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350 Cards in this Set
- Front
- Back
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What do isotropy and lusitropy refer to?
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Contraction and relaxation of the heart, respectively.
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The definition of cardiac failure is?
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mechanical failure of the heart to maintain perfusion and meet requirements of tissues
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CCF stands for what? What does it denote?
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CCF stands for Congestive Cardiac Failure, and denotes combined RHF and LHF
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What is the definition of low output cardiac failure?
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Inadequate output (<35% ejection fraction), or only adequate with high filling pressures
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Concentric hypertrophy occurs from what stressor?
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Pressure overload; increased systolic pressure
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Eccentric hypertrophy occurs from what stressor?
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Volume overload; increased diastolic pressure
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What cardiac drugs can contribute to heart failure?
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Beta-blockers (inadequate heart rate); anti-arrythmic drugs (negatively inotropic drugs)
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What presenting complaint is common to both low output and congestive heart failure?
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Sleep disturbances
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The two tests that can rule out heart failure are?
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ECG combined with BNP (brain/b-type natriuretic peptide)
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On chest x-ray, how will CCF appear?
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A cardiothoracic ratio of >50% will be seen, bat-wing shadows, prominent upper lobe veins, pleural effusions, Kerley B lines
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What are the three types of natiuretic peptides?
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atrial natriuretic peptide (ANP, from the atria), brain natriuretic peptide (BNP, from ventricles) and C-type natriuretic peptide (from endothelia)
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What is the function of the natriuretic peptides?
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They are released by the heart under increased P or V, to reduce BP
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What two hormones do natriuretic peptides suppress?
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RAAS and Endothelin
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The 6-year prognosis for heart failure patients, upon diagnosis, is?
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<20%
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What are the basic management strategies for heart failure?
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Treat medical/iatrogenic causes; cease smoking; reduce weight; proper nutrition (reduce salt)
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what is the most likely cause of chest pain, if no risk factors are known?
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reflux
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what is the best initial test for a patient presenting with chest pain?
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ECG
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in a patient presenting with chest pain, which is reproduced with palpation, what is the likely cause?
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costochondritis
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what can provide relief from chest pain, if it is due to reflux?
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antacids
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what are the likely causes of chest pain if it is epigastric?
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Dyspepsia (more common) OR Peptic Ulcer
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If chest pain is localized to the RUQ, with tenderness, what is the likely cause?
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Gallbladder disease
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what are the characteristic of chest pain that indicate a pulmonary embolism?
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tachypnoea/dyspnoea, cough, pleuritic pain, haemoptysis
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sudden onset of chest pain and dyspnoea is associated with what pathology?
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pneumothorax
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what are the distinguishing trademarks of chest pain in a myocardial infarction?
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severe pain, lasting >20min
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what clinical picture of chest pain is typical of aortic stenosis?
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angina*, syncope, CHF, systolic ejection murmus
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what is the typical clinical picture of chest pain from myocarditis?
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vague/mild pain
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sharp chest pain that is worse when supine, and relieved by sitting up is typical of?
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pericarditis
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sharp chest pain radiating to the back, with a 'tearing' sensation is likely?
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aortic dissection
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what is the most common risk factor for coronary artery disease?
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hypertension
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what lifestyle factor can provide the greatest immediate improvement, for coronary artery disease?
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smoking cessation
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at what age is a parents' myocardial infarction considered a risk factor for an individual?
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dad < 55; mom < 65
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what is the most common location for myocardial infarction pain to present?
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substernal
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what drug can be administered for alleviation of pain from myocardial infarction?
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nitroglycerine
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if a patient is given nitroglycerine for chest pain and it worsens, what is the cause?
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GORD (relaxes the lower esophogeal sphincter)
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why do some patients get nause/vomiting, diarrhoea & bradycardia with an MI?
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inflammation of the inferior wall of the heart irritates the diaphragm, which aggrevates the vagus nerve
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what is the most common physical finding for a patient with a myocardial infarction?
