Pathophysiology Flashcards
definition of shock
Circulatory failure that results in inadequate cellular oxygen utilisation
- Low arterial blood pressure leading to
- Inadequate tissue perfusion resulting in
- Cellular hypoxia
- If shock not corrected it will end in Death!
main causes of schock
Distributive
- (generalised vasodilatation – “leaky pipes”)
- mainly caused by sepsis
- can sometimes be caused by anaphylaxis
Hypovolaemic (loss of circulating blood volume)
- internal or external losses (blood, plasma, gastrointestinal fluids)
Cardiogenic - (pump failure)
- myocardial infarction, cardiomyopathy, arrhythmia, valvular heart failure
Obstructive - (mechanical interference with blood flow)
- pulmonary embolism, cardiac tamponade, tension pneumothorax
(ordered most to lest likely)
direct consequences of shock
Reduced Arterial Blood Pressure“Hypotensive”
(BP = CO x PR)
- Distributive: decreased PR (vasodilation)
- Hypovolaemic: decreased CO
- Cardiogenic: decreased CO
- Obstructive: decreased CO
- Reduced BP - reduced systemic blood flow
- Decreased cerebral blood flow (brain dysfunction) - confusion, restlessness
- Decreased renal perfusion (kidney failure) - fall in glomerular filtration rate (GFR) and urine volume
- Decreased tissue perfusion (tissue hypoxia) - switch to anaerobic metabolism and development of lactic acidosis
signs and symptoms of shock
Low blood pressure
- In adults, systolic BP < 90mmHg or mean arterial pressure <70 mmHg
Skin changes
- cold, clammy, mottled, cyanosed, prolonged capillary refill time
Altered mental state
- altered level of consciousness, disorientation, confusion, restless
Organ dysfunction
- decreased urine output, acute kidney injury
Increased sympathetic tone
- tachycardia, sweating
Respiratory compensation for metabolic acidosis
- Hyperventilation “air hunger” to increase excretion of CO2
describe the autonomic nervous system’s compensatory physiological response to a fall in blood pressure
a. Increased sympathetic tone & catecholamine release
b. Decreased parasympathetic tone
- fall in bp
- Decreased baroreceptor output
(+ increased chemoreceptor output) - Increased sympathetic nervous system activity
- Increased adrenaline and noradrenaline release
- Increased
vasoconstriction
(increase in PR) and Increased heart rate and cardiac contractility (increase in CO) - Decreased parasympathetic nervous system activity - Increased heart rate (increase in CO)
describe the renin-angiotensin-aldosterone system (RAAS) compensatory physiological response to a fall in blood pressure
- Fall in BP - decreased in kidney perfusion
- Decrease in glomerular filtration sensed by macula densa
- Increased Renin released from juxtaglomerular apparatus
- Renin cleaves Angiotensinogen to Angiotensin I
- Angiotensin I converted to Angiotensin II by ACE
- Angiotensin II vasoconstricts arterioles
- Angiotensin II increases release of Aldosterone
- Aldosterone increases sodium and water retention
describe the Vasopressin (anti-diuretic hormone) compensatory physiological response to a fall in blood pressure
Pathophysiology of shock lecture slide 48
• Outline the main causes of heart failure
The main causes of heart failure are: • Ischaemic heart disease, which results in myocardial damage and fibrosis - scar tissue - can't contract properly • Dilated cardiomyopathy • Hypertension - overworking heart • Disease of the cardiac valves
• Provide a functional classification of heart failure
• the side of the heart involved (left heart failure or right heart failure)
• the phase of the cardiac cycle which is mainly
affected, i.e. systolic dysfunction versus diastolic
dysfunction
• whether the main features are those caused by
increased atrial and venous pressure proximal to the ventricles (backward failure) or decreased arterial perfusion (forwards failure)
• whether there is low cardiac output with a
compensatory increase in peripheral resistance
(low output failure) or high cardiac output in the
face of chronically low peripheral resistance (high output failure). (Eventually, cardiac function deteriorates in the face of the increased load and cardiac output falls.)
• the level of functional limitation experienced by the patient.
