Small Animal Medicine: Cardiology: Pathophysiology Of Heart Failure

Front 1

What is circulatory failure?

Back 1

Insufficient delivery of oxygenated blood to meet tissue requirements.
May result from failure of heart, vascular bed, blood volume, or concentration of oxygenated hemoglobin

Front 2

What is the definition of heart failure?

Back 2

A Pathophysiologic state resulting when the heart is injured and unable to pump blood at a sufficient rate to meet metabolic needs of tissue and to maintain normal arterial and venous pressures at rest or with exercise.
Ex. Ruptured chordae tendonae

Front 3

What is the definition of myocardial failure?

Back 3

Heart failure caused by myocardial contractility defect (= systolic pump failure)
Ex. Dilated cardiomyopathy

Front 4

List 6 reliable signs of heart disease.

Back 4

1. Loud systolic murmurs, palpable thrills
2. Diastolic murmurs
3. Generalized venous engorgement
4. Pericardial effusion or friction rubs
5. Gross cardiomegaly - generalized or particular chambers
5. Certain arrhythmias (atrial fib or flutter, APCs or VPCs, paroxysmal tachycardia, high grade heart block)

Front 5

What are 6 clinical signs of left sided heart failure?

Back 5

1. Exercise intolerance
2. Tachypnea, dyspnea
3. Orthopnea, nocturnal dyspnea
4. Rales
5. Cyanosis
6. Weaknes or collapse

Front 6

What are 6 clinical signs of right sided heart failure?

Back 6

1. Exercise intolerance
2. Venous engorgement
3. Hepatomegaly, splenomegaly
4. Ascites, peripheral edema
5. Weight loss, GI disturbances
6. Weakness or collapse

Front 7

What systemic alterations occur in heart failure?

Back 7

Increased plasma volume
Mild to moderate hypoproteinemia
Mild anemia
Mild to moderate azotemia
Modest elevations of liver enzymes
Hyponatremia with severe CHF
Effusions associated with CHF are usually modified transudates
Chylothorax is common in cats with cardiogenic pleural effusions

Front 8

At what RA pressure do animals develop ascites?

Back 8

>15 mmHg

Front 9

What are some clinical signs of R sided heart failure?

Back 9

Jugular distention
Abdominal distention
Ascites
Anorexia
Diarrhea
Malabsorptive signs dt venous congestion of GIT

Front 10

Why does pulmonary congestion often present acutely in L sided heart failure?

Back 10

Blood retained in the splanchnic vv. moves to the pulmonary circuit due to sympathetic tone and stress.

Front 11

When might you see high output related heart failure?

Back 11

Hyperthyroidism
Anemia
Relatively uncommon

Front 12

What is different between the congestive lung patterns of dogs and cats?

Back 12

Dogs: perihilar edema
Cats: variable

Front 13

What is the equation for fractional shortening calculation from an echo?

Back 13

EDD-ESD/EDD x 100 = fractional shortening (diameter)

Front 14

What is the equation for ejection fraction calculation from an echo?

Back 14

EDV-ESV/EDV x 100 = ejection fraction (volume)

Front 15

What are the four functional classifications of heart failure?

Back 15

1. Impeded cardiac filling = diastolic failure = compliance failure
2. Increased resistance to ejection = pressure overload = afterload mismatch (can be systolic or diastolic failure)
3. Impaired ejection = systolic failure dt volume overload = pump failure
4. Conduction failure = arrhythmias/conduction disorders

Front 16

Give some examples of diseases that result in impeded cardiac filling/diastolic failure/compliance failure.

Back 16

Constrictive pericarditis
AV valve stenosis
Hypertrophic cardiomyopathy
Inflow obstructions: mitral valve stenosis
Pericardial ds: effusion, coccidiomycosis pericarditis
Myocardial dz: hypertrophic cardiomyopathy, restrictive CM (cats!)

Front 17

Give some examples of diseases that result in increased resistance to ejection/pressure overload/afterload mismatch.

