A. Acute pericarditis; perform an echocardiogram in 1 week to confirm diagnosis
B. Acute pericarditis; start a non-steroidal anti-inflammatory drug (NSAID)
C. Acute pericarditis; start prednisolone
D. ST elevation myocardial infarction; start thrombolytics
E. Pericardial tamponade; requires pericardiocentesis
10. A 21-year-old Aboriginal woman presents with a sore throat for 2 days. She has fever (38° C) and coryza. On physical examination, the patient appears well but has a markedly infected posterior pharynx and exudates over her tonsils. Streptococcal pharyngitis is suspected. Which one of the following approaches to management is most appropriate?
A. A throat swab is adequate to establish diagnosis in Aboriginal patients
B. Intravenous benzylpenicillin 1.2 g four times a day for 10 days is the treatment of choice in eradicating Group A streptococci from the nasopharynx
C. Treatment should be started within 9 days of the onset of symptoms to prevent acute rheumatic fever
D. Aspirin can prevent rheumatic chorea
E. Asymptomatic family contacts of patients with streptococcal pharyngitis should have throat swabs for streptococcal infection
11. A 50-year-old man presents with a 2-h history of severe chest pain. The pain started suddenly while eating, was constant and radiated to the back and interscapular region. His past medical history includes hypertension and hyperlipidaemia. On examination, his heart rate is 120 beats/min and his blood pressure is 80/40 mmHg. Jugular venous pressure is not visualised. All peripheral pulses are present and equal. While stabilising the patient, which one of the following investigations should be undertaken?
A. Serum lipase
B. Computed tomography (CT) angiography of the chest
C. D-dimer
D. Lung ventilation–perfusion scan
E. Upper gastrointestinal endoscopy
12. Which one of the following best describes the use of plasma brain natriuretic peptide (BNP) in the assessment of congestive heart failure (CHF)?
A. BNP level is more useful in detecting diastolic heart failure than systolic heart failure
B. Measurement of BNP is recommended as routine in the diagnosis of CHF
C. BNP offers additional diagnostic information beyond that provided by echocardiogram
D. BNP levels have been shown to predict all-cause mortality, including sudden death
E. Plasma BNP or N-terminal pro-BNP measurement is not useful in patients presenting with new-onset breathlessness
13. A 46-year-old woman presents with a 2-week history of shortness of breath and ankle swelling. On examination her jugular venous pressure (JVP) is elevated and there are fine crackles at the bases of both lungs on auscultation. She was diagnosed with breast cancer a year ago and has been treated with surgery, doxorubicin, cyclophosphamide and radiotherapy. She has no cardiac risk factors or family history of cardiac disease. Computed tomography pulmonary angiography (CTPA) is normal and chest X-ray shows interstitial pulmonary oedema. What is the most likely cause for this presentation?
A. Anthracycline cardiotoxicity
B. Constrictive pericarditis
C. Pulmonary fibrosis
D. Radiation-induced cardiomyopathy
E. Pulmonary embolism
14. All of the following drugs can be utilised in patients with heart failure. Which one is the most effective in improving systolic function?
A. Spironolactone
B. Angiotensin converting enzyme (ACE) inhibitor
C. Digoxin
D. Frusemide
E. Hydralazine
15. A 72-year-old man describes substernal chest pressure while walking for more than 100 m and this is relieved by rest. His medical history is remarkable for hypertension and a myocardial infarction 3 years ago. His medications include aspirin 150 mg daily; metoprolol 50 mg twice daily; atorvastatin 40 mg daily; perindopril 5 mg daily; and isosorbide mononitrate 120 mg daily. He had a cardiac catheterisation 1 month ago that showed a left main coronary artery stenosis of 85%, a proximal left anterior descending artery stenosis of 70% and a 80% stenosis of the first obtuse marginal branch. His left ventricular ejection fraction (LVEF) was estimated at 45%. Which one of the following therapies would be most beneficial for this patient?
A. Addition of clopidogrel
B. Regular exercise programme
C. Percutaneous transluminal angioplasty (PCTA)
D. Coronary artery bypass grafting (CABG)
E. Transmyocardial revascularisation procedure (TMR)
16. The use of computed tomography coronary angiography (CTCA) is most appropriate in which one of the following patients?
