Exam 2 Flashcards
Lecture 1
Clinical Cardiovascular Structure and Function
What are some signs of cardiac disease?
Objective signs
-Cardiac murmurs
-Rhythm disturbances
-Jugular pulsations
-Cardiac enlargement
Exemptions
-Non-pathologic murmurs
-Normal irregularity of sinus arrhythmia
What are some signs of cardiac disease that can occur with other non-cardiac diseases?
-Syncope
-Excessively weak or strong arterial pulses
-Cough or respiratory difficulty
-Exercise intolerance
-Abdominal distention
-Cyanosis
How can we evaluate (diagnose) CV disease presence?
-Thoracic radiographs
-Cardiac biomarkers tests
-Echocardiography
Electrocardiography (ECG)
What are the C/S of HF?
Congestive signs LEFT (Increased Heart filling pressure)
-Pulmonary venous congestion
-Pulmonary edema = tachypnea, Increase Respiratory effort, cough, orthopnea ( shortness of breath), pulmonary crackles, tiring, cyanosis, hemoptysis (discharge of bloody mucus)
-Postcapillary pulmonary hypertension
-Second right-sided heart failure
-Cardiac arrhythmias
Congestive signs RIGHT (Increased Heart filling pressure)
-Systemic venous congestion = causes central venous pressure, jugular vein distention.
-Hepatic +/- splenic congestion
-Pleural effusion (causes increase respiratory effort, orthopnea, cyanosis)
-Ascites
-Small pericardial effusion
-Subcutaneous edema
-Cardiac arrhythmias
Low cardiac Output
-Tiring
-Exertional weakness
-Syncope
-Pre renal azotemia
-Cyanosis (from peripheral circulation)
- Cardiac arrhtyhmias
What are CV Causes of Syncope or Intermittent Weakness?
Other causes of Syncope
Cardiovascular Causes
-Bradyarrhythmias = 2nd or 3rd degree AV block, sinus arrest, sick sinus syndrome, atrial standstill.
-Tachyarrhythmias = paroproximal atrial or ventricular tachycardia, reentrant supraventricular tachycardia, atrial fibrillation.
-Congenital ventricular outflow obstruction = pulmonic stenosis, subaortic stenosis.
-Acquired ventricular outflow obstruction = HTW disease, other causes of pulmonary hypertension, hypertrophic obstructive cardiomyopathy, intracardiac tumor, thrombus.
-Cyanotic heart disease = Tetralogy of Fallot, pulmonary hypertension, “reversed” shunt.
-Impaired forward CO = severe valvular insufficiency, dilated cardiomyopathy, myocardial infarction or inflammation
-Impaired cardiac filling = cardiac tamponade, constructive pericarditis, hypertrophic or restrictive cardiomayopathy, intracardiac tumor, thrombus.
-Cardiovascular drugs = DIURETICS, VASODILATORS
-Neurpcardiogenic reflexes (vasovagal, cough-syncope, other situational syncope).
What are the characteristics of CV syncope? see previous card
Transient unconsciousness with loss of postural tone (collapse) from insufficient oxygen or glucose delivery to the brain
-Rear limb weakness
-Sudden collapse
-Lateral recumbency
-Stiffness of the forelimbs with opisthotonos (state of severe hypertension, tenanus-like muscle spasms) and micturition (urination)
NOT
-Postictal dementia
-Neurologic deficits
-Defecation
Syncope
Predisposed Breeds
-Activation of vasodepressor reflexes
-Excessive CV drugs dosage
-Very fast or very slow HR
-Weakness of CO - inappropriate reflex bradychardia and hypotension
Doberman Pinschers
Boxers
-Postural hypotension
-Sudden bradycardia
-Hypersensitivity of carotid sinus receptors
What is cough syncope?
Occurs in some dogs with LA enlargement and bronchial compression or primary respiratory disease
-Cough fit that leads to acute decrease in cardiac filling and output.
-Peripheral vasodilation after cough
-Increased intracranial venous compression, increased cerebrospinal fluid.
Severe pulmonary disease, ANEMIA, and certain metabolic abnormalities, primary neurologic disease can also cause it
CHF and other respiratory signs
(Heartworm disease and Pulmonary vascular pathology)
How is the cough different in dogs and cats?
What stimulates dry hacking cough?