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a normal physical
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does MI pain ever present as positional, pleuritic or tender?
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no, none of these symptoms
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if one is suffering from an aortic dissection, what is the expected difference in BP between arms?
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>20mmHg
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what is the only cause of a fixed S2 split?
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ASD
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hearing an S4 gallop is associated with what pathology? How does it affect treatment?
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S4 gallop is caused by left-ventricular hypertrophy. It does not change management, as hypertension is the cause and would be addressed regardless!
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what is the cause of an S3 gallop? How does it affect treatment?
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S3 gallop is caused by fluid overload (CHF), and an ACE-I & diuretic should be given to the patient
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an aortic dissection is associated with the new appearance of what heart sound?
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Aortic regurgitation
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a new onset of mitral regurgitation, associated with chest pain, if caused by what? How is it managed?
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Papillary rupture. Management: surgery
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how is an ECG used to tell if a myocardial infarction has occurred?
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Either 1) ST elevation in 2 leads, or 2) ST depression or T-wave inversion or normal ECG, with positive bloodwork
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how long does it take troponins and CK-MB to elevate after a myocardial infarction? How long until they peak?
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3-4 hours to rise. 12 hours to peak.
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how long do troponins remain elevated post-MI? How long for CK-MB?
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troponins: several weeks. CK-MB: 3-4 days. (Hence why CK-MB useful for re-infarction detection)
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what pathology also commonly see raised troponins, besides MI?
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renal failure, as normal trononin turnover accumulates in the bloodstream
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what are typical physical findings of an aortic dissection?
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1) loss of pulses, 2) aortic insufficiency, 3) BP difference between R/L
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what is the best initial test for a suspected aortic dissection?
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chest X-ray (widening of mediastinum)
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after a CXR for a suspected aortic dissection, what tests can be used to confirm diagnosis? Which is the most accurate?
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Tests: TEE, CT angiogram, MR angiogram. Most accurate: CT angiogram
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with sudden onset of dyspnoea and chest pain (which is worse on exertion) what is the most accurate test for diagnosis of PE?
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angiogram
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in pregnancy, what test is used to confirm a suspected PE?
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V/Q scan
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what is specific to ECG readings in a PE?
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ECG readings are non-specific (trick Q)
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what is the most common cause of pericarditis?
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viral illness
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on ECG, what is PR-segment depression characteristic of?
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pericarditis
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what ECG findings are characterisitic of pericarditis?
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diffuse ST-elevation without Q-waves, and PR-segment depression
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what is first line treatment for pericarditis?
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NSAIDs
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what is second line treatment for pericarditis?
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steroids (given if patient re-presents)
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what is the most common cause of viral myocarditis in North America?
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Coxsackie virus
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how is the pain of myocarditis described?
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vague and mild
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how do cardiac enzymes appear in myocarditis?
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CK/CK-MB may be elevated
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how is myocarditis diagnosed?
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cardiac biopsy
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what test is used to confirm the diagnosis of pneumothorax?
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CXR
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how does pneumothorax present?
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abrupt onset of dyspnoea and sharp pleuritic chest pain; breath sounds absent
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what is the first line treatment for pleuritis?
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NSAIDs
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in clot formation, what compound stabilizes platelets?
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fibrin
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what compound degrades cross-linked fibrin? What is it's precursor?
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plasmin (plasminogen)
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what clotting factor is also known as 'platelet stabilizing factor' and prevents their degradation?
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Factor XIII
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why must tPA be given quickly for an MI?
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as it must be administered before Factor XIII stabilizes the clot
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what is the most important risk factor for improving mortality in ischaemic heart disease?
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lowering LDL < 100 (< 70 in diabetics)
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what is the target range for LDL for reducing mortality from IHD?
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< 100
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what is the relative risk of IHD from smoking?
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2x
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what is the target range for HDL to reduce the risk of IHD?