Back 17

Aortic stenosis
Hypertrophic obstructive cardiomyopathy
Hypertension
Pulmonary stenosis and subaortic stenosis
Thromboembolism
Hypertension: Hearworm

Front 18

Give some examples of diseases that result in Impaired ejection/systolic failures dt volume overload/pump failure.

Back 18

Dilated cardiomyopathy (large and giant breed dogs)
Myocardial dz (nutritional/infection/toxic/ischemic)
Valve insufficiency (mitral insufficiency = most common heart failure in small dogs)
Dilative cardiomyopathy (secondary myocardial dz)
Shunting defects

Front 19

Give some examples of diseases that result in conduction failure.

Back 19

Atrial fibrillatin
Supraventricular tachycardia
Complete heart block

Front 20

What is systolic failure?

Back 20

Failure of the heart to propel blood forward through pulmonary and systemic venous reservoirs. Impaired emptying.
Predominates in most dogs with heart failure

Front 21

What are some causes of systolic failure?

Back 21

Primary myocardial failure
Chronic volume overload
Chronic pressure overload (obstruction or hypertension)

Front 22

What is diastolic failure?

Back 22

Failure of the heart to receive blood from the pulmonary and systemic venous reservoirs
Impaired filling
Predominates in cats suffering from myocardial diseases

Front 23

What are some causes of diastolic failure?

Back 23

Pericardial restraint
Venous inflow disorders
Impaired myocardial relaxation or reduced ventricular compliance

Front 24

What is backward failure?

Back 24

"back up and leak out"
Increased vent diastolic pressure --> increased mean atrial pressure --> increased venous pressure --> increased capillary pressure --> edema!

Front 25

What is forward failure?

Back 25

Decreased CO --> decreased tissue perfusion --> decreased flow to muscle/kidney/brain --> weakness/edema/confusion?

Front 26

What is the modern integration of the backward and forward failure concepts?

Back 26

Cardiac injury --> decreased CO and decreased tissue perfusion --> maladaptive compensatory response --> Na and water retention/vasconstriction/cardiac and vascular remodeling --> congestion, increased afterload, early myocyte death

Front 27

What are the 5 determinants of cardiac output?

Back 27

HR
Preload
Afterload
Contractility
Ventricular synchrony

Front 28

What are the benefits and drawbacks of the Frank-Starling mechanism?

Back 28

Benefit: Increased vetricular volume (stretch) --> more forceful contraction and larger stroke volume
Drawbacks:
Not intended for chronic changes
Doesn't work if there is excess dilation, fibrosis, hypertrophy

Front 29

What are the benefits and draw backs of sympathetic input on the CV system?

Back 29

Benefit: Increased symp. tone --> increased heart rate and myocardial contractility --> increased CO
Drawbacks:
NE synthesis decreased in heart failure
Too much peripheral vasoconstriction during heart failure
Beta adrenergic receptors down regulated in heart failur
Excessive HR decreases diastolic filling time, CO
Some arrhythmias are aggravated by symp. tone
Chronic catacholamine exposure --> premature myocyte death

Front 30

What is the function of natriuretic peptides?

Back 30

Atrial distention --> ANP/BNP release from the atria which promotes salt and water excretion and act as vasodilators to delay congestive signs/improve CO/limit salt and water overload.

Front 31

What happens with natriuretic peptides in heart failure?

Back 31

Chronic heart failure --> decreased levels of mature ANP/BNP
Renal ANP/BNP receptors become refractory under chronic stimulation
RAAS eventually overcomes ANP/BNP dt increased ADH (vasopressin) and redistribution of renal blood flow

Front 32

What is the process of remodeling due to volume overload?

Back 32

Eccentric hypertrophy
Increased diastolic pressure --> increased diastolic wall stress --> replication of sarcomeres in series --> decreased collagen and eccentric hypertrophy
Chamber size enlarges

Front 33

What is the process of remodeling due to pressure overload?

