle/wall length d/t volume overload. as seen in dilated cardiomyopathies b/c it takes ^ muscle length to keep up with ^ preload

Front 24

Compensatory Mechanisms
HF
Eccentric Hypertrophy

Back 24

leads to decreased ventricular wall thickness, less strength of the muscle, and increases diastolic volume & wall tensions

Front 25

HF

Causes?

Back 25

acute MI, hypertension, cardiomyopathy, renal failure, thyrotoxicosis, severe anemia, polycythemia vera-

Front 26

HF Type

High-Output?

Back 26

is uncommon, caused by excess need for CO: caused by severe anemia, thyrotoxicosis

Front 27

HF Type

Low-Output?

Back 27

is caused by disorders that impair the pumping ability of the heart: caused by severe ischemia, cardiomyopathies, MI, sudden tamponade

Front 28

HF Type

Systolic Dysfunction?

Back 28

involves a decrease in cardiac contractility and ejection fraction. decreased CO symptoms dominate

Front 29

Ejection Fraction (EF)

Back 29

a normal heart ejects apprx. 65% of the blood that is in the LV when it contracts. This is the ejection fraction-

Front 30

HF Type

Diastolic Dysfunction?

Back 30

accounts for 40% of HF-
characterized by smaller ventricular size, hypertrophy, & poor compliance. congestive symptoms dominate

Front 31

HF Type

Right side fail?

Back 31

impairs the ability to move deoxygenated blood from the systemic circulation into the pulmonary circulation-

Front 32

HF Type

Right side fail. Cause?

Back 32

left side fail, pulmonary diseases, cor pulmonale, valvular diseases. result in ^ R atrial, ^ R ventricular, & ^ systemic venous pressures

Front 33

HF Type

Right side fail. SXS?

Back 33

peripheral PITTING edema, anorexia
GI congestion, Jug distention
liver congestion/ enlargement/ impairment, ascites, wt gain.
1 pt fl = 1 lb. wt.

Front 34

HF Type

Left side fail?

Back 34

impairs the pumping of blood from the low-pressure pulm. circulation into the high-pressure systemic circulation

Front 35

HF Type

Left side fail. Cause?

Back 35

AMI, valvular defects (mitral regurg., aortic stenosis, aortic regurg.) hypertension. result in ^ L atrial, & ^ L ventricular end-diastolic pressures; and congestion in pulm. circulation

Front 36

HF Type

Left side fail. SXS?

Back 36

decreased CO, pulm. congestion, orthopnea, frothy pink sputum, paroxysmal nocturnal dyspnea

Front 37

HF

Fluid & Edema?

Back 37

d/t fluid retention by the kidneys by way of Renin release, and as a result of ^ capillary pressure

Front 38

HF

Treatment?

Back 38

goal of tx is directed at relieving symptoms and improving life quality, long-term goal slow, halt, or reverse cardiac dysfunction; decrease preload and afterload; restrict salt and fluid intake, weigh daily

Front 39

HF

Treatment- Pharmaco?

Back 39

for moderate to severe HF;
diuretics- most freq, reduce preload & afterload
digoxin- + inotropic effect to ^ force/strength of ventricle contractions:
angio converting enzyme (ACE)- prevent angio conversion (side effect cough)
B-Blockers- decrease SNS activation

Front 40

Acute Pulm. Edema

Back 40

accumulatiuon of fluid in the lungs. most dramatic symptom in HR.

Front 41

Acute Pulm. Edema

SxS

Back 41

SOB, cyanosis, tachycardia, cool, frothy pink sputum, crackles

Front 42

Acute Pulm. Edema

Treatment?

Back 42

digoxin, diuretics, vasodilators, O2 on mask, Morphine to decrease anxiety and reduce pulmonary r eflex & spasm: Let PT stand up!

Front 43

Cardiogenic Shock

most common cause is AMI

Back 43

Failure of heart to pump. results in hypotension, decrease CO, later ^ vasoconstriction, ^ preload

Front 44

Cardiogenic Shock

Treatment?

Back 44

most common cause is AMI
decrease workload, O2, vasodilators (venous=Nitro), aortic balloon pump to ^ aortic diastolic pressure

Front 45

Hypovolemic Shock

Back 45

Diminished blood volume d/t hemorrhage, severe burns, vomiting or diarrhea. Acute loss of 15-20%, loss of < 10% without loss of fx.

Front 46

Hypovolemic Shock

Stages?

Back 46

nonprogressive: normal compensatory mechanisms prevent large changes in circulatory fx
progressive: shock becomes progressively worse
irreversible: shock has progressed to an extent that therapy is insufficient to save the persons life

Front 47

Hypovolemic Shock

SxS

Back 47

thirst, tachycardia, cool and clammy skin, decreased urine output, restlessness, can led to apathy, stupor and coma

Front 48

Hypovolemic Shock

Treatment?

Back 48

#1. is response of SNS to preserve HR & CO-
Treat cause, O2, give fluids, blood, Vasoconstrictors. 350 mL blood store in liver, more in gut

Front 49

Distributive Shock

Back 49

Characterized by loss of vessel tone, enlargement of vascular compartment, and displacement of vascular volume away from the heart and circulation

Front 50

Distributive Shock

3 types: 1) Neurogenic Shock 2) Anaphylactic Shock 3) Septic Shock

Back 50

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Front 51

Neurogenic Shock?

What?

Back 51

caused by decreased SNS control of vessel tone d/t defect in vasomotor center or sympathetic output.HR is often slow and skin is warm and dry

Front 52

Neurogenic Shock?

Causes?

Back 52

brain injury, drugs, anesthesia, hypoxia, lack of glucose. 'spinal shock' in spinal cord injuries

Front 53

Anaphylactic Shock

Back 53

the most severe allergic reaction. releases vasodialtors. accompanied by life dangering laryngeal edema, bronchospasm, and circulatory collapse

Front 54

Anaphylactic Shock

Characterized by?

Back 54

abdominal cramps, burning, flushing, warming, & itching sensations of skin: wheezing, difficulty breathing, alterations in BP-

Front 55

Anaphylactic Shock

Treatment?

Back 55

decrease absorption of agent, Epi, O2, antihistamines, corticosteroids

Front 56

Sepsis/Septic Shock

Back 56

most common type of vasodilatory shock, it is associated with severe infection and release of inflammatory mediators

Front 57

Sepsis/Septic Shock

Back 57

most freq w/ gram-negative bacterial- unlike other forms of shock it is commonly linked to patho complications-

Front 58

Sepsis/Septic Shock

SxS

Back 58

fluctuations in body temp.
tachypnea, hyperventilation, tachycardia, WBC counts high or low, altered BP, altered mental status

Front 59

Sepsis/Septic Shock

Treatment?

Back 59

control cause, support circulation. antibiotics, IV fluids, vasopressors,