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Cardiovascular System Disorders > Diagnostic Tests For Cardiovascular System > Flashcards

Diagnostic Tests For Cardiovascular System Flashcards

1
Q

Thoracic radiographs

A
  • Assess heart size and shape
  • Pulmonary vessels
  • Lung parenchymal and surrounding structures
  • Laterals and VD
  • Peak inspiration
  • On expiration heart appears larger, diaphragm overlap caudal heart border, pulmonary vessels poorly delineated
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2
Q

Chest conformation and cardiac shadow

A

-Round or barrel-shaped chest has greater sternal contact on lateral view, oval shape on DV or VD
-Narrow or deep-chested dogs have upright, elongated appearance on lateral view and small circular shape on VD or DV

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3
Q

Vertebral Heart Score

A

-Ventral border of left mainstem bronchus to the most ventral aspect of cardiac apex
-Distance compared to thoracic spine beginning at cranial sacral edge of T4
-Maximum perpendicular short axis is measured in the central third of the heart shadow, and measured in number of vertebrae beginning from T4
- 8.5 a 10.5 consider normal for most breeds

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4
Q

Cats Vertebral Heart Score

A

-lateral view less than or equal to 2 ICS in width and <70% of height of thorax
-DV view no more than half the width if thorax
-7.3 to 7.5 vertebra is normal
-Short axis cardiac dimension on VD 3.4 to 3.5

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5
Q

Small heart shadow (microcardia)

A

-Reduced venous return (shock or hypovolemia)

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6
Q

Enlargement of heart shadow on plain radiographs

A

-True cardiomegaly
-Pericardial distension
-Contours if different chambers evident normally
-Massive RV and RA dilation can cause a round cardiac silhouette
-Fluid, fat, viscera within pericardium obliterate contours and create globoid heart shadow

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7
Q

Generalised enlargement of Cardiac Shadow

A

Pericardial effusion
Dilated cardiomyopathy
Hypertrophic cardiomyopathy?
Pericardial effusion
Mitral and tricuspid insufficiency
Peritoneopericardial diaphragmatic hernia
Tricuspid dysplasia
Ventricular or atrial septal defect
Patent Ductus Arteriosus

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8
Q

Left Atrial Enlargement

A

Early mitral insufficiency
Hypertrophic Cardiomyopathy
Subaortic stenosis
Early dilated cardiomyopathy (Doberman Punschers)

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9
Q

Left Atrial and Ventricular Enlargment

A

DCM
Mitral insufficiency
Subaortic stenosis
Aortic insufficiency
HCM
Patent Ductus Arteriosus
Ventricular septal defect
Systemic hypertension
Hyperthyroidism

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10
Q

Right Atrial and Ventricular Enlargement

A

Chronic severe pulmonary disease
Advanced heartworm disease
Tricuspid insufficiency
Pulmonic stenosis
Tetralogy of fallot
Pulmonary hypertension (with or without reversed shunting congenital defect)
Atrial septal defect
Mass lesion within right heart

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11
Q

Left atrium

A

-Most dorsocaudal chamber of heart
-Auricular appendage extends to the left and craniad
-Enlarge LA bulges dorsally and caudally on lateral view, elevating L and sometimes R mainstem bronchi (compression in severe enlargement)
-DV or VD mainstem bronchi pushed laterally and curve slightly around a markedly enlarged LA (bowed-legged cowboy sign) + bulge in 2-3 o clock position (concurrent L auricular enlargement) + large rounded soft tissue opacity superimposed over LV apical area

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12
Q

Rupture chordae tendinae

A

Acutely cause severe valvular regurgitation, pulmonary oedema with relatively normal LA size (rapid increase in atrial pressure)

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13
Q

Left Ventricle Enlargement

A

Taller cardiac silhouette
Elevation of carina and caudal vena cava
Convex caudal heart boder
Enlargement in 2-5 o clock in VD
Caudal apical in lateral

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14
Q

Right atrium enlargement

A

Expands cranial heart border and widens cardiac silhouette on lateral view
Tracheal elevation
Bulging of cardiac shadow on DV/VD in 9-11 clock

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15
Q

Right ventricle enlargement

A

Increase convexity of cranioventral heart border and elevation of trachea on lateral view
Apex elevated from the sternum
Carina and caudal VC also elevated

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16
Q

Great vessels

A

-Aorta and main pulmonary artery dilate in response to chronic arterial hypertension or increased turbulence
-main pulmonary trunk dilation associated with pulmonic stenosis or pulmonary hypetension

