Chapter 2 Cardiovascular System

Question 1

Which of the following is MOST likely to be associated with decreased central venous pressure (CVP)? A. Vasoconstriction B. Congestive heart failure C. Pericardial effusion D. Hypovolemia

Answer 1

D. CVP is a reflection of intravascular blood vol., cardiac function, venous tone and compliance, and intrathoracic pressure.

Question 2

Congestive heart failure

Answer 2

Increases CVP due to cardiac dysfunction and poor forward blood flow

Question 3

Pericardial effusion

Answer 3

Causes increase in CVP due to impaired diastolic function in the heart causing backup into the venous system

Question 4

Vasoconstriction

Answer 4

Decreases venous compliance thus increasing CVP even in the face of hypotension

Question 5

A five year old corgi was presented to your hospital and on physical examination is found to have a Doppler BP of 120/90 & HR of 80bpm. Calculate his MAP.

Answer 5

MAP = average blood pressure / time ( through systole and diastole). Diastole counts twice as much as systole as 2/3 of the cardiac cycle is spent in diastole. MAP= ((2 x diastolic) + systolic) / 3 = ( (2X 90) + 120 ) /3 = 100 OR 1/3 of pulse pressure added to diastolic pressure Pulse pressure is the difference between systolic and diastolic pressure MAP=diastolic + (systolic - diastolic) = 90 + (120-90)

Question 6

Which medications is most likely to decrease after load in the heart? A. Hydralazine B. Furosemide C. Atenolol D. Lidocaine

Answer 6

After load = how hard to push the blood out fo the heart A. Hydralazine is a potent arterial dilator and by dilating the aorta, it will decrease the amount of pressure it takes to push blood out of the heart

Question 7

Furosemide

Answer 7

Decreases vol. and therefore decreases preload

Question 8

Atenolol

Answer 8

Beta 1 blocker and therefore slows HR, decreases contractility and slows conduction through the AV node

Question 9

Lidocaine

Answer 9

Anti-arrhythmic and has no effect on afterload

Question 10

Which of the following groups of medications would not be appropriate to use in a patient experiencing super ventricular tachyarrhythmia?

Answer 10

Vagolytic agents as it would block the vagus nerve from slowing the heart down and in some cases will actually increase HR i.e.Atropine

Question 11

What do Calcium channel blockers, Beta blockers and digitalis glycosides have in common?

Answer 11

They all conduction through the AV node and could be used to treat a supraventricular tachyarrhythmia

Question 12

What is a Tetralogy of Fallot?

Answer 12

A congenital defect that consist of 4 defects: Pulmonary stenosis (narrowing of the exit from the right ventricle) Ventricular Septal Defect (a hole between the two ventricles) Secondary right ventricular hypertrophy (thickening of the right ventricular wall) Over-riding aorta ( blood from both ventricles to enter the aorta)

Question 13

According to the RECOVER CPR Guidelines, which of the following therapies should be used first in a patient in pulseless ventricular tachycardia (VT or vfib)? A. Biphasic defibrillation B. Vasopressin C. Lidocaine D. Epinephrine

Answer 13

Defibrillation. Then resume compressions and ventilation. EPI and vasopressins are second line treatment if there is prolonged pulse less ventricular tachycardia.

Question 14

Which of the following heart conditions or disease states is NOT appropriately paired with a frequently associated clinical sign? A. Tricuspid valve dysplasia: ascites B. Feline hypertrophic cardiomyopathy: distal aortic thrombus C. Dilated cardiomyopathy: coughing and respiratory distress D. Pulmonic stenosis: Pulmonary oedema

Answer 14

D. Pulmonic stenosis is the narrowing of the right side of the ventricles which will likely show as ascites instead of pulmonary oedema

Question 15

Tricuspid valve dysplasia

Answer 15

Leads to right sided heart failure signs = ascites

Question 16

Feline HCM

Answer 16

Usually shows up in emergency for a thromboembolic event

Question 17

Dilated cardiomyopathy

Answer 17

Left sided heart failure signs: Pulmonary oedema Coughing Lung congestion

Question 18

Which of the following arrhythmias would be the least likely to auscultation in a rhythmic pattern? A. First degree AV block B. Second degree AV block C. Third degree AV block D. Bundle branch block

Answer 18

B. Second degree AV block would sound irregular due to dropped QRS’s

Question 19

First degree AV block

Answer 19

Prolonged P-R intervals Regular rate and rhythm

Question 20

Third degree AV block

Answer 20

All atrial impulses are blocked.

