PBL Topic 2 Case 4 Flashcards
Describe the movement of ions through the sodium potassium pump
- 3 sodium ions out
- 2 potassium ions in
What is the value of the resting potential?
- -90 mV
What occurs during depolarisation?
- Membrane becomes permeable to sodium ions
- Large numbers of sodium ions diffuse into the axon
- Reaches around +35mV
What occurs during repolarisation?
- Sodium channels close
- Membrane becomes permeable to potassium ions
- Large numbers of potassium ions diffuse into the axon
Describe the structure of a voltage gated sodium channel
- Activation (m) gate near outside of channel
- Inactivation (h) gate near inside of channel
Why is the conductance of potassium ions much greater than that of sodium ions?
- Presence of leak channels
What are intercalated discs?
- Cell membranes that separate cardiac cells from one another
- That form gap junctions
Why do intercalated discs allow easy transfer of action potentials between cells?
- Intercalated discs form gap junctions
- Allowing mostly free diffusion of ions
Why is cardiac muscle described as syncytium?
- Cardiac cells are so interconnected
- That when one cells
What causes the plateau seen in a cardiac action potential
- L-Type Calcium Channels
- Which are slower to open and remain open for longer
Which type of potassium channel is responsible for repolarisation in cardiac muscle?
- Inward rectifier channels
What is the absolute refractory period and what is its duration?
- Period in which cardiac impulse cannot re-excite an already excited area
- 0.2 to 0.3 seconds in ventricles
- 0.15 seconds in atria
What is the relative refractory period and what is its duration?
- Period in which only large impulses can re-excite an already excited area
- 0.05 seconds
What is a T tubule?
- Modified voltage-sensitive calcium channel
- Known as the dihydropyridine receptor
What occurs when an action potential passes over a T tubule?
- Calcium ions enter sarcoplasm
- Which bind to ryanodine receptors on sarcoplasmic reticulum
- Causing release of calcium into sarcoplasm
Explain how calcium ions exposure myosin binding sites
- Calcium enters myofibrils
- Calcium binds to troponin
- Troponin moves away from tropomyosin
- Exposing myosin binding site
Explain the process of power stroke
- Cross bridge head of myosin binds to active site on actin
- Head tilts forward and drags actin filament with it
- Head breaks away and process is repeated at a distant site
How is sarcoplasmic calcium concentration restored (and hence muscle relaxation)?
- Calcium-ATPase pumps
What is the cardiac cycle?
- The events that occur from the beginning of one heartbeat to the beginning of the next
Where does the cardiac cycle begin?
- Sinus node
What is the duration of the delay between the atria and ventricles and what is the purpose of this delay?
- 0.1 seconds
- Allows atria to fully contract ahead of ventricular contraction
What is the difference between systole and diastole?
- Systole refers to the period of contraction
- Diastole refers to the period of relaxation
What causes the P wave?
- Atrial depolarisation
What is the duration between the P wave and QRS complex?
- 0.16 seconds
What causes the QRS wave?
- Ventral depolarisation
What causes the T wave?
- Ventricular repolarisation
What percentage of blood flows directly into the atria?
- 80 per cent
What causes the a wave?
- Atrial contraction
What causes the c wave?
- Ventricular contraction (causing backflow of blood)
What causes the v wave?
- Ventricular relaxation (passive flow of blood into the atria)
What is meant by isometric contraction?
- Period required for ventricles to build up sufficient pressure to open semi-lunar valves?
What is the duration of isometric contraction and at what pressure do the semi-lunar valves open?
- 0.02 to 0.03 seconds
- Above 80 mm Hg
What is meant by the term rapid ejection?
- First 1/3 of ventricular contraction
- Emptying 70 per cent of ventricular volume
What is meant by isometric relaxation and what is the duration of this process?
- Period in which ventricles continue to relax even though the ventricular volume does not change
- 0.03 - 0.06 seconds
What is the value of end-diastolic volume?
- 110 - 120 ml
What is the value of the stroke volume ouptut?
- 70 ml
What is the value of the end-systolic volume?
- 50 ml
What is the ejection fraction?
- The fraction of end diastolic volume that is rejected
- Usually 60 per cent
Where is the tricuspid valve located?
- Between the right atrium and ventricle
Where is the mitral valve located?
- Between the left atrium and ventricle
Why is closure of the AV-valves described as passive?
