Pathology of the Cardiovascular System (8-11) Flashcards
1
Q
What is hypertension?
A
Persistent high blood pressure
→ normal blood pressure: 120/80 mm Hg
Treat when systolic (contracting) > 140
and diastolic (resting) > 90
→ level of hypertension above which the use of antihypertensive treatment does more good than harm (if its marginally high side effects might not be worth it)
2
Q
How is blood pressure measured?
A
Arterial blood pressure is normally measures in the brachial artery in arm
→ Ambulatory blood pressure monitoring (ABPM) - 24hour blood pressure measurement
3
Q
What is white coat hypertension?
A
When you blood pressure is abnormally high
→ due to anxiety around doctors
Can be overcome with home BP measurement but they’re not calibrated
4
Q
What are you measuring when you take a blood pressure?
A
Ausculation and Korotkoff sounds
→ specific sounds found in the artery
Inflate cuff so high you stop all blood flow - no sound
→ slowly release pressure
→ point when you hear a first sound = systolic BP
→ as you turn it down further reach a point of no sound - no turbulence = diastolic BP
5
Q
What is mean arterial pressure?
A
MAP = (SP + (2 x DP)) / 3
→ not just average BP as uneven amount of time spent at rest
→ ~2/3 diastolic and ~1/3 systolic
→ mean closer to diastolic
6
Q
What are the causes of hypertension?
A
90-95% primary of essential hypertension → no known cause, probably a complex genetic disorder
Secondary hypertension → renal causes, endocrine disorders, aortic coarctation, preeclampsia, neurogenic hypertension, endocrine tumours, drug induced
7
Q
Why treat hypertension?
A
Hypertension increases the risk of:
→ stroke - occlusion in the brain
→ coronary events - MI, angina
→ aortic aneurysm - bulging in blood vessel, can rupture
→ heart failure
→ renal failure
→ end organ damage
8
Q
What are the symptoms and signs of hypertension?
A
Symptoms (patient describes)
→ headaches
→ dizziness
→ flushing
→ awareness of heart beat
→ epistaxis - nose bleeds
→ none (silent killer)
Signs (clinician observes)
→ level of blood pressure
→ cardiomegaly/left ventricular hypertrophy (echocardiogram) - heart has to work harder so increases in mass
→ abnormal renal function
→ hypertensive retinopathy
9
Q
How is hypertension managed?
A
- Patient education/lifestyle changes
→ stop smoking, los of weight, exercise, reduce salt intake, diet, relaxation therapy - Drug treatment
- Surgery (for secondary causes if appropriate)
10
Q
What is the effect of weight on blood pressure?
A
Weight and blood pressure are linked
→ its likely that weight interacts with various factors controlling blood pressure at different points over a lifetime
11
Q
What determines blood pressure?
A
Pressure depends on:
How much blood is ejected → cardiac output
→ heart rate and stroke volume (contractility and filling pressure)
How small the lumen is → total peripheral resistance
→ diameter of arterioles
12
Q
What are the two major mechanisms for controlling blood pressure?
A
- Barorectpor/sympathetic nervous system
→ controls BP minute to minute - ECF volume/plasma renin activity
→ longer term effects
13
Q
What is the baroreceptor reflex?
A
A physiological mechanism that helps to regulated blood pressure - baroreceptors are specialised sensory receptors located in certain blood vessels → walls of the carotid sinuses and aortic arch
Fall in BP detected by baroreceptors due to decrease in stretch
→ reduces frequency of nerve impulses to vasomotor centres in the medulla
→ inhibits parasympathetic nervous system
→ stimulates sympathetic nervous system
Leads to increased heart rate and contraction of arteries → increase in cardiac output and total peripheral resistance
→ ultimately increasing blood pressure
14
Q
What things can you aim to change to reduce blood pressure?
A
- Cardiac output (stroke volume * heart rate)
→ diuretics - reduce blood volume and therefore stroke volume
→ ACE inhibitors - reduce blood volume
→ angiotensin II receptor antagonists - reduce blood volume
→ beta-blockers - reduce heart rate and contractility - Reduce total peripheral resistance
→ vasodilators
→ calcium channel antagonists
→ ACE inhibitors
→ angiotensin II receptor antagonists
→ alpha-adrenoceptor blockers
Some drugs to both
15
Q
How do ACE inhibitors and angiotensin II receptor antagonists work?