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> 40
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what is the target range for total-cholesterol to minimize the risk of IHD?
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< 4
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smoking cessation has the greatest impact on what component of serum lipids?
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HDL
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what is the most common risk factor for IHD?
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hypertension
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what is the target blood pressure for reducing risk of IHD? (In diabetes or renal failure?)
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<140/90 (<130/80)
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what is the second line treatment for hypercholesterolaemia, after a statin?
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another statin!
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what percent of T2DM can be controlled with diet and exercise alone?
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25%
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what component of serum lipids is improved most from exercise?
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HDL
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the impact of 1kg loss of body mass on blood pressure is?
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a decrease of 1mmHg (linear relationship)
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what lifestyle factor has the greatest impact on BP of all?
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physical exercise (1mmHg/kg loss!)
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how does stable angina appear on ECG?
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normal
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what is ST-depression representative of, on ECG?
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ischaemia
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in an exercise stress test, what is the target HR?
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85% of maximum (220 - age)
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what are the contraindications to an exercise stress test?
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1) beta-blockers, 2) digoxin, 3) unstable angina, 4) baseline abnormalities, 5) immobility
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what positive inotropes are used in pharmacological stress tests?
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adenosine or dobutamine
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what population of patients has a false positive rate in stress tests?
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females (+/- 2%)
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how is ischaemia differentiated from infarction on radio stress test?
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thallium is not taken up during stress in either scenario, but upon cessation it is taken up by ischaemic tissue (not infarcted)
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how are angina patients identified as candidates for CABG?
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1) stress test: positive -> 2) angiogram: 3-vessel disease or left main coronary disease or 2-vessel disease/diabetes
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what is the management of an angina patient with 2-vessel disease?
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angioplasty/stent
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acute pharmacological treatment for stable angina includes?
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1) nitroglycerine, 2) oxygen
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what medication is given long-term for stable angina?
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1) long-acting nitrates or beta-blockers, 2) aspirin, 3) statins
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what two medications have the greatest impact on mortality in stable angina?
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1) beta-blockers and 2) aspirin
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following PCI angioplasty, what the restenosis rate without a stent? With a stent?
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without: 1/3. with: 1/5
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acute coronary syndrome encompasses what three disorders?
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Unstable angina (UA), STEMI and non-STEMI
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all patients presenting with acute coronary syndrome (ACS) are given what treatment?
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ASA/clopidogrel, heparin, beta-blockers, statin, morphine, ACE-I, oxygen, GPIIb/IIIb inhibitors
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only this type of ACS is a candidate for tPA (or other thrombolytics) for treatment:
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STEMI
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in ACS, which patients are candidates for CABG?
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(on angiogram) those with a) 3-vessel disease, b) 2-vessel disease and diabetes, c) left main coronary disease
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what two investigations are used to differentiate acute coronary syndromes?
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1) ECG, and 2) cardiac enzymes
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what are the ABCDE's for discharging a patient with ACS?
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aspirin/anti-anginals, beta-blocker/BP drugs, cholesterol(statin)/cigarettes, diet/diabetes, education/exercise
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describe an exercise stress test used for someone with chest pain
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performed when stable; ECG while on treadmill; attain 70% of HRmax (220-age, 85% if 3-6wks post-MI); positive = ischaemic ECG changes, or hypotension (drop of sysBP > 10mmHg)
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after an ACS presenation, how long should one wait before taking a cardiac stress test?
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5-7 days
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how long must one wait for having sexual intercourse after being discharged from an MI?
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no waiting; stress test is more demanding of the heart than intercourse
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what is the most common reason for erectile dysfunction after an MI?
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psychological
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if one is taking Viagra (sidenifil) after an MI, for erectile dysfunction, what medication must be ceased?
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nitrites
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after ACS, what is the best long-term therapy to avoid VT/VF and sudden cardiac death?
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beta-blockers
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how do cardiac enzymes and ECG compare between unstable angina and a NSTEMI?