- Backward pressure gradient forces them to close
What do the papillary muscles attach to?
- The vanes of the atrioventricular valves
- By the chordae tendinae
How do the papillary muscles prevent the budding of the valves toward the atria during ventricular contraction?
- Pull vanes of valves inward toward ventricles
Where is the aortic valve located?
- Between left ventricle and aorta
Where is the pulmonary valve located?
- Between right ventricle and pulmonary trunk
Identify four ways in which semilunar valves to A-V valves
- Snap to closed position
- Velocity of blood ejection is far greater
- Subjected to greater abrasion
- Not supported by chordae tendinae
What is meant by preload?
- Degree of tension on the muscle when it begins to contract
- Corresponds with end diastolic pressure
What is meant by afterload
- Degree of tension of the muscle against which the muscle exerts its contractile forces
- Corresponds with systolic pressure
What is the Frank-Starling mechanism?
- The greater the heart muscle is stretched during filling (end-diastolic volume) the greater the force of contraction
- The greater quantity of blood pumped into the aorta
Identify two effects of sympathetic innervation on cardiac output
- Increases the heart rate
- Increases the force of contraction
Which regions of the heart are innervated by sympathetic stimulation?
- The entire heart
Explain how sympathetic stimulation causes these changes
- Noradrenaline binds to beta-adrenergic receptors
- G proteins activate Adenylate Cyclase
- Which converts ATP to cAMP
- Which acts as a second messenger activate protein kinases
- Protein kinases phosphorylate L-type calcium channels
- Which causes influx of calcium ions for muscle contraction
How does sympathetic stimulation enhance myocyte relaxation and what is the significance of this?
- Phosphorylation of Troponin I
- Which inhibits myocyte interaction
- Myocyte is ready for next interaction more quickly
What is the role of phospholambin?
- Regulates return of calcium ions to sarcoplasmic reticulum
Which regions of the heart are innervated by the parasympathetic stimulation?
- Atria
Explain how parasympathetic stimulation causes these changes
- Acetylcholine binds to muscarinic receptors
- Negative coupling to adenylate cyclase so inhibit L-type calcium channels
- Open potassium channels and therefore have a hyper-polarising effect
Identify two effects of sympathetic innervation on cardiac output
- Decrease heart rate
- Slightly decrease force of heart contraction
What is the resting potential of the sinus node and why is this value different to that of a ventricular muscle? What is the importance of this?
- -55 to - 60 mV
- Leaky channels for sodium and calcium
- Which is responsible for self-excitation
Identify the regions of atrial tissue where conduction is rapid
- Anterior interatrial band
- Anterior, middle and posterior internodal pathways
The transmission has a delay of:
[A] after its origin in the sinus node
[B] in the A-V node
[C] in the penetrating tissue
For a total delay of [0.16’ before the signal reaches the ventricles
- [A] = 0.03
- [B] = 0.09
- [C] = 0.04
- [D] = 0.16
What causes the delay in the A-V node?
- Diminished number of gap junctions
Identify 2 reasons why Purkinje fibres transmit action potentials at high velocity
- High level of permeability of the gap junctions
- Few myofibrils so little contraction
How long is the delay between the bundle branches in the ventricular septum to the terminations of the Purkinje fibres?
- 0.03 seconds
How long is the delay between the endocardial and epicardial surfaces of the ventricles?
- 0.03 seconds
What is cardiac output and what is the average value?
- Volume of blood pumped into aorta per minute
- 5 L/ min
Identify four factors that determine cardiac ouput
- Metabolism
- Exercise
- Age
- Size
In which direction does an increase in intrapleural pressure shift the cardiac output curve? Why does this occur?
- To the right
- External cardiac pressure = Intrapleural pressure
- An increase in intrapleural pressure increases cardiac output
What is cardiac tamponade?
- Accumulation of fluid in pericardiac cavity
Opening of the thoracic cage increases the intrapleural pressure to 0 mm Hg, determine:
- The direction in which the cardiac output curve will shift
- How many mm Hg the cardiac output will shift in that direction
External cardiac pressure = Intrapleural pressure
Normal cardiac output pressure / intrapleural = -4 mm Hg
0 - -4 = +4 mm Hg
- To the right due to an increase (positive) pressure
Identify the three principal factors that determine venous return
- Right atrial pressure
- Systemic filling pressure
- Resistance to blood flow
Describe how mean systemic filling pressure occurs
- Backward force of rising right atrial pressure decreases venous blood flow to heart
- Pumping by heart approaches zero because of decreased venous return
- Arterial and venous pressures come to equilibrium at 7 mm Hg (Psf)
Describe how mean circulatory filling pressure occurs.