A
Target different components of the renin-angiotensin-aldoerstone system → lead to vasodilation and reduction in blood pressure
Liver secretes angiotensinogen
Kidneys secretes renin → converts angiotensinogen to angiotensin I (inactive)
Converting enzyme → converts to angiotensin II (active)
→ causes adrenal cortex to secrete aldosterone a vasoconstrictor
ACE inhibitors → block converting enzyme
Angiotensin II receptor antagonists → block action of angiotensin II
16
Q
What are the effects of angiotensin II?
A
→ vasoconstriction of arterioles
→ stimulates Na+ reabsorption in the proximal tubule (Cl- and water follow passively)
→ stimulates aldosterone secretion (adrenal cortex)
→ stimulates vasopressin secretion from the posterior pituitary gland
→ stimulates thirst
17
Q
What are some examples of ACE inhibitors?
A
Ending in -pril → enalapril, lisinopril, ramipril
→ lower arterial resistance
→ reduce blood volume
Side effects → cause very rapid fall in blood pressure, can cause persistent dry cough (bradykinin - mediator released in response to inflammation - also blocked by ACE)
18
Q
What are some examples of angiotensin II receptor antagonists?
A
Ending in -sartan → losartan, candesartan, valsartan, ibesartan
→ well tolerated side effect profile
→ once daily dosing
→ cost effective
19
Q
What are calcium channel antagonists?
A
Block Ca2+ channel in muscles - needed for contraction
→ cause vasodilation - reduce peripheral resistance
For hypertension: dihydropyridines - nifedipine, amlodipine
Side effects → headache, flushing, ankle swelling
20
Q
What are thiazide diuretics?
A
Cause mild diuresis → e.g. bendroflumethiazide
Work at the beginning of the distal convoluted tubule in the kidneys to increase water and sodium loss → more excretion from kidneys
→ reduce blood volume, cardiac output and mean arterial pressure
→ take in morning to avoid nocturnal diuresis
→ use low doses
→ can cause hypokalaemia - loss of K
→ most effective in elderly or patients of African origin
21
Q
What are beta adrenoreceptor blockers?
A
Block beta receptors on the heart
→ -olol e.g. atenolol
→ no longer first line therapy - large clinical trial showed people still dying despite reduced BP
→
22
Q
What is the coronary circulation?
A
The circulation of blood that supplies the heart muscle (myocardium) with O2 and nutrients
Coronary arteries → arise from root of aorta, supply O2-rich blood to heart muscle, main arteries on the surface smaller penetrate into muscle
Coronary veins → collects deoxygenated blood after utilised by the myocardium, drain into the coronary sinus which empties into the right atrium
1/10 mm of endocardial surface can obtain nutrients from blood inside chambers
23
Q
Why is there phasic blood flow through the coronary circulation?
A
There is little coronary blood flow during systole (contraction) but it increases during diastole
→ when the hear contracts the coronary vessels squeeze shut restricting blood flow
24
Q
How is coronary blood flow reduced?
A
Reduction in diastolic interval (e.g. during exercise)
Rise in ventricular end-diastolic pressure
Fall in arterial pressure
25
How do you change coronary blood flow?
Need to increase coronary blood flow when there is greater demand for O2 from the heart (e.g. during exercise)
→ by dilating blood vessels - controlled by local metabolites
→ drop in O2 releases vasodilator substances from cardiac muscle
→ ado sine is a potent dilator - build up in low O2 because ATP not produces - dilates blood vessels - oxygen consumption matched by blood flow
26
What is the major cause of ischemic heart disease?
Ischemic heart disease (or coronary artery disease) → reduced blood flow / glucose to the heart muscle
Major cause is atherosclerosis - build up of plaque
→ genetic predisposition
→ excessive cholesterol/sedentary life style
→ cholesterol deposited in arteries (beneath endothelium), invaded by fibrous tissue / calcified
→ atherosclerotic plaques protrude into lumen and block/partially reduce blood flow
27
What are the different types of coronary syndromes caused by different atherosclerotic plaques?
