tag training version 1.0
TRANSCRIPT
Normal Heart Function Maintain blood pressure Perfuse lung and tissues Maintain normal venous pressure Maintain systemic and pulmonary
capillary pressures
Abnormal Heart Function
Low blood pressure Decreased tissue perfusion Increased venous pressures Increased capillary pressures
Factors of Cardiac Performance
Cardiac output = heart rate X stroke volume
Stroke volume = end diastolic volume-end systolic volume
Stroke VolumeSV = contractility X preload afterloadSince CO = HR X SV
ThenCO = heart rate X contractility X PL afterload
Preload Force that stretches ventricular
fibers Increases contractility at first Increases stroke volume Estimated as end diastolic
volume
Afterload Impedes ventricular contraction
and ejection of blood Due to vascular resistance Increases ventricular wall stress Increases work load of heart Decreases stroke volume
Contractility Sarcomere contraction Many factors affect it—cardiac
and systemic factors Increased contractility increases
stroke volume and vice versa
Compliance Pliability of the ventricles so that
they can fill. Influenced by wall thickness Also influenced by pericardial
diseases
Heart Rate Influenced by many factors Increased heart rate will increase
cardiac output up to a point Decreased heart rates can
decrease cardiac output
Synergy
Coordinated function of the atria and ventricles to optimize heart function
Arrhythmias disrupt synergy and decrease cardiac output
Heart Disease Abnormal heart Heart may or may not be in
failure Congenital Acquired 10% of dogs have heart disease
Heart Failure Heart cannot pump blood
presented to it-congestive Or heart cannot meet body’s
needs- output failure
Heart Failure Normal heart=low diastolic size
and low venous pressure Failing heart=high diastolic size
and high venous pressure Failing heart=cardiac reserve is
used at rest
Left sided Congestive Heart Failure
Left sided congestive heart failure (CHF)
Cascade of events that starts with increased left ventricular diastolic pressure
Left sided congestive heart failure
Increased LV diastolic pressure Increased LA diastolic pressure Increased pulmonary venous
pressure
Left sided congestive heart failure
Increased pulmonary capillary hydrostatic pressure
Fluid into interstitial and alveolar areas
Pulmonary edema
Causes of increased LV diastolic pressure
Increased preload Decreased compliance Increased afterload Combinations of the above
Right sided congestive heart failure
Increased right ventricular diastolic pressures
Increased right atrial diastolic pressure
Increased central venous pressure
Right sided Congestive Heart Failure
Increased systemic capillary bed pressure
Edema (pleural effusion, ascites)
Causes of Right Sided CHF
Increased preload Decreased compliance Increased afterload Combination of above
Low output failure Either right or left side cannot
pump enough blood to perfuse tissues
Dilated cardiomyopathy (end stage)
Pressure Overload Excessive afterload diastolic dysfunction Contractility ok Examples: subaortic stenosis,
pulmonic stenosis, hypertension
Volume Overload Excessive preload Systolic dysfunction Contractility ok at first Examples: Mitral regurgitation,
patent ductus arteriosus
Pump Failure Insufficient contractility Systolic dysfunction Low output failure Also, congestive failure
Arrhythmias Changes in rate, rhythm, or
conduction Affects heart rate, synergy, and
ventricular filling Examples: tachycardias,
bradycardias, heart blocks
Myocardial Restriction Interferes with ventricular filling Diastolic dysfunction Contractility ok Examples: hypertrophic
cardiomyopathy, pericardial effusion
High output states Increased need for tissue blood
flow Heart is normal until later Examples: hyperthyroidism,
chronic anemia, chronic fever
Sympathetic Nervous System
Heart rate increased due to stimulation of Beta1 receptors on SA and AV nodes
Increases cardiac output at up to 2 ½ times normal rate
Sympathetic Nervous System
Increased contractility by stimulation of Beta1 receptors and epinephrine and norepinephrine
Effects blunted in chronic disease and can make things worse
Sympathetic Nervous System
Causes peripheral arteriolar vasoconstriction by stimulation of Alpha1 receptors
Prevents hypotension Creates increased afterload and
increased workload on the heart
RAAS System Increases preload to try to
increase cardiac output Activated by decreased renal
perfusion Renin released, converted to
angiotension I converted to angiotension II by ACE