A. An asymptomatic patient who has a strong family history of ischaemic heart disease
B. A patient with coronary stents presenting with chest pain in whom you suspect in-stent restenosis
C. A patient presenting with severe crushing chest pain and an ECG showing ST-elevation myocardial infarction (STEMI)
D. A patient presenting with chest pain and palpitations and an ECG showing rapid atrial fibrillation (heart rate: 125 beats/min)
E. A patient with chest pain with normal serial cardiac enzymes and ECGs who you think has a low-to-intermediate pre-test probability of coronary artery disease
17. An 86-year-old woman with a history of ischaemic heart disease, atrial fibrillation and type 2 diabetes presented to the emergency department with flank pain and symptomatic anaemia with haemoglobin of 69 g/L. After abdominal CT imaging, she was found to have a retroperitoneal haemorrhage. Three weeks prior to the presentation she had been changed from warfarin to dabigatran (taking a standard dose of 150 mg twice a day) for stroke prevention. Prior to this change, her INR has been within the target range for 6 years. What is the most likely explanation for the significant haemorrhagic complication in this patient after commencing dabigatran?
A. She is also taking phenytoin
B. She has impaired renal function
C. Her atrial fibrillation had reverted to sinus rhythm
D. Her INR has not been checked during the 3 weeks on the new medication
E. She is also taking digoxin
18. A 60-year-old man has had an inferior myocardial infarction 5 days ago. Today he is feeling lightheaded and his pulse rate is 40 beats/min. Blood pressure is 85/65 mmHg. An ECG is done immediately. Which one of the following findings is an indication for temporary pacing?
A. (ECG A)
B. (ECG B)
C. (ECG C)
D. (ECG D)
E. (ECG E)
19. During pregnancy, which one of the following heart diseases is associated with the highest maternal mortality?
A. Aortic stenosis
B. Atrial septal defect
C. Coarctation of aorta
D. Eisenmenger syndrome
E. Mitral stenosis
20. A 22-year-old man who is known to have hypertrophic cardiomyopathy undergoes physical and echocardiographic examination. Which one of the following findings is most predictive of this patient’s risk of sudden cardiac death?
A. Hypertension
B. Double apex beat
C. Atrial dilatation
D. Intensity of systolic murmur
E. Septal wall thickness of 3 cm or greater
21. Which is the commonest organism causing prosthetic valve infective endocarditis?
A. Staphylococcus aureus
B. Coagulase-negative staphylococcus
C. Streptococcus bovis
D. Candida
E. Streptococcus viridans
22. A 16-year-old girl has a cardiac arrest while visiting her grandmother in hospital and has the ECG shown below. She revives after DC shock and all the subsequent ECGs show a prolonged QT interval. Blood tests rule out any metabolic derangement. Two of her first-degree relatives died suddenly at a young age. She should be treated with:
A. An implantable cardioverter–defibrillator
B. Beta-blocker
C. Quinidine
D. Sotalol
E. Verapamil
23. A 35-year-old man who is from an indigenous community in New Zealand has had mitral stenosis due to rheumatic heart disease. He has experienced some exertional dyspnoea recently. He attends a cardiology clinic with his most recent echocardiography results. Which one of the following features should prompt a referral for him to have a percutaneous balloon mitral valvuloplasty (PBMV)?
A. Mitral orifice area of 1.2 cm2 with minimal calcification
B. The presence of severe mitral regurgitation
C. Dyspnoea classified as New York Heart Association functional class I
D. Mitral orifice area of 3 cm2 with fusion of the subvalvular apparatus
E. Large left atrial thrombus
24. A 68-year-old male farmer is transferred from a country hospital following a late presentation with acute myocardial infarction. He suffered severe chest pain 2 days ago but did not seek medical treatment. While you are examining the patient you hear a pericardial rub and make a diagnosis of peri-infarction pericarditis. Which one of the following statements is correct?