• Describe the pathophysiological responses to heart failure
Characteristic pathophysiological features of heart failure are:
• Increased venous pressure and ventricular dilatation. The reasons for this are best understood in terms
of the Starling curve for the heart. Stroke volume and cardiac output are depressed at any given filling pressure when cardiac pumping is impaired. In mild heart failure the stroke volume and cardiac output can still be maintained but this is only achieved at the cost of increased venous pressure and end diastolic volume.
• Reduced ejection fraction. Since the end diastolic volume is increased but the stroke volume is unchanged in the new steady state, the fraction of the end diastolic volume ejected during each beat (the ejection fraction) is
reduced below the normal value (>50%).
In moderate heart failure one may expect:
• Normal or reduced stroke volume
• Normal or increased heart rate (to compensate for the reduced stroke volume)
• Normal cardiac output at rest (Cardiac output = stroke volume x heart rate)
• Reduced exercise tolerance.
As cardiac function deteriorates further a state of severe cardiac failure becomes inevitable, in which ventricular function is so depressed that normal stroke volume and cardiac output can no longer be maintained even at rest (see Starling curve for severe heart failure). This has a series of consequences that further exacerbate the situation.
Moderate heart failure:
•Normal or reduced SV
•Normal or increased HR
•Normal CO at rest (CO = SV x HR) •Reduced exercise tolerance
Severe heart failure:
•Reduced SV
•Reduced CO at rest
describe the signs and symptoms of heart failure
These can be mapped onto the pathophysiological consequences of ventricular failure.
- Increased venous pressure:
a. In left ventricular failure this causes increased pulmonary venous pressure, which increases capillary filtration leading to:
- Pulmonary oedema, which interferes with pulmonary gas exchange, and
- Reduced lung compliance
The symptoms and signs which result from this are:
o dyspnoea (breathlessness or difficulty breathing): this may be exertional at first but is present at
rest in more severe disease
o orthopnoea (breathlessness when lying down): caused by the increased venous return and
increased pulmonary pressure which make pulmonary oedema worse when lying as opposed to
standing
o paroxysmal nocturnal dyspnoea: episodic breathless which may waken a patient from sleep and
which is usually lessened by sitting or standing upright. The mechanisms are probably similar to
those in orthopnoea.
o bilateral basal crackles on auscultation of the chest
o central cyanosis (due to impaired gas exchange in the lungs caused by pulmonary oedema)
• In right ventricular failure this causes increased systemic venous pressure and increased capillary filtration.
Symptoms and signs are:
o elevated jugular venous pressure, and
o dependent oedema (ankle oedema if ambulant)
o ascites
o tender hepatomegaly
- Decreased cardiac output.
Symptoms and signs are:
o fatigue
o hypotension
o reduced peripheral perfusion (advanced stage), resulting in
o peripheral cyanosis (can only be diagnosed in the absence of central cyanosis) - Ventricular dilatation/hypertrophy.
Sign is:
a. displaced apex beat - Sympathetic compensation.
Sign is:
a. sinus tachycardia
describe the compensatory mechanisms associated with heart failure
- Attempted compensation for low cardiac output: The compensatory mechanisms that maintain a stable blood pressure with changes in posture from minute to minute, and which help limit the hypotensive effects of hypovolaemia, are also activated in severe heart failure.
• Reduced renal blood flow resulting from the
reduced cardiac output leads to Na+ and H2O retention through a number of mechanisms:
o Reduced GFR reduces urinary fluid loss
o Reduced blood flow activates
renin/angiotenisin/aldosterone
signalling. The increased angiotenisin 2
causes vasoconstriction (increasing the
afterload against which the failing heart
must pump) and stimulates aldosterone
secretion (2 ̊ hyperaldosteronism),
leading to increased Na+/H2O
reabsorption in the distal convoluted
tubule, so increasing blood volume and
venous return (preload). This further increases venous pressure.
• Reduced cardiac output leads to increased sympathetic activity, increasing heart rate and peripheral resistance (vasoconstrictor nerves).