RAAS System Angiotension II is potent
vasoconstrictor which increases afterload and preload
Angiotension II has adrenals release aldosterone so that sodium and water retained which also increases preload
RAAS System In early heart disease, can return
CO to normal In later heart disease, increases
preload which increases cardiac work load and increases failure
RAAS System Antidiuretic hormone (ADH)
released by increased angiotension II
ADH causes renal retention of fluid which increases preload
Myocardial Remodeling Chronic volume overload
increases diastolic stress Heart lays down more sarcomers
end to end Result is dilation of the heart and
eventually some hypertrophy (eccentric hypertrophy)
Myocardial Remodeling Chronic pressure overloads Heart lays down more sarcomers
in parallel so that wall becomes thicker
Concentric hypertrophy
Side Effects of Remodeling Dilated ventricle eventually has
decreased contractility Excessively hypertrophied
ventricle results in decreased lumen size, stiff ventricle, and decreased coronary artery filling
Clinical Signs of Heart Failure
Decreased cardiac output (exercise intolerance)
Pulmonary congestion (coughing, dyspnea)
Physical Exam Findings with Left Heart Failure
Possible murmur or gallop Tachycardias or bradycardias Coughing and/or dyspnea are the
main 2 signs
Physical Exam Findings with Left Heart Failure
Pulmonary crackles (rales), not always
Prolonged capillary refill time => decrease CO
Weak femoral pulses (not always)
Physical Exam Findings with Right Heart Failure
Systemic congestion (ascites in dogs, pleural effusion in cats, peripheral edema in horses, cows)
Hepatomegaly, splenomegaly Distended jugular veins Cardiac cachexia
Cats with Left or Right Heart Failure
Dyspnea is primary sign** Cats may or may not cough with
left heart failure (usually not detected)
Therapy Goals Reduce congestion Increase cardiac output Decrease cardiac work load Control arrhythmias, heart rate Treat cause of heart failure
Therapy Goals Modify the neurohormonal
compensation Modify cardiac remodeling Improve the patient’s quality of
life Increase patient’s longevity
RAAS Beta blockers decrease renin
release ACE inhibitors interupt
conversion of AGI to AGII ARBs (angiotension receptor
blockers) Aldosterone antagonists
Sympathetic Stimulation Beta blockers prevent stimulation
of heart by sympathetic system Alpha antagonists block alpha
one receptors in arterioles (over 50% dogs will get hypotensive). ACE I don’t cause hypotension.
Cardiac Remodeling ACE inhibitors and aldosterone
antagonists Beta blockers Arteriolar dilators to reduce
afterload Reduce preload with ACE
inhibitors and diuretics
Reduce Preload Diuretics ACE inhibitors Venodilators Low salt diet Do not reduce preload too much!
b/c these rely on preload for CO
Afterload Reduction ACE inhibitors - dilate Arteriolar dilators Must treat other diseases causing
the increased afterload. Hyperthyroid in cats
Don’t overdo it as get hypotension.
Increase Contractility Digoxin (wk. positive inotrope) Pimobendan (st. pos. inotrope) Catetcholamines IV Increases myocardial oxygen
demand and ATP consumption (down side)
Find and treat underlying disease
Increasing Compliance Calcium channel blockers may
relax heart Decrease heart rate so heart can
fill Remove pericardial effusion. This
is easy to do and rewarding. Find cause and treat
Heart Rate Must treat tachycardias or
bradycardias Antiarrhythmic therapy if needed. Find and treat any underlying
systemic problem contributing to the change in heart rate.
Positive Inotropes Affect calcium in some manner Used only with systolic function
with decreased contractility Increases oxygen and energy
used by heart, so heart works harder
Arrhythmogenic
Positive Inotropes Do not cure disease!!*** Efficacy varies b/t patients Give symptomatic improvement
is the goal of Tx
Digitalis Increases contractility in normal
and failing hearts Only increases cardiac output in
failing hearts Weak positive inotrope
Digitalis Negative chronotrope Increases myocardial excitability Better for volume overloads and
myocardial disease. Not good for pressure overloads.
Digoxin ECG Changes Seen mainly with toxicity Slower heart rate First degree heart block Mild ST changes (depression) Arrhythmias
Digitalis Digoxin Digitoxin Oral drugs Well absorbed but, absorption
decreased by food, drugs, and malabsorption states
Digitalis Digoxin eliminated by kidneys Slow oral method of dosing Cats (sick) are more intolerant of
digoxin. Don’t use it.
