Exam 2 Flashcards

Question

Cardiac Murmurs Grade 4

Answer 1

-Loud murmur but without precordial thrill -Radiates widely and usually can be heard over most precordial regions

Answer 2

-Loud murmur with palpable precordial thrill -Radiates widely and usually can be heard clearly over all precordial regions

Answer 3

-Very loud murmur with a precordial thrill -Radiates widely -Generally is clearly heard over all precordial areas, and also can be heard with the stethoscope chestpiece slightly 1cm from chest wall

Answer 4

PDA: Patent ductus arteriosus MR: mitral regurgitation (insufficiency) SAS: subaortic stenosis (left and right) PS: Pulmonic Stenosis TR: tricuspid regurgitation VSD: ventricular septal defect

Answer 5

-Over the left heart base -Soft to moderate intensity -Decrescebdo or crescendo-decrescendo configuration Causes -Hypoproteinemia -Fever -High sympathetic tone -Anemia -Hyperthyroidism -Marked bradycardia -Peripheral arteriovenous fistule -Athletic hearts

Answer 6

-Aortic dilation (from hypertension) -Dynamic RV outflow obstruction

Answer 7

-Left base of heart -Ventricular outflow obstruction -Subaortic stenosis = low left base and also at the right base bc it radiates up the aortic arch, which curves toward the right. -Pulmonic stenosis = cranial left base -Dynamic muscular obstruction They become louders as cardiac output or contractile strength increases **Pulmonic stenosis: occurs when flow volume through normal valve is abnormally increased as with left-to-right shunting atrial or ventricular septal defect**

Answer 8

-At the right apex over the valve -It can be noticeably different from concurrent mitral valve insufficiency -It is accompanied by jugular pulsations

Answer 9

-Ventricular septal defects -PMI is the right sternal border

Answer 10

-Near the sternal border -Many are associated with dynamic left or right ventricular outflow obstruction -Congenital Cardiac malformations are also a common cause of murmurs in cats. -NT-proBNP measurement can help screening

Answer 11

-Uncommon in cats and dogs -They are always pathologic **Aortic valve insufficiency from infective endocarditis is the most common cause** -Pulmonic valve insufficiency is rare, but heard during pulmonary hypertension -Diastolic murmurs are heard at the beginning of S2 -Best heard at the left base -Decrescendo in configuration

Answer 12

-"Machinery" -Throughout the cardiac cycle **Indicate substantial pressure gradient exists continuously between two connecting vessels** -It becomes softer toward the end of diastole, and at slow heart rates, may become inaudible PDA: the most common cause -Heard best at the left base, dorsal to the pulmonic valve -Radiates cranially, ventrally and to the right

Answer 13

Cardiac troponins -Regulatory proteins attached to the cardiac actin (thin) contractile filaments -Myocyte injury allows their leakage -Cardiac troponin 1 (cTnI) -Half life = 6 hrs, persistent increase in serum indicate ongoing damage. -Gastric dilation/volvulus = increased cTnI minimal -Older animals - mild increase <2.0 ng/ml normal Natriuretic Peptides -NT-proBNP: Brain NP -Atrial ANP: atrial - ANP

Answer 14

Idexx Canine or Feline Troponin I It can be used to detect chronic mitral valve disease

Answer 15

Increased circulation occurs with -Increased vascular volume expansion -Decreased Renal clearance Due to -Atrial stretch -Ventricular strain -Ventricular Hypertrophy -Hypoxia -Tachyarrhythmias -Ectopic non-cardiac production ANP & BNP **Help regulate blood volume and pressure** -Antagonize the RAAS axis -Synthesized as prehormones -Cleaved to PROHORMONE -Inactive form NT-pro- -Active carboxyterminal (C-) fragments **The N-terminal fragments remain in circulation longer and reach higher plasma concentrations than active hormone molecules**

Answer 16

NT-pro-BNP -Inactive form = N-terminal higher concentration in plasma -They can also indicate non cardiac disease -Hyperthyroidism in cats -Renal dysfunction -Pulmonary hypertension Low risk <800-900 pmol/L in dogs <100 pmol/L in cats High risk for CHF >1400-1800 pmol/L in dogs >1500 pmol/L in small breeds **Doberman pinchers occult cardiomyopathy can show <800 pmol/L** Low risk CHF Cats with respiratory signs and 100-269 pmol/L

