To understand the heart and mind of a person, look not at what he has already achieved, but at what he aspires to

1. To understand the heart and mind of a person, look not at what he has already achieved, but at what he aspires to -Kahlil Gibran

2. VC > RA > Triscuspid valve > RV > Pulmonary valve: pulmonary a. > Lungs > pulmonary v. > LA > Mitral v. > LV > Aortic v. > Aorta > SYSTEMIC CIRCULATION > VC • http://www.bostonscientific.com/templatedata/imports/HTML/lifebeatonline/winter2007/learning.shtml#fig1

4. CARDIAC CYCLE • The atria contract in unison and the ventricles contract in unison • The atria and ventricles do not contract at the same time (as one group contracts, the other relaxes) • ATRIAL contraction sends blood into the ventricles through the bicuspid and tricuspid valves • While this is occurring, the semilunar valves close • The ventricles relax at this time  • VENTRICULAR contraction sends blood through the semilunar valves into the aorta and pulmonary artery • While this is occurring, the bicuspid and tricuspid valves close • The atria relax at this time and blood enters the atria from the vena cava and pulmonary veins • SYSTOLE – contraction of the atria and ventricles • blood is being ejected from the heart • DIASTOLE – relaxation of the atria and ventricles -heart is filling with blood

5. HEARTBEAT: Lub-dub: S1 and S2 • S1: Beginning of systole (pulse) • increase in intraventricular pressure during contraction exceeds the pressure within the atria • closing AV valves (mitral first) • contraction forces blood semilunar valves. • S2: Beginning of Diastole (no pulse) • ventricles begin to relax • pressures within the heart become less than the semilunar valves, • causes the semilunar valves to snap shut (aortic first)

6. STROKE VOLUME • Contractility:  Contractility is the intrinsic ability of cardiac muscle to develop force for a given muscle length.  It is also referred to as inotropism. • Preload:  Preload is the muscle length prior to contractility, and it is dependent of ventricular filling (or end diastolic volume.)  This value is related to right atrial pressure.  The most important determining factor for preload is venous return. • Afterload:  Afterload is the tension (or the arterial pressure) against which the ventricle must contract.  If arterial pressure increases, afterload also increases. Afterload for the left ventricle is determined by aortic pressure, afterload for the right ventricle is determined by pulmonary artery pressure.      

7. 2.5 – 3.5 rib spaces CANINE WITH CARDIOMEGALY NORMAL CANINE HEART Stroke Volume (SV) = EDV – ESV Cardiac Output (Q) = SV × HR

8. MURMURS • I - Lowest intensity, difficult to hear even by expert listeners • II- Low intensity, but usually audible by all listeners • III - Medium intensity, easy to hear even by inexperienced listeners, but without a palpable thrill • IV - Medium intensity with a palpable thrill • V - Loud intensity with a palpable thrill. Audible even with the stethoscope placed on the chest with the edge of the diaphragm • VI - Loudest intensity with a palpable thrill. Audible even with the stethoscope raised above the chest.

9. Failure of pump • Myocardial dysfunction • Cardiomyopathy • Myocarditis • Taurine deficiency cat • Circulatory Failure • Hypovolemia: shock, hemorrhage, dehydration • Anemia • Valvular dysfunction • Congenital shunts or defects

10. DISEASES OF THE CARDIOVASCULAR SYSTEM: ‘Failure of pump’ Cardiomyopathies CHF Valvular disease Congenital malformation Infectious

11. DX Heart Disease • HISTORY: cats usually acute • PHYSICAL EXAMINATION: cyanosis: R to L shunt • ANCILLARY TESTS- electrocardiography- radiography- echocardiography (including Doppler Echocardiography)- cardiac catheterization • RESPONSE TO THERAPY

12. CANINE DILATED CARDIOMYOPATHY 90% of cases occur in Doberman Pinschers and Boxers OTHER BREEDS INCLUDE WOLFHOUNDS, GREAT DANES, AND COCKER SPANIELS