Myocardial infarction (heart attack) → plaque + thrombus causing complete occlusion
Stable angina → plaque causing partial occlusion
Unstable angina → plaque + thrombus attach that can happen periodically causes almost complete occlusion
28
What is myocardial infarction?
Heart attack - sudden blockage of blood flow to a part of the myocardium
causes: ischemia → loss of blood supply - no O2 and no nutrients
leads to: necrosis → cell of tissue death
→ one of the most common causes of morbidity and mortality
→ 123,000 heart attacks per year
29
What causes myocardial infarction?
Atherosclerosis plaque rupture (chemical/mechanical stress) in coronary arteries
→ intraplaque hemorrhage - reduces vessel lumen diameter
→ release of tissue factor - activation of coagulation cascade
→ exposure of subendothelial collagen/turbulent blood flow - platelets aggregation - activation of coagulation cascade
→ coronary thrombus producing complete occlusion
30
What is the myocardial infarction process?
Blood flow beyond occlusion ceases
→ local dilation/collateral flow overfilling with stagnant blood
→ use up oxygen: deoxygenated haemoglobin
→ vessel walls become highly permeable - allowing fluid to leak into surrounding tissues
→ muscle cells swell - diminished cellular metabolism
→ within ~20 mins (without supply) the cardiac muscle cells die
31
How does ischemia lead to myocardial cell death?
Ischemia causes fall in ATP - impaired Na+ K+ ATPase
→ decreases membrane potential depolarisation - arrhythmias
→ intracellular edema
→ increases intracellular [Ca2+] - proteases lipases
Ischemia also leads to anaerobic metabolism
→ increases intracellular [H+] (acidity) - protein denaturation
all lead to cell death
32
What is collateral circulation?
Development of new blood vessels in response to blocked or narrowed arteries
→ as vessels slowly narrow (atherosclerosis) collateral vessels develop
→ may reroute blood flow around obstruction - alternative pathway for blood to reach tissues
33
How does myocardial infarction cause death?
Cardiac shock → decreased cardiac output
→ insufficient force to pump blood into the peripheral arterial tree
→ systolic stretch - heart wall damaged - buldges out - can't push blood out
Pulmonary oedema → build up of fluid in the lungs
→ heart unable to pump blood away - reduced systemic blood circulation, blood pools in atria and lung blood vessels
→ build up of pressure in lung capillary - increases capillary pressure
Ventricular fibrillation → completely chaotic rhythm, heart quivering - not ejecting any blood
→ ECG has no certain peaks
34
How is myocardial infarction diagnosed?
History → heavy, crushing chest pain radiating down left arm (nervous supply to heart and left arm in the same spinal segment)
Unrelated to exercise - pain exists after exertion
Associated with nausea and vomiting, sweating
ECG changes
Biochemical markers
35
What is the characteristic change to ECGs during myocardial infarction?
ST elevation - ST interval above baseline
STEMI → ST-segment elevation MI
ECG measures flow of current - when there is no flow the line is at baseline
→ if areas of heart aren't depolarised or have short AP current will flow
Within hours can develop abnormal Q wave - can be present throughout life (Q-wave infarctions)
36
What are the biochemical markers used to determine myocardial infarction?
Troponins → part of the muscle, involved in coupling of actin to myosin - regulate muscle contraction
→ cardiac muscle dying - release of troponins into blood
Two isoforms specific to myocardium: T and I
T → structures and maybe expressed in skeletal muscle *in utero*
I → catalytic and only ever in myocardium
Can detect very small infarctions (~0.003g non-STEMI)
→ measures 12 hours after infarction
→ long time to return to normal levels - cannot detect re-infarction
37
How is myocardial infarction treated?
1. Confirm diagnosis (ECG and biomarkers)
2. Relieve ischemic pain
3. Stabilise hemodynamic abnormalities - ensure blood flow to organs
4. Save as much myocardial tissue as possible
→ oxygen, diamorphine, aspirin, GTN (vasodilator), thrombolytic drugs, surgery (angioplasty/coronary bypass surgery)
Long term → aspirin/warfarin, beta blockers, ACE inhibitors, statins
38
How does recovery from MI occur?