Answer 17

-VD, DV, and lateral (right usually) -VD: heart more elongated, -DV: better ihilar area and pulmonary arteries definition -Exposure at peak of inspiration -Excess pericardial fat may mimic the appearance of cardiomegaly Vertebral Heart Score -Using lateral view in adults -Long axis -Short axis -Values added Dogs normal: 8.5 - 10.5 vertebrae Cats normal: 7.3 - 7.5 vertebrae, 9 suggests heart disease

Answer 18

-Hypovolemia: reduced venous return can cause microcardia

Answer 19

Generalized Enlargement of the Cardiac Shadow -Dilated cardiomyopathy -Chronic mitral and tricuspid insufficiency -Pericardial effusion -Peritoneopericardial diaphragmatic hernia -Tricuspid dysplasia -Ventricular or Atrial septal defect -Patent ductus arteriosus LA enlargement alone -Early mitral insufficiency -Early dilated cardiomyopathy (Doberman pinchers) -Hypertrophic cardiomyopathy -(Sub) Aortic Stenosis LA & LV enlargement -Dilated cardiopmyopathy - Hypertrophic cardiomyopathy -Mitral insufficiency -Aortic insufficiency -Ventricular septa defect VSD -PDA -(Sub) Aortic stenosis -Systemic hypertension -Hyperthyroidism RA & RV enlargement -Advanced HTW disease -Chronic severe pulmonary disease -Pulmonic stenosis -Tetralogy of Fallot -Atrial septal defect -Pulmonary Hypertension -Mass lesion within the right heart

Answer 20

Association 1. LV & LA 2. RV, main pulmonary artery bulge, and often RA dilation 3. Severe LA enlargement 4. Mainstem bronchi displaced laterally due to enlarged LA 5. Marked LA enlargement LA enlargement -Severity influenced by volume load or pressure. Ex: no pulmonary edema but LA enlargement = early mitral valve deficiency while rapture of cordae tendinae = acute pressure and valvular regurgitaion leading to pulmonary edema.

Answer 21

-Pulmonary veins enlarged -LA enlargement -LV enlargement DDx: mitral valve insufficiency, mitral valve regurgitation

Answer 22

-Taller cardiac silhouette with elevation of the carina and caudal vena cave (CdVC) -Apical sternal contact is maintained -DV/VD rounding at 2-5 O'clock position

Answer 23

-Cranial heart border -Widen cardiac silhouette on lateral view -Tracheal elevation -Bulging shadow at 9 - 11 O'clock position on DV/VD

Answer 24

-Dilation or hypertrophy -Increased convexity of cranioventral heart border on lateral view -Sometimes apex elevated from sternum -Carina and CaVC also elevated -VD/DV tends to be reversed-D especially when no Lt-sided enlargement -Right border may bulge to the right

Answer 25

1. Aorta and main pulmonary artery 2. PDA: localized dilation in the descending aorta just caudal to the arch where the ductus exits. Seen on DV/VD 2 - 3 O'clock position. Prominent Aortic arch -Systemic hypertension should also be considered 3. Severe dilation of pulmonary trunk = bulge superimposed over the trachea. Main pulmonary trunk enlargement 1-2 O'clock area DV in dogs. 4. CaVC enlargement, pushed dorsally with enlargement of ventricles. 5. Thin CaVC

Answer 26

Located "ventral and central" 1. Overcirculation and yes both promienent 2. Undercirculation 3. Prominent pulmonary arteries 4. Prominent pulmonary veins 5. In cats when pulmonary veins and arteries are enlarged during acute cardiogenic pulmonary edema is present.