Back 33

Concentric hypertrophy
Increased systolic pressure --> increased systolic wall stress --> replication of sarcomeres in parallel (angiotensin II) --> increased collagen and concentric hypertrophy
Chamber dimensions stay the same

Front 34

How is the RAAS system beneficial?

Back 34

Decreased CO --> decreased renal perfusion which activates the RAAS to increase blood volume
The idea is that increased circulating volume will lead to increased preload and CO.
RAAS also causes release of Angiotensin II which acts on CNS to increase water intake, to stimulate the sympathetic system, to vasoconstrict, and to promote myocardial hypertrophy

Front 35

What are some ways that the RAAS system is deleterious to cardiac output and heart function?

Back 35

1. Aldosterone, Angiotensin II, and endothelin-1 --> excessive ventricular and vascular remodeling --> decreased myocardial perfusion, myocardial fibrosis, deterioration of the left ventricle
2. In CHF, effects of increased preload dt RAAS activation contribute to congestion and edema
3. Vasoconstriction mediated by ADH, Angiotensin II and endothelin --> excess afterload (resulting in mismatch with deficit in myocardial contractility)

Front 36

What is the kidney's response to heart failure?

Back 36

Decreased renal perfusion (decreased GFR dt decreased CO) --> increased Na resporption by proximal convoluted tubules + redistribution of blood flow within the kidney (away from outer cortex) --> sodium and water retention to increase circulating volume and increased CO and preload.

Front 37

What deleterious effects does the kidney's response to heart failure have?

Back 37

1. Kidney loses its ability to regulate plasma volume
2. Kidney becomes refractory to ANP/BNP --> RAAS overpowering ANP/BNP even in the face of excessive plasma volume --> life threatening congestion

Front 38

What is the benefit of the arterial-mixed venous oxygen difference?

Back 38

The oxygen content of mixed venous blood is lower than normal due to an increase in 2,3-DPG --> progressive decrease in the affinity of HgB for O2

Front 39

What is a limitation of the arterial-mixed venous oxygen difference?

Back 39

The normal arterial-mixed venous O2 difference is 4 mL/dL (75% venous O2 saturation). Maximal O2 difference equals 7 mL/dL (35% venous O2 saturation)

Front 40

What are the 3 mechanisms responsible for sodium and water retention in patients with heart failure?

Back 40

Innate renal autoregulatory mechanisms
Aldosterone
ADH

Front 41

How does the innate renal autoregulatory mechanisms work?

Back 41

Decreased GFR, increased Na reabsorption by proximal convoluted tubules + redistribution of blood flow within the kidney (away from cortex) all lead to sodium and water retention to increase circulating volume to increase CO and preload

Front 42

How does Aldosterone cause a net increase in sodium?

Back 42

Aldosterone binds mineralocorticoid receptors inside distal collecting duct epithelial cells --> increased absorption of Na and excretion of K. Water follows Na.
Aldosterone release is stimulated by angiotensin II, elevated K, and ACTH.

Front 43

How does ADH release cause an increase in plasma volume?

Back 43

ADH release is stimulated by an increase in plasma osmolality, hypovolemia, decreased stimulation of stretch receptors in atria and large veins, sympathetic stimulation, and angiotensin II.
ADH acts to mediate vasoconstriction and stimulates water resorption in the kidney.

Front 44

What are the 4 substances that mediate excess vasoconstriction observed in patients with heart failure?

Back 44

1. Angiotensin II
2. NE
3. Endothelin
4. ADH

Front 45

What are the causes of sodium retention that contribute to the development of congestion in animals with heart disease?

Back 45

1. Innate renal autoregulatory mechanisms
2. Aldosterone
3. ADH
4. Declining response for ANP

Front 46

What are the effects of angiotensin II on tissue and systemically?

Back 46

Tissue effects: pathologic remodeling
Systemic effects: excessive vasoconstriction, excessive Na/H2O retention via aldosterone

Front 47

What is renin release stimulated by?

Back 47

Under perfused kidney
Increased sympathetic stimulation
Hyponatremia
Furosemide