Cardiology and respiratory medicine Flashcards
what are the common presenting problems that suggest cardiac or respiratory disease?
cough respiratory noise increased RR or effort lethargy/exercise intolerance syncope
what cardiac disease are Cavalier King Charles Spaniels predisposed to?
myxomatous degenerative valvular disease (mitral valve disease)
what breeds are predisposed to dilated cardiomyopathy?
dobermans and other giant breed dogs
what cardiac disease are cats predisposed to?
hypertrophic cardiomyopathy
what should be found out about the history of a cough (if present)?
when it coughs
if it is productive
length of cough
when it started
what should be found out about the history of a rapid/laboured breathing (if present)?
if it is constant/intermittent
if the animal can lie down
if it has adopted a new sleeping position
what might a change in voice of an animal suggest?
problem with the larynx
what part of the respiratory tract does breathing noises suggest there is a problem with?
upper airway
what is it important to do before handling the patient in suspected cardio-respiratory cases?
get RR and pattern
note if animals is dyspnoeic
what is the normal RR of dogs/cats when calm?
20-30 respirations/minute
what are the two types of dyspnoeic patterns?
obstructive
restrictive
if an animal has cyanotic MM, what should be done?
avoid stress
give oxygen
what may a slow CRT be due to?
shock or reduced cardiac output
what can be checked on a clinical exam as a sign of cardiac output?
MM colour
CRT
femoral pulse quality
warmth of extremities
what two abnormalities can be seen with the femoral pulse?
weak or bounding
what is a possible cause of a bounding femoral pulse?
some congenital heart defects such as patent ductus arteriosus
what are some clinical signs off forward heart failure?
lethargy exercise intolerance weak femoral pulse pale MM and slow CRT quiet heart sounds cold extremities
what are the clinical signs of left sided congestive heart failure?
tachypnoea hyperpnoea dyspnoea restrictive breathing pattern soft inspiratory crackles on auscultation
what is the major clinical sign of right sided congestive heart failure?
fluid accumulations in body cavities (ascites)
what are the clinical signs of right sided congestive heart failure?
ascites (abdominal distention) - wave on ballotment
hepatomegaly
distended jugular veins
pleural effusion
why is hepatomegaly a clinical sign of right sided congestive heart failure?
due to hepatic venous congestion
what reflex should be checked in animals with suspect right sided congestive heart failure?
hepatojugular
why does the hepatojugular reflex need checking in patients with suspected right sided congestive heart failure?
gentle cranial abdominal pressure will increase caudal vena cava flow to the heat to there will be increased distention of the jugular veins
what is the normal HR for a cat?
120-200bpm
what is a normal HR for a dog?
80-140bpm
what is a regularly irregular rhythm of the heart associated with in dogs?
sinus arrhythmias
how are heart tumours categorised?
location timing grade character radiation
how are murmurs characterised by location?
point of maximal intensity
what are the locations the valves of the heart can be auscultated on?
left side 3rd intercostal space - pulmonic 4th intercostal space - aortic 5th intercostal space - mitral left side tricuspid valve
what can the location of murmurs be divided into in smaller patients?
basilar and apical
what are the three ways timing can be used to characterise murmurs?
systolic
diastolic
continuous
what are two examples of left basilar systolic murmurs?
aortic stenosis
pulmonic stenosis
what is a left apical systolic murmur often due to?
mitral regurgitation
what is a continuous murmur usually due to?
patent ductus arteriosus
where are continuous murmurs due to patent ductus arteriosus heard most intensely?
dorsally and cranially (push stethoscope into axilla)
what is a possible causes of a diastolic murmur?
aortic regurgitation
what is used to grade heart murmurs?
the loudness of them
how are heart murmurs graded?