In cardiac failure, where inadequate cardiac pumping means that normal perfusion cannot be restored, these mechanisms actually contribute to the pathophysiology. Thus, fluid retention exacerbates the increase in venous pressure while the peripheral vasoconstriction further reduces cardiac output.
describe some
Non-cardiac factors which contribute to the pathophysiology of cardiac failure
- Attempted compensation for low cardiac output: The compensatory mechanisms that maintain a stable blood pressure with changes in posture from minute to minute, and which help limit the hypotensive effects of hypovolaemia, are also activated in severe heart failure.
• Reduced renal blood flow resulting from the
reduced cardiac output leads to Na+ and H2O retention through a number of mechanisms:
o Reduced GFR reduces urinary fluid loss
o Reduced blood flow activates
renin/angiotenisin/aldosterone
signalling. The increased angiotenisin 2
causes vasoconstriction (increasing the
afterload against which the failing heart
must pump) and stimulates aldosterone
secretion (2 ̊ hyperaldosteronism),
leading to increased Na+/H2O
reabsorption in the distal convoluted
tubule, so increasing blood volume and
venous return (preload). This further increases venous pressure.
• Reduced cardiac output leads to increased sympathetic activity, increasing heart rate and peripheral resistance (vasoconstrictor nerves).
In cardiac failure, where inadequate cardiac pumping means that normal perfusion cannot be restored, these mechanisms actually contribute to the pathophysiology. Thus, fluid retention exacerbates the increase in venous pressure while the peripheral vasoconstriction further reduces cardiac output.
- Myocardial remodelling: This refers to structural and
molecular changes which occur within the failing heart. Many of these further impair cardiac contractility. This area is currently a major area of clinical research. Some typical abnormalities include:
• Ventricular hypertrophy (eg in response to hypertension) and/or dilatation are often seen.
• Individual myocytes also undergo hypertrophy
• Myocyte apoptosis (programmed death not just necrosis)
• Interstitial fibrosis
• Changes in myosin expression
• Abnormailities in Ca2+-signalling in myocytes which may
impair excitation-contraction coupling - Endothelial dysfunction: Endothelial production of the
physiological dilator nitric oxide is reduced in cardiac failure, while the endothelial constrictor peptide endothelin is increased in levels. This contributes to peripheral vasoconstriction, further reducing cardiac output and tissue perfusion. - Antidiuretic hormone (vasopressin): this may be released in increased amounts in severe chronic cardiac failure. It causes H2O retention (increased absorption in the renal collecting ducts), vasoconstriction and hyponatraemia, and elevated levels are a very poor prognostic indicator.
describe the role of natriuretic peptides in heart failure
These peptides promote fluid loss (diuresis), Na+-loss (natriuresis) and vasodilataion. They are, therefore, potentially beneficial in cardiac failure, although their therapeutic use is not well established. Levels of these peptides are raised in the circulation. Three main peptides have been identified:
• Atrial natriuretic peptide (ANP): secreted by the atria under conditions of stretch, as occur in cardiac failure.
• Brain natriuretic peptide (BNP; so named because that was where it was first identified): released from the ventricles.
• C-type peptide: released from vascular endothelium.
describe the Investigations in heart failure
The aim is to identify evidence of cardiac damage and assess cardiac function. This will include:
• blood tests looking for anaemia, elevated cardiac enzymes if ischaemic damage is suspected in acute
failure, and BNP levels, which increase as severity increases
• chest x-ray to assess cardiomegaly
• ECG, looking for ischaemic changes, arrhythmias or evidence of hypertrophy in hypertension (left axis deviation)
• Echocardiogram and other imaging techniques allow assessment of cardiac size, ventricular systolic and diastolic function, ejection fraction, cardiac output, etc
• Cardiac catheterisation to measure relevant pressures;
o catheter introduced through systemic vein to assess pressures in right atrium and ventricle, pulmonary artery and left atrium (pulmonary artery occlusion pressure)
o catheter introduced retrogradely via systemic artery to assess left ventricular end diastolic
pressure
• Blood gases or pulse oximeter to assess oxygenation
• Exercise testing to assess VO2 max: this is a very sensitive prognostic indicator.
describe the treatment of heart failure
Treatment targets the pathophysiological processes contributing to the symptoms and signs of cardiac failure by reducing venous congestion (preload), reducing peripheral resistance (afterload), or improving myocardial contractility.