MI causes dead figures and non functions sections of myocardium
→ area of dead fibres enlarges
→ non-functional muscle recovered - collateral blood flow
→ respiration of dead tissue by macrophages
→ fibrous tissue develops
→ gradual progressive contraction of fibrous tissue over years
→ hypertrophy of normal areas to compensate
→ recovers either partially/completely within a few months
Often pumping capacity permanently reduced
→ normal cardiac reserve 300-300% more blood/min than at rest
→ reserve may be reduced to 100%, but still function normally
39
What is angina pectoris (stable angina)?
Cardiac pain due to insufficient blood supply to the heart during increased load (exercise)
→ pain felt beneath upper sternum over the heart - also left arm, shoulder, neck, side of face
→ lasts 2-10 minutes
→ common in the cold and after large meals
→ released by rest and GTN
→ described as pressure, tightness, burning
Caused by partial occlusion of blood vessels due to fixed obstructive atheromatous plaques
→ imbalance of the demand for oxygen and the supply
Diagnosed → patient history, changes to ECG during attack, stress test, angioplasty, nuclear imaging
40
How is stable angina treated?
Balance O2 supply with demand - most agents work by reducing myocardial demand
Vasodilators → NO donors, calcium channel blockers
→ major effect - dilation means less blood comes back to heart - reduce stroke volume - heart has to do less work
→ reduced myocardial oxygen demand
Beta blockers → reduce heart rate
→ block sympathetic enhancement of heart rate and cardiac metabolism during exercise
Surgical intervention → aortic-coronary bypass surgery
→ coronary angioplasty - inflating balloon catheter in a vessel - stent keeps arteries open, contains drugs to prevent plaque growth around it
41
What is unstable and variant angina?
Plaque partially occluding vessel - thrombus periodically attaches
→ causes complete occlusion - pain
→ central pain radiating to the neck, jaw or arms - heavy crushing
→ 10-20 mins
→ onset with progressively less exercise or at rest - not associated with exercise
→ relieved by GTN
→ non-STEMI - short lived - no real pattern
42
What is heart failure?
Failure of the heart to pump enough blood to satisfy the requirements of the body
→ acute (come on quickly) or chronic (over several years)
→ clinical syndrome: characteristic pattern of harm-dynamic, renal, neural and hormonal responses
→ a multisystem disorder
43
What causes heart failure?
Diminished coronary blood flow → ischemic heart disease, damages part of the heart - pumps inefficiently
Damaged heart valves → reduce cardiac output
Thyrotoxicosis → too much thyroid hormone
Vitamin B deficiency
Cardiac muscle disease
44
What are the acute effects of moderate heart failure?
Sudden damage (MI)
→ reduced cardiac output (fatigue) - not enough blood and O2 to muscles
→ fall in arterial pressure
→ damming of blood in veins (congestion) - blood returning to heart but heart can't pump away
Compensation methods kick in → body can deal with mild heart failure by evoking some compensation methods
45
What are the sympathetic reflexes to compensate for heart failure?
Baroreceptor reflex → diminished arterial pressure
Central reflexes and reflexes from damaged heart
Sympathetic nervous system stimulated - parasympathetic inhibited
Two major effects:
→ direct effect on the heart - positive inotropic and chronotropic (speeds up)
→ increases venous return (vasoconstriction) - raising systemic filling pressure so more blood coming back to the heart - increased right atria pressure and increases cardiac output
Fall in cardiac output so body tried to increase cardiac output and BP
46
What does Starling's curve show?
As you increase filling pressure in the heart you get a bigger cardiac output
Stretching muscle of myocardium → push out more blood
47
What effect does the sympathetic nervous system have on Starling curves in response to heart failure?
Fall in BP due to lack of cardiac output
Shifts curve right → increase in filling pressure - more blood returning to heart due to vasoconstriction
Shifts curve up → increased contractility increases efficiency of pumping - for a given pressure you get a bigger cardiac output
48
How to compensation mechanisms help with heart failure in general?
Push heart to work harder
→ help to compensate in the short-term
→ although heart failing still pushed - can worsen condition
49
How is fluid retention used to compensate for heart failure?
