What is angina?
A restriction in blood supply (most often talked about in heart but can even occur in the mouth!)
What is abdominal angina?
Post prandial (after eating) abdominal pain
What is ludwig's angina?
A serious infection of the floor of the mouth
What is vincent's angina?
trench mouth and necrotic gum tissue
What is angina tonsillaris?
An inflammation of the tonsils
What is herpangina?
Pharyngeal blisters caused by Coxsackie A virus or echovirus
What is angina pectoris?
Pain localised to the chest
Acute or chronic (on tablets)
What causes angina?
Restricted blood supply = increased metabolite build up = decreased oxygen supply and increased cardiac work
narrowing of the coronary artery (atheroma, thrombus etc.)
vasospasm of the coronary artery (overly reactive vessels and drugs - e.g. cocaine & smoking)
severe anaemia (cannot carry enough oxygen to the heart)
What are the 3 types of angina pectoris?
Chronic stable = exercise induced -> normally take medication
Unstable = sudden rupture of athleroscelrotic plaque -> blocks down stream arteries
Prinzmetal's (angina inversa) = vasospasm = oversensitivity to vasoconstrictors
From which age do athlerosclerotic plaques start to build up from?
10 years old
What are the risk factors for coronary heart disease (8)?
- Family history
- high blood pressure
- High LDL cholestrol & low HDL cholestrol
- Lack of regular exercise
What is coronary heart disease?
Athlerosclerosis in the coronary arteries
(most common cause of death in UK)
Which is more important... having good (LDL) or bad (HDL) lipoproteins or having the right balance of LDL and HDL?
Having the right balance
What happens to the HDL:LDL ratio with age?
Decreases = increased MI risk
What happens to HDL:LDL ratio with statins?
Increases = less MI risk
(although other drugs that increase the ratio )
Does eating fewer saturated fats in your diet increase or decrease your risk for CHD?
Decrease because less obese!
What are the 3 stages of developing atheroma?
- Damage to epithelia
- Cholesterol accumulation = inflammatory response -> produces foam cells
- Foam cell degeneration = increased stiffness of artery wall = shear stress = continued worsening damage
What causes activation of platelets?
- contact with intima matrix (sheds microparticles = attracts monocytes = proliferate & differentiate = phagocytes)
What is a coronary artery bypass graft?
takes a blood vessel from another part of the body
List 3 alternative treatments for surgical treatment of atheroma:
- Rotational bur
- Stent (wire coil)
What diastolic blood pressure is required for someone to be hypertensive?
What are the potential complications of hypertension (6)?
- Stroke (athlerosclerosis)
- kidney disease
- eye disease
- pre-eclampsia (hypertension & protein in urea, swelling of feet, ankles, face & hands, severe headache, vision problems & pain just below ribs -> occurs if problem with placenta)
- erectile dysfunction
What is primary hypertension:
what % of cases does it make up?
What are its two main causes?
- 90-95% cases (essential/idiopathic)
- obesity (BMI>25)
What is secondary hypertension:
what % of cases does it make up?
What are the 4 main causes?
- 10% of cases
- renal/renovascular disease
- endocrine disease (e.g. phaeochomocytoma- tumour of adrenal medulla, cushings syndrome - excess cortisol, acromegaly - excess aldosterone, hypo/hyperthyroidism, pregnancy)
- coarcation of aorta (malformation of aorta)
- iatrogenic (hormonal/oral contraceptive & NSAIDs)
What are the consequences of hypertension?
Hypertrophy of ventricular (esp. left) wall -> muscle has to work harder for long time = increased risk of sudden cardiac death
What does ALLHAT trial stand for?
The antihypertensive and lipid lowering to prevent heart attack trial
why in the ALLHAT trial was the alpha blocker doxazosin discontinued?
There was an excess no. of deaths
In the ALLHAT trial what was discovered about the efficacy of the following drugs:
Thaizide diuretic (chlorthalidone)
ACE inhibitor (lisinopril)
Ca channel blocker (amlodipine)
All of equal efficacy
Which type of diabetes is hypertension often found in conjunction with?
Which % of type II diabetic patients die from cardiovascular disease?