- Reducing venous pressure. This is achieved by reducing the total extracellular fluid volume and thus, the circulating blood volume. This will reduce the symptoms and signs of venous hypertension, particularly dyspnoea due to pulmonary oedema.
The JVP should fall and systemic (eg
ankle) oedema will be reduced as
well. It is important to realise that
this will not increase cardiac output,
in fact, this is likely to fall further due
to the reduced filling pressure (see
the Starling curve again). However,
the stroke volume v venous pressure
relationship is often quite flat in the
high venous pressure range in cardiac
failure, so the effect on stroke
volume is limited. The improvement
in function due to reduced venous congestion (decreased backwards failure) outweighs any losses due to any further reduction in tissue perfusion (increased forwards failure). Venous loading can be reduced using:
• diuretics (increased renal Na+/H2O loss)
• ACE inhibitors (reduced angiotensin 2 formation (also reduces vasoconstriction)
• Angiotensin 2 receptor blockers (blocks A2 actions; also reduces vasoconstriction)
• aldosterone antagonists - Reducing peripheral vasoconstriction: This increases cardiac output by reducing the afterload, which is pathologically elevated in cardiac failure. Vasodilator agents are usually used, such as nitrates (which mimic the actions of endothelial NO, deficiency of which contributes to the endothelial dysfunction seen in heart failure) and hydralazine, which also acts directly to relax vascular smooth muscle.
- Cardiac acting drugs, including:
• β−adrenoceptor blockers, which inhibit the effects of increased sympathetic drive on the heart.
This drive, beneficial in short term cardiovascular control, increase cardiac work leading to permanent myocyte damage in the longer term. Reducing the heart rate with β-blockers may also improve diastolic filling, especially if diastolic dysfunction is a major feature.
• digoxin and other inotropic drugs, act directly on ventricular myocytes, increasing stroke work by shifting the Starling curve up and towards the left, thereby reversing the defining pathophysiological characteristics of cardiac failure itself (see diagram). This increases cardiac output while also reducing
venous pressures.
In summary, medical treatment targets the pathophysiological processes already identified as contributing to cardiac failure. - Cardiac transplant: This is most likely to be considered in younger patients with very a poor prognosis. The usual problems of antigen matching and rejection apply. It is of physiological
interest to note that the transplanted heart is denervated and so has no parasympathetic or sympathetic nerve supply. This results in:
• a higher than normal resting heart rate, since parasympathetic tone is normally dominant at rest.
• very restricted increase in heart rate during exercise
(no sympathetic drive)
• an increased stroke volume during exercise (the only
way to achieve an increase in cardiac output).
This is the reverse of the situation in normal individuals in which most of the exercise induced increased in cardiac dependent is achieved through a tachycardia, with only a limited increase in stroke volume.
describe how you may monitor heart failure
This is based on assessment of the key features of the disease and involves:
• clinical evaluation of the symptoms and signs, looking for improvement or deterioration
• assessment of body fluid status: as with any cause of oedema the extracellular fluid volume is
increased. Oedema can be assessed clinically, acute changes in body weight recorded, and plasma biochemistry checked, eg looking for hyponatraemia, which may reflect inappropriate ADH secretion in sever cases and has a poor prognosis.
• checking cardiac rhythm (arrhythmias may contribute to cardiac failure): ECG and possibly a 24-hr ECG tape.
• functional testing: such as echocardiography, exercise testing and maximal oxygen consumption (VO2 max) determination.
definition of hypertension
Arterial blood pressure, like most biological variables, is not
exactly the same in all normal people, nor is it the same in
any given person over time, eg it changes during exercise and
with aging. This means that the definition of a ‘normal’ blood
pressure has to be based on appropriate population studies
carried out under defined conditions. The distribution of
resting blood pressure in the population follows a bell-
shaped, or normal distribution. Epidemiological studies have
shown that the risk of cardiovascular complications increases
with blood pressure. Based on these studies and consideration of the likely population benefit of treatment, hypertension is currently defined as >140 mmHg and >90 mmHg. This equates to 20-30% of the population in western communities.
describe the causes and pathogenesis of primary or ‘essential hypertension’ hypertension
Causes:
• This is a multifactorial condition with no specific cause
identifiable.