I-VI
describe a grade I murmur
very quiet only heard in optimal conditions
describe a grade II murmur
less loud than heart sounds
describe a grade III murmur
as loud as heart sounds
describe a grade IV murmur
louder than heart sounds
describe a grade V murmur
loud heart murmur with precordial thrill
describe a grade VI murmur
very loud murmur with precordial thrill that can be detected with stethoscope lifted off the chest
what ways can the precise character of the murmur be described?
early systolic
mid systolic
holosystolic
pansystolic
what is a holosystolic murmur?
between the first and second heart sound
what does the radiation of a heart murmur describe?
describes where the murmur is the next loudest (eg. aortic stenosis radiates to the carotids and thoracic inlet)
what are murmurs due to?
turbulent flow of blood
what are innocent murmur in puppies/kittens?
usually left basilar and low grade that disappear by 20 weeks
(thought to be due to changes from foetal to adult haemoglobin)
what causes the S1 heart sound?
closure of the atrioventricular valves
what causes the S2 heart sound?
closure of semilunar valves
what heart sounds are heard in the healthy dog/cat?
S1 and S2
what heart sounds can sometimes be detected in dogs/cats?
diastolic sounds - S3 and S4
what is the best way of detecting the diastolic heart sounds in cats/dogs?
using the bell of the stethoscopes
what is S3 associated with?
early diastolic filling of the left ventricle
what causes the S3 to be louder than in normal animals?
high left atrial pressure
stiff poorly compliant left ventricle
what is S4 associated with?
late diastolic filling with atrial contraction
what causes S4 to be louder in some animals?
animals that are more dependant on atrial contraction to achieve ventricular filling
when are crackles usual heard in the lungs?
inspiration (when the airways open)
what does crackles in the lung field indicate?
indicates the presence of fluid
when are wheezes in the lung field heard?
during expiration
what are wheezes in the lung field associated with?
airway narrowing
what is thoracic percussion?
gently tapping on the chest wall checking for resonance
when is resonance normally heard in the lung?
air-filled lungs usually are
what might increased resonance of the lungs be evident of?
pneumothorax
what might cause decreased resonance of the lungs?
pleural effusion
what can cause reduced thoracic compressibility in cats?
cranial mediastinal mass
large pleural effusion
in the dog what is a good way to differentiate cardiac and respiratory disease?
heart rate and rhythm
in dogs with congestive heart failure what is reduced/absent?
vagal tone (compared to respiratory disease when the vagal tone is enhanced)
how is HR effected by cardiac disease?
normal or increased
how is HR effected by respiratory disease?
normal or decreased
how is the rhythm of the heart effected by cardiac disease?
sinus rhythm
sinus tachycardia
arrhythmias
how is the rhythm of the heart effected by respiratory disease?
sinus arrhythmia
what is a sinus arrhythmia?
an irregular heart rhythm/rate that originates from the SAN
when is coughing mainly seen in animals with cardiac disease?
at night
when is coughing mainly seen in animals with respiratory disease?
when excited/exerted
what are diastolic gallops?
S3 and S4
what is the ACVIM ABCD classification used for?
staging cardiac disease
what is the criteria for A in the ACVIM classification?
at risk but with no structural abnormalities (such as all CKCS)
what is the criteria for B in the ACVIM classification?
structural abnormalities detected but no clinical signs of congestive heart failure
what can the B criteria of the ACVIM be subdivided into?
B1 - no evidence of significant remodelling such as ventricular dilation
B2 - evidence of significant remodelling in response to volume overload
what is the criteria for C in the ACVIM classification?
congestive heart failure (acute or chronic)
what is the criteria for A in the ACVIM classification?
persistent endstage congestive heart failure
what is preload?
resistance that has to overcome for venous return to the heart
what is afterload?
resistance that has to be overcome for ventricular ejection during systole
define heart failure?
clinical syndrome caused by heart disease resulting in systolic/diastolic function severe enough to overwhelm the normal compensatory mechanisms of the heart resulting in poor cardiac output causing oedema and effusions
what are the four major consequences of congestive heart failure?