Answer 27

-Interstitial and alveolar patterns -Located dorsal in perihilar areas, often bilaterally asymmetric -Some dogs can have concurrent ventral distribution and unilateral **The infiltrates can be distributed unevenly and patchy in cats**

Answer 28

-Anatomic relationships and cardiac function -Cardiac chamber evaluation -Wall thickness -Wall motion -Valve configuration and motion -Proximal great vessels and other parameters -Pericaldial and pleural fluid -Mass lesions 2-D: stronger echoes when ultrasound beam is perpendicular to the imaged structure M-mode: stronger echoes when ultrasound beam is perpendicular to the imaged structure Droppler: provides additional information

Answer 29

4- chamber inflow view 5-chamber LV inflow view

Answer 30

Generally represents the electrical depolarization and repolarization of cardiac muscle. Provides information regarding -Hear rhythym -Heart rate -Intracardiac conduction -May suggest specific chamber enlargement -Myocardial disease -Ischemia -Pericardial disease -Certain electrolyte imbalance -Some drug toxicities Normal ECG waveforms -Normal cardiac rhythym originates in SA node -P-QRS-T are generated as heart muscle is depolarized and then repolarized -QRS complex represents ventricular muscle electrical activation. It does not necessarily have individual Q, R, S wave components. -Variation of the QRS complex depends on the lead being recorded, as well as the animal's intraventricular conduction characteristics.

Answer 31

P: depolarization (activation) of atrial muscle; normally positive in leads II and aVf. PR interval: time from the onset of atrial activation, through conduction over AV node, Bundle of HIS, and Purkinje Fibers; Also called PQ interval QRS complex: depolarization of ventricular muscle; by definition, Q is the first negative deflection (if present), R the first positive deflection, and S is the negative deflection after the R wave. J point: end of QRS complex ( and ventricular muscle activation); junction of QRS and ST segment ST segment: represents the period between ventricular depolarization and repolarization (correlates with phase 2 of action potential) T wave: ventricular muscle repolarization QT interval: total time of ventricular depolarization and repolarization Lead Systems A positive deflection will be recorded in a lead if the cardiac activation wave travels toward the positive pole (electrode) of that lead. If the wave of depolarization travels away from the positive pole, a negative deflection will be recorded.

Answer 32

-Right lateral recumbency -On nonconducting surface If regulat rhythyms -Count QRS complexes: heart ventricular rate = beats. RR intervals -3-6 secs and multiply by 20 or 10 in 25 mm/sec paper -300 divided by # of larger boxes -1500/#small boxes in 25mm/sec -3000/#small boxes in 50mm/sec paper -Presence and relationship between P wave and QRS complex is evaluated -Amplitude: mV -Speed/duration sec 25 mm/sec -Small box = 0.04 sec -Large box 0.2 sec 50 mm/sec -Small box = 0.02 sec -Large box = 0.1 sec -10 small boxes vertically = 1mV -1 small box = 0.1 mV

Answer 33

HR 60-160 bpm (adults) to 220 bpm (puppies) MEA (mean electrical axis) Frontal Plane +40 to +100 degrees Measurements (Lead II) P wave 0.04 sec (0.05 sec large/giant breeds) P wave height (max) 0.4 mV PR interval 0.06-0.13 sec QRS comples duration (max) 0.05 sec (small breeds) 0.06 sec (large breeds) R wave height (max) 2.5 mV (small breeds) 3 mV (large breeds) ST segment deviation <0.2 mV depression <.015 mV elevation T wave Usually <25% or R wave height; can be positive, negative, or biphasic QT interval duration 0.15-0.25 (to 0.27) sec; varies inversely with heart rate

Answer 34

HR 120-240 bpm MEA (mean electrical axis) Frontal Plane +0 to +160 degrees Measurements (Lead II) P wave 0.035-0.04 sec P wave height (max) 0.2 mV PR interval 0.05-0.09 sec QRS comples duration (max) 0.04 sec R wave height (max) <1.2mV ST segment deviation <0.1mV T wave Maximum 0.3 mV can be positive (most common), negative or biphasic QT interval duration 0.12-0.18 (range 0.07-.020) sec; varies inversely with heart rate