13. CANINE DILATED CARDIOMYOPATHY: PATHOPHYSIOLOGY • DECREASED CONTRACTILITY FROM AN UNKNOWN CAUSE (viral?, carnitine deficiency?) • Decreased contractility = decreased cardiac output CO (CARDIAC OUTPUT) = SV (STROKE VOLUME) X HR (HEART RATE) Amt. of blood ejected with Each cardiac contraction (affected by afterload, preload, and inherent contractility) How often the heart contracts The amt. of blood that leaves The heart

14. CANINE DILATED CARDIOMYOPATHY: PATHOPHYSIOLOGY • THE BODY COMPENSATES BY: 1.INCREASING THE HEART RATE *this is done by sympathetic nervous system stimulation 2.TRYING TO INCREASE STROKE VOLUME BY INCREASING PRELOAD (this means that the body increases filling of the heart) *This is done by activation of the Renin-angiotensin-aldosterone system which leads to sodium and water retention

15. THE WALLS OF THE HEART ARE WEAK, FLABBY, AND DILATED – THIS DILATION MAY CAUSE SEPARATION OF THE MITRAL VALVE LEAFLETS LEADING TO MITRAL REGURGITATION

16. CANINE DILATED CARDIOMYOPATHY: CLINICAL SIGNS LETHARGY, EXERCISE INTOLERANCE, COUGHING, WEIGHT LOSS, TACHYPNEA, SYNCOPE, SOFT MURMUR (WHERE?)

17. CANINE DILATED CARDIOMYOPATHY:DIAGNOSIS Enlarged, round heart DOBERMANS ARE DEEP CHESTED AND MAY NOT APPEAR TO HAVE SUCH AN ENLARGED HEART ON RADIOGRAPHS

18. CANINE DILATED CARDIOMYOPATHY: DIAGNOSIS PULMONARY EDEMA OCCURS IN LEFT-SIDED HEART FAILURE PLEURAL EFFUSION OCCURS IN RIGHT SIDED HEART FAILURE PATIENT MAY SHOW SIGNS OF LEFT-SIDED, RIGHT-SIDED, OR HEART FAILURE FROM BOTH SIDES

19. CANINE DILATED CARDIOMYOPATHY: PATHOPHYSIOLOGY, DIAGNOSIS • Constant stimulation of the heart by the sympathetic nervous system causes ventricular arrhythmias and myocyte death • Most common arrhythmias: VPC’s and ventricular tachycardia, esp. in boxers & Dobies; other dogs may have APC’s and atrial fibrillation ONE VPC MULTIPLE VPCs CAUSING TACHY-CARDIA

20. CANINE DILATED CARDIOMYOPATHY: DIAGNOSIS: ECHOCARDIOGRAM http://www.youtube.com/watch?v=7TWu0_Gklzo&feature=related http://www.youtube.com/watch?v=NSnh3qN2kR4&NR=1 PERFORMING AN ECHOCARDIOGRAM IS THE DEFINITIVE WAY TO DIAGNOSE DILATED CARDIOMYOPATHY

21. CANINE DILATED CARDIOMYOPATHY: TREATMENT INCREASES CONTRACTILITY REDUCES FLUID RETENTION DIURETIC-ELIMINATES EXCESS FLUID

22. CANINE DILATED CARDIOMYOPATHY: TREATMENT TAURINE – USED IN COCKER SPANIELS AND CATS, MAINLY L-CARNITINE COENZYME Q10 DIETARY SUPPLEMENTS THAT MAY HELP IMPROVE HEART FUNCTION, ESP IF THERE IS A DEFICIENCY

23. FELINE DILATED CARDIOMYOPATHY A globular-shaped heart with severe dilation of all four chambers. Depressed ventricular contractile performance occurs. Ventricular dilation distorts the atrioventricular valves leading to mitral regurgitation and atrial enlargement ABNORMALLY THIN VENTRICULAR WALLS ATROPHIED PAPILLARY MUSCLES

24. FELINE DILATED CARDIOMYOPATHY • In the 1980’s DCM in cats was one of the most commonly diagnosed heart diseases. It was discovered that this was caused by a deficiency of TAURINE, an amino acid. • Since that time commercial foods have added taurine to feline diets, which has significantly decreased the number of cases of feline DCM

25. FELINE HYPERTROPHIC CARDIOMYOPATHY (HCM) NEUTERED MALE CATS BETWEEN 1-16 YRS. OF AGE THE MOST COMMON CARDIOMYOPATHY IN CATS!