Dogs
-Cough cardiopulmonary edema
-Soft and moist cough
Cats
-Rarely cough from pulmonary edema
PLEURAL & PERICARDIAL effusions
- Main stem bronchus collapse or compression from LA enlargement = DRY HACKING COUGH from Chronic mitral valve disease, a heart base tumor, enlarged hilar lymph nodes, or other masses that impinge on an airway
- Generalized cardiomegaly, LA enlargement, pulmonary venous congestion, lung infiltrates (that resolve with diuretic therapy), or positive HTW test.
Congenital Basilar ejection murmur What breeds?
-Greyhounds
-Sighthounds
What does the PE for CV specific evaluates?
-Peripheral circulation = MMs,
MMs: petechia = platelet disfunction, Icterus = yellow (hemolysis, hepatobiliary disease)
- Systemic veins (jugular)
-Systemic arterial pulses
-Precordium (left and right chest wall over the ehart)
-Auscultation of heart and lungs
-Palpating for abnormal fluid accumulation
Respiratory patterns
-Dyspnea: respiratory difficulty
-Hyperpnea: increased depth of respiration, can result in hypoxemia, hypercarbia, or acidosis.
-Tachypnea: rapid, shallow breathing, associated with pulmonary edema (stiff lungs).
Increased resting RR without respiratory disease is and early indicator of pulmonary edema
Upper airway obstruction: prolonged, labored inspiration
Lower airway obstruction: prolonged expiration (edema)
Open mouth breathing = severe respiratory distress in CATS
Jugular Pulsations
How to differentiate from carotid pulsations?
What are they related to?
What disease can be present if visible jugular pulsations occur?
Abnormal when
-Extend higher than one third of the way up the neck
Carotid vs Jugular pulsations
-Lightly occlude jugular below area of visible pulsation, if it disappears = jugular pulsation. If it continues = carotid.
Jugular pulses are related to Atrial contraction and filling, EX: Hypervolemia
-Tricuspid insufficiency (after S1 during ventricular contraction)
-Hypertrophied right ventricle (just before S1, during atrial contraction)
-Arrhythmias
Arterial Pulses
Give examples of causes for strong and weak pulses
What can cause very strong, bounding pulses?
How do cardiac arrhythmias affect arterial pulses?
-Hypokinetic: Pressure difference is small, weak pulse upon palpation
Ex: severe subaortic stenosis
-Hyperkinetic: pressure difference is wide, strong pulses upon palpation
-Both femoral pulses should be compared: Thromboembolic disease can cause difference between the two.
Cardiac Arrhythmias
-Induce pulse deficits by causing heart to beat before adequate ventricular filling has occurred = minimal or no blood is ejected for those beats = absent palpable pulse
Bigeminy
(a normal heartbeat alternating with a premature beat) & Severe Myocardial failure
-Causes reduced ventricular filling and ejection = alternately weak then strong pulsations
Cardiac Tamponade
(fluid collects in pericardial sac, increasing pressure, which prevents ventricles from expanding fully)
-Decreased arterial pressure during inspiration = weak pulse during inspiration.
Precordium Pulses
Precordium: chest area that overlies the heart on both sides of the thorax
Should be stronger in the left chest wall
Decreased pulse
-Obesity, weak cardiac contractions, pericardial effusions, intrathoracic masses, pleural effusion, or pneumothorax
Abnormally strong Right pericordium pulse
-RV hypertrophy, or displacement of heart to the right by a hemithorax, mass lesion, lung atelectasis, or chest deformity.
Cardiac murmurs
-Very loud ones can cause pulsations/vibrations “buzzing” sensation
Auscultation and Cardiac Cycle Diagram
Transient sounds
-Short duration
-S1: closure and tensing AV valves (Tricuspid and mitral) and structures at the onset of systole
-S2: Closure of Aortic and Pulmonic valves following ejection.
Cardiac murmurs
-Longer sounds occurring during a normally silent part of the cardiac cycle.
Characteristics
-Frequency (pitch)
-Amplitude of vibrations (intensity/loudness)
-Duration
-Quality (timbre): affected by the physical characteristics of the vibrating structures
Stethoscope
-Diaphragm: applied firm
-Bell: applied lightly
-One piece stethoscope: firm pressure and light pressure against the skin
Large Breeds - normal splitting of S2
During inspiration, increased venous return to the RV tends to delay closure of the pulmonic valve, whereas reduced filling of the LV accelerates Aortic closure
What can cause Pathophysiologic S2 Splitting?