Answer 35

-Normal cardiac rhythym originates in the sinus node -P waves are positive in caudal leads (II and aVF) -PR intervals are consistent -Characterized by <10% deviation in the timing of QRS to QRS complexes (or R to R) -QRS normally narrow and upright (wide and abnormally shape when intraventricular conduction disturbance or enlargement is present) -Characterized by slowing (inspiration) and speeding up (exhalation) as a result of vagal tone -There may also be a "wandering pacemaker" P waves become taller and spiked during inspiration and flatter during expiration **Pronounced sinus arrhythmias can be associated with pulmonary disease** Sinus Tachycardia causes -Hyperthermia/fever -Hyperthyroidism -Anemia/hypoxia -Hypotension -Shock -Sepsis -Anxiety/fear -Excitement -Exercise -Pain -Drugs (e.g., anticholinergics, sympathomimetics) -Toxicities (e.g., chocolate, amphetamines, theophylline) -Electric shock Sinus Bradycardia causes -Hypothermia -Hypothyroidism -Drugs (e.g., some tranquilizers, anesthetics, B-clockers, calcium entry blockers, digoxin) -Increased intracranial pressure -Brainstem lesions -Ocular pressure -Carotid sinus pressure -Other causes of high vagal tone (e.g., airway obstruction) -Sinus node disease -Severe metabolic disease (e.g., hyperkalemia, uremia) -Normal variation (athletic dog) -Cardiac arrest (before and after) -Both are conducted normally, however HR is either fast or slower than normal. Sinus Arrest -It is the absence of sinus activity lasting at least twice as long as the animal's longest expected QRS to QRS interval An escape complex -Usually interrupts the resulting pause if sinus activity does not resume -Long pauses in sinus activity can cause fainting or weakness

Answer 36

A. Sinus tachycardia B. Sinus arrhythmia with wandering pacemaker C. Sinus bradycardia D. Intermittent periods of sinus arrest.

Answer 37

-Impulses originate from outside the SA node -Are abnormal and create an arrhythmia (dysrrhythmia) -Described based on the site of origin and timing -Timing refers to whether the impulse occurs earlier than the next expected sinus impulse (premature) Origin -Atrial -Junctional -Supraventricular -Ventricular Timing -Premature -Escape: represent activation of a subsidiary pacemaker and function as a rescue mechanism for the heart Premature Ectopic complexes -Occur singly or in multiples; groups of three or more constitute and episode of tachycardia. Episodes of tachycardia -Can consist of a brief run of ventricular premature complexes or can be quite prolonged VPCs -Ventricular premature complexes: episode of brief run Paroxysmal Tachycardia -brief run of VPCs Sustained tachycardia -prolonged VPCs Bigeminy -When a VPCs follows each normal sinus QRS

Answer 38

-Normal-appearing QRS. -Abnormal P wave usually precedes a complex originating in atrial tissue -No P wave (or retrogate) is common with an impulse originating from AV junction -Ventricular-origin QRS complexes have a different configuration from the normal sinus

Answer 39

A. Supraventricular premature complex (Doberman pinscher) B. Short paroxysm of supraventricular tachycardia with 1 single premature complex (mixed-breed dog with mitral regurgitation) C. Sustained atrial tachycardia (Irish setter with mitral stenosis) Note negative, abnormal P wave D. Rapid supraventricular tachycardia in Retriever puppy E. Sinus rhythm in a cat with two isolated ventricular premature complexes, patient with hypertrophic cardiomyopathy F. Intermittent paroxysms of ventricular tachycardia demonstrating fusion complexes (arrows) in a dog G. Accelerated idioventricular rhythm interspersed with a background sinus arrhythmia in a dog H. Paroxysmal, rapid ventricular tachycardia in a dog with dilated cardiomyopathy

Answer 40

Atrial Flutter ->400 impulses/min -Rapid waves of electrical activation cycling through the atria -Response may be regular or irregular **"Saw tooth" pattern on ECG** -Often degenerates into atrial fibrillation Atrial Fibrillation -Common arrhythmia -Rapid chaotic electrical activation within the atria -Baseline: small, irregular undulations -Lack of atrial contraction -QRS complexes usually normal bc intraventricular conduction usually is normal -Often a consequence of marked atrial enlargement, intermittent tachyarrhythmias and atrial flutter

Answer 41

-Usually not conducted backward through the AV node into atria, the sinus rate continuous undisturbed and VPC is followed by a "Compensatory pause" -QRS complexes are usually wider because of their slower intramuscular conduction -They can be monomorphic or polymorphic Ventricular tachycardia -Non-conducting P waves may be superimposed -Fusing complex are often observed at the onset or end of paroxysm (run) of ventricular tachycardia. Preceded by a P wave and shortened PR interval Ventricular Fibrillation -Lethal rhythm -Multiple reentrant circuits causing chaotic electrical activity within the ventricles