- Right atrial pressure falls
- This sucks the walls of the veins together
- Pressure everywhere in the circulation becomes equal
In the healthy human:
- Venous return = [A] L/min
- Mean systemic filling pressure = [B] mm Hg
- Right atrial pressure = [C] mm Hg
- Resistance to venous return = [D] mm Hg
- [A] = 5
- [B] = 7
- [C] = 0
- [D] = 1.4
Identify the three main causes of heart failure
- Ischaemic Heart Disease
- Dilated Cardiomyopathy
- Hypertension
For each of the following causes of heart failure, identify a condition associated with it:
[A] Reduced Ventricular Contractility
[B] Ventricular outflow obstruction
[C] Ventricular inflow obstruction
[D] Arrhythmia
- [A] = Myocardial Infarction
- [B] = Hypertension
- [C] = Mitral / Tricuspid Stenosis
- [D] Atrial Fibrillation
With regards to the body’s compensatory mechanisms to heart failure:
How does the body deal with a reduced ejection fraction?
- Tachycardia
- Increase in venous pressure
Outline the compensatory mechanisms involved in heart failure and how they are caused
- Impaired ventricular function leads to a fall in cardiac output
- This activates renin-angiotensin-aldosterone system
- Which leads to vasoconstriction, salt and water retention and sympathetic nervous activation
- All of which increase blood pressure and cardiac output
What is the pathological outcome of increased salt and water retention? How is this compensated for?
- Pulmonary Oedema
- Natriuretic Peptides
What is the pathological outcome of increased sympathetic activation? How is this compensated for?
- Cardiac Myocyte Apoptosis
- Down-regulation of B-receptors
What is the typical right-sided heart failure?
- Chronic Lung Disease (Cor Pulmonale)
Outline the pathophysiology of right-sided heart failure
- Reduction in right ventricular output for any given right atrial pressure
Outline four signs of right-sided heart failure
- Raised jugular venous pressure
- Hepatomegaly
- Ascites
- Peripheral pitting oedema
What is the typical cause of left sided heart failure?
- Ischaemic Heart Disease
Outline the pathophysiology of left-sided heart failure
- An acute increase in left atrial pressure causes pulmonary oedema
OR
- A gradual increase in left atrial pressure causes pulmonary vasoconstriction which protects against pulmonary oedema at the cost of increasing pulmonary hypertension
Outline five signs of right-sided heart failure
- Raised jugular venous pressure
- Pulmonary Oedema
- Cardiomegaly
- Pleural Effusions
- Pitting oedema
Identify three general symptoms of heart failure
- Dyspnoea
- Orthopnoea (dyspnoea while lying down)
- Fatigue
Identify a clinical finding from a blood test in the diagnosis of heart failure?
- Increased brain natriuretic peptide
Identify three clinical findings from a CXR in the diagnosis of heart failure
- Enlarged cardiac silhouette
- Enlarged hilar vessels
- Pulmonary Oedema
- Septal Kerley B lines
Identify a clinical finding from echocardiography in the diagnosis of heart failure?
- Valvular disease e..g occult mitral stenosis
Identify the four classes of hear failure according to the NYHA
- Class 1: Normal exercise does not cause fatigue, dyspnoea or palpitations
- Class 2: Normal physical exercise produces fatigue,, dyspnoea or palpitations
- Class 3: Gentle physical activity produces marked symptoms of heart failure
- Class 4: Symptoms of heart failure even at rest
Outline four aspects of management of pulmonary oedema
- Administer a loop diuretic e.g. furosemide
- Administer nitrates e..g glyceryl trinitrate
- Sit the patient up
- Oxygen e.g. CPAP
Why are patients with ischaemic heart disease induced heart failure advised not to take sildenafil?
- Patients with ischaemic heart disease are prescribed nitrates as vasodilators
- Sildenafil is an erectile dysfunction tablet and is an example of a phosphodiesterase type 5 inhibitor, which also lower blood pressure
- Administration of both may lead to profound hypotension
Identify three essential aspects of monitoring a patient with heart failure
- Functional capacity e.g. exercise tolerance
- Fluid states e.g. body weight.