• It accounts for 80-90% of all hypertension
• There is a genetic pre-disposition to hypertension
• Developmental factors in utero increase the risk (eg association with low birth weight)
• Environmental factors increase the risk of hypertension, eg:
o Obesity
o Excess alcohol intake o Excess Na+ intake
• Hypertension is associated with diabetes, particularly in Type 2 diabetes with insulin resistance. A combination of features including hypertension, obesity and insulin resistance is often seen together and has been labelled metabolic syndrome.
Pathogenesis of essential hypertension:
• Cardiac output is normal in chronic hypertension
• As predicted from BP=COxPR, peripheral resistance is increased.
• This results from a reduction in the lumen size in resistance arteries and arterioles.
• Wall thickness is increased in these resistance vessels, a pathological change known as arteriosclerosis.
• It can be difficult to untangle causes and consequences in essential hypertension. For example, there is
evidence that in genetically predisposed individuals, high Na+ intake is associated with an increased risk of hypertension. Now increased total body Na+ would be expected to lead to an increased volume of extracellular fluid and blood, causing an increase in cardiac output and so raising blood pressure. However, as we’ve seen, cardiac output is not chronically elevated in essential hypertension. This has led to the suggestion that high Na+ may lead to an initial increase in BP via an increase in cardiac output. This may result in arteriolar sclerosis with a subsequent increase in resistance that maintains the increased pressure in the long term.
• Baroreceptor reflexes normally help ensure that shifts in blood pressure are minimised in amplitude and reversed as quickly as possible. However, in the face of a chronic elevation of BP, the baroreceptors become adapted to the higher pressure, with a reduced sensitivity to arterial stretch. The baroreceptors still help to minimise pressure fluctuations in an individual (BP variance) but do not affect the mean arterial pressure.
describe the causes of secondary hypertension
Renal disease
Endocrine diseases
- Primary hyperaldosteronism (Bilateral Adrenal hyperplasia (rarer – unilateral adrenal tumour = Conn’s syndrome)
- Phaeochromocytoma
- Cushing’s syndrome
Coarctation of the aorta
Pregnancy
Drugs
Pathogenesis of hypertension secondary to renal disease
Damage to renal tissue results in decreased renal perfusion and glomerular filtration. This elevates BP through at least 2 mechanisms:
• Activation of the renin/angiotensin/aldosterone signalling system though increased renin secretion by
the juxtaglomerular apparatus. This results in increased peripheral resistance (vasoconstriction by angiotensin 2) and increased cardiac output (aldosterone stimulates Na+/H2O re-absorption, increasing ECF and blood volume, leading to increased venous return), both of which increase BP (BP=COxPR).
• Reduced filtration leads to fluid retention, which also increases blood volume and cardiac output.
Pathogenesis of hypertension in endocrine disease
In each case, high blood pressure reflects the actions of a hormone produced in excess.
• Primary hyperaldosteronism (Conn’s syndrome): the increased aldosterone levels increase blood
volume and cardiac output. [Na+] may be elevated (aldosterone directly stimulates renal Na+ re- absorption), while [K+] is reduced (aldosterone stimulates renal K+-secretion and urinary excretion). [H+] may also be reduced (aldosterone stimulates renal H+-secretion: metabolic alkalosis).
• Phaeochromocytoma: this is a catecholamine secreting tumour often (but not always) found in the adrenal medulla. Elevated adrenaline/noradrenaline increases heart rate and myocardial contractility, increasing cardiac output. Catecholamines (particularly noradrenaline) also cause vasoconstriction, increasing peripheral resistance. The hypertension may be extreme and intermittent (episodic catecholamine release). The breakdown products of catecholamines are excreted in the urine, and 24 hour excretion can be measured if a phaeochromocytoma is suspected. Imaging studies may reveal the tumour itself.