Results from
-Delayed ventricular activation or
-Prolonged RV ejection secondary to PREMATURE BEATS
-Right bundle branch block
-Ventricular or Atrial Septal Defect or
-Pulmonary Hypertension
Gallop Sounds
When are they usually heard?
Bell or diaphragm of stethoscope?
What does an audible S3/S4 indicate? when does each occur?
S3 and S4
-During diastole
-Not Normal
Heart sounds like a galloping horse when S3 and S4 present
-Best heard with bell (light pressure)
-Lower frequency than S1 and S2
S3 ventricular gallop
-Low frequency vibrations
-At the end of rapid ventricular filling
Audible = ventricular dilation with myocardial failure, CHF, advanced mitral valve disease
-Heard best over the cardiac Apex
S4 Atrial or presystolic gallop
-Low frequency vibrations
-Triggered by blood flow into the ventricles during Atrial Contraction (just after P-wave)
Increased ventricular stiffness and hypertrophy, such as with hypertrophic cardiomyopathy or HYPERTHYROIDISM in cats
-Sometimes in stressed or anemic cats
What sound is associated with Degenerative Valve disease?
Systolic clicks
Mid-to-late systolic sounds that are heard best over the mitral valve area
-Murmur that develops over time
Associated also with congenital mitral dysplasia, concurrent mitral insufficiency, mitral valve prolapse
-Valvular pulmonic stenosis: early systolic high pitched ejection sound at the base. Diseases that cause dilation of a great artery. Sound can be from fused pulmonic valve or rapid filling of dilated vessel during ejection.
Pericardial Knock
-Restrictive pericardial disease causes an audible pericardial knock.
-Diastolic sound arises from sudden checking of ventricular filling by the constructive pericardium
-Timing similar to S3
Cardiac Murmurs
Are they always pathologic?
Which murmurs are systolic in timing? What are some reason non-pathologic murmurs can occur?
Phonocardiography
What usually causes:
- holosystolic murmurs,
- Crescendo-decresendo murmurs,
- Systolic decrescendo,
- Diastolic decrescendo, and
- Continous murmurs?
-Not always pathologic
-Most involve structural cardiac abnormality and are considered pathologic
FUNCTIONAL MURMURS = Non-pathologic = systolic in timing
-Anemia: blood viscosity decreased
-Fever, CO increased
-Hyperthyroidisms, etc.
-Puppies
Phonocardiography
- Plateau shape “regurgitant” murmur
Turbulent blood flow begins at the time AV valve closing and continues through systole
(AV valve insufficiency and Interventricular septal defects)
-Begins at S1 and remains fairly uniform intensity throughout systole. AKA HOLOSYSTOLIC becuase is consistent throughout systole.
Loud holosystolic can mask S1 and S2 sounds
- Crescendo-decrescendo murmur or Diamond shape.
(Ventricular outflow obstruction)
-Starts softly and builds intensity in midsystole, and diminishes; the S1 and S2 sounds usually can be heard before and after murmur.
AKA EJECTION MURMUR
- Descrecendo (systolic or Diastolic)
-Decreases initial intensity overtime.
- Continous (machinery)
-Occurs throughout systole and (well into or) throughout diastole.
Cardiac Murmurs Grade 1
-Very soft murmur
-Heard only over its site of origin, after prolonged listening, in quiet surroundings
Cardiac Murmurs Grade 2
-Soft murmur but easily heard over its site of origin (usually a particular valve area)
Cardiac Murmurs Grade 3
-Moderate-intensity murmur
-Usually radiates to other precordial/valve areas too
Cardiac Murmurs Grade 4
-Loud murmur but without precordial thrill
-Radiates widely and usually can be heard over most precordial regions
Cardiac Murmurs Grade 5
-Loud murmur with palpable precordial thrill
-Radiates widely and usually can be heard clearly over all precordial regions
Cardiac Murmurs Grade 6
-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
Point of Maximal Intensity
PDA: Patent ductus arteriosus
MR: mitral regurgitation (insufficiency)
SAS: subaortic stenosis (left and right)
PS: Pulmonic Stenosis
TR: tricuspid regurgitation
VSD: ventricular septal defect
Where can functional murmurs can be best heard?
What is the expected sound and intensity?
-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
What conditions are associated with systolic murmurs in cats?