Which % of type II diabetes patients are obese?
Which % of type II diabetic patients need polypharmacy to achieve tight control of their hypertension?
What is polypharmacy?
using low doses of different drugs to produce a synergistic effect on blood pressure and have few side effects (each drug has its own unique side effects)
What are arrhythmias?
Regional differences in action potentials between nodal tissue, atria and ventricles
What depolarises in the PQ wave?
the atria & AV node
What depolarises in the QRS complex?
what repolarises in the T wave?
What happes in phase 4? (DIASTOLIC)
NaK pump = inward flow of K+
Na channel closed
= gradual depolarisation of cells
What happens in Phase 0?
Na channels open = inward influx of Na = rapid depolarisation
What happens in phase 1?
= transient outward current
Cl current = SNS regulated
What happens in phase 2?
Plateu = balance of electrical charges (outward K current = inward Na & Ca current -> NaCa exchanger)
What happens in phase 3?
= increased K currents & inactivation of inward Na & Ca currents
What is a 'normal'/sinus arrhythmia?
Variations in heart rate with breathing (originate from SAN = normal conduction)
No cause for concern unless rate changes are extreme! Treatment not needed!
What is atrial flutter?
Atrial rentry without conduction block (not every p = qrs) -> cannot repolarise until after a contraction has occured
What is atrial fibrilation?
irregular but on finer physical state than flutter
What is paroxymal supraventricular tachycardia?
Episodic ventricular tachycardia from nodal re-entry
What is ventricular tachycardia?
High ventricular rate (atrial driven or re-entry) e.g. after ischaemic heart disease -> heart failure
What is polymorphic ventricular tachycardia?
Ventricular tachycardia with unstable (changes with time) ECG
What is ventricular fibrillation?
- frequently follows polymorphic ventricular tachycardia
= fine re-entry = fatal! Completely unco-ordinated pumping of the heart = no blood pumped (CPR helps in this case)
What are the main 3 causes of arrythmias?
- Abnormality in action potential
(genetic, drugs, ischaemia, electrolyte disturbances)
- Abnormality in conduction
(anatomy, ischaemia, electrolyte disturbances, secondary to AP and electrial activity)
- Abnormality in excitability
(increased sympathetic drive & surgery)
What does EAD stand for?
Early after depolarisation
What is an EAD?
the heart is reactivated (it fails to depolarise fully = longer action potential = increased following refractory period following contraction)
What does DAD stand for?
Delay after depolarisation
What is a DAD?
spontaneous Ca release inside cell = too much Ca = activates Ca/Na exchanger = another depolarisation
How can purkinje fibres cause a ectopic focus?
Anterograde movement of abnomal electrical activity = interferes with normal conduction & heart contraction
What is a unidirectional block?
A cell can only depolarise other cells it is touching
What is re-entry?
Re-entered beat passes the conduction defect before the next normal beat = cycles & changes rhythm of heart
What is a circus rhythm?
A region of slow conduction = part of AP reaches tissue after its conducted (after the refractory period) = second small AP
How can we correct unidirectional blocks, re-entry and circus rhythm?
= forces depolarisation of tissue = total resynchronisation (if timing is wrong must reapply!)
Which 4 things determine the refractory period (4)?
Average membrane potential (recruitment of ion channels -> must return to resting)
Recovery time of Na channel
What are the 6 mechanisms of anti-arrhytmic drugs?
Stop automaticity (the tissue becoming a pacemaker):
- Increase membrane threshold
- Hyperpolarise membrane
- Block sympathetic activity
- Inhibit Na & Ca entry
- Convert unidirectional block to bidirectional block
- Abolish unidirectional block
What is the mneumonic for Antiarrhythmic drugs?
Quick Lids Flecking At Amiable Dilatants
Quinone Lidocaine Flecainide Atenolol Amidorone Diltiazem
What type of drugs are 1a, 1b & 1c?
Na channel blockers
What type of drugs is II?
What type of drug is III?
K channel blocker
Which type of block is IV?
Ca channel blocker
How does magnesium effect electrical activity?