A. Aspirin and heparin infusion should be stopped immediately
B. The patient should be commenced on ibuprofen
C. Reperfusion therapies are associated with a reduced incidence of peri-infarction pericarditis
D. The patient should be commenced on high-dose prednisolone
E. The echocardiogram is likely to show preserved ejection fraction
25. A 35-year-old man presents to the emergency department with a 1-h history of feeling his heart racing and slight chest discomfort. He has had two similar episodes previously following alcohol binges. An electrocardiography shows a regular narrow complex tachycardia with a rate of 180 beats/min. He otherwise feels well, his blood pressure is 98/68 mmHg and pulse oximetry on air shows oxygen saturation of 97%. What treatment should be administered?
A. Electrical cardioversion
B. Intravenous lignocaine
C. Intravenous adenosine
D. Intravenous digoxin
E. Intravenous verapamil
26. A 45-year-man presents with a 24-h history of palpitations and chest discomfort. He had one similar episode 5 years ago. He is known to have asthma since childhood and uses a salbutamol inhaler two to three times a week. His initial examination reveals blood pressure of 110/60 mmHg, pulse rate 152 beats/min and oxygen saturation on room air of 95%. There is a scattered expiratory wheeze but no cardiac murmur. His ECG taken 5 years ago when he was admitted with an acute asthma attack is shown below (A) and his current ECG (B). His biochemistry results are unremarkable and the troponin T level is normal. Which one of the following medications should be administered to achieve rate control?
A. Intravenous adenosine
B. Intravenous atenolol
C. Intravenous loading dose of digoxin
D. Intravenous flecainide
E. Intravenous verapamil
27. A 75-year old man presents to hospital with a 2-week history of malaise and low-grade fever. He also has had chronic diarrhoea for the past 3 months and a 5-kg weight loss. On examination, his blood pressure is 100/70 mmHg, heart rate 110 beats/min and temperature of 38.4° C. A diastolic murmur (3/6) is heard at the left sternal edge. He is mildly anaemic with mean cell volume (MCV) of 76 fL (normal reference range 80–100 fL). Blood cultures grow Streptococcus bovis and transoesophageal echocardiography reveals vegetations on the aortic valve. What additional investigations should be undertaken?
A. Cardiac magnetic resonance imaging
B. Computed tomography of the abdomen
C. Orthopantomogram (OPG)
D. Colonoscopy
E. White cell scan
28. Which one of the following disorders does NOT cause high-output heart failure?
A. Hyperthyroidism
B. Paget disease
C. Brachio-cephalic arteriovenous fistula
D. Cirrhosis
E. Amyloidosis
29. A 60-year-old woman is diagnosed with Streptococcus viridians endocarditis involving the mitral valve. Which one of the following is a poor prognostic factor?
A. Left ventricular ejection fraction of 50%
B. Perivalvular extension of infection
C. Recent dental extraction
D. Previous adverse drug reaction to penicillin
E. Previous abdominal aortic aneurysm repair
30. A 72-year-old man presents with a 2-day history of pain in his toes. He presented to another hospital with chest pain and received a coronary angiography 7 days ago. His other medical problems include hypertension, type 2 diabetes, chronic kidney disease with a serum creatinine of 156 μmol/L and osteoarthritis. He is taking aspirin, clopidogrel, metformin, atorvastatin and perindopril. On examination, he is afebrile, peripheral pulses are difficult to palpate and toes are painful to touch. His initial blood test results are shown below. Which one of the following diagnoses is most likely?
| Value | Reference range | |
|---|---|---|
| Haemoglobin | 82 g/L | 115–155 g/L |
| White blood cells | 13.0 × 109 cells/L | 4.0–11.0 × 109 cells/L |
| Platelet count | 593 × 109 cells/L | 150–400 × 109 cells/L |
| Lactate dehydrogenase | 344 U/L | 110–230 U/L |
| Creatinine | 287 μmol/L | 80–120 μmol/L |
| Urate | 0.69 μmol/L | 0.21–0.48 μmol/L |
A. Contrast nephropathy
B. Renal embolus
C. Cholesterol emboli
D. Cryoglobulinaemia
E. Metformin-induced renal failure
31. A 72-year-old man who was admitted with an inferior myocardial infarction has a cardiac arrest on the way to the angiogram suite. After three cycles of cardiopulmonary resuscitation (CPR), two boluses of 1 mg epinephrine (adrenaline) and two defibrillator shocks, his electrocardiography remains unchanged and is shown below. What is the next most appropriate step?