-Aortic dilation (from hypertension)
-Dynamic RV outflow obstruction
Where are systolic Ejection murmurs best heard at?
What are the typical causes?
-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
Where is Tricuspid valve insufficiency murmur best heard at?
-At the right apex over the valve
-It can be noticeably different from concurrent mitral valve insufficiency
-It is accompanied by jugular pulsations
Holosystolic murmurs other casuses?
-Ventricular septal defects
-PMI is the right sternal border
Where is the PMI of most feline murmurs?
-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
Diastolic Murmurs
What is the most common cause?
When are they heard?
-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
Continuous Murmurs
When are they heard?
What do they indicate?
-“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
Cardiac Biochemical Markers
What are cardiac troponins and natriuretic peptides?
What are the biomarkers measured clinically?
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
Give an example of an avialble in house cardiac biomarkers test
Idexx Canine or Feline
Troponin I
It can be used to detect chronic mitral valve disease
What does natriuretic peptides (for their precursors) identify when their presence is abnormal?
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
Which natriurectic peptide is often most measured because its degree of elevation generally correlates with cardiac disease severity?
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
Cardiac Radiography
-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
Microcardia
What can cause an abnormally small heart shadow?
-Hypovolemia: reduced venous return can cause microcardia
Cardiomegaly DDx
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
Cardiac Chamber Enlargement Patterns
- Mitral valve insufficiency/regurgitation
- Pulmonic stenosis
- Collapse of the mainstem bronchus
- Bowed legged cowboy Sign
- Valentine - shaped in cats
What influences LA enlargement severity?
Association
- LV & LA
- RV, main pulmonary artery bulge, and often RA dilation
- Severe LA enlargement
- Mainstem bronchi displaced laterally due to enlarged LA
- 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.
What do you see in the radiographs? DDx?
-Pulmonary veins enlarged
-LA enlargement
-LV enlargement
DDx: mitral valve insufficiency, mitral valve regurgitation
LV enlargement
-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
RA enlargement
-Cranial heart border
-Widen cardiac silhouette on lateral view
-Tracheal elevation
-Bulging shadow at 9 - 11 O’clock position on DV/VD
RV enlargement
-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
Intrathoracic vessels
Great Vessels
- Which vessels dilate in response to chronic arterial hypertension or increased turbulence (postenotic dilation)?
- PDA causes what dilation and where in radiographs is it seen?
- Pulmonic Stenosis or pulmonary hypertension vessels enlargement
- RV failure, cardiac tamponade, pericardial constriction, obstruction of the right heart inflow.
- Hypovolemia, poor venous return, or pulmonary overinflation
- Aorta and main pulmonary artery
- 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 - Severe dilation of pulmonary trunk = bulge superimposed over the trachea. Main pulmonary trunk enlargement 1-2 O’clock area DV in dogs.
- CaVC enlargement, pushed dorsally with enlargement of ventricles.
- Thin CaVC
Lobar pulmonary vessels
- What is the pattern associated with hyperperfused lungs as with left-to-right shunting, overhydration or other hyperdynamic states, and are both pulmonary arteries and veins prominent?
- … Thin arteries and veins, along with increased pulmonary lucency> Severe dyhydrations, hypovolemia, obstruction to RV inflow, right-sided CHF and Tetralogy of Fallot? Some animals with pulmonic stenosis.
- … Pulmonary arterial hypertension, dilated, tortuous and blunted. Associated with HTW disease in addition to causing diffuse interstitial pulmonary infiltrates?
- Pulmonary venous congestion, usually from left-sided CHF. Dilated tortuous entering the dorsocaudal aspect of LA in cases of chronic pulmonary venous hypertension.
- When and in what species if acute cardiogenic pulmonary edema associated with enlargement of vessels?
Located “ventral and central”
- Overcirculation and yes both promienent
- Undercirculation
- Prominent pulmonary arteries
- Prominent pulmonary veins
- In cats when pulmonary veins and arteries are enlarged during acute cardiogenic pulmonary edema is present.
What are the patterns associated with cardiogenic pulmonary edema? where is it located?
-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
What can be assessed with Echocardiography?
What are some of the modalities available?
-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
Long axis 4-chamber view
Long axis LV outflow view
4- chamber inflow view
5-chamber LV inflow view
Electrocardiography (ECG)
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.
Normal Cardiac Waveforms
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.