oedema/effusions
peripheral vasoconstriction
tachycardia/arrhythmias
remodelling/fibrosis of myocardium
what is the four major consequences of heart failure a result of?
neuro-hormonal activation
what does decreased cardiac output cause a decrease in?
blood pressure
where is a decreased blood pressure detected?
baroreceptors
what do the baroreceptors mediate when they detect a drop in blood pressure?
increase in sympathetic drive
what three things does increased sympathetic drive stimulate as a result of decreased blood pressure?
increased HR (tachycardia) activation of renin-angiotensin-alosterone-system (RAAS) vasoconstriction
what is stimulated by the increased sympathetic drive to cause tachycardia?
cardiac beta1 adrenal-recepotors
why is tachycardia detrimental in the long term?
causes reduced coronary perfusion (blood to the heart muscle)
what is stimulated by the increased sympathetic drive due to decreased blood pressure to cause rennin to be released?
beta1 receptors on the juxtaglomerular apparatus
what are the two aims of vasoconstriction when associated with decreased blood pressure?
increased arteriole constriction - increases blood pressure
increased vena-constriction - increases venous return to the heart
what causes vasoconstriction when associated with increased sympathetic drive due to a drop in blood pressure?
alpha1 adrenal-receptors on the vascular smooth muscle cells
what cells release rennin?
juxtaglomerular cells
what triggers rennin release?
reduced kidney perfusion
reduced sodium concentration
beta1 stimulation
what is rennin?
an enzyme
what does rennin do?
converts angiotensinogen into angiotensin I in the liver
what is angiotensin I converted to?
angiotensin II
what converts angiotensin I to angiotensin II?
ACE (angiotensin converting enzyme)
what are the actions of angiotensin II?
vasoconstriction
potentiates sympathetic activity
release of vasopressin
hypertrophy and fibrosis of cardiomyocytes (myocardial remodelling)
where is vasopressin released from?
posterior pituitary
what is vasopressin?
an antidiuretic hormone
how does angiotensin II potentiate sympathetic activity?
enhances adrenergic tone
facilitates ganglionic transport
enhance release of noradrenaline from adrenergic neurons
where is aldosterone released from?
zona glomerulosa of adrenal cortex
what is the effect of aldosterone?
acts on the distal convoluted tubules of the nephron to cause sodium/water retention
what is the effect of vasopressin?
result in water retention leading to excessive retention causing oedema and effusions
other than sodium/water retention, what is an effect of aldosterone?
myocardial fibrosis and remodelling
what are the two types of natriuretic peptide?
atrial and brain
what are atrial natriuretic peptide released due to?
atrial stretch
what are brain natriuretic peptide released due to?
as a result of ventricular stretch
what do natriuretic peptides do?
adverse effects of angiotensin II (counteract the RAAS - diuresis, natiuresis, vasodilation)
what can be used to demonstrate the presence of heart failure?
atrial and brain natriuretic peptides
what does endothelin cause?
vasoconstriction
what mediates the release of endothelin?
elevated angiotensin II and endothelial damage
other than vasoconstriction, what does endothelin have a role in?
myocardial fibrosis and remodelling
what does volume overload of the heart chambers lead to?
chamber dilation and compensatory hypertrophy
what is compensatory hypertrophy due to volume overload called?
eccentric hypertrophy
what is compensatory hypertrophy due to pressure overload called?
concentric hypertrophy
how do sarcomeres replicate in eccentric hypertrophy?
in series
how do sarcomeres replicate in concentric hypertrophy?
in parallel
what are some examples that pressure overload?
aortic stenosis
systemic hypertension
pulmonic stenosis
pulmonary hypertension
define adaptive remodelling of the heart
changes in heart chamber and wall dimensions as a consequence of underlying lesions which normalise wall stress compensatory mechanisms
define maladaptive remodelling of the heart
change in relative wall thickness or altered geometry of a heart chamber due to increased wall stress
what mediates tachycardia and arrhythmias?