Retention of fluid by kidneys
Effects of aldosterone and anti-diuretic hormone (ADH)
Increase blood volume increases venous return
Increased systemic filling pressure
Reduced venous resistance which eases flow of blood to the heart
→ moderate fluid retention is beneficial - large amounts are not
50
How do compensation methods increasing right atrial pressure work in a healthy heart compared to damaged hearts?
In a healthy heart increasing right atrial pressure massively increases cardiac output to a plateau → big cardiac reserve utilised by increasing filling pressure
In a partially recovered heart the effect on cardiac output is more gradual but can compensate → there is no cardiac reserve - at rest looks normal but exercise creates problem
In damaged hearts and acutely damages hearts the effect on cardiac output is even slower and cannot fully compensate
51
What effect does congestive heart failure have on cardiac reserve?
Cardiac reserve - the ability of the heart to increase cardiac output in response to increased demand e.g. during exercise or stress
→ in healthy individuals this is 300-400%
→ inherit failure this is greatly reduced - patients fine at rest but exercise creates problems
→ due to muscle weakness reducing contractility - also impairs ability to refill
Can be seen with a stress test: treadmill
→ shortness of breath
→ muscle fatigue (muscle ischemia)
→ excessive increase in heart rate
52
What happens with severe cardiac failure?
If the heart is severely damages then no amount of compensation can produce adequate cardiac output
→ fluid is continually retained because of inadequate kidney perfusion
→ patient develops oedema and this state can eventually lead to death
Sympathetic stimulation increases atrial pressure thus cardiac output
Fluid accumulation also increases atrial pressure
→ does reach the critical cardiac output level for normal fluid balance
Then heart muscle overstretches → oedema of heart muscle, fall in cardiac output - not enough O2 to organs
Cardiac output very low but atrial pressure very high
53
What 3 effects does long term fluid retention have?
Three causes of reduced renal urine output
1. Decreased glomerular filtration → decreases in atrial pressure
2. Renin-angiotensin system → constriction
3. Aldosterone secretion → retain fluid
54
How is reduced kidney perfusion compensated?
Fall in pressure of blood perfusing kidney detected
Increases renin secretion from kidneys → activates RAAS cascade leading to angiotensin II (vasoconstrictor) production constrict vessels - increasing peripheral pressure and venous tone (push blood back to heart to increase CO)
→ angiotensin II also stimulates aldosterone - promotes sodium and water retention, expands ECF and plasma volume increasing filling pressure
Sympathetic nervous system activated → increase in frequency of impulses, norepinephrine and epinephrin released - vasoconstriction
→ also stimulates renin secretion
55
What is unilateral left heart failure?
Blood is pumped to lungs normally (right side normal)
But left side not pumped effectively
→ rise in mean pulmonary filling pressure
Pulmonary capillary pressure increases
→ once above ~28 mm Hg - fluid pushed out capillaries and enters lung interstitial space and alveoli
Leads to pulmonary vascular congestion
→ can't breath
or pulmonary oedema
→ bubbling rales, dyspnea, orthopnea
56
How is acute pulmonary oedema treated?
Rapidly flowing oxygen
Rapidly acting diuretic → remove liquid so can breathe again
→ furosemide - potent works on loop of Henle
Propped up position
In extreme:
→ rotating tourniquets (arms and legs) to sequester blood and decrease workload on left side of heart
→ bleed the patient
57
What are the signs/symptoms of chronic heart failure?
A cough
Shortness of breath on exertion
Shortness of breath at night (nocturnal dyspnea)
Otheropnea (lie down - can't breathe)
Mild oedema (swollen ankles)
Unusual fatigue (reduces perfusion of skeletal muscle)
A swollen jugular vein in the neck
Adcites (accumulation of fluid in the abdomen)
Diagnosed → a third heart sound or a loud P2
→ enlarged heart seen with chest X-ray or echocardiogram
→ no ECG specific features
58
What is the New York Heart Association classification?
4 causes of heart failure for easy communication
NYHA class 1 → little or no limit of physical activity
NYHA class 2 → dyspnea and palpitations/increased heart rate with ordinary physical activity, comfortable at rest
NYHA class 3 → marked limitation of physical activity, comfortable at rest, dyspnoea while getting in/out of bed
NYHA class 4 → unable to carry out physical activity, dyspnoea at test and rapid/irregular heart beat, many physical activity increases discomfort
59
What are the aims of treating chronic congestive heart failure?