Answer 42

-A escape complex occurs only after a pause in the dominant (usually sinus) rhythm -Originate from subsidiary pacemaker cells within the atria, the AV junction, or the ventricles -Protection when ventricular asystole occurs -Usually <40-50 bpm -should never be suppressed with antiarrhytmetic drugs Conduction Disturbances -SA block prevents impulse transmission from the SA node to adjacent atrial muscle **Hard to differentiate from Sinus Arrest** -Interval between P waves is a multiple of the normal P-P interval -An atrial, junction, or ventricular escape rhythm should take over the cardiac rhythm if there is a prolonged sinus arrest or black. A. First degree AV block B. Second Degree AV block C. Third degree AV block Atrial Standstill -Occurs when diseased atrial muscle prevents normal electrical and mechanical function, regardless of Sinus node activity, consequently a junctional or ventricular escape rhythm results **Hyperkalemia can mimic atrial standstill bc it interferes with atrial function**

Answer 43

Abnormalities of AV conduction from excessive vagal tone. Organic disease of AV node and/or atrioventricular conduction system can also result in disturbances First Degree AV block -Mildest -Atrial to ventricular conduction time is prolonged -PR interval is longer than normal Second Degree AV block -Intermittent AV conduction; some P waves are not followed by QRS complex Second degree type 1 -Progressive PR interval prolongation until conduction fails -Usually associated with high vagal tone Second degree type 2 -Uniform PR intervals preceding the blocked impulse -Escape complexes commonly appear during long pauses Third degree AV block -Complete failure of AV conduction, no sinus or supraventricular impulses are conducted into the ventricles. Although a regular sinus rhythm or sinus arrhythmia is often evident, the P waves are completely dissociated from QRS complexes, which result from regular ventricular escape rhythms

Answer 44

LBBB: usually clinically relevant underlying LV disease RBBB: sometimes in otherwise healthy dogs and cats although RV distention can occur from disease -A block in all three major banches results in 3rd (complete) heart block. -QRS complexes appear wide and abnormal, similar to ventricular origin QRS complexes.

Answer 45

-Wide P wave

Answer 46

-Tall, spiked P wave

Answer 47

-Increased R wave amplitude -Sometimes widen QRS complex -Displacement of ST segment -T-wave enlargement may also occur

Answer 48

-Deep S wave

Answer 49

- Deep S wave -Prolonged terminal QRS

Answer 50

-R wave in lead I taller than R wave in leads II and aVf

Answer 51

Left Atrial Enlargement Mitral insufficiency (acquired or congenital) Cardiomyopathies Patent ductus arteriosus Subaortic stenosis Ventricular septal defect Mitral stenosis (rare) Right Atrial Enlargement Tricuspid insufficiency (acquired or congenital) Chronic respiratory disease Interatrial septal defect Pulmonic stenosis Left Ventricular Enlargement (Dilation) Mitral insufficiency Dilated cardiomyopathy Aortic insufficiency Patent ductus arteriosus Ventricular septal defect Subaortic stenosis Left Ventricular Enlargement (Hypertrophy) Hypertrophic cardiomyopathy Subaortic stenosis Right Ventricular Enlargement Pulmonic stenosis Tetralogy of Fallot Tricuspid insufficiency (acquired or congenital) Severe heartworm disease Severe pulmonary hypertension (of other cause)

Answer 52

-Hypothyroidism -Pleural or pericardial effusions -Obesity -Intrathoracic mass lesions -Hypovolemia

Answer 53

In dogs and cats this segment tends to slope into the T wave that follows without clear demarcation. Abnormal J-point and ST segment elevation often is clinically significant. -Myocardial ischemia and other types of myocardial injuries are possible causes. -Atrial enlargement or tachycardia can cause pseudodepression of the ST segment because of prominent T waves. -Other secondary causes of ST segment deviation include ventricular hypertrophy, slowed conduction, and some drugs (e.g., digoxin). The T wave represents ventricular muscle repolarization; it may be positive, negative, or biphasic in normal cats and dogs. Changes in T wave size, shape, or polarity from previous recordings in a particular animal are probably clinically important.