elevated catecholamine levels, increased sympathetic drive and reduced vagal tone
what is the main immediate problem associated with congestive heart failure?
excessive sodium/water retention - oedema…
what are three things the owner should be aware of when treating congestive heart failure?
it is palliative - not curable
it is life long treatment once started
aim is to improve animals quality of life
what is left sided backwards congestive heart failure due to?
elevated filling pressures in the left side of the heart
what is the primary sign of left sided backwards congestive heart failure?
pulmonary oedema
why does pulmonary oedema occur in left sided backwards congestive heart failure?
increased left sided filling pressure is transmitted into the pulmonary vasculature leading to fluid leaving the pulmonary veins and capillaries
what are the two types of pulmonary oedema?
interstial oedema - fluid in interstitium
alveolar oedema - air filled spaces of lungs
what are the clinical signs of pulmonary oedema?
tachypnoea
dyspnoea
(inspiratory and expiratory)
where is elevated right heart filling pressure transmitted to in right sided backward congestive heart failure?
great veins
how may increased pressure in the great veins due to right sided backwards congestive heart failure be seen on a physical examination?
jugular vein distention
jugular pulsations seen cranial to thoracic inlet
how do elevated central venous pressures effect the liver?
effects venous return from the liver so results in hepatomegaly
what can cause ascites due to hepatomegaly?
sinusoids may leak fluid and some proteins into the abdominal cavity
what type of reflex can may be identified in right sided backwards congestive heart failure?
positive hepatojugular reflex
what effect can fluid leakage into pleural space have on lymphatics?
can overwhelm the lymphatics ability to return fluid to the cranial vena cava, this can result in pleural effusions
what drugs are always indicated for congestive heart failure?
diuretics
what diuretic is used for patients with severe pulmonary oedema?
furosemide
what type of diuretics are most useful for treatment of oedema and effusions?
high ceiling loop diuretics
what type of diuretic is furosemide?
high ceiling loop diuretics
how is furosemide administered in life threatening pulmonary oedema cases?
IV
what should be monitored when giving furosemide to cases of life threatening pulmonary oedema?
respiratory rate and urine production
what effects does intravenous furosemide have?
diuretic
venodilator
why should diuretics never be used as long term monotherapy for heart failure?
they result in further activation of the RAAS and accelerate the deterioration of congestive heart failure
what are some common side effects of furosemide?
pre-reanl azotaemia
hypokalaemia
what should be monitored when administering furosemide or patients with congestive heart failure?
renal function - urea and creatinine
electrolytes
what conditions makes controlling congestive heart failure very difficult?
renal failure
if furosemide is not adequately controlling congestive heart failure, what can be used?
a more potent loop diuretic with better/more reliable bioavailability (torasemide)
if diuresis using furosemide or torasemide doesn’t control congestive heart failure, what can be done?
additional diuretic drugs can be used, normally ones that act on a different part of the nephron
what is the use of two diuretics working on different parts of the nephron called?
sequential nephron blockade (synergistic effect)
what are three diuretics that can be used alongside furosemide/torasemide in sequential nephron blockades?
spironolactone
hydrochlorothiazide
amiloride
what is the mechanism of action of spironolactone when used as a diuretic?
competitively antagonises aldosterone - weak potassium sparing diuretic
other than a diuretic, what additional effect does spironolactone have on congestive heart failure?
blocks aldosterone mediated myocardial remodelling and fibrosis (aldosterone antagonist)
what type of diuretic is hydrochlorothiazide?
thiazide diuretic
what type of diuretic is amiloride?
potassium sparing diuretic
what should be done in cases of pleural effusion?
thoracocentesis (drain) - diagnostic and therapeutic benefit
what should be done with abdominal effusions associated with congestive heart failure?
do not drain (unless very uncomfortable or breathing is compromised)
why should abdominal effusions associated with congestive heart failure not e drained?