No communication between atria and ventricles, so each act completely independent of each other.

Requires the heart to function on an escape rhythm. Consistent P-P intervals Consistent R-R intervals Irregular P-R intervals

Question 21

Right bundle branch blocks

Answer 21

Regular and fully functioning beats despite altered electrical pathways

Question 22

What is an atrial standstill?

Answer 22

A rhythm created by the inhibition of atrial myocardial depolarisation secondary to hyperkalemia (K is greater than 7.5mEq/L) ECG most commonly shows absence P waves and wide bizarre QRS complexes with an overall slow rate. Rare cases: no P waves & narrow complexes, with biphasic T waves and a U wave after the T wave

Question 23

What are the common diseases associated with the development of an atrial standstill?

Answer 23

Addison’s disease (Hypoadrenocorticism) Anuric or oliguric renal failure Uncontrolled DKA Metabolic acidosis Urethral obstruction Ruptured bladder

Question 24

Which of the following cardiac conditions is primarily associated with a diastolic dysfunction? A. Dilated cardiomyopathy B. Heart worm disease C. Patent ductus arteriosus D. Feline hypertrophic cardiomyopathy

Answer 24

D. Diastolic dysfunction is the relaxation phase of the heart where it is allowed to stretch and fill. Hypertrophic cardiomyopathy is an issue of the ventricular walls stiffening and no longer stretching or allowing ventricular filling. Dilated cardiomyopathy is more related to the systolic phase and impaired contraction. Heart worm disease is an obstructive issue that leads to right side overload and right side systolic failure. Patent ductus arteriosus is a shunt issue between aorta and pulmonary artery creating a vol. overload to the left side of the heart and leading to pulmonary congestion and potentially oedema.

Question 25

Based on a patient with atrial standstill, which of the following is the least likely the patient’s diagnosis? A. Hypoadrenocorticism (Addison’s disease) B. Inflammatory bowel disease C. Anuric renal failure D. Ruptured bladder

Answer 25

B. Inflammatory bowel disease causes severe diarrhoea which leads to a decrease in serum potassium due to GI losses Atrial standstill is due to hyperkalemia. Hypoadrenocorticism causes eleveated K levels. Anuric renal failure patients are no longer able to excrete potassium and therefore start developing hyperK. Patients with ruptured bladder will reabsorb K from the urine that is leaked back into the abdomen causing hyperK.

Question 26

What is colloid oncotic pressure(COP)?

Answer 26

COP is a way of measuring the holding power of fluids within the vascular fluid compartment.

Question 27

What is the normal COP measurement?

Answer 27

18-25mm Hg

Question 28

At what COP measurement would synthetic colloids be used?

Answer 28

Below 3.5g/dL

Question 29

Congenital Cardiac diseases or conditions

Answer 29

Patent ductus arteriosus (hole between pulmonary trunk and aorta) Ventricular septal Defect Tricuspid valve dysplasia Mitral valve dysplasia Tetralogy of Fallot (4 defects) Pulmonary stenosis

Question 30

Specific acquired diseases or conditions

Answer 30

Feline hypertrophic cardiomyopathy (left ventricular hypertrophy) Canine dilated cardiomyopathy (ventricular dilation) Degenerative valvular disease (accumulation of mucopolysaccharides on Mitral valve) Infective endocarditis (bacterial colonization of heart valves and endocardium) Heart worm disease

Question 31

Patent ductus arteriosus

Answer 31

Arterial duct that shunts fetal blood from pulmonary artery directly to the aorta results in appropriate flow of blood between aorta and pulmonary artery Congestive heart failure Need furosemide (diuretic) to reduce edema Left atrial enlargement can lead to atrial fibrillation - digoxin Watch for hypokalemia due to being on diuretic and digoxin Auscultable murmur of mitral regurgitation

Question 32

Ventricular septal defect (VSD)

Answer 32

Hole in the interventricular septum which separates the left and right ventricles Most common cardiac anomalies in cats 4th most common in dogs Leads to left to right shunting May lead to right or left or biventricular failure

Question 33

Tricuspid valve dysplasia (right atrial ventricular valve)

Answer 33

Congenital malformation of the tricuspid valve due to pathologic lesions to the valve. Leads to tricuspid valve regurgitation and possibly tricuspid stenosis. Leads to right ventricular volume overload and dilation and ultimately right sided heart failure.