→ relive symptoms
→ improve exercise tolerance - can lead a normal life
→ reduce acute exacerbations
→ reduce mortality
treated by:
→ life style changes
→ first line treatment: ACE inhibitors/angiotensin-II receptor antagonists, beta-adrenoreceptor blockers
→ second line treatment: aldosterone antagonist, cardiac glycosides
→ used alone or in combination
60
How do ACE inhibitors and angiotensin II receptor antagonists (-sartan) work to treat heart failure?
Reduce peripheral resistance (afterload)
Reduce blood volume (preload) via reduction in aldosterone release
Increase blood [K+] counteracting lord via diuretics
Helps to prevent cardiac remodelling - reduce increase in heart size
Strong evidence that increase survival
→ remove compensation mechanisms - can shift along plateau of starling curve for a bit before being below necessary cardiac output - no symptoms
→ reduces heart workload as compensation methods make heart work harder
61
How to beta-blockers (-lol) work to treat heart failure?
Reduce heart rate and contractility
Reduce work of heart and slow disease progression
Reduce renin-angiotensin-aldosterone
Some also block alpha receptors on blood vessels - vasodilaton
Start at low dose and slowly titrate
Only use in stable heart failure
62
How do diuretics work to treat heart failure?
Mild diuretics (thiazide) → mild heart failure
Loop diuretic (furosemide) → severe heart failure
→ reduce blood volume
→ hypokalaemia (loss of K+) is a potential problem
63
What are not first line therapies for heart failure?
Aldosterone antagonists → spironolactone, reduce mortality but linked to hyperkalemia
Cardiac glycosides → increase contractility of the myocardium, block Na+/K+ exchange leading to greater Ca2+ influx
→ for patients with CHF and atrial fibrillation
→ or with worsening or severe heart failure due to left ventricular systolic dysfunction despite ACE inhibitor, beta-blocker and diuretic therapy
64
What are the types of trials involved with testing medication efficiency for heart failure?
Consensus trial → enalapril reduces progression, improves symptoms
SOLVD trial → enalapril in asymptotic LV dysfunction reduce incidence of hospitalisation
Charm trial → candersartan reduced mortality in CCF
DIG → digoxin reduced CCF hospitalisation but not mortality
RALES → spironolactone reduces mortality and symptoms in NYHA class 3 patients
Evidence based medicine → trials to see if the medical treatments working as we think they might
65
What is intractable heart failure?
Heart failure you can't treat with medication
→ requires transplantation
→ can be on ventricular assist device (VAD) while they wait for transplant
66
What is the conduction pathway through the heart?
Beat arises in the SA node (native pacemaker) → AV node → bundle of His → purkinje fibres → ventricles
67
What are latent pacemakers?
Cells which have the potential to generate electrical impulses
Normal heart rate (SA node) → 60-100 BMP
Latent (ectopic pacemakers):
AV node → 50-60 BMP
Bundle of His → 50-60 BMP
Purkinje fibres → 30-40 BMP
→ if heart rate driven by these it beats too slowly - overridden by SA node
68
How is the cardiac impulse transmitted?
From SA node spreads rapidly through the atria - 30ms
→ delayed at the atria for 0.1s - 130ms
→ spreads through bundle of HIs via Purkinje fibres to endocardial surfaces of ventricles 30-40ms
69
Why is there a delay of the cardiac impulse at the AV node?
You don't want the atria and ventricles to contract at the same time
→ allows for ventricles to fill
70
How is heart rate controlled?
The heart is myogenic - it produces its own beat
In the SA node membrane potential doesn't just sit flat - slowly depolarises due to gradual ion influx
→ reaches threshold then AP fires
→ AP carried by Ca2+ influx, then K+ efflux on repolarisation
The gradient of depolarisation determines rate of the heart
→ the autonomic nervous system can control this
→ sympathetic activity opens channels - steeper gradient - increased heart rate
→ parasympathetic (vagal activity) - decreases channels - gradual gradient - reduces heart rate
71
How is heart rhythm measured?