they are protein rich, therapies associated with reabsorption is preferred
what should always be considered in animals with right sided congestive heart failure?
whether the animal has a pericardial effusion or not
why does the possibility of pericardial effusion always need to be considered in animals with right sided congestive heart failure?
they will have cardiac tamponade which compromises preload and impairs cardiac output, giving diuretics can compromise preload further and may be fatal
why do some patients on very high doses of furosemide not become azotaemic or have adequate control of their congestive heart failure?
may be diuretic resistant
what clinical sign in patients being administered diuretics would make you suspect diuretic resistance?
no obvious PU/PD
how can diuretic resistance possibly be bypassed?
IV/IM administration instead of oral
what can chronic repeated diuretic administration lead to?
distal nephron tubular cell hypertrophy and increased sodium absorption (genuine diuretic resistance)
what are the two licensed products of torasemide?
upcard
isemid
why does care need to be given when administering torasemide?
can cause azotaemia (acute kidney injury)
what can be used to counteract neurological-endocrine activation in congestive heart failure cases?
ACE inhibitors
angiotensin II blockers
anti-aldosterone drugs
what are the favourable effects of ACE inhibitors?
vasodilators
reduce the release of aldosterone (counteracting sodium/water retention)
prevent angiotensin II mediated myocardial fibrosis and remodelling
reduce vasopressin release
prevents bradykinin breakdown
counteract increased glomerular filtration pressure
what effect does bradykinin have, making the blocking of its breakdown by ACE inhibitors useful?
potent vasodilators (beneficial to renal function)
what does bradykinin mediate its vasodilatory action through?
nitric oxide
vasodilatory prostaglandins
how does aldosterone cause increased glomerular filtration pressure?
causes greater vasoconstriction in the efferent glomerular arteriole than the afferent
what are the 4 ACE inhibitors licensed in dogs?
benazepril
enalapril
ramipril
imidapril
when are ACE inhibitors indicated for use in congestive heart failure?
always (whatever the cause) - avoided when very hypotensive and shouldn’t be started until renal function is stable
when may angiotensin II receptor blocker be indicated for use?
in cats that often show side effects when using ACE inhibitors
what is an angiotensin II receptor blocker?
telmisartan
what is the anti-aldosterone drug used in dogs?
spironolactone
how does spironolactone work as an anti-aldosterone drug?
competitive aldosterone antagonist
how should spironolactone be given?
with food (improves bioavailability)
what is done to counteract vasoconstriction in congestive heart failure?
vasodilators given
what do arteriodilators do to counteract vasoconstriction in congestive heart failure?
reduce mean arterial pressure which reduces the resistance against which the left ventricle has to pump
what effect does reducing afterload have on controlling congestive heart failure?
reduce wall stress and myocardial oxygen consumption
what effect do ventilators have on controlling congestive heart failure?
reduced preload which means left sided filling pressure is reduced and blood is diverted away from the cardiopulmonary circuit which alleviates pulmonary oedema
what is used for emergency treatment of pulmonary oedema?
furosemide and nitroglycerine
how does nitroglycerine work to control pulmonary oedema?
applied topically and results in venodilation
what are balanced vasodilators?
drugs that effect with arteries and veins equally
what are two examples of balanced vasodilators?
ACE inhibitors
pimobendan
what can be used to improve mitral regurgitation?
arteriodilators
how do arteriodilators help to improve mitral regurgitation?
reduce afterload so will improve the fraction of forward stroke volume (reduces left atrial size/pressure to alleviate pulmonary oedema)
what are three arteriodilators used for mitral valve disease?
pimobendan
amlodipine
hydralazine
what drug can be used to improve cardiac output in congestive heart failure cases?
pimobendan
describe the mode of action of pimobendan
increases the sensitivity of the contractile apparatus to intracellular calcium levels
what actions does pimobendan have?
positive inotrope
balanced vasodilator
how should pimobendan be given?
orally on an empty stomach (absorption impaired by food)
how fast does pimobendan act?
