Pathology of the Cardiovascular System (8-11)

Question 1

What is hypertension?

Answer 1

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)

Question 2

How is blood pressure measured?

Answer 2

Arterial blood pressure is normally measures in the brachial artery in arm
→ Ambulatory blood pressure monitoring (ABPM) - 24hour blood pressure measurement

Question 3

What is white coat hypertension?

Answer 3

When you blood pressure is abnormally high
→ due to anxiety around doctors

Can be overcome with home BP measurement but they’re not calibrated

Question 4

What are you measuring when you take a blood pressure?

Answer 4

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

Question 5

What is mean arterial pressure?

Answer 5

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

Question 6

What are the causes of hypertension?

Answer 6

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

Question 7

Why treat hypertension?

Answer 7

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

Question 8

What are the symptoms and signs of hypertension?

Answer 8

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

Question 9

How is hypertension managed?

Answer 9

1. Patient education/lifestyle changes
   → stop smoking, los of weight, exercise, reduce salt intake, diet, relaxation therapy
2. Drug treatment
3. Surgery (for secondary causes if appropriate)

Question 10

What is the effect of weight on blood pressure?

Answer 10

Weight and blood pressure are linked
→ its likely that weight interacts with various factors controlling blood pressure at different points over a lifetime

Question 11

What determines blood pressure?

Answer 11

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

Question 12

What are the two major mechanisms for controlling blood pressure?

Answer 12

1. Barorectpor/sympathetic nervous system
   → controls BP minute to minute
2. ECF volume/plasma renin activity
   → longer term effects

Question 13

What is the baroreceptor reflex?

Answer 13

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

Question 14

What things can you aim to change to reduce blood pressure?

Answer 14

1. 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
2. Reduce total peripheral resistance
   → vasodilators
   → calcium channel antagonists
   → ACE inhibitors
   → angiotensin II receptor antagonists
   → alpha-adrenoceptor blockers

Some drugs to both

Question 15

How do ACE inhibitors and angiotensin II receptor antagonists work?

Answer 15

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

Question 16

What are the effects of angiotensin II?

Answer 16

→ 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

Question 17

What are some examples of ACE inhibitors?

Answer 17

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)

Question 18

What are some examples of angiotensin II receptor antagonists?

Answer 18

Ending in -sartan → losartan, candesartan, valsartan, ibesartan
→ well tolerated side effect profile
→ once daily dosing
→ cost effective

Question 19

What are calcium channel antagonists?

Answer 19

Block Ca2+ channel in muscles - needed for contraction
→ cause vasodilation - reduce peripheral resistance

For hypertension: dihydropyridines - nifedipine, amlodipine

Side effects → headache, flushing, ankle swelling

Question 20

What are thiazide diuretics?

Answer 20

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

Question 21

What are beta adrenoreceptor blockers?

Answer 21

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
→

Question 22

What is the coronary circulation?

Answer 22

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

Question 23

Why is there phasic blood flow through the coronary circulation?

Answer 23

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

Question 24

How is coronary blood flow reduced?

Answer 24

Reduction in diastolic interval (e.g. during exercise)

Rise in ventricular end-diastolic pressure

Fall in arterial pressure

Question 25

How do you change coronary blood flow?

Answer 25

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

Question 26

What is the major cause of ischemic heart disease?

Answer 26

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

Question 27

What are the different types of coronary syndromes caused by different atherosclerotic plaques?

Answer 27

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

Question 28

What is myocardial infarction?

Answer 28

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

Question 29

What causes myocardial infarction?

Answer 29

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

Question 30

What is the myocardial infarction process?

Answer 30

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

Question 31

How does ischemia lead to myocardial cell death?

Answer 31

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

Question 32

What is collateral circulation?

Answer 32

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

Question 33

How does myocardial infarction cause death?

Answer 33

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

Question 34

How is myocardial infarction diagnosed?

Answer 34

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

Question 35

What is the characteristic change to ECGs during myocardial infarction?

Answer 35

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)

Question 36

What are the biochemical markers used to determine myocardial infarction?

Answer 36

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

Question 37

How is myocardial infarction treated?

Answer 37

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

Question 38

How does recovery from MI occur?

Answer 38

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

Question 39

What is angina pectoris (stable angina)?

Answer 39

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

Question 40

How is stable angina treated?

Answer 40

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

Question 41

What is unstable and variant angina?

Answer 41

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

Question 42

What is heart failure?

Answer 42

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

Question 43

What causes heart failure?