ECG - electrocardiogram recording
→ records changes in current flow
Started with patient with hands in jars of salt solution
Now 12 lead ECG
→ 6 chest leads, 6 limb leads
→ looking at heart from different angles
72
What are the components of an ECG recording?
P wave → depolarisation of atria
QRS complex → depolarisation of the ventricles
T wave → repolarisation of the ventricles
QT interval → duration of cardiac action potential, ventricular systole
RR-QT → diastole
Heart rate → (n-1 / dt) x 60, n = number of r waves, dt = time between them
Current flow too small to detect in; SA node, AV node, bundle of His, bundle branches and purkinje fibres
73
What is a cardiac arrhythmia?
Any change from 'normal' sinus rhythm
→ some are okay and others potentially life threatening
74
What are the causes of arrhythmias?
1. Increased sinus node automaticity → tachycardia
2. Decreased sinus node automaticity → SA node depolarising too slowly
3. Escape rhythms → beating from another pacemaker
4. Enhanced automaticity of latent pacemakers (ectopic beats/rhythms) → heartbeat coming from another site
5. Triggered activity (after depolarisation) → 2nd beat after, hypokalaemia (low K), drug toxicity
6. Conduction abnormalities → areas of the heart that can't conduct
7. Unidirectional block and re-entry → very fast heart beat
75
What is sinus tachycardia?
Heart rate faster than normal > 100BMP, 100-180
→ still in rhythm
→ still driven by SA node
→ decreased vagal or increases sympathetic tone
→ seen in frightened individual or during normal exercise
→
Can be pathological: acute hyperthyroidism, heart failure, haemorrhage, fever, anaemia, hypovolepia, drug induced
→ never 'treat' sinus tachycardia, treat the cause of it
76
What is sinus bradycardia?
Heart rate slower than normal < 60BMP
→ normal during sleep/fit athlete
Can occur:
→ following MI (blood supply to SA node interrupted)
→ drug induced (beta blockers, digoxin)
→ hyperkalemia, hyperthyroidism, hypothermia
Tolerate as low as 45 BMP
Treat underlying condition, stop medication
77
What is sinus arrest?
Missing beats → occasionally so PQRST complex, otherwise normal ECG
Sinus pause → 1-2 missing beats, arrest (3 or more)
Maybe no symptoms
Causes: drug induces, MI, SA disease, increased vagal tone
78
What is sick sinus syndrome?
SA node fails to excite the atria in a regular manner
→ resulting in a slow resting heart rate
→ heart rate does not increase with exercise
→ can be: drug induced, intense vagal activity, degeneration of the pacemaker following schema
Treated → by insertion of artificial pacemaker - gives heart a shock
79
What is sinus arrhythmia?
Normal phenomenon → subtle change in heart rate with each respiratory cycle
→ speeding and slowing of the heart during breathing - expiration slows heart rate
→ normal in children and young adults, disappears with age
→ fluctuations in vagal activity
80
What are premature ventricular contractions (PVCs)?
Ventricles contracting separate from beat
→ can vary from 0.5% to 3% of the normal heart beats in 24 hours
→ % of PCVs typically increases with age
Triggers: medications that have a stimulant effect on the heart, caffeine, alcohol. illicit drugs, states of heightened sympathetic activity like stress or exercise
81
What are the 2 major causes of conduction abnormalities?
1. Depolarisation → tissue depolarised if injured
→ need an intact semi-permeable membrane for resting membrane potential
→ depolarised tissue - inactivation of Na and K channels - can't conduct well
→ less excitable (partial block), completely inexcitable (complete conduction block)
2. Abnormal anatomy → presence of aberrant conduction pathway
→ e.g. can bypass AV node which normally imposes conduction delay
→ second conduction pathway between atria and ventricles predisposes to supra ventricular arrhythmias
82
What is Wolff-Parkinson-White syndrome?
A cardiac arrhythmia disorder - an accessory pathway in the heart that allows the electrical current to bypass the AV node
→ beat can go backwards into atria - excites atria, another beat can go prematurely to the ventricles - creates strange QRS complex
→ loop of activity can lead to tachycardia
83
What is first-degree block?