Answer 54

Depression of J Point/ST Segment Myocardial ischemia Myocardial infarction/injury (LV subendocardial) Hyperkalemia or hypokalemia Cardiac trauma Secondary change (ventricular hypertrophy, conduction disturbance, VPCs) Digitalis (“sagging” appearance) Pseudodepression (prominent Ta wave) Elevation of J Point/ST Segment Pericarditis Left ventricular epicardial injury Myocardial infarction (transmural) Myocardial hypoxia Secondary change (ventricular hypertrophy, conduction disturbance, VPCs) Digoxin toxicity Prolongation of QT Interval Hypocalcemia Hypokalemia Secondary to prolonged QRS Hypothermia Central nervous system abnormalities Ethylene glycol poisoning Quinidine toxicity Shortening of QT Interval Hypercalcemia Hyperkalemia Digitalis toxicity Large T Waves Myocardial hypoxia Ventricular enlargement Intraventricular conduction abnormalities Hyperkalemia Metabolic or respiratory diseases Normal variation Tented T Waves Hyperkalemia VPC, Ventricular premature complex.

Answer 55

Digoxin PR prolongation Second-degree (2°) or third-degree (3°) AV block Sinus bradycardia or arrest Accelerated junctional rhythm Ventricular premature complexes Ventricular tachycardia Paroxysmal atrial tachycardia with block Atrial fibrillation with slow ventricular rate Lidocaine AV block Ventricular tachycardia Sinus arrest β-Blockers Sinus bradycardia Prolonged PR interval AV block Quinidine/Procainamide Atropine-like effects Prolonged QT interval AV block Ventricular tachyarrhythmias Widened QRS complex Sinus arrest Medetomidine/Xylazine Sinus bradycardia Sinus arrest/sinoatrial block AV block Ventricular tachyarrhythmias (especially with halothane, epinephrine) Barbiturates/Thiobarbiturates Ventricular bigeminy Halothane/Methoxyflurane Sinus bradycardia Ventricular arrhythmias (increased sensitivity to catecholamines, especially halothane)

Answer 56

Hypokalemia Prolonged QT interval ST segment depression Small, biphasic T waves Tachyarrhythmias

Answer 57

Hypercalcemia Few effects Short QT interval Prolonged conduction Tachyarrhythmias

Answer 58

Hypocalcemia Prolonged QT interval Tachyarrhythmias

Answer 59

Hyperkalemia Peaked (tented) T waves (can be large or small) Short QT interval Flat or absent P waves Widened QRS ST segment depression

Answer 60

Congestive heart failure (CHF) is characterized by high cardiac filling pressure, which leads to venous congestion and tissue fluid accumulation. -Cardiac remodeling is inherent to heart failure. -Secondary to valvular disease, genetic mutation, acute inflammation, ischemia, increased systolic pressure load, and other causes. -Ventricular hypertrophy can increase chamber stiffness, impair relaxation, and increase filling pressures. These abnormalities of diastolic function also can have a negative effect on systolic function. Promotes development of arrhythmias -A ventricular systolic pressure load induces concentric hypertrophy; myocardial fibers and ventricular walls thicken as contractile units (sarcomeres) are added in parallel. Perfusion may become inadequate = myocardial hypoxia and schemia -Chronic volume loading increases diastolic wall stress and leads to eccentric hypertrophy; myocardial fiber elongation and chamber dilation occur as new sarcomeres are laid down in series.

Answer 61

-Although these mechanisms support circulation in the face of acute hypotension and hypovolemia, their chronic activation accelerates the deterioration of cardiac function. Sympathetic Stimulation -Increased contractility -Increased HR -Increased venous return -Results in increased afterload stress and myocardial oxygen requirements = fibrosis, arrhythmias

Answer 62

-Normal feedback regulation of sympathetic nervous and hormonal systems depends on arterial and atrial baroreceptor function. -Baroreceptor responsiveness becomes attenuated (reduced) in chronic heart failure, which contributes to sustained sympathetic and hormonal activation and reduced inhibitory vagal effects. -Baroreceptor function can improve with reversal of heart failure, increased myocardial contractility, decreased cardiac loading conditions, or inhibition of angiotensin II and aldosterone (which directly attenuate baroreceptor sensitivity). -Digoxin has a positive effect on baroreceptor sensitivity.