Question 34

How do you treat tricuspid valve dysplasia?

Answer 34

Decreasing preload using diuretics and ACE inhibitors Treat ascites with abdominocentesis Nitrate venodilators (nitroglycerine) Thiazide diuretics (hydrochlorothiazide) Calcium channel blockers (anti-hypertensive drug) Digoxin (anti-fibrillation) Surgical - ring annuloplasty or valve replacement

Question 35

What is mitral valve dysplasia?

Answer 35

Leaflet deformity, adherence to adjacent structure, cleft leaflet, inappropriate length of chordae tendonae, abnormal papillary muscles, abnormal valve annulus, or a fibrous ring or membrane located above the valve Leads to left sided heart failure, hypertrophy of the left atrium and ventricle

Question 36

How do you treat tricuspid valve dysplasia?

Answer 36

Decreasing preload using diuretics and ACE inhibitors Treat ascites with abdominocentesis Nitrate venodilators (nitroglycerine) Thiazide diuretics (hydrochlorothiazide) Calcium channel blockers (anti-hypertensive drug) Digoxin (anti-fibrillation) Surgical - ring annuloplasty or valve replacement

Question 37

What is mitral valve dysplasia?

Answer 37

Leaflet deformity, adherence to adjacent structure, cleft leaflet, inappropriate length of chordae tendonae, abnormal papillary muscles, abnormal valve annulus, or a fibrous ring or membrane located above the valve Leads to left sided heart failure, hypertrophy of the left atrium and ventricle

Question 38

How to treat mitral valve dysplasia?

Answer 38

ACE inhibitors - relaxes blood vessels and decreases blood vol. Congestion - diuretics Atrial arrhythmia - digitalis glycosides Stenotic valve - balloon valvuloplasty Severe - Valve repair and replacement

Question 39

What is Tetralogy of Fallot?

Answer 39

Tetralogy = 4 Congenital defect that consist of 4 defects 1) Pulmonary stenosis 2) Ventricular septal defect 3) Tricuspid valve dysplasia 4) over-riding aorta

Question 40

What is a pulmonary stenosis?

Answer 40

A congenital abnormality characterized by obstruction to blood flow from the right ventricle to the pulmonary artery. Obstruction is caused by narrowing (stenosis) at one or more points from the right ventricle to the pulmonary valve, stenosis of the valve itself, or stenosis of the pulmonary artery above the valve. Leads to right sides heart failure.

Question 41

What is feline hypertrophic cardiomyopathy(HCM)?

Answer 41

HCM is an acquired disease that affects the left ventricle and its functional ability to pump blood into the aorta. Abnormal thickened or enlarged left ventricle. Leads to heart failure and inadequate stroke volume. Atrial enlargement. Circulatory stasis Thromboembolism Pulmonary congestion Edema Pleural effusion

Question 42

What is canine dilated cardiomyopathy?

Answer 42

Enlarged heart where both upper and lower chambers with one side being worse than the other leading to CHF.

Question 43

What do patients with DCM present with?

Answer 43

Respiratory distress due to pulmonary congestion Coughing Ascites Weakness History: Exercise intolerance Lethargy Anorexia Weight loss

Question 44

What is the goal of treating DCM?

Answer 44

Goal is to decrease preload using loop diuretics to reduce congestion and decrease afterload using vasodilator (Nitroprusside) to improve forward flow, and to improve contractility

Question 45

What is degenerative valvular disease?

Answer 45

Most common cardiac disability in dogs characterised by accumulation of mucopolysaccarides on the AV valve leaflets especially on the mitral valve (left atrial ventricular valve). This leads to mitral valve regurgitation = volume overload of the left atrium and ventricle=hyperthrophy= left sided heart failure. If tricuspid valve is affected (right atrial ventricular valve) = right sided heart failure.

Question 46

How do you treat degenerative valvular disease?

Answer 46

ACE inhibitors for its vasodilation effects and inhibition of aldosterone. Calcium channel blockers Nitroprusside or nitroglycerin for acute phase Diuretics for pulmonary oedema If CHF= hydralazine or amlodipine Surgical = mitral valve repair or replacement

Question 47

What is an infective endocarditis?

Answer 47

Bacterial colonization of the heart valves and adjacent endocardium with associated tissue destruction. Most commonly affecting the aortic and mitral valve leading to CHF.