- Cardiac rhythm e.g. ECG
Identify an example of a loop diuretic
- Furosemide
Identify the mechanism of action of loop diuretics
- Combine with Cl- binding site in ascending limb
- Natriuresis
Identify three unwanted effects of loop diuretics
- Hypotension
- Hypovolaemia
- Hypokalaemia
Identify an example of an ACE Inhibitor
- Ramipril
Identify the mechanism of action of action of ACE Inhibitors
- Inhibiting Angiotensin Converting Enzyme
- Blocks the formation of angiotensin II, a powerful vasoconstrictor
- Blocks the formation of aldosterone, resulting in natriuresis
Identify three unwanted effects of ACE Inhibitors
- Hypotension
- Hyperkaleamia
- Renal Dysfunction
- Cough
Identify three contraindications to the use of ACE Inhibitors
- Renal artery stenosis
- Pregnancy
- Previous angiodema
Identify an example of an Angiotensin II Receptor Antagonists and outline when they are used
- Valsartan
- Second line therapy in patients intolerant to ACE Inhibitors
- Since they do not affect bradykinin metabolism or produce cough
Identify two examples of beta blockers and provide a brief description of each
- Carvedilol, non selective b-receptor antagonist with additional a1-blocking activity
- Nebivolol, a b1-receptor antagonist
Identify the mechanism of action of beta blockers
- Antagonise B-adrenergic receptors
- Prevent binding of noradrenaline
- Reducing heart rate and contractility
Identify three adverse side effects of beta blockers
- Bronchoconstriction
- Bradycardia
- Fatigue
- Hypoglycaemia
Identify an example of a cardiac glycoside
- Digoxin
Identify the mechanism of action of cardiac glycosides
- Cardiac slowing + increased force of contraction
- Inhibition of Na/K pump
- Increased intracellular sodium, which slows extrusion of calcium
- Therefore increased intracellular calcium for storage in sarcoplasmic reticulum
Identify five conditions that can be detected using an ECG
- Myocardial Ischaemia
- Myocardial Infarction
- Arrhythmia
- Pericarditis
- Chamber Hypertrophy
What is the voltage and time of the P wave?
- 0.1 - 0.3 mV
- Less than 0.12 seconds
What is the voltage and time of the QRS complex?
- 1 - 1.5 mV
- Less than 0.1 seconds
What is the voltage of the T wave?
- 0.25 - 0.35
What is the time of the PR interval?
What can a long and short PR interval suggest?
- 0.16 seconds
- Long = AV nodal conduction
- Short = Wolf-Parkinson-White syndrome
What is the time of the QT interval?
- 0.35 seconds
Describe how the current flow occurs in relation to direction
- Flows with negativity towards the base of the heart
- Flows with positivity towards the apex of the heart
What does the term bipolar mean in relation to limb leads?
- Two electrodes
- On different sides of the heart
In lead 1, where are the electrodes placed?
What is the axis of lead 1?
- Negative terminal connected to right arm
- Positive terminal connected to left arm
- 0 degrees
In lead 2, where are the electrodes placed?
What is the axis of lead 2?
- Negative terminal connected to right arm
- Positive terminal connected to left leg
- 60 degrees
In lead 3, where are the electrodes placed?
What is the axis of lead 3?
- Negative terminal connected to left arm
- Positive terminal connected to left leg
- 120 degrees
Using Einthoven’s law, determine the electrical potential of lead 3 when:
Lead 1 = +0.5 mV
Lead 2 = -0.3 mV
(+0.5) - (-0.3) = +0.8 mV
Where do V1 and V2 lie?
- Over the right ventricle
Where do V3 and V4 lie?
- Over the interventricular septum
Where do V5 and V6 lie?
- Over the left ventricle
Are the QRS recordings of V1 and V2 positive or negative? Why is this the case?
- Negative
- These leads are nearer to the base of the heart
Are the QRS recordings of V4,5 and 6 positive or negative? Why is this the case?
- Positive
- These leads are nearer to the apex of the heart
Describe the pattern of the R wave in the chest leads
- Grows from V1 - V4
Describe the pattern of the S wave in the chest leads
- Grows from V1 to V3
- Disappear in V6
In which leads should the P wave be upright?