very quickly - in about 2 hours of oral administration
what drug is used to counteract the high sympathetic drive of congestive heart failure?
digoxin
when is digoxin use indicated in congestive heart failure cases?
atrial fibrillation and other supraventricular tachyarrhythmias
as an antiarrhythmic
patients with reduced systolic function (poor contractility)
what are the effects of digoxin?
vagomimetic
favourable autonomic effects
mild positive inotrope
how does digoxin do as a vagomimetic?
enhances vagal tone and reduces sympathetic drive
how does digoxin act as a vagomimetic?
stimulating CNS vagal centres
sensitise baroreceptors to BP change
enhance cardiac pacemaker response to acetylcholine
what do the vagomimetic effects of digoxin result in?
slowing the rate of discharge of SAN so slows the sinus rate
slows conduction through AVN and increased the refractory period
(negative chronotrope)
what favourable autonomic effects does digoxin have?
can stop syncope episodes in animals with postural/tussive syncope
what are some tips to avoid digoxin toxicity?
start with low oral dose rate
assess blood levels every week
warn owners of clinical signs
what conditions is digoxin toxicity more likely to be seen with?
cachexia obesity hypoproteinaemic hypokalaemia hypothyroidism renal dysfunction
what are the clinical signs of digoxin toxicity?
dull
excessive stomach noises
inappetance
vomiting/diarrhoea
what is the standard quadruple therapy for congestive heart failure in dogs?
furosemide
ACE inhibitor
pimobendan
spironolactone
how are dobermans with preclinical dilated cardiomyopathy treated?
pimobendan
ACE inhibitors
how are dogs with preclinical myxomatous degenerative mitral valve disease with cardiomegaly treated?
pimobendan
what should never be used to counteract high sympathetic drive in patients with congestive heart failure?
beta blockers
what does an ECG record?
changes in electrical potential difference in the heart occurring during depolarisation and repolarisation of the myocardium plotted against time
what is the pacemaker of the heart?
SAN
what is the P wave on an ECG?
atrial depolarisation
what is the speed of the wave of depolarisation across the atria?
1m/s
what happens to the speed of the wave of depolarisation when it reaches the AV node?
slows to 0.1m/s
what does the P wave prompt?
atrial contraction
what is the P-R interval?
the slowed wave passing through the AV node
what does the P-R interval allow?
ventricular filling
where does the wave reach after the AV node?
bundle of his which branches into purkinje fibres throughout the ventricles
how fast do electrical impulses travel through the ventricles?
4m/s
what does the QRS complex show?
ventricular depolarisation
how fast is conduction during ventricular depolarisation?
1m/s
what does the T wave show?
ventricular repolarisation
what does an increase in the amplitude of a P wave indicate?
increased size of one/two atria
what does an increase in the amplitude of a QRS complex indicate?
increased size of one/two ventricles
what species is P wave and QRS complex amplitude associated with atria/ventricle size?
small animals and humans
can ECG be used to determine which chamber is enlarged when increase P wave or QRS complex is increased?
no (need echocardiography)
what colour is the right fore electrode?
red
what colour is the left fore electrode?
yellow
what colour is the left hind electrode?
green
what colour is the earth lead of an ECG?
black
what are the six leads (channels) of the ECG?
I, II, II, aVR, aVL, aVF
what is the most important lead of an ECG?
II
what does lead I of the ECG connect?
right fore (negative) to left fore (positive)
what does lead II of the ECG connect?
right for (negative) to left hind (positive)
what does lead III of the ECG connect?
left fore (negative) to left hind (positive)
why is lead II of the ECG the most important in assessing the heart?
it is roughly parallel to the portion of the heart so has the largest QRS complex in the normal heart
what should be checked when assessing an ECG?
paper speed and sensitivity
what is assessed when looking at and ECG?
what the heart rate is
if the P:QRS ratio is 1:1
what is the predominant rhythm
what does a wide and bizarre QRS complex indicate?
a rhythmic disturbance of ventricular origin or a conduction disturbance
how can T waves look in a dog?
negative, positive or biphasic
asymmetrical
what does a tall, spikey, symmetrical or a change in the T wave indicate?
underlying blood gas, acid-base or electrolyte disturbance
what is the standard speed and sensitivity of an ECG?