Question 48

How is infective endocarditis treated?

Answer 48

Digoxin ACE inhibitors Diuretics Diet and exercise restriction Severe= hydralazine and/or amlodipine

Question 49

What causes heart worm disease?

Answer 49

Filarid nematode - Dirofilaria immitis transmitted by mosquitoes They mostly reside in the pulmonary arteries (blood to the lungs), but can also be found in right atrium and ventricle and vena cava. Obstruction of pulmonary circulation = pulmonary hypertension Pressure overload of the right ventricle = tricuspid regurgitation and systolic myocardial failure of the right side of the heart Caval syndrome = large numbers of worms localized in the cranial and caudal vena cava and right atrium

Question 50

How do you treat heart worm disease?

Answer 50

Adulticide therapy, then microfilaricidal therapy within 4-6 weeks Heparin to reduce incidence of pulmonary thromboembolism Aspirin to reduce pulmonary endothelial damage and reduce severity of thromboembolism Strict cage rest Surgical removal of worms in caval syndrome patient CHF=furosemide and ACE inhibitor

Question 51

Furosemide

Answer 51

Loop diuretic 2-4mg/kg q1-8hours CRT 0.1mg/kg/hr

Question 52

Spironolactone

Answer 52

Potassium-sparing diuretic Aldosterone receptor blocker Slow onset - takes 2-3 days to peak effect More of a long term treatment 2-4mg/kg/day PO Must monitor renal function as can lead to hyperkalemia

Question 53

What is a positive inotrope?

Answer 53

They increase myocardial contractility, hence increasing cardiac output. The four groups are: Sympathomimetic amines (dobutamine & dopamine) Phosphodiesterase inhibitors (Milrinone, Amrinone, Sildenafil and pimobendan) Calcium sensitized Digitalis glycosides (Digoxin, digitoxin)

Question 54

What are vasodilators?

Answer 54

Nitroglycerin and hydralazine Nitroprusside potent arterial and venous dilator (CRI 0.5-10mcg/kg/min) Calcium channel blockers (dihydropyridine (Amlodipine) and non-dihydropyridine (Diltiazem))

Question 55

What are beta-adrenergic blockers?

Answer 55

They bind to the beta receptors of the sympathetic nervous system. Beta-1 receptors causes increased heart rate, increase in AV nodal conduction velocity and increase in strength of myocardial contraction. Beta-2 receptors causes vasodilation in skeletal muscles and bronchodilation in airways. Beta blockers stops these. Examples: Propranolol (1 &2) Atenolol (1) Metoprolol (1) Esmolol (1)

Question 56

What is an atrial fibrillation ? (Add photo)

Answer 56

Uncoordinated activity of the atria. ECG: no defined P waves irregular R to R intervals Treatment: Cardioversion and/or Digoxin Calcium blockers or Beta blockers

Question 57

Second degree AV block, Mobitz Type 1

Answer 57

Progressive prolongation of P-R interval until a dropped beat occurs P wave without a QRS after a series of prolonging P-R intervals Also known as Wenckebach Less likely to progress into third degree AV block Causes: Increased vagal tone Fibrosis drugs Electrolyte imbalance

Question 58

Second degree AV block Mobitz Type 2

Answer 58

P-R interval remains constant with intermittent P waves without QRS More likely to progress to a 3rd degree AV block QRS rhythm may or may not be regular depending on ratio of blocked beats Hemodynamic compromise may occur if numerous dropped beats occurs

Question 59

What are atrioventricular blocks?

Answer 59

Arrhythmias that occur due to communication issue between SA node and AV node and exist in different degrees first, second and third heart blocks

Question 60

Atrial flutter

Answer 60

Rapid atrial rate where atrial repolarization is altered resulting in saw-toothed atrial complexes = F waves QRS appear normal Causes: Valvular disease Cardiomyopathy Digitalis

Question 61

Secondary AV block

Answer 61

Occurs because of intermittent interruptions of AV conduction causing loss of ventricular activation \*Sometimes the message from SA node does make it to the AV node

Question 62

Atrial Premature Complexes (APC’s)

Answer 62

Premature atrial beats that originate out of the SA node ECG normal but rhythm is irregular due to premature P waves (P’ waves) QRS normal or abnormal Dangerous if P’ occur within S-T segment and disrupts heart depolarization Causes: Mitral valve insufficiency Atrial diease Chronic obstructive Pulmonary disease Hypoxia

Question 63

Bundle Branch Blocks

Answer 63

\*3 bundle of brunches in the heart: right, left posterior and left anterior branches \*Obstruction of any of these branches causes an altered ECG due to altered electrical path in the heart

Question 64

Right bundle branch block

Answer 64

Causes late depolarisation of the right ventricle. Widening of ECG complex. Alters direction of the current flow = Deep wide S wave. Unaffected P and P-R interval. No treatment required.