• Cushing’s syndrome: increased glucocorticoid secretion or aggressive glucocorticoid treatment can lead to hypertension since these hormones also have some mineralocorticoid action.
Pathogenesis of hypertension secondary to co-arctation of the aorta:
Co- arctation of the aorta is a congenital abnormality in which the aorta is narrowed, usually close to the site of the ductus arteriosus in fetal life.
• The resulting increase in resistance leads to hypertension in all
arteries branching off the aorta proximal to the narrowing, while pressure is normal or low in vessels that originate distal to it. A classical finding is hypertension in the right arm with low pressures and weak pulses in the legs. The left arm may be hypertensive or normo-hypotensive, depending on whether the narrowing is distal or proximal to the root of the left subclavian artery.
• If undiagnosed, reduced perfusion to the kidneys will eventually lead to generalised systemic hypertension through the renal mechanisms described above.
pathogenesis of Hypertension secondary to pregnancy
Normally, the increase in maternal cardiac output during pregnancy is more than compensated for by a fall in peripheral resistance, resulting in a decrease in blood pressure around mid-term of pregnancy. For reasons that are not understood, however, a life-threatening rise in blood pressure is sometimes seen in the second half of pregnancy. This is part of a syndrome known as pre- eclampsia.
Pathophysiology of Hypertension caused by drugs:
prescribed medication may lead to an increase in blood pressure, often reflecting their mode of action.
eg NSAIDS Steroids COC pill Sympathomimetics Substance abuse Herbal remedies
describe the consequences of hypertension
• Left ventricular hypertrophy and cardiac failure. This may be discovered/confirmed:
o On clinical examination (displaced apex beat, triple rhythm, bilateral crackles on ausculataion)
o On chest X-ray
o On the ECG, which classically shows left axis deviation, reflecting the increased muscle mass in
the left ventricular wall
• Arterial wall thickening and reduced wall compliance: This results in an increased pulse wave velocity,
which shows up as a decreased lag time between the pulse recorded at 2 different sites, one close to
and the other further from the heart.
• Atheroma: with increased risk of coronary artery disease and myocardial ischaemia, cerebral arterial
disease (see below), and peripheral artery disease.
• Endothelial dysfunction: Features of this dysfunction include:
o Reduced production of endothelial dilators such as NO and prostacyclins.
o Increased production of endothelial constrictors such as endothelin
o Increased risk of atheroma and thrombus formation
• Renal damage: This is referred to as hypertensive nephropathy and is characterised by narrowing of the renal vessels
(nephrosclerosis). This results in:
o Reduced renal perfusion and filtration
o Positive feedback via the renin/angiotensin/aldosterone
signalling pathways.
o Further increases in BP.
• Cerebrovascular disease: also contributed to by atheroma and thrombus formation. Clinical outcomes include:
o Vascular dementia
o Transient ischaemic attacks o Stroke
• Hypertensive retinopathy: the eye provides an opportunity to observe the effects of hypertension on the vasculature directly. Hypertensive retinopathy is characterised by:
o Thickening of the arterial walls (arteriosclerosis) o Haemorrhages
o Retinal infarcts (soft exudates)
signs and symptoms of hypertension
Uncomplicated hypertension has few symptoms, other than headache and nosebleed. The relevant signs are:
• Elevated BP (may be detected on screening)
• Hypertensive retinopathy
• Symptoms and signs of the complications of hypertension:
o Cardiac
o Renal
o Cerebrovascular
o Peripheral vascular disease
Principles of management of hypertension
Drugs that reduce blood pressure must act on either the cardiac output or peripheral resistance. There is considerable overlap with the treatments used in cardiac failure.
- Drugs which reduce cardiac output: The main drugs currently used are:
• Thiazide diuretics (the action on cardiac output is transient, these agents lower peripheral
resistance in the long term)
• β-adrenoceptor blockers (reduce sympathetic stimulation of the heart)
• ACE inhibitors
• Angiotensin 2 receptor blockers
• Renin inhibitors
The last 3 agents all inhibit aldosterone production, reducing renal Na+/H2O reabsorption. They also reduce angiotenisin 2 induced vasoconstriction, and so also reduce peripheral resistance.
