21 – Cardiovascular Disease

Question 1

How does an arrythmia cause clinical signs?

Answer 1

• Rate is too fast or too slow

Question 2

What determines cardiac output/cardiac performance?

Answer 2

• SV: amount of blood ejected with each heart beat
• HR

Question 3

Heart rate

Answer 3

• Sinus node=pacemaker
• Rate can be increased as demand increases
  o Sinus node is species dependent
  o Will increase with adrenergic, sympathetic stimulation
• With increased rate (to an upper limit), CO will increase
• With sustained elevations in HR, myocardial oxygen demand will increase

Question 4

Preload

Answer 4

• Force of cardiac contraction is dependent on level at which it is stretched prior to contraction
• Based on Frank-Starling Law of Heart
• Once stretch exceeds a certain level=CO falls (fibers are pulled too far apart)

Question 5

Afterload:

Answer 5

• Resistance to ejection
  o Determined by impedance (minor) and **systemic vascular resistance
• Increased=decreased CO
• Increased by increased chamber size
• Decreased by increasing wall thickness
• Ex. catecholamines and Ang II =have high systemic vascular resistance

Question 6

Contractility

Answer 6

• Intrinsic ability of hear to contract independent of preload
• Can be altered by outside factors
  o Catecholamines increase contractility
  o Beta blockers=decrease contractility
  o Few drugs are available to increase in failure that are safe and easy to use

Question 7

What are the main determinants of BP?

Answer 7

• CO
  o Increase CO=increase BP
  o Ex. hypermetabolic states (hyperthyroidism)
• SVR
  o Increase SVR=increase BP
  o Ex. in Cushings disease sensitivity to adrenergic hormones is increase
  o Ex. RAAS activation (Ang II) vasoconstricts

Question 8

What is heart disease?

Answer 8

• Any abnormality of the heart
• Many can remain compensated

Question 9

What is heart failure or cardiac insufficiency?

Answer 9

• Present when heart cannot meet the demands of the body at normal or elevating filling pressures
• Forward and backward failure can COEXIST

Question 10

Endocarditis vs. endocardiosis

Answer 10

• Endocarditis: bacteria present
• Endocardiosis: change in cartilage
  o Inflammatory due to hypoperfusion organs and bacteria crosses the gut

Question 11

What are you trying to achieve when treating a dog with heart failure?

Answer 11

• Maintain BP
• *do the normal things so can have a good quality of life
  o Usually euthanasia due to poor quality of life
  o Sometimes it is a combination of what is possible by the owner (not many owners will be able to give the drugs 3x a day at regular intervals)
• “improve the duration of life”

Question 12

Backward congestive heart failure (ex. mitral valve disease)

Answer 12

• pulmonary edema: L-sided heart disease (increased P in left atrium and pulmonary veins) **MOST COMMON
• ascites: R-sided heart disease (ex. tricuspid valve disease, heartworm)
• **treat with diuretics (ex. furosemide)
  o Decreased preload=decreased SV

Question 13

Forward congestive failure (ex. DCM)

Answer 13

• Inability to maintain adequate CO (low output)
• Ex. weak, cold, CRT prolonged, poor pulses
• Can have syncope
• *progression to cardiogenic shock with organ dysfunction possible
• If give furosemide=put into cardiogenic shock
  o Give something to increase contractility to avoid that

Question 14

What are different compensation CV mechanisms?

Answer 14

• Frank-starling mechanism
• Ventricular hypertrophy
• Neurhumporal mechanisms
  o RAAS
  o Adrenergic NS
  o ADH
  o ANP
  o *combating neurohumoral activation=PROLONGS LIFESPAN

Question 15

Frank-Starling: compensation mechanism

Answer 15

• SV decreased for same preload
  o Each beat pumps out less blood=increase preload (next beat has better preload)
• *eventually results in EDP that is HIGH enough to cause edema

Question 16

RAAS compensation system

Answer 16

• Give ACE inhibitors (block Ang II and aldosterone)
  o Not used as much anymore (use Pimobendan)
  o Humans: coughing
• *major determinant of survival in cardiac heart failure

Question 17

RAAS: determinant of survival in cardiac heart failure

Answer 17

• Potent vasoconstrictor (increases BP which improves perfusion at cost of increased afterload)
• Increases aldosterone which increases salt and water retention
• Increased thirst
• Increased GFR by post glomerular capillary vasoconstriction
• Myocardial hypertrophy

Question 18

Adrenergic nervous system: compensation

Answer 18

• increased sympathetic tone
• increases contractility and HR
• vasocontricts to increase BP
• long term deleterious to survival (beta-blockage seems counterintuitive though)
• increases afterload and oxygen demand

Question 19

Pathophysiological classification of heart failure

Answer 19

• Volume overload: eccentric hypertrophy
  o Valvular insufficiency, shunts like PDA, VSD
• Pressure overload: concentric hypertrophy
  o Stenotic lesions, systemic or pulmonary hypertension
• Myocardial failure: contractility decreased
  o Idiopathic DCM
  o End stage CHF regardless of cause
  o Adriamycin, taurine deficiency
• Diastolic dysfunction: heart cannot relax
  o HCM (cats 2-6 years old, response to something), RCM
  o Pericardial disease
  o Tachycardias