A. 3 mg of epinephrine (adrenaline)
B. 40 units of vasopressin
C. 10 ml of 10% calcium chloride
D. 10 ml of magnesium sulphate
E. 300 mg of amiodarone
32. A 66-year-old woman is admitted for fixation of a left hip fracture. She has a history of osteoporosis and hypertension, but is otherwise in good health. She has no history of chest pain, but she says she experiences dyspnoea after walking about 400 m. She has a 30 pack-year smoking history but stopped 5 years ago. She is currently taking an angiotensin converting-enzyme inhibitor for her hypertension. What is the next most appropriate step in her assessment?
A. Transthoracic echocardiography
B. Dobutamine stress echocardiography
C. Coronary angiography
D. No further cardiac investigation
E. Cardiac magnetic resonance imaging
33. Which one of the following is the modality of choice for diagnosing and monitoring transplant coronary artery disease after orthotopic heart transplantation?
A. Clinical history
B. Coronary angiography
C. Exercise electrocardiography (ECG)
D. Myocardial contrast echocardiography
E. Intravascular ultrasound
34. A 53-year-old woman presents with dyspnoea and ankle oedema for 1 month. Her blood pressure is 110/80 mmHg. On examination, her jugular venous pressure rises with inspiration. She has a soft systolic murmur and a third heart sound. Electrocardiography (ECG) shows poor R-wave progression. An echocardiogram shows no pericardial effusion, increased ratio of early diastolic filling-to-atrial filling and systolic function is mildly impaired. Which one of the following is the most likely diagnosis?
A. Restrictive cardiomyopathy
B. Dilated cardiomyopathy
C. Constrictive pericarditis
D. Ischaemic cardiomyopathy
E. Pulmonary embolus
35. A patient with acute fulminant myocarditis is most likely to present with:
A. Dyspnoea
B. Palpitations
C. Hypotension
D. Fever
E. Chest pain
36. A 63-year-old woman is worried because her elder sister has just had a disabling stroke. Her blood pressure is 148/94 mmHg and her BMI is 30 kg/m2. She wishes to reduce her blood pressure by non-pharmacological means. You should recommend which one of the following evidence-based measures?
A. Weight reduction and a sodium intake of 5 g/day
B. A diet reduced in sodium intake to less than 1 g/day
C. Insist on starting an antihypertensive medication
D. A diet reduced in potassium and sodium intake
E. Weight reduction and the Dietary Approaches to Stop Hypertension (DASH) diet
Theme: Congenital heart disease (for Questions 37–40)
A. Ostium secundum atrial septal defect
B. Ventricular septal defect
C. Patent ductus arteriosus
D. Eisenmenger syndrome
E. Tetralogy of Fallot
F. Pulmonary stenosis
G. Bicuspid aortic valve
H. Coarctation of the aorta
For each of the following patients, select the most likely diagnosis.
37. A 32-year-old man presents to a hospital with fatigue and fever of 2 weeks’ duration. He has no chest pain, dyspnoea or orthopnoea. He is known to have a ‘heart murmur’ since birth. On physical examination the only abnormal findings are a temperature of 38.3° C; a harsh systolic murmur is heard in the left lower sternal border; and the presence of small tender nodules are noted on two fingers. Which cardiac anomaly is most consistent with this patient’s clinical presentation?
38. A 21-year-old woman is being evaluated for exertional dyspnoea. She has been having these symptoms for the past 4 months. Her medical history includes one episode of atrial fibrillation 1 month ago. Her physical examination shows fixed splitting of the second heart sound and a systolic murmur in the pulmonic area. An electrocardiogram shows slight right axis deviation and incomplete right bundle-branch block. A chest X-ray reveals an enlarged right atrium and main pulmonary artery. Which cardiac anomaly is the most likely diagnosis for this patient?
39. An 18-year-old man is being evaluated for a murmur and hypertension. He is asymptomatic. On physical examination his blood pressure is 170/100 mmHg in the right arm. The femoral pulses are diminished in amplitude compared to the radial pulses. His cardiac examination reveals a short mid-systolic murmur in the left infrascapular area. Which cardiac anomaly is the most likely diagnosis for this patient?