Slowed conduction through AV node → long PR interval
→ structural defect or transient influence
→ still 1:1 relationship with P and QRS
Benign condition → many young people show this pattern, especially during sleep, when there is high vagal tone, does not require treatment
84
What is second-degree block?
Periodic failure at AV node - intermittent block
Mobitz type I → slow lengthening of PR interval until AV node fails completely - beat failure
→ atrial rhythm regular
→ benign condition, no specific treatment, symptoms rare; dizziness, syncope
Mobitz type II → PR interval consistent, but every nth cycle ventricular depolarisation is missing, failure of AV - no QRS
→ may progress rapidly to complete heart block
85
What is branch bundle block?
One of the bundle of His fails - ventricular conduction fails often at high heart rate
→ still get contraction of whole heart as myocardium coupled - not as efficient
→ slow depolarisation - wide QRS
Right branch bundle block → dip in QRS below baseline
→ occurs in conditions such as blood clots to the lung, chronic lung disease, cardiomyopathy and atrial/ventricular septal defects
Left branch bundle block → small dip in QRS
→ usually indicates underlying cardiac pathology - seen in dilated cardiomyopathy, hypertrophic cardiomyopathy, hypertension, aortic valve disease
→ more dangerous, not as often seen in healthy people
86
What is this degree (complete) block?
Complete block at AV node → don't trigger ventricular contraction
→ failure of conduction between atria and ventricles
→ ventricles beat via latent pacemakers
→ no relationship between PR waves and QRS
→ P waves regularly spaced, QRS irregular
caused by: acute MI, drug toxicity, chronic degeneration with age
Escape rhythm → a heart rhythm initiated by lower centres when the SA node fails to initiate impulses
Symptoms → bradycardia, signs of congestive heart failure (decreased cardiac output), signs of hyper fusion - mental confusion, lethargy -
87
What is unidirectional block and re-entry?
An area of damage to heart muscle which is non-conducting with a unidirectional block
→ only allows AP of beat to move in one direction
Can create re-entrant circuit - slowed retrograde conduction velocity
88
What is atrial flutter?
Rapid regular atrial activity (180-350 BMP)
→ many impulses reach the AV node but do not conduct to ventricles
→ caused by re-entry over anatomically fixed circuit, ectopic focus -beat going round and round atria
→ can be transient or permanent
→ risk of atrial thromboembolism - atria don't eject block well, possible clotting
Treatment : electrical cardio version,pacemaker, pharmacological therapy, catheter ablation
89
What is atrial fibrillation?
Chaotic rhythm atrial rate (350-600 discharges PM)
→ P waves so quick don't see falls and rises - wobbly base line
→ ony some reach ventricles - ventricular rate 140-160 BPM
→ due to wandering re-entrant circuits
Causes: enlarged atria, heart failure, hypertension, CAD, thyrotoxicosis, alcohol
Dangerous → rapid ventricular rates reduce cardiac output, blood stasis can lead to thrombus/emboli
Treatment → anti arrhythmic drugs, electrical cardio version, catheter ablation, maze procedure
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What is ventricular tachycardia?
Rapid heart rhythm originating from the ventricles
→ sustained or not sustained
→ structural heart disease, MI, heart failure
→ wide QRS, 100-200 BPM
→ regular (monomorphic): re-entrant circuit in ventricle
→ irregular (polymorphic): delayed repolarisation long QT
Symptoms: syncope, pulmonary oedema, cardiac arrest
Dangerous → can deteriorate into ventricular fibrillation
Treatment: electrical cardio version, IV anti arrhythmic drugs
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What is ventricular fibrillation?
Disordered rapid stimulation of the ventricles (quiver but don't contract)
→ life threatening
→ loss of cardiac output
Causes: heart disease, low K+, electric shock, some drugs
Often initiated by episodes of ventricular tachycardia
Treatment: prompt electrical defibrillation, IV antiarrythmic drug to prevent recurrence, survivors may receive ICD (implantable cardioverter defibrillator)
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What is congenital long-QT syndrome?
Prolonged ventricular depolarisation
→ many different types
→ different mutations (many in K+ channels) - heart not repolarised properly
→ can be asymptomatic
→ can lead to ventricular arrhythmias
→ SADS - sudden arrhythmic death syndrome
Cardiac AP very wide
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