- Drugs which reduce peripheral resistance: Major drugs used include:
• L-type Ca-channel blockers. These agents reduce intracellular [Ca2+] and so inhibit smooth
muscle contractility. They have a similar action on the heart and may reduce cardiac contractility, tending to reduce cardiac output. (L-type Ca2+-channel blockers also tend to shorten the plateau phase of the cardiac action potential and so may shorten systole.)
• α1-adrenoceptor blockers. These inhibit the constrictor action of sympathetically released noradrenaline on smooth muscle in blood vessels, leading to dilatation.
• Other vasodilators eg hydralazine or minoxidil.
Pathophysiology of arrhythmias
Principles of management of arrhythmias
.
describe what the different letters in an ECG waveform correspond with
P: Generation and spread of depolarization through atria
PR interval: Time taken for conduction of depolarization from SA node through atria and AV node, to ventricles
QRS: Spread of depolarization through bundle of His and Purkinje system within ventricles
T: ventricular repolarization
QT interval: Total time for depolarization and repolarization of ventricles
what do cardiac arrhythmias usually result from
Abnormal action potential initiation
Abnormal conduction
what are the values for bradycardia and tachycardia
Bradycardia
<60 beats per minute
Tachycardia
>100 beats per minute
describe the extrinsic and intrinsic causes of sinus bradycardia
Arrthymia lecture slide 9
Extrinsic causes (normal SA node): - Hypothermia - Hypothyroidism - Drugs, eg b-blockers - Neurally mediated o Increased vagal tone (athletes) o Carotid sinus syndrome o Vasovagal attacks
Intrinsic causes (abnormal SA node):
- Ischaemia/infarction
- Degeneration/fibrosis (sick sinus syndrome)
describe the three types of AV blocks
First-degree:
- (prolonged PR interval: >0.20s)
Second degree:
- Type 1 (Wenckebach) eg 6:5 = 6 P waves and only 5 QRS complexes
- that is, one fewer QRS than P wave (3:2 or 4:3 or 5:4 or 6:5….)
- Type 2 eg 3:1 = 3 P waves for 1 QRS complex
- (or could be 2:1 or 3:1 or 4:1 or 5:1…)
- more serious
Third degree
- p waves all over the place
- some of the t waves change shape - mixture of p wave and t wave
- no relationship between p waves and QRS complexes
symptoms of cardiac arrythmias
May result from hypotension and reduced cerebral blood flow
- Dizziness
- Syncope
- Stokes-Adams attacks (complete heart block)
Note - BBB is usually asymptomatic
briefly describe management of cardia arrythmias
Identify and treat extrinsic causes sinus bradycardia
Temporary or permanent pacemaker
what are the three main mechanisms of tachycardia
Arrhythmia lecture slide 19 and 20
- Accelerated automaticity:
- Sinus tachycardia
o Exercise
o Postural orthostatic tachycardia
- AV nodal rhythms - Triggered activity (after depolarizations):
- early (E) / delayed (D) - Re-entry (see next slide)
- Re-entry (‘circus’) movements
o Anterograde conduction in one limb blocked
o Retrograde conduction maintained
o May reflect reduced conduction velocity or prolonged refractory period
what are the three main mechanisms of tachycardia
Arrhythmia lecture slide 19 and 20
- Accelerated automaticity:
- Sinus tachycardia
o Exercise
o Postural orthostatic tachycardia
- AV nodal rhythms - Triggered activity (after depolarizations):
- early (E) / delayed (D) - Re-entry (slide 20):
- Re-entry (‘circus’) movements
o Anterograde conduction in one limb blocked
o Retrograde conduction maintained
o May reflect reduced conduction velocity or prolonged refractory period
describe some causes of atrial fibrillation
Causes include hypertension, ischaemic heart disease, thyrotoxicosis, rheumatic heart disease, alcohol