Approach to ECG Interpretation
-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
Normal ECG Reference Ranges for Dogs
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
Normal ECG Reference Ranges for Cats
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
Sinus Rhythms
-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
What type of sinus rhythms?
A. Sinus tachycardia
B. Sinus arrhythmia with wandering pacemaker
C. Sinus bradycardia
D. Intermittent periods of sinus arrest.
Ectopic Rhythms
Are they normal?
Where does not the impulse originate?
How are they categorized?
What are the types of timing?
How often do premature ectopic complexes can occur?
What is paroxysmal tachycardia, sustained tachycardia, ventricular bigeminy?
-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
A. Supraventricular: Above AV node origin or from within the ventricles
B. The timing of Ectopic complexes
What is their appearance?
-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
What complexes?
Sinus or Ectopic? Supraventricular, ventricular, junctional, or Atrial? Premature, or escape? Sustanined or short? Bradycardia or tachycardia? Paroxysmal, bigemy?
P wave or retrogade?
A.
B.
C.
D.
E.
F.
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
Atrial Flutter & Atrial Fibrillation
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
Ventricular Premature Complexes - VPCs
-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
Escape Complexes and Conduction Disturbances
A.
B.
C.
-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
What effect can digoxin, xylazine, medetomidine, verapamil, anesthetic agents have on conduction within AV node?
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
RBBB (right bundle branch block)
LBBB
LAVFB: cats with hypertrophic cardiomyopathy cocentric
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.
What is the classic pattern of LA enlargement?
-Wide P wave
What is the classic pattern of RA enlargement?
-Tall, spiked P wave
What is the classic pattern of LV dilation and eccentric hypertrophy?
-Increased R wave amplitude
-Sometimes widen QRS complex
-Displacement of ST segment
-T-wave enlargement may also occur
What is the classic pattern of RV enlargement?
-Deep S wave
What is the classic pattern of RBBB?
- Deep S wave
-Prolonged terminal QRS
Left Ventricular (Cocentric) Hypertrophy (e.g., pulmonic stenosis, aortic stenosis) classic pattern?
-R wave in lead I taller than R wave in leads II and aVf
Common ventricular enlargement
Clinical Associations of Electrocardiographic Enlargement Patterns
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)
What are some causes of abnormally reduced amplitude QRS complexes?
-Hypothyroidism
-Pleural or pericardial effusions
-Obesity
-Intrathoracic mass lesions
-Hypovolemia
ST-T Abnormalities
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.
Causes of ST Segment, T Wave, and QT Abnormalities
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.
What effects do lidocaine, B-blockers, Quinidine/procainamide, Medetomidine/Xylazine, Barbiturates/Thiobarbiturates, Halothane/Mehoxyflurane have on ECG?
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)
Hypokalemia ECG
Hypokalemia
Prolonged QT interval
ST segment depression
Small, biphasic T waves
Tachyarrhythmias
Hypercalcemia
Hypercalcemia
Few effects
Short QT interval
Prolonged conduction
Tachyarrhythmias
Hypocalcemia
Hypocalcemia
Prolonged QT interval
Tachyarrhythmias
Hyperkalemia
Hyperkalemia
Peaked (tented) T waves (can be large or small)
Short QT interval
Flat or absent P waves
Widened QRS
ST segment depression
CHF
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.
Neurohormonal Mechanisms - Systemic response that contributes to cardiac remodeling
-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
How do baroreceptors work?
-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.
RAAS
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.
Endothelium and Others
-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.
ANP, BNP
-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.
NOS
-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.
Renal effects CHF
Why do diuretics can magnify azotemia and electrolyte loss?
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.
Common Causes of CHF
Common Causes of CHF
Common Causes of CHF
Common Causes of CHF
Classification Systems for HF Severity Modified AHA/ACC
A.
B.
B1.
B2.
C.
D.
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)
Which two breeds are predisposed to DCM and CMVD?
risk for DCM in Doberman Pinschers, and CMVD in Cavalier King Charles Spaniels
Pimobendan therapy and Preclinical heart Disease
-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
When is an ACEI advocated?
-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
Mild or Early CHF signs
What is the indicated therapy and Dx?
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
Treatment for Acute Congestive HF
What is Fulminant CHF characterized by?
-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)
Why are catecholamines only used for acute CHF?
-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.
Monitoring and Follow up
-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.
Management of Chronic Heart Failure
General Considerations
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.