17
Q

Electrocardiogram

A
  • Electrical depolarisation and repolarisation of cardiac muscle
  • Information of HR, rhythm, intracardiac conduction
  • suggest specific chamber enlargement, myocardial disease, ischemia, pericardial disease, electrolyte imbalances, drug toxicities
18
Q

Normal ECG waveforms

A
  • Originates in the sinoatrial node
  • specialised conduction pathways facilitate activation of atria and ventricles
  • SA node, AV node, bundle of his, R and L bundle branch
  • P activation of atrial muscle
  • PR interval: time from atrial activation through conduction over the AV node, bundle of his, purkinje fibres
  • QRS is ventricular muscle electrical activation
  • ST: period between ventricular depolarisation and repolarisation
  • T: ventricular repolarisation
19
Q

Sinus rhythms

A

Originates from sinus node
Produces P-QRS-T waveforms
Regular sinus rhythm less than 10% variation in timing of QRS to QRS (R to R)
QVS complexes are narrow and upright

20
Q

Sinus arrhythmia

A

Cyclic slowing and speeding of sinus rate
Associated with respiration
Sinus rate increase on inspiration and decrease with expiration
Result of fluctuations in vagal tone
Cyclic change in P-wave- taller and spiked during inspiration and flatter in expiration

21
Q

Sinus bradycardia and tachycardia

A

Originate in sinus node and are conducted normally
But HR slower or faster than normal

22
Q

Sinus arrest

A
  • 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 in time
  • Long pauses cause fainting or weakness
  • Sinus arrest cannot be differentiated with certainty from SA block
23
Q

Ectopic rhythms

A
  • Impulses originating from outside the sinus node (ectopic impulse)
  • Are abnormal and create an arrhythmia
  • described based on origin (atrial, junctional, supraventricular, ventricular) and their timing
  • Timing: whether impulse occurs earlier than the next expected sinus impulse (premature) or after a longer pause (late or escape)
  • Escape complexes represent activation of a subsidiary pacemaker and function as a rescue mechanism for the heart
  • Premature ectopic impulses (complexes) occur singly or multiples; group if 3 or more constitute an episode of tachycardia (paroxysmal vs prolonged tachycardia)
  • If one premature complex follows each normal QRS, a bigeminal pattern exists (atrial/ventricular bigeminy)
24
Q

Supraventricular premature complexes

A
  • Impulses that originate ABOVE the atrioventricular (AV) node, either in atria or the AV junctional area
  • Conducted into and through the ventricles via the normal conduction pathway, QVS configuration is normal
  • Premature complexes arising within the atria usually preceded with an abnormal P wave (positive, negative or biphasic) called P’ wave
  • If ectopic P’ wave occurs before AV node has completely repolarised, impulse may not be conducted into the ventricles = physiologic AV block
  • Junctional complexes = no P’ wave, but sometimes negative P’ wave due to retrograde conduction into atria
25
Q

Supraventricular tachycardias

A
  • Often involve a reentrant pathway using the AV node (either within AV node or using an accessory pathway)
  • A premature supraventricular or ventricular impulse can initiate reentrant supraventricular tachycardia (SVT)
  • Atrial tachycardia caused by rapid discharge of an abnormal atrial focus or by atrial reentry (abnormal circuit within atria)
  • In dogs atrial activation rate usually btn 260-380/min
  • P’ wave often hidden in QRS-T complexes
  • Paroxysmal or sustained
  • Usually regular rhythm unless rate is too fast for AV node to conduct every impulse; physiologic AV block and irregular ventricular activation result
  • A consistent ratio of atrial impulses to ventricular activation (2:1 or 3:1 AV conduction) preserves the regularity of this arrhythmia
26
Q

Atrial flutter

A
  • Caused by a rapid (> 400 impulses/min) wave of electrical activation regularly cycling through the atria
  • ventricular response may be irregular or regular
  • ECG baseline consists if “sawtooth” flutter waves that represent fast, recurrent atrial activation
  • Not a stable rhythm, often degenerates into atrial fibrillation or convert back to sinus rhythm
27
Q

Atrial fibrillation

A
  • Characterised by rapid and chaotic and electrical activation within the atria
  • No P waves, because there is no uniform atrial depolarisation wave
  • Baseline shows irregular undulations (fibrillation waves)
  • Lack of organised electrical activity prevents effective atrial contraction
  • AV node being bombarded by chaotic electrical impulses, conducts as many as possible to ventricles- determined by conduction velocity and recovery time- influenced by prevailing autonomic tone
  • Usually normal QRS complexes, minor variation in QRS complex amplitude is common. Intermittent or sustained bundle branch blocks can occur
  • Tend to be consequence of marked atrial enlargement in dogs and esp. in cats; usually preceded by intermittent atrial tachyarrhythmias and perhaps atrial flutter
  • Can occur spontaneously in giant breed dogs with no cardiac disease
28
Q