26. FELINE HYPERTROPHIC CARDIOMYOPATHY • THE PREDOMINANT PATHOLOGY OF THIS DISEASE IS LEFT VENTRICULAR HYPERTROPHY • CAUSE: • +/- genetics • related to abnormal myocardial myosin or calcium transport within the muscles of the heart

27. FELINE HYPERTROPHIC CARDIOMYOPATHY Blood backs up LA enlarged

28. FELINE HYPERTROPHIC CARDIOMYOPATHY: DIAGNOSIS http://www.youtube.com/watch?v=yNj-lQaUBao http://www.youtube.com/watch?v=KvUFb4qZwmw&feature=related http://www.youtube.com/watch?v=xlsq5tJpj04&feature=related

29. FELINE HYPERTROPHIC CARDIOMYOPATHY: Pathophysiology PROBLEM #1: The walls lose compliance and resist filling during diastole! (diastolic failure)

30. FELINE HYPERTROPHIC CARDIOMYOPATHY: Pathophysiology • PROBLEM #2: If the left ventricle cannot fill adequately with blood, the blood backs up into the left atrium (enlargement) → pulmonary veins → pulmonary edema! • PROBLEM #3: The left atrium becomes dilated with blood → the blood becomes static → blood stasis leads to clot formation → clot becomes dislodged and trapped elsewhere in the arterial system → thromboembolism! ***90% of thrombi become lodged in the aortic trifurcation causing “saddle thrombus”***

31. FELINE HYPERTROPHIC CARDIOMYOPATHY: SADDLE THROMBUS ACUTE, PAINFUL CONDITION CAUSING PARESIS, COLD REAR LEGS/FEET!

32. FELINE HYPERTROPHIC CARDIOMYOPATHY: SADDLE THROMBUS

33. FELINE HYPERTROPHIC CARDIOMYOPATHY: CLINICAL SIGNS and DIAGNOSIS • Soft, sytolic murmur (grade 2-3/6) • Gallop rhythms or other arrhythmias • ECG: ↑ p wave duration, ↑ QRS width, sinus tachycardia • Echo: shows ↑ ventricular wall thickness, dilated left atrium • Acute onset of heart failure • Acute onset of systemic thromboembolism • Hindlimb paresis • Cold rear legs • Painful rear legs

34. FELINE HYPERTROPHIC CARDIOMYOPATHY: TREATMENT FUROSEMIDE (DIURETIC) ASPIRIN ANTICOAGULANT Relax so Time to fill OR DILTIAZEM (CALCIUM CHANNEL BLOCKER) Inhibits contractility: low BP and cardiac afterload PROPRANOLOL (B-BLOCKER) Slows HR

35. FELINE HYPERTROPHIC CARDIOMYOPATHY: TREATEMENT • LASIX (furosemide): a diuretic used to treat pulmonary edema • DILTIAZEM: a calcium channel blocker used to inhibit cardiac and vascular smooth muscle contractility; reduces blood pressure and cardiac afterload; overall improvement in diastolic function • Or Propranolol: a beta-blocker to decrease heart rate and myocardial oxygen demand • ASPIRIN: an anticoagulant used to thin blood and help prevent clot formation in HCM • TPA (Activase): serves as a fibrolysin resulting in the breakdown of clots that have already formed • Or Heparin, Warfarin: acts on the coagulation factors to inhibit the formation of a stable clot

36. FELINE HYPERTROPHIC CARDIOMYOPATHY: CLIENT INFO • There is no cure! • Cats with HCM may experience heart failure, arterial embolism, or SUDDEN DEATH! • Cats whose heart rates stay below 200 beats/min have a better prognosis than those whose heart rate is >200 beats/min

37. CANINE HYPERTROPHIC CARDIOMYOPATHY: • An UNCOMMON canine disease, but the cause appears to be heritable • CLINICAL SIGNS: • Fatigue • Sudden death • Tachypnea • Syncope • Cough • BREEDS: German Shepherds, Rottweilers, Cocker Spaniels, and others