- 1, 2, V2-V6
In which leads should the ST segment start isoelectric?
- V3-V6
In which leads should there be no Q wave?
- 1, 2, V2-V6
In which leads should the T wave be upright?
- 1, 2, V2-V6
What is the mean QRS vector?
+59 degrees
In Augmented Unipolar limb leads, where is the aVR lead connected?
What is the axis in this lead?
- Right arm
- Positive 210 degrees
In Augmented Unipolar limb leads, where is the aVL lead connected?
- Left arm
- Negative 30 degrees
In Augmented Unipolar limb leads, where is the aVF lead connected?
- Left leg
- Positive 90 degrees
The normal QRS axis sits in between which angles?
- Negative 30 to Positive 90 degrees
The QRS axis with left axis deviation sits in between which angles?
- Negative 30 to Negative 90 degrees
The QRS axis with right axis deviation sits in between which angles?
- Positive 90 to Positive 180 degrees
Identify three normal causes of left axis deviation
- After deep expiration
- When a person lies down
- In stocky, fat people
Identify three normal causes of right axis deviation
- After a deep inhalation
- When a person stands up
- In tall, lanky people
Identify two pathological causes of left axis deviation
- Aortic valvular stenosis
- Aortic valvular regurgitation
Identify two pathological causes of right axis deviation
- Congenital pulmonary valvular stenosis
- Tetralogy of Fallot
With regards to atrial fibrillation:
- What does the ECG show?
- How is the pulse described?
- Normal but irregular QRS complexes
- No P wave
- Irregularly Irregular Pulse
With regards to ventricular fibrillation:
- What does the ECG show?
- What is the clinical significance of this condition?
- Shapeless, rapid oscillations
- It is fatal
How does one determine heart rate of a regular rhythm from an ECG?
- Rule of 300
- Large Squares / 300
How does one determine heart rate of an irregular rhythm from an ECG?
- 10 Second Rule
- Number of QRS complexes x 6
What is the typical cause of Rheumatic Fever?
- Pharyngeal Infection
- By Group A streptococci
In which countries is Rheumatic Fever more common and why is this the case?
- Developing countries
- Poorer hygiene and antibiotics
Explain the pathophysiology of Rheumatic Fever
- Group A Streptococci antigens cross react with cardiac myosin and sarcolemmal membrane protein
- Inflammation of endocardium, myocardium and pericardium and joints of the skin
What are Aschoff nodules?
- Multinucleate giant cells surrounded by macrophages and T lymphocytes
- Pathognomonic symptom of Rheumatic Fever
Identify four clinical features of Rheumatic Fever
- Fever
- Anorexia
- Lethargy
- Joint Pain
How is Rheumatic Fever diagnosed?
- Revised Jones Criteria
- More than 2 major manifestations e.g. carditis, polyarthritis
What is the mainstay treatment of Rheumatic Fever?
What drugs can treat the arthritis of Rheumatic Fever?
- Oral phenoxymethylpenicillin 500 mg four times daily
- NSAIDs
In longstanding left atrial regurgitation, why is there little increase in left atrial pressure?
- Hypertrophy of left atrium
- To accommodate the left atrial dilation
What is the significance of acute mitral regurgitation?
- There is no hypertrophy
- So atrial pressure increases
- Resulting in pulmonary oedema
Identify three symptoms of mitral regurgitation and briefly explain their cause
- Palpitation (increased stroke volume)
- Dyspnoea (pulmonary hypertension)
- Fatigue and lethargy (decreased cardiac output)
In the later stages of mitral regurgitation, the symptoms of which condition occur ?
- Right sided heart failure
Identify three signs of mitral regurgitation
- Soft first heart sound
- Prominent third heart sound
- Mid-systolic click
- Laterally displaced diffuse apex beat
- Pansystolic murmur
With mitral regurgitation, what would an ECG show?
- Left ventricular / atrial hypertrophy
With mitral regurgitation, what would a CXR show?
- Enlarged left ventricle / atrium
- Pulmonary oedema / congestion
With mitral regurgitation, what would echocardiography show?
- Dilated left ventricle / atrium
Identify the treatment of mitral regurgitation
- Mitral valve repair / replacement
- ACE Inhibitors
- Diuretics
- Anticoagulants