Answer 63

The renin-angiotensin system (RAAS) has far-reaching effects. -Renin release from the renal juxtaglomerular apparatus occurs secondary to low renal artery perfusion pressure, renal β-adrenergic receptor stimulation, and reduced Na+ delivery to the macula densa of the distal renal tubule. -Inhibition of ACE can reduce NH activation and promote vasodilation and diuresis. -Increased aldosterone concentration can promote hypokalemia, hypomagnesemia, and impaired baroreceptor function. It can potentiate the effects of catecholamines by blocking NE reuptake.

Answer 64

-Endothelin is a potent vasoconstrictor whose precursor peptide is produced by vascular endothelium. -Endothelin production is stimulated by hypoxia and vascular mechanical factors and also by angiotensin II, ADH, norepinephrine, cytokines (including TNFα and interleukin-I), and other factors. -Endogenous mechanisms that oppose the vasoconstrictor responses also are activated. -These include natriuretic peptides, adrenomedullin, nitric oxide (NO), and vasodilator prostaglandins. Normally, a balance between vasodilator and vasoconstrictor effects maintains circulatory homeostasis, as well as renal solute excretion. - As heart failure progresses, the influence of the vasoconstrictor mechanisms predominates despite increased activation of vasodilator mechanisms.

Answer 65

-Natriuretic peptides are synthesized in the heart and play an important role in regulating blood volume and pressure. -Atrial natriuretic peptide (ANP) is synthesized by atrial myocytes as a prohormone, which is then cleaved to the active peptide after its release. -Mechanical stretch of the atrial wall stimulates ANP release. -Brain natriuretic peptide (BNP) also is synthesized in the heart, mainly by the ventricles in response to myocardial dysfunction or ischemia. -Natriuretic peptides promote diuresis, natriuresis, and peripheral vasodilation. They act to antagonize the effects of the RAAS, and also can alter vascular permeability and inhibit growth of smooth muscle cells.

Answer 66

-NO, produced by the vascular endothelium in response to endothelial-nitric oxide synthetase (NOS), is a functional antagonist of endothelin and angiotensin II. -This response is impaired in patients with heart failure.

Answer 67

Higher oncotic and lower hydrostatic pressures develop in the peritubular capillaries, enhancing the reabsorption of tubular fluid and sodium. -Angiotensin II–mediated aldosterone release further promotes sodium and water retention. -Continued activation of these mechanisms leads to clinical edema and effusions. Afferent arteriolar vasodilation mediated by endogenous prostaglandins and natriuretic peptides can partially offset the effects of efferent vasoconstriction, but progressive impairment of renal blood flow leads to renal insufficiency. -Diuretics not only can magnify azotemia and electrolyte loss but also further reduce cardiac output and activate NH mechanisms.

Answer 68

Common Causes of CHF

Answer 69

Common Causes of CHF

Answer 70

A. No apparent structural disease, yet considered “at risk” for developing heart disease (for example, breed-associated risk for DCM in Doberman Pinschers, and CMVD in Cavalier King Charles Spaniels) B. Structural cardiac abnormality is evident (such as a murmur), but no clinical signs of heart failure have occurred B1. Asymptomatic disease, with no/minimal radiographic or echo evidence of cardiac chamber enlargement/remodeling B2. Asymptomatic disease, but cardiac chamber enlargement is evident C. Structural cardiac abnormality evident, with clinical signs of heart failure either in the past (resolved with therapy) or currently present Note: Some clinicians subdivide stage C based on current signs of CHF into C1 – No current signs; C2 – mild congestive signs (low/medium grade); C3 – overt/severe CHF (high grade) D. Persistent or end-stage heart failure signs, refractory to standard therapy (e.g., require ≥ 8-12 mg/kg/day of furosemide)