Decreases Ca reentry through sarcolemma
= ATP binding agent
n.b. magnesium levels are decreased in ischemic cells = ventricular arrhythmias
How does Adenosine effect electrical activity?
Increases K in atrial tissues
What is adenosine used for?
Used for supraventricular tachycardia
What are the side effects of adenosine?
transient flushing & breathlessness
What is the sicilian gambit?
Anti-arrythmic therapy logically based on know sites of action of a drug and arrhythmias mechanism (pattern recognition)
What is a syndrome?
a number of associated symptoms
What are the 6 main characteristics for heart failure?
- Progressive cardiac dysfuntion
- Neurohormonal disturbances (e.g. corticotropin releasing hormone, vasopresssin, growth hormone releasing hormone)
- Odema (pitting odema = press thumb firmly & doesnt bounce back)
- sudden death
What % of the population odes heart failure effect?
Why does the risk of heart failure increase with age?
Loss of ability to repair itsnelf
What are the causes of heart failure (4)?
Volume overload (valve regurgitation)
Pressure overload (systemic hypertension/outflow obstruction)
Loss of muscle (post MI, chronic ischaemia, connective tissue diseases, infection & poisons)
Restricted filling (pericardial disease = stiff heart, restrictive cardiomyopathy & tachyarrhythmia)
What is the 5 year mortality rate for heart failure?
In which two ways can you determine increased right atrial pressure?
Distended jugulars in neck
Peripheral odema (pulmonary)
What is the outcome of increased right atrial pressure (3)?
Inadequate tissue perfusion (stress causes heart dilation = decreased coronary output)
Cardiac remodelling (enlarged ventricles, spherical shape & decreased efficiency of contraction = easier to distend further)
What are the two main treatment aims?
Which drugs do we use to improve the symptoms of heartfailure (3)?
Diuretics (decrease blood volume)
Angiotensin Converting Enzyme (ACE) inhibitors
Which 3 drugs do we use to improve survival for heart failure patients?
List 3 classes of inotropic drugs:
Cardiac glycosides (e.g. digoxin) = cardiotonic steroids
Sympathomimetics e.g. dobutamine
List 5 adrenoreceptor sympathomimetics:
- Adrenaline (β > α)
- Noradrenaline (β1=α1 > β2=α2)
- Dopamine (β1=β2 > α1)
- Dobutamine (β1 > β2 > α1)
- Isoproterenol (β1=β2)
What is the effect of adrenaline at low dose?
What is the effect of adrenaline at high dose?
What are 3 clinical uses of adrenaline?
What are 2 clinical uses of noradrenaline?
What can reflex bradycardia mask?
direct stimulation on SAN
What are 3 clinical uses of dopamine?
Acute heart failure
Acute renal failure
what does a low dose of dopamine cause (2)?
Decreased vascular resistance
what does a high dose of dobutamine cause?
n.b. = vasodilation in kidneys via D1 receptors
What are 3 clinical uses of dobutamine?
Acute heart failure
Refractory heart failure
What does dobutamine do?
Cardiac stimulation with modest vasodilation
What are 2 clinical uses of isoproterenol?
What are the effects of isoproterenol?
Vasodilation with little change in pressure
When are sympathomimetics used to treat heart failure?
Last ditch treatment for those in hospital awaiting a transplant
When are transduction sympathomimetics useful?
When other therapies fail (no real benefit over other treatment and 27% increase in morbidity)
When are loop diuretics useful in treating heart failure?
Pulmonary and refractive odema
What are the side effects of loop diuretics (4)?
What is the action of thiazide diuretics?
Distal tubule = direct vasodilator
What are the 2 side effects of thiazide diuretics?
When are K sparing diuretics useful in heart failure?
control K loss (aldosterone antagonist)
What are the side effects of K sparing diuretics (2)?
Oestrogen like effects (with spirolactone)
What do ACE inhibitors control?
What are the side effects of ACE inhibitors?
Why are angiotensin II receptor blockers preferable to ACE inhibitors (3)?
No cough (no effect on bradykining)
What is the key side effect of angiotensin II receptor blockers?
tetragenic (birth defects)
n.b. it also has less vasodilation than ACE