Flashcards in Cardiology Deck (70):
Briefly describe the ionic basic of the cardiac action potential (in the pacemaker cells of the heart)
1. The permeability of the pacemaker cells does not remain constant between action potentials - this means that there is a pacemaker potential (the line is always sloping upwards between action potential firing) This is due to less pottasium efflux, the funny current (sodium and pottasium influx) and transient calcium influx (due to T type calcium channels)
2. Once threshold is reached there is the rising phase of action potential depolarisation (caused by L type calcium influx and this causes depolarisation)
3. The following phase of action potential repolarisation in caused by inactivation of L type calcium channels and activation of pottasium channels resulting in pottasium efflux
What are the junctions that exist between cardiac myocytes?
Gap junctions - no neuromuscular junctions
What is meant by excitation contraction coupling?
The ability of the action potential to cause cardiac muscle contraction.
1. Influx of calcium through the L type gap junction causes release of stored calcium in the sarcoplasmic reticulum to be released (calcium induced calcium release)
2. This calcium then binds to the actin filaments and induces contraction
3. After the contraction calcium comes off the myolfilaments and is reabsorbed back into the sarcoplasmic reticulum
What causes the plateau phase of the ventricular muscle action potential?
Calcium influx through L type calcium channels
What is stroke volume?
The volume of blood ejected by each ventricle each heartbeat
What determines the end diastolic volume?
The venous return to the heart
What factors influence the stroke volume of the heart?
Intrinsic factors - cardiac preload
Extrinsic factors - nervous and hormonal control
What is afterload of the heart?
The resistance into which the heart in pumping (this would be increased in hypertension and result n hypertrophy
What effect does an increase in sympathetic stimulation have on the heart?
1. Increases the force of contraction (Positive inotropic effect)
2. Increases the heart rate (Positive chronotrophic effect)
What is cardiac output?
The volume of blood pumped out by each ventricle each minute
What division of the nervous system dominates the resting tone of the heart?
- Vagus nerve supplies the SA node and the AV node.
- Vagus nerve does not control the ventricles
- Vagus nerve controls the rate, not the force of contraction
How does sympathetic stimulation affect the heart? Where does it supply?
Ventricular muscle is supplied by sympathetic nerve fibres
What is a normal cardiac output?
5litres per minute
What are the five parts of the cardiac cycle?
1. Passive filling of the atria
2. Atrial contraction
3. Isovolumetric ventricular contraction
4. Ventricular ejection
5. Isovolumetric ventricular relaxation.
What valves are closing when you hear the first heart sound?
Mitral and tricuspid (the start of systole)
What valves are closing when you hear the second heart sound?
Aortic and pulmonary (the start of diastole)
What is the calculation for working out mean arterial pressure? What is the normal range?
(2 x diastolic pressure) + (systolic pressure) /3
Normal is 75 - 105.
What part of the vasculature contributes most to the regulation of blood pressure? Why?
They are heavily innervated with autonomic nerves and are sensitive to hormonal changes.
What controls the short term regulation of blood pressure (ie from lying to standing) explain this mechanims.
Baroreceptors. They are stretch receptors situated in the aortic arch and the carotid sinus and they sense changes in the blood pressure.
So if blood pressure decreases there is less firing of baroreceptors. This then induces changes in the tone of the heart (So if BP is low the vagal tone decreases and the sympathetic tone increases, causing an increase in the heart rate and the stroke volume)
What causes postural hypotension?
Failure of the baroreceptor reflex to respond to gravitational shifts in the blood.
Describe the renin angiotensin aldosterone system.
1. Renin is released from the kidney is response to low pressure in the juxtaglomerular cells in the macula densa of the kidney.
2. This causes the conversion of angiotensin (produced in the liver) into angiotensin 1.
3. Angiotensin 1 is then converted to angiotensin 2 by angiotensin converting enzyme (ACE)
4. Angiotensin 2 acts on the adrenal gland to produce aldosterone.
5. Aldosterone causes systemic vasoconstriction, thirst and increase sodium and water retention in the kidneys. It also causes the excretion of potassium in order to maintain electrolyte balance. It also stimulates the action of ADH
What is ANP and what does it do with regards to blood pressure?
1. Synthesised and stored by atrial myocytes and released in response to atrial distention. ie when you have hight blood pressure causing a high venous return to the atria.
2. Causes the excretion of salt and water in the kidneys and reduces blood pressure
3. Acts as a vasodilator
4. Decreases renin release
(Opposite of the RAAS system)
What is ADH and what does it do?
Peptide hormone synthesised in the hypothalamus and stored in the posterior pituitary.
- Stimulation by increased plasma osmolarity and reduced extracellular volume.
- Acts on the kidney tubules to increase reabsorption of water (urine is more concentrated) and this increases the extracellular and plasma volume and increases the cardiac output.
- Also causes a small degree of vasoconstriction
What is the NICE guidelines regarding a diagnosis of hypertension?
If clinic blood pressure is over 140/90 then ambulatory blood pressure (ABPM) is needed to confirm a diagnosis of hypertension.
- This consists of at least 2 measurements per hour during the waking hours
- Then hypertension can be diagnosed if the average blood pressure reading is over 135/85mmHg.
What are the definitions for stage 1, stage 2 and severe hypertenion?
Stage 1: Clinic BP over 140/90. ABPM over 135/85
Stage 2: Clinic BP 160/100. ABPM over 150/95.
Severe: Clinic BP is 180mmHg or diastolic BP is 110mmHg or higher.
What tests might you do in clinic to assess for end organ damage as a result of hypertension?