Answer 43

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

Question 44

What are the acute effects of moderate heart failure?

Answer 44

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

Question 45

What are the sympathetic reflexes to compensate for heart failure?

Answer 45

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

Question 46

What does Starling’s curve show?

Answer 46

As you increase filling pressure in the heart you get a bigger cardiac output

Stretching muscle of myocardium → push out more blood

Question 47

What effect does the sympathetic nervous system have on Starling curves in response to heart failure?

Answer 47

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

Question 48

How to compensation mechanisms help with heart failure in general?

Answer 48

Push heart to work harder
→ help to compensate in the short-term
→ although heart failing still pushed - can worsen condition

Question 49

How is fluid retention used to compensate for heart failure?

Answer 49

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

Question 50

How do compensation methods increasing right atrial pressure work in a healthy heart compared to damaged hearts?

Answer 50

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

Question 51

What effect does congestive heart failure have on cardiac reserve?

Answer 51

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

Question 52

What happens with severe cardiac failure?

Answer 52

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

Question 53

What 3 effects does long term fluid retention have?

Answer 53

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

Question 54

How is reduced kidney perfusion compensated?

Answer 54

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

Question 55

What is unilateral left heart failure?

Answer 55

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

Question 56

How is acute pulmonary oedema treated?

Answer 56

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

Question 57

What are the signs/symptoms of chronic heart failure?

Answer 57

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

Question 58

What is the New York Heart Association classification?

Answer 58

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

Question 59

What are the aims of treating chronic congestive heart failure?

Answer 59

→ 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

Question 60

How do ACE inhibitors and angiotensin II receptor antagonists (-sartan) work to treat heart failure?

Answer 60

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

Question 61

How to beta-blockers (-lol) work to treat heart failure?

Answer 61

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

Question 62

How do diuretics work to treat heart failure?

Answer 62

Mild diuretics (thiazide) → mild heart failure
Loop diuretic (furosemide) → severe heart failure

→ reduce blood volume
→ hypokalaemia (loss of K+) is a potential problem

Question 63

What are not first line therapies for heart failure?

Answer 63

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

Question 64

What are the types of trials involved with testing medication efficiency for heart failure?

Answer 64

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

Question 65

What is intractable heart failure?

Answer 65

Heart failure you can’t treat with medication
→ requires transplantation
→ can be on ventricular assist device (VAD) while they wait for transplant

Question 66

What is the conduction pathway through the heart?

Answer 66

Beat arises in the SA node (native pacemaker) → AV node → bundle of His → purkinje fibres → ventricles

Question 67

What are latent pacemakers?

Answer 67

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

Question 68

How is the cardiac impulse transmitted?

Answer 68

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

Question 69

Why is there a delay of the cardiac impulse at the AV node?

Answer 69

You don’t want the atria and ventricles to contract at the same time
→ allows for ventricles to fill

Question 70

How is heart rate controlled?

Answer 70

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

Question 71

How is heart rhythm measured?

Answer 71

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

Question 72

What are the components of an ECG recording?

Answer 72

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

Question 73

What is a cardiac arrhythmia?

Answer 73

Any change from ‘normal’ sinus rhythm
→ some are okay and others potentially life threatening

Question 74

What are the causes of arrhythmias?

Answer 74

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

Question 75

What is sinus tachycardia?

Answer 75

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

Question 76

What is sinus bradycardia?

Answer 76

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

Question 77

What is sinus arrest?

Answer 77

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

Question 78

What is sick sinus syndrome?

Answer 78

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

Question 79

What is sinus arrhythmia?

Answer 79

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

Question 80

What are premature ventricular contractions (PVCs)?

Answer 80

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

Question 81

What are the 2 major causes of conduction abnormalities?

Answer 81

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

Question 82

What is Wolff-Parkinson-White syndrome?

Answer 82

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

Question 83

What is first-degree block?

Answer 83

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

Question 84

What is second-degree block?

Answer 84

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

Question 85

What is branch bundle block?

Answer 85

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

Question 86

What is this degree (complete) block?

Answer 86

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 -

Question 87

What is unidirectional block and re-entry?

Answer 87

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

Question 88

What is atrial flutter?

Answer 88

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

Question 89

What is atrial fibrillation?

Answer 89

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

Question 90

What is ventricular tachycardia?

Answer 90

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

Question 91

What is ventricular fibrillation?

Answer 91

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)

Question 92

What is congenital long-QT syndrome?

Answer 92

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