50mm/s
1mV = 1cm
what abnormality in lead II suggests left atrial enlargement?
prolonged P wave
what abnormality in lead II suggests right atrial enlargement?
tall P wave
what abnormality in lead II suggests left ventricular enlargement?
tall R wave
what abnormality in lead II suggests ventricular enlargement/hypertrophy?
prolonged QRS complex
what is the normal heart rhythm called?
sinus rhythm
when can sinus rhythm vary slightly?
with respiration
what is it called when sinus rhythm varies with respiration?
sinus arrhythmia
is sinus arrhythmia normal?
yes its normal in dogs and indicates normal/high vagal tone
describe how a sinus arrhythmia appear on an ECG?
R-R interval rhythmically decreases with inspiration and increases with expiration
what is a sinus tachycardia?
normal ECG with a heart rate faster than normal
what is sinus bradycardia?
normal ECG with a heart rate slower than normal
what is sinus arrest?
ECG shows a gap with no electrical activity for a period exceeding two normal R-R intervals
what are the types of AV block?
first degree
second degree
third degree
what is an AV block?
AV node blocks/slows conduction of atrial depolarisation into the ventricles
what is a first degree AV block?
the P-R interval is longer than normal for the species
what does a second degree AV block look like on ECG?
some P waves aren’t followed by a QRS complex
what can cause second degree AV block?
disease of AVN
normal/physiological (especially horses)
what are the types of second degree AV block?
mobitz I
mobitz II
what is a mobitz I AV block?
single non-conducted P waves in the ECG
what is a mobitz II AV block?
multiple (every) non-conducted P wave
are mobitz I or II AV blocks more serious?
II - usually represent pathology
how does a third degree AV block appear on ECG?
one in which the P waves have no relationship to the QRS complex - they occur at their own normal rate
what cause atrial fibrillation?
atria being large or stretched then normal cell to cell conduction is lost
they will randomly reach the AV node and be conducted into the ventricles
what is seen on the ECG of animals with atrial fibrillation?
QRS and T waves are normal but the rate is fast and R-R interval is random (chaotic)
no P waves
what is the most common rhythmic disturbance of the heart?
atrial fibrillation
what is another name for supraventricular tachycardia?
supraventricular premature complexes
what is a supraventricular tachycardia?
an ectopic focus in the atria or atrioventricular junction depolarises the atria prematurely then a complex with the appearance of a normal QRS complex is produced
what is another name for ventricular tachycardia?
ventricular premature complex
what is a ventricular tachycardia?
ectopic focus arise in the ventricular myocardium, this depolarisation spreads cell by cell (instead of by Purkinje fibres) causing a slow spread making a wide and bizarre complex
what are the hallmarks of a ventricular tachycardia ECG?
wide bizarre complex that slurs into an oppositely directed T wave
where does a ventricular premature complex with a positive T wave in leads I and II originate?
left ventricle
where does a ventricular premature complex with a negative T wave in leads I and II originate?
right ventricle
what is ventricular fibrillation?
complete loss of coordinated ventricular depolarisation/repolarisation
(chaotic ECG results)
how does the autonomic nervous system influence an ECG?
vagal tone and sympathetic drive affects heart rate and rhythm
how can electrolyte disturbances influence ECGs?
electrical activity of the heart depends on intra- and extra-cellular concentration gradients of electrolytes - potassium, sodium and calcium
how can hyperkalaemia show on an ECG?
sinoventricular rhythm
no discernible P wave
relatively normal QRS complex
tall spikes T waves
what is echocardiography?
cardiac ultrasound