1. Test urine for protein
2. Blood to look at glucose, U & E, eGFR and cholesterol
3. Fundoscopy for hypertensive retinopathy
4. 12 lead ECG (LVH)
What are examples of things you might see on a fundoscopy of a patient with hypertension?
Cotton wool spots
What are the target blood pressures for people under 80 and over 80 being treated for hypertension?
140/90mmHg in people under 80.
150mmHg in people over 80
List some diseases than can cause secondary hypertension
1. Renal disease (eg tumour)
2. Obstructive sleep apnoea
4. Reno vascular disease
8. Aortic coarctation
9. Intracranial tumour
What is conns disease (primary aldosteronism)
Excess production of aldosterone by the adrenal glands. This results in high blood pressure, low pottasium levels and low levels of renin.
Can be due to an enlargement of the adrenal glands, adenoma or can be familial.
What is a phaechromocytoma?
Neuroendocrine tumour of the medulla of the adrenal glands that secretes high levels of catecholamines (mostly norephrine) This causes sympathetic overactivity causing high blood pressure and heart rate as well as headaches and palpitations.
What is renal artery stenosis and how does it cause secondary hypertension?
Narrowing of the renal arteriesmost often caused by atherosclerosis. This blocks that blood flow to the kidney. This means that the kidneys think the blood pressure is low and release increased levels of renin. This results in secondary hypertenion.
What are the classical symptoms of angina?
Heavy, squeezing visceral pain which occurs on exertion. It is relieved by rest and GTN.
What is stable angina pectoris?
Chest pain caused by obstruction/spasm of the coronary arteries, most often caused by atherosclerosis.
What is unstable angina?
A form of acute coronary syndrome that occurs at rest, in severe and has a crescendo pattern.
What is prinzmetals angina?
Angina caused by coronary artery spasm (tends to occur in young people and it not related to risk factors or exercise. It may be assoicted with migraine or raynauds.
What drugs might be used to treat prinzmetals angina?
Calcium channel blockers
What is the frank starling law?
The stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (EDV) This is because when the myocardial sarcomeres are stretched to higher volumes there is greater contracility of the sarcomeres.
What are sodium channel blockers, how do they work and when would they be used?
- Sodium channel blockers are part of the class 1 anti-arrhythmic drugs.
- Bind to the sodium channels that are responsible for the rapid depolarisation phase (phase 0) of the action potential of non nodal cardiomyocytes. This decreases the slope of phase 0, which leads to a decrease in the amplitude of the action potential.
They affect the rate and magnitude of depolarization and slow down the heart rate/ They are used in SVT, AF and WPW.
An ejection systolic murmur heard best in the right upper sternal border and radiated to the carotids. There is also a forceful displaced apex beat.
A pansystolic 'blowing' murmur best heard at the apex radiating to the axilla.
Where is the abnormal blood flow in mitral regurgitation?
Blood is being allowed to go back up from the left ventricle to the left atria.
An ejection systolic murmur heard best in the left upper sternal border.
Where is the abnormal blood flow in aortic reguritation?
Blood is flowing backwards from the aorta into the left ventricle
What are the two main pathologies that cause aortic valve disease?
1. Problems with the valve leaflets (rheumatic heart disease, endocarditis, degeneration)
2. Problems with the aortic root(aortic dissection, connective tissue disease)
An early diastolic 'blowing' 'decresendo' murmur heard best at the left sternal edge.
What are the general characteristics of a physiological murmur?
No associated symptoms
Located between the apex and left lower sternal border
Occur in early to mid systole
Cresecndo decresendo shape
What is a malar flush?
Red discolouration of the cheeks that is classically associated with mitral stenosis due to the CO2 retention that this condition causes.
Mid diastolic murmur which is localised to the apex and is associated with a tapping apex beat.
What symptoms do patients with aortic stenosis complain of?
What causes a raised JVP with a prominent A wave?
The A wave is an indicator of right atrial contraction. Pulmonary hypertension
Right atria thrombus.
What type of MI can cause arrhythmias after infarction? why is this?
The right coronary artery supplied the AV ode so can cause arryhthmias after infarction
How logn does chronic pericarditis last?
More than 6 months
How much fluid is in th pericardial cavity?
What causes acute pericarditis?
Viral - coxsackie B
Autoimmune disease such as SLE
Why doy people with pericarditis need an echocardiogram?
Risk of pericardial effusion and tamponade
What happens in chronic pericarditis?
Fibrin starts to accumulate in pericardial space and leads to constriction of the heart and over time the stroke volume decreases and the heart rate has to go up to compensate.
What are the signs and symptoms of acute pericarditis?
Chest pain better on sitting forwards
Decreased heart sounds
ST segment elevation and PR depression
Inverted T waves
Low QRS volume in effusion
What is the treatment of acute pericarditis?
What is kussmalls sign and what does it show?
Raised JVP that doesn't fall with inspiration.
What is the secondary prevention after an MI
Dual antiplatelet therapy + Beta blocker + ACEi + Statin
What causes a slow rising pulse?
What causes a collapsing pulse?
What causes a pulsus paradoxus?
Severe astham or cardiac tamponade
What causes pulsus alterans (regular alternation of the force of the arterial pulse?
What causes a bisferiens pulse (double pulse)
Mixed aortic valve disease
What causes a jerky pulse?
Hypertrophic obstructive cardiomyopathy
What are the four main side effects of GTN spray?
How do nitrates work?
Release nitric oxide ins mooth muscle which increases cGMP which leads to a fall in intracellular calcium levels. In angina this causes dilation of the coronary arteries and a reductionin venous return which reduces ventricular work and myocardial oxygen dem,ande