40. A 19-year-old woman presents with breathlessness on exertion and mild fatigue. She has no significant medical history. She does not smoke and is not on regular medication. Her cardiac examination reveals a systolic murmur at the second left intercostal space, which increases with inspiration. What is the most likely diagnosis for this patient?
Answers
Basic Science
1. Answer D
The beneficial effects of beta-blockers in stable angina are secondary to reduction in myocardial oxygen demand. Myocardial oxygen demand varies directly according to the heart rate, contractility and left ventricular wall stress, each of which is decreased by beta-blockers.
Catecholamine activation of the beta-1 receptors, which are primarily found in the heart muscle, leads to increased heart rate, contractility and atrioventricular (AV) conduction, with a decrease in AV node refractoriness. Beta-blockers act by competitively inhibiting catecholamines from binding to these receptors.
No randomised trials have studied the effect of beta-blockers on survival in patients with angina, but survival benefits have been seen in patients with systolic heart failure and following myocardial infarction.
In the treatment of patients with angina, titrating the dose of beta-blocker to achieve a target resting heart rate of 55–60 beats/min is recommended. Adverse side effects can include bradycardia, AV node conduction problems, reduced contractility, bronchoconstriction (notably in patients who are taking a beta-2 adrenergic agonist), worsening of peripheral vascular disease, Raynaud phenomenon, fatigue, nightmares and erectile dysfunction.
The beneficial effects of beta-blockers in stable angina are secondary to reduction in myocardial oxygen demand. Myocardial oxygen demand varies directly according to the heart rate, contractility and left ventricular wall stress, each of which is decreased by beta-blockers.
Catecholamine activation of the beta-1 receptors, which are primarily found in the heart muscle, leads to increased heart rate, contractility and atrioventricular (AV) conduction, with a decrease in AV node refractoriness. Beta-blockers act by competitively inhibiting catecholamines from binding to these receptors.
No randomised trials have studied the effect of beta-blockers on survival in patients with angina, but survival benefits have been seen in patients with systolic heart failure and following myocardial infarction.
In the treatment of patients with angina, titrating the dose of beta-blocker to achieve a target resting heart rate of 55–60 beats/min is recommended. Adverse side effects can include bradycardia, AV node conduction problems, reduced contractility, bronchoconstriction (notably in patients who are taking a beta-2 adrenergic agonist), worsening of peripheral vascular disease, Raynaud phenomenon, fatigue, nightmares and erectile dysfunction.
2. Answer D
Compensatory mechanisms that are activated in heart failure include:
These processes are controlled mainly by activation of neurohormonal vasoconstrictor systems, including the renin–angiotensin–aldosterone system, the adrenergic nervous system, and non-osmotic release of arginine–vasopressin. These and other mechanisms contribute to the symptoms, signs and poor natural history of heart failure. In particular, an increase in wall stress along with neurohormonal activation facilitates pathological ventricular remodelling; this process has been closely linked to heart failure disease progression. Management of chronic heart failure targets these mechanisms and, in some instances, results in reverse remodelling of the failing heart (Krum and Abraham, 2009).
Compensatory mechanisms that are activated in heart failure include:
- Increased ventricular preload with ventricular dilatation and volume expansion
- Peripheral vasoconstriction, which initially maintains perfusion to vital organs
- Myocardial hypertrophy to preserve wall stress as the heart dilates
- Renal sodium and water retention to enhance ventricular preload
- Activation of the adrenergic nervous system, which increases heart rate and contractile function.
These processes are controlled mainly by activation of neurohormonal vasoconstrictor systems, including the renin–angiotensin–aldosterone system, the adrenergic nervous system, and non-osmotic release of arginine–vasopressin. These and other mechanisms contribute to the symptoms, signs and poor natural history of heart failure. In particular, an increase in wall stress along with neurohormonal activation facilitates pathological ventricular remodelling; this process has been closely linked to heart failure disease progression. Management of chronic heart failure targets these mechanisms and, in some instances, results in reverse remodelling of the failing heart (Krum and Abraham, 2009).