Digitoxicity Vomiting, diarrhea, anorexia Arrhythmias Negative inotrope Enhanced by hypokalemia, low
magnesium, hypercalcemia, and alkalosis
Digoxin Drug Interactions
Quinidine Aspirin (high levels) Amiodarone (same class w/
Sotalol) Spironolactone Cimetidine (decreases absorp of
Dig) Verapamil Chronic phenobarbital (increases
Dig levels)
Digoxin Crosses placenta Older dogs less tolerant of
digoxin Giants breeds need less Hypothyroid dogs have problems
unless being treated
Indications for Digoxin
SVT (Supraventricular tachycardia) or
Hearts with decreased contractility
Does not prevent progression of the disease process
Contraindications for Digoxin
Ventricular arrhythmias (severe) Animals with just a murmur Pericardial disease Restrictive cardiomyopathy Sinus node disease
Contraindications for Digoxin
AV blocks Hypertrophic cardiomyopathy Aortic stenosis Pulmonic stenosis Pulmonary hypertension
Pimobendan Inodilator = positive inotrope and
peripheral vasodilator Increases cardiac output Decreases preload and afterload Increases efficiency of cardiac
cells
Pimobendan Oral drug Well absorbed Out via feces Used in addition to other
medications (instead of digoxin)
Pimobendan No drug interactions But, it is a vasodilator so when
using other vasodilators, be careful of hypotension.
Negative inotropes may attenuate its positive inotropic effects
Pimobendan Side Effects Uncommon – yea! Vomiting/diarrhea-uncommon Polyuria/polydipsia-uncomon Anorexia-uncommon Sinus tachycardia at high doses Usually doesn’t worsen VPCs,
but can cause them at high doses
Pimobendan Efficacy in cats being studied Does not stop the progression of
the disease process Can accelerate the progression
of mitral regurgitation (murmurs) if used too soon in the disease. Don’t start p on this drug if just has murmurs.
Catecholamines Stimulates beta receptors and
cyclic AMP Synergistic with digoxin Metabolized in the liver (IV drugs)
Catecholamines Contraindications
Hypotension or hypertension Sinus tachycardia Arrhythmias Cardiac disease with mechanical
obstruction (aortic stenosis) With beta blockers
Epinephrine Increases heart rate (thru beta
receptors) Increases blood pressure Increases cardiac output
(contractility thru beat receptors) Increases arrhythmias Used mostly in CPR
Isoproterenol Increases contractility Increases heart rate Increases cardiac output Causes hypotension Used for heart block
Dopamine Increases contractility Increases heart rate (sinus
tachycardia) Increases blood pressure
(vasoconstricts) (dose dependent)
Dopamine Side Effects Tachycardias--high doses Arrhythmias--high doses Hypotension--low doses Hypertension--high doses
(vasoconstriction) Increases pulmonary capillary
pressure--high doses. Right heart to work against increased pressure
Dobutamine Hydrochloride
Increases contractility No vasodilatation or
vasoconstriction Cats can seizure or vomit Dogs can vomit
Dopamine versus Dobutamine
Same price now Dobutamine does not induce
tachycardias or affect peripheral vasculature
Both cannot be used more than 72 hours b.c they up regulate beta receptors and the receptors then become ineffective
Types of Diuretics Xanthine derivative Thiazides Aldosterone inhibitors Ethacrynic acid Loop diuretics—furosemide –
used the most - Lasix
Xanthines Bronchodilators
Weak diuretics Weak positive inotropes Dilates coronary, pulmonary ,
renal, and systemic arterioles and veins (v little effect)
Bronchodilator
Bronchodilators
Metabolized in the liver Side effects: vomiting, sinus
tachycardia, hyperexcitability (MAY happen and could last for 8 hrs.)