Question 65

What are the causes of right bundle of branch block?

Answer 65

Incidental finding, no Tx needed as beats are fully functional \*Congenital heart disease, valvular disease, neoplasia, heartworm, pulmonary embolism, and hypokalemia

Question 66

Left bundle branch block

Answer 66

Conduction delay or a block in both posterior and anterior fascicles of the left branch. ≈ \*Right ventricle is activated first and then left ventricle activated late -causes Wide QRS with positive deflection.

Question 67

Causes of left bundle branch block

Answer 67

Cardiomyopathy, congenital defects, neoplasia, trauma or fibrosis

Question 68

Sick Sinus Syndrome (SSS)

Answer 68

\*Encompasses a number of sinus nodal abnormalities \*Can include sinus bradycardia, sinus arrest, sinoatrial block, alternating bradycardia/tachycardia and combination of SA and AV conduction disturbances or combination thereof

Question 69

Causes of Sick Sinus Syndrome (SSS)

Answer 69

Ischemia, inflammation, fibrosis, metastatic disease, idiopathic, and hereditary

Question 70

Treatment for sick sinus syndrome (SSS)

Answer 70

Propatheline bromide if atropine responsive. If not: Aminophylline Theophylline Albuterol If medical therapy doesn’t work: Pacemaker

Question 71

Atrial fibrillation

Answer 71

Numerous unorganised ectopic foci in the atria that discharge at very high rates causing uncoordinated activity in the atria. ECG: No defined P waves Undulating baseline with erratic atrial activity Irregularly irregular R to R intervals due to unpredictable communication to AV node.

Question 72

Treatment for atrial fibrillation

Answer 72

Cardioversion, and/or digoxin, calcium channel blockers, or beta blockers

Question 73

Supraventricular tachycardia

Answer 73

Supraventricular = everything from AV node and above in the heart. So it includes sinus tachycardia, atrial tachycardia and AV junctional tachycardia. Regulat rhythm and between 260-350bpm. Abnormal or irregular P waves, but hard to see as they are buried in T wave.

Question 74

Treatment for supraventricular tachycardia

Answer 74

\*Occasionally, a vagal maneuver (ocular or carotid sinus pressure) can convert the patient out of this rhythm back to a normal sinus rhythm. \*If above doesn’t work: use calcium channel blocker, beta blocker, or digoxin

Question 75

Sinus arrest and escape rhythms

Answer 75

Sinus arrest: a pause between two normal complexes that is greater than two times the normal R to R interval due to lack of sinus node discharge. Escape rhythms: If pauses are long enough, the heart’s natural defence system will “escape” out of the natural pathway and initiate a beat from another region of the heart. - AV node (junctional escapes): negatively deflected P wave or no discernible P wave and narrow complex QRS wave. 60-75% of patient’s normal sinus rate. - Ventricles (ventricular escapes): no P wave and a wide and bizarre QRS complex. 1/2 of a normal sinus rhythm.

Question 76

Ventricular Bigeminy

Answer 76

Repeated pairing of two beats over a period of time \*\*Atrial bigeminy: two beats are atrial \*\*Ventricular bigeminy: when one beat is ventricular \*\*\*Trigeminy: three repeated beats over time \*Usually no tx needed \*Pulse variability can be felt

Question 78

Left anterior fasicular block

Answer 78

\*causes altered activation sequence of left ventricle \*ECG: normal QRS width, but S wave very deep (exceed R wave)

Question 79

What is a left anterior fasicular block associated with?

Answer 79

\*Hypertrophic cardiomyopathy, left ventricular hypertrophy, hyperkalemia, ischemic cardiomyopathy

Question 80

First degree AV block

Answer 80

\*Impulse is delayed between SA node and AV node but always makes it to the AV node \*ECG: prolonged P-R intervals \*Rate and rhyming usually regular \*Causes: drug that delays AV conduction, hyperkalemia, increased vagal tone, myocarditis, doxorubicin therapy and cardiomyopathies