Krum, H. and Abraham, W.T. (2009). Heart failure. Lancet 373, 941–955.
3. Answer E
Ventricular tachycardia without structural heart disease is often referred to as idiopathic ventricular tachycardia (John et al., 2012). Idiopathic ventricular tachycardia in the absence of structural heart disease most often originates from the right ventricular outflow tract. Diseases such as arrhythmogenic right ventricular cardiomyopathy and sarcoidosis often need to be excluded before a diagnosis is made. Idiopathic ventricular tachycardia must be distinguished from ventricular tachycardia with structural heart disease, because the latter often warrants an implantable cardioverter defibrillator (ICD). Detection of ventricular scar on cardiac imaging can be helpful. Although idiopathic monomorphic ventricular tachycardia can cause syncope, sudden death is rare. Beta-blockers, calcium-channel blockers or catheter ablation are often effective.
Catheter ablation is a reasonable first-line therapy for many patients with symptomatic idiopathic ventricular tachycardias. Success rates approach 80–90% in experienced centres. Success rates are lower for those tachycardias arising in less common locations, such as along the aortic annulus, within the aortic sinuses, within the great cardiac vein or from the epicardium. Failure of ablation is usually due to the inability to induce the arrhythmia for precise localisation, or ventricular tachycardia origin in a location that is inaccessible or in close proximity to a coronary artery, which precludes safe ablation.
Ventricular tachycardia without structural heart disease is often referred to as idiopathic ventricular tachycardia (John et al., 2012). Idiopathic ventricular tachycardia in the absence of structural heart disease most often originates from the right ventricular outflow tract. Diseases such as arrhythmogenic right ventricular cardiomyopathy and sarcoidosis often need to be excluded before a diagnosis is made. Idiopathic ventricular tachycardia must be distinguished from ventricular tachycardia with structural heart disease, because the latter often warrants an implantable cardioverter defibrillator (ICD). Detection of ventricular scar on cardiac imaging can be helpful. Although idiopathic monomorphic ventricular tachycardia can cause syncope, sudden death is rare. Beta-blockers, calcium-channel blockers or catheter ablation are often effective.
Catheter ablation is a reasonable first-line therapy for many patients with symptomatic idiopathic ventricular tachycardias. Success rates approach 80–90% in experienced centres. Success rates are lower for those tachycardias arising in less common locations, such as along the aortic annulus, within the aortic sinuses, within the great cardiac vein or from the epicardium. Failure of ablation is usually due to the inability to induce the arrhythmia for precise localisation, or ventricular tachycardia origin in a location that is inaccessible or in close proximity to a coronary artery, which precludes safe ablation.
John, R.M., Tedrow, U.B., Koplan, B.A., et al. (2012). Ventricular arrhythmias and sudden cardiac death. Lancet 380, 1520–1529.
4. Answer A
Myocarditis is most commonly caused by a viral infection in developed countries (Magnani and Dec, 2006). Enteroviruses, including the Coxsackie virus, are the most commonly associated viral species. The Coxsackie virus has a myocardial affinity because of its easy entrance into the myocardial cell through the Coxsackie–adenoviral receptor, which triggers the host immune response.
Cytomegalovirus is commonly associated with post-transplantation myocarditis. Influenza myocarditis is often associated with haemorrhagic pulmonary oedema. HIV has been reported to cause myocarditis. However, it may be difficult to determine the exact cause of cardiac dysfunction because symptoms may be due to the inflammatory response to HIV; the HIV infection itself; or coexisting opportunistic infections, side effects of anti-retroviral treatment, or a combination of these causes.
Hepatitis C, adenovirus, parvovirus B19 and Epstein–Barr virus (EBV) have been reported to cause myocarditis.
Myocarditis is most commonly caused by a viral infection in developed countries (Magnani and Dec, 2006). Enteroviruses, including the Coxsackie virus, are the most commonly associated viral species. The Coxsackie virus has a myocardial affinity because of its easy entrance into the myocardial cell through the Coxsackie–adenoviral receptor, which triggers the host immune response.