Thiazide Diuretics
Effects are not dose dependent Not as potent as furosemide but
have a more sustained diuretic effect
New lipid soluable ones Not effective with compromised
renal function
Thiazides
Side effects uncommon Cheap No drug tolerance develops Can be used with other diuretics Well tolerated Effects aren’t dose related
Aldosterone InhibitorsSpironolactone
Takes 2-3 days to be effective Weak diuretic Used in combination with other
diuretics Other benefits being explored Drug interactions—ACE inhibitors
Furosemide
Loop diuretic Effect is dose dependent Will dehydrate animal Comes in IV and oral forms Inexpensive
Furosemide
Side effects--hypokalemia, hyponatremia, dehydration, prerenal azotemia
Tolerance develops Drug interactions--cephaloridine,
polymixins, aminoglycosides
Arterial dilators Counteract reflex
vasoconstriction of heart failure Decreases work load of left
ventricle Improves tissue perfusion Decreases mitral regurgitation
(indirectly) Side effect is hypotension
Venodilators Increase vascular capacity Decrease venous pressure (less
bld goes back to the heart) Decrease preload Decreases pulmonary edema
indirectly Side effect is decreased CO (be
careful with this)
Vasodilator Uses Chronic, congestive heart failure Valvular heart disease (leaky
valves) Congenital heart problems (PDA,
VSD) Pulmonary hypertension (some) Cardiac arrhythmias due to
hypoxia Hypertension
Vasodilator Contraindications
Hypotension Coronary artery disease (some) Poor cardiac contractility Tachycardias
Vasodilator Net Effects Decreased preload Decreased afterload Increases cardiac output Decreased workload of heart Antiarrhythmic
Hydralazine
Pure Arterial dilator Uses--dogs with mitral
regurgitation, hypertension Side effects in 50%--hypotension,
GI side effects, increased pulmonary artery pressures
Nitrates
Nitroglycerine ointment--venodilator, no side effects, topical
Sodium nitroprusside--IV, mixed vasodilator, metabolized to cyanide
Prazosin Arterial and venous dilator Metabolized in the liver Does not cause a reflex
tachycardia Unknown if animals develop a
tolerance to it or not.
Angiotension Converting Enzyme
Inhibitors (ACE)
Captopril (not used much b/c had many problems)
Enalapril Benazapril Lisinopril Other “Pril” drugs
ACE Inhibitors Stop conversion of angiotensin I
to angiotensin II in lungs Decreases plasma aldosterone
levels Increases blood flow to kidneys Effects are progressive
ACE Inhibitors Increases effects of thiazide
diuretics Causes retention of potassium Does not cross blood brain
barrier
ACE Inhibitors Used in: Dilated cardiomyopathy Mitral regurgitation Volume overloaded hearts
(shunts such as PDA, VSD) Advanced heart disease in
people
Enalapril Side effects uncommon--
hypotension Improves heart failure and
increases survival Takes 7-10 days to reach
maximum benefits Only one clinically tested in
animals
Enalapril Hard to use in renal patients so
use benazepril Improves dog’s quality of life and
increases longevity Use in cat needs more study Not effective in horses, not
absoped well in their GI tract
Beta Blockers’ Actions Decrease contractility (negative
inotrope) Decrease heart rate Decreases myocardial oxygen
consumption Blocks sympathetic stimulation of
heart
Beta Blockers
Used to slow AV conduction and slow heart rate with SVT
Also used in hypertrophic cardiomyopathy
Beta Blockers Side Effects Blocking beta 1 receptors in heart
will decrease contractility and heart rate
Blocking beta 2 receptors cause bronchoconstriction
Heart blocks Heart failure
Carvedilol Blocks beta 1 and beta 2
receptors Extends life span in people May help in dogs—studies
ongoing
All Beta Blockers Start at low dose and increase
gradually Do not stop abruptly Don’t start until heart failure
under control
Acute Pulmonary Edema Diuretics Cage rest with oxygen Nitrol ointment ACE inhibitors Hydralazine or nitroprusside Catecholamines
Chronic CHF Therapy Diuretics Venodilators—ACE inhibitors Treat the underlying heart
disease with appropriate drugs Beta blockers
Pressure Overload
Excessive afterload Systolic dysfunction Subaortic stenosis or pulmonic
stenosis Pulmonary hypertension Systemic hypertension
Volume Overload
Excessive preload Systolic dysfunction Mitral or tricuspid regurgitation Shunts--PDA, VSD
Pump Failure Systolic dysfunction Cardiomyopathies--dilated,
myocarditis Chronic heart disease Dysynergy Drugs
Arrhythmias Changes in rate, rhythm, or
conduction Affects heart rate, synergy and
filling of the ventricles Effect depends on ventricular
heart rate Bradyarrhythmias,
tachyarrhythmias
Myocardial Restriction
Diastolic dysfunction Restrictive cardiomyopathy Pericardial disease Tumors infiltrating myocardium Hypertrophic cardiomyopathy