Answer 71

risk for DCM in Doberman Pinschers, and CMVD in Cavalier King Charles Spaniels

Answer 72

-For dogs with stage B2 chronic mitral valve disease, pimobendan has been shown to delay onset of CHF; pimobendan therapy is recommended for those dogs with clear evidence for cardiac enlargement that have not yet developed signs of CHF

Answer 73

-An ACEI generally is not advocated for dogs with preclinical mitral valve disease, unless it is used to reduce elevated blood pressure. -Some dogs with advanced stage B2 disease might benefit from them. Doberman Pinschers, Irish Wolfhounds, and probably other dogs with occult DCM also benefit from the introduction of pimobendan and an ACEI before overt CHF develops

Answer 74

Signs -Moderate to increased persistent resting respiratory rate (RRR) -Reduced exercise tolerance -Excessive panting -Occassional cough -Mild pulmonary edema Dx -Thoracic radiographs are indicated when signs suggestive of decompensating CHF appear, especially if this is the first episode. When radiographic findings are consistent with mild cardiogenic pulmonary edema, initial therapy for CHF (furosemide, an ACEI, and pimobendan, if indicated), along with exercise restriction, often can be instituted on an outpatient basis. -An NT-proBNP test also can help in unclear cases -If the radiographs are nondiagnostic, but CHF is suspected, a furosemide trial (such as 2 mg/kg/day) with or without an ACEI can be given for a week or so, with RRR monitoring Tx -Furosemide -ACEI, and -Pimobendan, if indicated

Answer 75

-Fulminant CHF is characterized by severe cardiogenic pulmonary edema, with or without pleural and/or abdominal effusions or poor cardiac output. -It can occur in stage C or D patients. -Therapy is aimed at rapidly clearing pulmonary edema, improving oxygenation, and optimizing cardiac output Tx -Thoracocentesis should be performed expediently if marked pleural effusion exists. -Likewise, large-volume ascites should be drained, at least partially, to improve ventilation. -Environmental stresses such as excess heat and humidity or extreme cold should be avoided. -Improve oxygenation -Diuresis: Furosemide -Support cardiac pump function (inodilator): Pimobendan -Reduce anxiety: butorphanol, morphine, buprenorphine. +/- Additional vasodilators: Nitroglycerin ointment, Sodium nitroprusside (if monitoring BP closely), Hydralazine (afterload reduction) +/- Additional inotropic support (if myocardial failure or persistent hypotension) Dobutamine Amrinone Digoxin For acute CHF from diastolic dysfunction (e.g., cats with hypertrophic cardiomyopathy): General recommendations, O2 therapy, furosemide, and sedation, as in the previous text. Thoracocentesis, if needed. ±Nitroglycerin If severe LV outflow obstruction or persistent and rapid sinus tachycardia, consider IV esmolol (200-500 µg/kg IV over 1 minute, followed by 25-200 µg/kg CRI) or diltiazem (0.15-0.25 mg/kg over 2-3 minutes IV) ±Pimobendan (see previous text) Monitor and manage abnormalities as possible (see previous text) ACE inhibitor (institute after appetite returns)

Answer 76

-Catecholamines enhance contractility via a cyclic adenosine monophosphate (cAMP)-mediated increase in intracellular Ca++. -They can provoke arrhythmias and increase pulmonary and systemic vascular resistance (potentially exacerbating edema formation). -Their short half-life (<2 minutes) and extensive hepatic metabolism necessitate constant IV infusion. -Concurrent use of a β-blocker also blunts the effect of the catecholamines.

Answer 77

-Hypotension or severe azotemia caused by excessive diuresis. -Mild azotemia is common. -Hypokalemia and metabolic alkalosis also can occur after aggressive diuresis. -Maintaining serum potassium concentration within the mid- to high-normal range is especially important for animals with arrhythmias. -Arterial blood pressure should be monitored, usually by indirect means because gaining arterial access can increase patient stress.

Answer 78

Long-term heart failure management in dogs with chronic mitral valve disease or DCM generally involves a combination of -Furosemide, pimobendan, an ACEI (usually enalapril or benazepril), and the addition of spironolactone. -A diet moderately reduced in salt -Exercise restriction helps reduce cardiac workload regardless of heart failure etiology.

Exam 2 Flashcards

(104 cards)