Cytomegalovirus is commonly associated with post-transplantation myocarditis. Influenza myocarditis is often associated with haemorrhagic pulmonary oedema. HIV has been reported to cause myocarditis. However, it may be difficult to determine the exact cause of cardiac dysfunction because symptoms may be due to the inflammatory response to HIV; the HIV infection itself; or coexisting opportunistic infections, side effects of anti-retroviral treatment, or a combination of these causes.
Hepatitis C, adenovirus, parvovirus B19 and Epstein–Barr virus (EBV) have been reported to cause myocarditis.
Magnani, J.W., and Dec, G.W. (2006). Myocarditis: current trends in diagnosis and treatment. Circulation 113, 876–890.
5. Answer B
Electrical propagation of the cardiac impulse is transmitted from the sino-atrial node to the anterior, middle, and posterior internodal tracts, to the AV node and to the bundle of His (AV bundle), and then via the right and left bundle branches to the Purkinje fibres and thence to the myocardium.
Myocytes have a negative membrane potential when at rest. Stimulation induces the opening of voltage-gated ion channels, leading to flow of cations into the cell. The positively charged ions enter the cell, causing the depolarisation characteristic of an action potential. The action potential spreads through the muscle network of T-tubules, depolarising the inner portion of the muscle fibre. The depolarisation activates L-type voltage-dependent calcium channels (dihydropyridine receptors) in the T-tubule membrane, which are in close proximity to calcium-release channels (ryanodine receptors) in the adjacent sarcoplasmic reticulum. Activated voltage-gated calcium channels physically interact with calcium-release channels to activate them, causing the sarcoplasmic reticulum to release calcium. Calcium release is the main trigger of muscle contraction by causing alterations in the binding of troponin and tropomyosin to actin and leading to the ATP-driven myosin–actin bonding, sliding and releasing interactions that generates contraction. Repolarisation occurs due to a flow of potassium out of the cardiac cells.
In an electrocardiogram the P wave corresponds to the depolarisation of the atria; the QRS complex to right and left ventricular depolarisation; the ST-T wave to ventricular repolarisation; the PR interval is the time from onset of atrial depolarisation (P wave) to onset of ventricular depolarisation (QRS complex); the QRS duration is duration of ventricular muscle depolarisation; and the QT interval is the duration of ventricular depolarisation and repolarisation.
During diastole the pressure within the left ventricle is lower than that in aorta, allowing blood to circulate into the heart itself through the epicardial coronary arteries.
Electrical propagation of the cardiac impulse is transmitted from the sino-atrial node to the anterior, middle, and posterior internodal tracts, to the AV node and to the bundle of His (AV bundle), and then via the right and left bundle branches to the Purkinje fibres and thence to the myocardium.
Myocytes have a negative membrane potential when at rest. Stimulation induces the opening of voltage-gated ion channels, leading to flow of cations into the cell. The positively charged ions enter the cell, causing the depolarisation characteristic of an action potential. The action potential spreads through the muscle network of T-tubules, depolarising the inner portion of the muscle fibre. The depolarisation activates L-type voltage-dependent calcium channels (dihydropyridine receptors) in the T-tubule membrane, which are in close proximity to calcium-release channels (ryanodine receptors) in the adjacent sarcoplasmic reticulum. Activated voltage-gated calcium channels physically interact with calcium-release channels to activate them, causing the sarcoplasmic reticulum to release calcium. Calcium release is the main trigger of muscle contraction by causing alterations in the binding of troponin and tropomyosin to actin and leading to the ATP-driven myosin–actin bonding, sliding and releasing interactions that generates contraction. Repolarisation occurs due to a flow of potassium out of the cardiac cells.
In an electrocardiogram the P wave corresponds to the depolarisation of the atria; the QRS complex to right and left ventricular depolarisation; the ST-T wave to ventricular repolarisation; the PR interval is the time from onset of atrial depolarisation (P wave) to onset of ventricular depolarisation (QRS complex); the QRS duration is duration of ventricular muscle depolarisation; and the QT interval is the duration of ventricular depolarisation and repolarisation.
During diastole the pressure within the left ventricle is lower than that in aorta, allowing blood to circulate into the heart itself through the epicardial coronary arteries.
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