38. DISEASES OF THE CARDIOVASCULAR SYSTEM: Cardiomyopathies CHF Valvular disease Congenital malformation Infectious

39. CONGENITAL DEFECTS: PATENT DUCTUS ARTERIOSUS CHIHUAHUAS, MALTESE, POODLE, POMERANIAN, SHELTIE PUPPIES COMMONLY AFFECTED (Table 1-1)

40. CONGENITAL DEFECTS: PATENT DUCTUS ARTERIOSUS Normally, the ductus arteriosus carries blood from the pulmonary artery to the aorta during fetal development. It bypasses the lungs of the fetus.

41. CONGENITAL DEFECTS: PATENT DUCTUS ARTERIOSUS The duct should close in the first 12-24 hours after birth. If it does not, the blood begins to shunt from the aorta into the pulmonary artery and hyperperfuse the lungs. The left side of the heart will have an increase in blood return and become volume overloaded. Left heart failure THIS IS CALLED A LEFT-TO-RIGHT SHUNT

42. CONGENITAL DEFECTS: PATENT DUCTUS ARTERIOSUS (PDA)

43. CONGENITAL DEFECTS: PATENT DUCTUS ARTERIOSUS • CLINICAL SIGNS: • A loud murmur best heard over the left base • Sometimes called a “machinery” murmur or a continuous murmur (btw S1 and S2) • If the shunt is small some animals may be asymptomatic • In large shunts the animal will develop left-sided heart failure • Pulmonary edema • Cough • Exercise intolerance • Tachypnea • Weight loss • ECG: wide range of arrhythmias including APCs and VPCs • Echocardiography (ultrasound) • Radiographs: left atrial and ventricular enlargement

44. PATENT DUCTUS ARTERIOSUS: TREATMENT EXCELLENT PROGNOSIS WITH SURGICAL CORRECTION: LIGATION OF THE DUCTUS ARTERIOSUS

45. PATENT DUCTUS ARTERIOSUS: TREATMENT • CLIENT INFO: • 64% OF ANIMALS WILL DIE WITHIN 1 YEAR IF NOT TREATED SURGICALLY • Dogs with this condition should not be used for breeding

46. ATRIAL AND VENTRICULAR SEPTAL DEFECTS~ Cats Atrial Septal Defect During fetal life, the foramen ovale is an openingi n the interatrial septum, allowing shunting of blood from the right atrium to the left atrium in order to bypass the nonfunctioning fetal lungs. It should close at birth. If it doesn’t, after birth, the blood will shunt from left to right resulting in overload of the right side of the heart.

47. CONGENITAL DEFECTS: ATRIAL AND VENTRICULAR SEPTAL DEFECTS • CLINICAL SIGNS: ATRIAL SEPTAL DEFECTS • Result in overload of the right side of the heart → dilation and hypertrophy of the right-sided chambers • Systolic murmur • Right-sided heart failure • Radiographs: right ventricular enlargement • Echo: right ventricular dilatation

48. CONGENITAL DEFECTS: ATRIAL AND VENTRICULAR SEPTAL DEFECTS Blood is shunted from the oxygen-rich left ventricle into the right ventricle. The blood goes through pulmonary circulation and right back into the left atrium and ventricle resulting in volume overload of the left side of the heart (LHF). The right ventricle may dilate as well.

49. CONGENITAL DEFECTS: ATRIAL AND VENTRICULAR SEPTAL DEFECTS • CLINICAL SIGNS: VENTRICULAR SEPTAL DEFECTS: • Animals with small defects may have minimal or no signs • Larger defects may result in acute left-sided heart failure, usually by 8 weeks of age • A harsh holosystolic murmur • CLIENT INFO: • Repair of these defects requires open-heart surgery or cardiopulmonary bypass. These procedures are uncommon in the dog and cat • Most of these animals will eventually experience development of congestive heart failure

50. VSD - Treatment • There are 2 current surgical options available.  • Before right-to-left shunting has developed, pulmonary artery banding • decrease the blood flow across the defect • reducing the overload on the lungs and the left heart.  • Repair of the defect, but this requires open heart surgery and carries a high risk.