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

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CARDIAC CYCLE The atria contract in unison and the ventricles contract in unison The atria and ventricles ___________ contract at the same time (as one group contracts, the other relaxes) ATRIAL contraction sends blood into the ventricles through the _________ and _______________ valves – While this is occurring, the __________________ valves close – The ventricles relax at this time VENTRICULAR contraction sends blood through the _______________ valves into the aorta and pulmonary artery – While this is occurring, the bicuspid and tricuspid valves close – The atria ___________ at this time and blood enters the atria from the vena cava and pulmonary veins SYSTOLE – ________________ of the atria and ventricles – blood is being _________________ from the heart DIASTOLE – _______________ of the atria and ventricles -heart is filling with blood

HEARTBEATHEARTBEAT: Lub-dub: S1 and S2Lub-dub: S1 and S2 – S1: Beginning of systole (pulse) increase in _________________ pressure during contraction exceeds the pressure within the atria closing ____valves (mitral first) contraction forces blood semilunar valves. – S2: Beginning of _________ (no pulse) ventricles begin to ___________ pressures within the heart become ________ than the semilunar valves, causes the semilunar valves to snap _________ (aortic first)

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.

NORMAL CANINE HEART CANINE WITH CARDIOMEGALY 2.5 – 3.5 rib spaces Stroke Volume (SV) = EDV – ESV Cardiac Output (Q) = ____ X ______

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 _________thrill IV - Medium intensity with a palpable thrill V - Loud intensity with a palpable thrill. Audible even with the stethoscope placed on the ________ with the edge of the diaphragm VI - Loudest intensity with a palpable thrill. Audible even with the stethoscope ___________ the chest.

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

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

FELINE HYPERTROPHIC CARDIOMYOPATHY THE PREDOMINANT PATHOLOGY OF THIS DISEASE IS ____________________ HYPERTROPHY CAUSE: – +/- genetics – related to abnormal ___________________ or ________________ transport within the muscles of the heart

FELINE HYPERTROPHIC CARDIOMYOPATHY Blood backs up LA enlarged

FELINE HYPERTROPHIC CARDIOMYOPATHY: DIAGNOSIS

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

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 → ___________________! PROBLEM #3: The left atrium becomes dilated with blood → the blood becomes __________→ blood stasis leads to clot formation → clot becomes dislodged and trapped elsewhere in the arterial system → _____________________! ***90% of thrombi become lodged in the aortic ___________ causing “saddle thrombus”***

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

FELINE HYPERTROPHIC CARDIOMYOPATHY: SADDLE THROMBUS

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

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

FELINE HYPERTROPHIC CARDIOMYOPATHY: TREATEMENT LASIX (furosemide): a diuretic used to treat ___________________ DILTIAZEM: a calcium channel blocker used to inhibit cardiac and vascular smooth muscle ____________; reduces blood pressure and cardiac afterload; overall improvement in ______________ – Or Propranolol: a beta-blocker to decrease heart rate and myocardial oxygen demand ASPIRIN: an anticoagulant used to thin blood and help prevent __________ formation in HCM TPA (Activase): serves as a ____________ 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

FELINE HYPERTROPHIC CARDIOMYOPATHY: CLIENT INFO There is no ____________! – 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

CANINE HYPERTROPHIC CARDIOMYOPATHY: An _____________ 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

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

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

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

CONGENITAL DEFECTS: PATENT DUCTUS ARTERIOSUS The duct should close in the first hours after birth. If it does not, the blood begins to shunt from the aorta into the pulmonary artery and _______________ the lungs. The left side of the heart will have an increase in blood return and become volume overloaded. ________________________ THIS IS CALLED A ___________________SHUNT

CONGENITAL DEFECTS: PATENT DUCTUS ARTERIOSUS (PDA)

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)machinery – If the shunt is small some animals may be asymptomatic – In large shunts the animal will develop ____________________ Pulmonary edema Cough Exercise intolerance Tachypnea Weight loss – ECG: wide range of arrhythmias including APCs and VPCs – Echocardiography (ultrasound) – Radiographs: _____________ and ventricular enlargement

PATENT DUCTUS ARTERIOSUS: TREATMENT EXCELLENT _____________ WITH SURGICAL CORRECTION: LIGATION OF THE DUCTUS ARTERIOSUS

PATENT DUCTUS ARTERIOSUS: TREATMENT CLIENT INFO: – 64% OF ANIMALS WILL DIE WITHIN _____ YEAR IF NOT TREATED SURGICALLY – Dogs with this condition should not be used for _______________

ATRIAL AND VENTRICULAR SEPTAL DEFECTS ~ Cats During fetal life, the _____________________ 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. Atrial Septal Defect

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 – _____________________ failure – Radiographs: right ventricular enlargement – Echo: right ventricular dilatation

CONGENITAL DEFECTS: ATRIAL AND VENTRICULAR SEPTAL DEFECTS 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. The right ventricle may dilate as well.

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 ________________, 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

VSD - Treatment There are 2 current surgical options available. – Before right-to-left shunting has developed, __________________________ 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.