Ventricular premature complexes

A
  • Originate below AV node, hence ventricular muscle activation does not occur via normal ventricular conduction pathway
  • QRS configuration of VPCs differs from normal sinus QVS complexes
  • Ventricular ectopic complexes are usually wider because of slower intramuscular conduction
  • VPCs not conducted backward thr AV node into atria, sinus rate continues undisturbed and VPCs followed by compensatory pause in sinus rhythm
  • Uniform/monomorphic vs multiform or polymorphic
29
Q

Ventricular tachycardia

A
  • Consists of a series of ventricular premature complexes (usually at a rate > 100 beats/min)
  • RR interval most often regular but some variations can occur
  • Non conducted sinus P waves may superimposed on or between ventricular complexes; unrelated to VPCs as AV node and/or ventricles are in refractory period (physiologic AV dissociation)
  • Capture beat refers to successful conduction of sinus P wave into ventricles uninterrupted by VPC; if interrupted is called a “fusion” complex
  • Identification of P waves or fusion complexes helps differentiating ventricular tachycardia from SVT with abnormal intraventricular conduction
30
Q

Accelerated ventricular rhythm

A
  • Also called idioventricular tachycardia
  • Ventricular-origin rhythm with a rate about 60-100/min in dogs, faster in cat
  • Rate is slower than true ventricular tachycardia, less serious rhythm disturbance
  • Can appear intermittently during sinus arrhythmia as sinus rate decreases
  • Common in dogs recovering from motor vehicle trauma
31
Q

Ventricular fibrillation

A
  • Lethal rhythm, characterised by multiple reentrant circuits causing chaotic electrical activity in ventricles
  • ECG consists of irregularly undulating baseline
  • Ventricles cannot function effectively as a pump because the chaotic electrical activation produces incoordinated mechanical activation
  • No coordinated ventricular muscle contraction due to chaotic impulses
  • May be preceded by ventricular flutter which appears as rapid sine-wave activity
32
Q

Escape complexes

A
  • Ventricular asystole is the absence of ventricular electrical (and mechanical) activity
  • Escape complexes and escape rhythms are protective mechanisms.
  • Occurs after a pause in the dominant (usually sinus) rhythm
  • If dominant rhythm does not resume, escape focus continues to discharge at its own intrinsic rate
  • Escape rhythm usually regular
  • Escape activity orginates from automatic cells within the atria, AV junction or the ventricles
  • Ventricular escape rhythms usually have intrinsic rate less than 40-50/min in dog and 100/min in cat
  • Junctional 40-60 in dogs, higher in cat
  • Important to differentiate escape from premature complexes
  • Escape activity should never be suppressed with anti-arrhythmic drugs
33
Q

Conduction disturbances

A
  • Sinoatrial (SA) block prevents pulse transmission from the SA node to the atrial muscle
  • cannot reliably be differentiated from sinus arrest
  • SA block interval between P waves is a multiple of normal P-P interval
  • Atrial, junctional or ventricular escape rhythm- take over after prolonged sinus arrest or block
  • Atrial standstill occurs when diseased atrial muscle prevents normal electrical and mechanical function, regardless of sinus node activity; junctional or ventricular escape rhythm results and P waves are not seen
  • Hyperkalemia interferes with normal atrial function and can mimic atrial standstill
34
Q

Conduction disturbances within the atrioventricular node

A
  • Abnormalities of AV conduction can occur from excessive vagal tone, drugs (digoxin, xylazine, medetomidine, verapamil, anaesthetic agents) and organic disease of AV node and/or intraventricular conduction system
  • 1st degree AV block: conduction from atria into the ventricles are prolonged; PR interval is longer than normal.
  • Second degree AV block characterised by intermittent AV conduction; some P waves not followed by QRS complex
  • Supraventricular or ventricular escape complexes are common during long pauses in ventricular activation
  • Third degree or complete AV block is complete failure of AV conduction, no sinus impulses conducted into ventricles; although regular sinus rhythm or sinus arrhythmia is often evident
    P waves are not related to QVS complexes, usually result from a regular ventricular escape rhythm
35
Q

Intraventricular conduction disturbances

A
  • Slowed or blocked impulse transmission in a major bundle branch or ventricular region
  • Right bundle branch or left anterior or posterior fascicles of L bundle branch
  • Activation of myocardium served by blocked pathway occurs relatively slowly from myocyte to myocyte; therefore QRS complexes appear wide and abnormal

Cardiovascular System Disorders (2 decks)

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