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ECG - ischaemic changes seen in both (ST-depression); cardiac enzymes - elevated in NSTEMI
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if left unmanaged, how will unstable angina progress with time?
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with more occlusion it may progress to a NSTEMI
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in Acute Coronary Syndrome, what are the 'high risk factors' used to determine who is a candidate for catheterization? (10)
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1) repetitive/prolonged chest pain (>10min), 2) elevated cardiac markers, 3) persistent ECG changes, 4) haemodynamic instability, 5) sustained ventricular tachycardia, 6) syncope, 7) LVEF < 40%, 8) prior PTCA/CABG, 9) diabetes, 10) chronic renal disease
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What are the names of some Glycoprotein IIb/IIIa inhibitors?
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abciximab, eptifibatide, tirofiban
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what form(s) of ACS are treated with thrombolytic therapy?
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only STEMI (if no contraindications in the patient)
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what is the most common cause of death from MI in the first 24 hours?
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(ventricular) arryhythmias
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what is the common presentation of someone experiencing an MI (STEMI/NSTEMI)?
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substernal pain/pressure with radiation (to jaw/arm/etc) lasting 20-30 minutes, experiencing presyncope, N/V, diaphoresis, dyspnoea
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what investigation is used to determine if thrombolytics are used to treat ACS?
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ECG - must have ST-elevation of >1mm
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which has a greater effect on mortality, in ACS: thrombolytics or angioplasty?
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angioplasty
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what is the time frame in which reperfusion of ACS must occur?
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12 hours
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by what time (after presentation) should angioplasty occur with ACS (ie. door-to-balloon)?
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90 min
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what class of drugs are GPIIb/IIIa inhibitors?
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antiplatelet
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what drugs have the greatest benefit if given early, before angioplasty?
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GPIIb/IIIa inhibitors
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in ACS, when are thrombolytics used instead of angioplasty?
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if facilities are unequipped and there is inadequate time to get patient to closest location that is
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which thrombolytic can only be used once, due to its allogenicity?
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streptokinase
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upon presentation to hospital, how soon should a patient with ACS be given thrombolytics? (ie. Door-to-needle)
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30 min
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contraindications to thrombolysis, for ACS, are?
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recent surgery, active bleeding, head trauma, suspected aortic dissection, prior intracranial haemorrhage, prolonged CPR, poorly controlled HTN (180/100)
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if a patient has stable angina, what is the preferred method of reperfusion therapy?
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(trick Q:) reperfusion therapy is not indicated for stable angina!
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if reperfusion therapy is deemed unsuccessful and the ACS patient is still unstable, what is the next best step in treatment?
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emegency CABG
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which tachyarrhythmia is worse: Atrial or Ventrical tachycardia?
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V-tach, as it can be lethal (SVT just presents with annoying symptoms)
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what is the most common cause of conduction defect between the SA and AV node?
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ischaemia
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on ECG, what is a prolonged P-R interval (>200ms) indicative of?
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first-degree heart block
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how is first degree heart block treated?
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first degree heart block requires no treatment
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on ECG, P-P & R-R intervals that are constant, but out of sync with each other are indicative of?
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third degree heart block
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what medication can be given for third-degree heart block, if the patient is symptomatic?
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atropine
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what therapy is given for third-degree heart block, regardless of symptomatology?
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PPM
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what is the best initial therapy for a symptomatic complete heart block?
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atropine
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if a QRS complex is >120ms the diagnosis is?
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Ventricular fibrillation or Ventricular tachycardia
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the next best step in management of ventricular fibrillation is?
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defibrillation
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the next best step in management of ventricular tachycardia is?
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(antiarrhythmic drugs:) lidocaine or amiodaone or procainamide
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what is Prinzmetal's angina?
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angina due to vasospasm, occuring at rest
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angina due to vasospasm (often during sleep) is called?
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Prinzmetal's angina
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Prinzmetal's angina is common in what patients?
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migrainers (usually women)
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ECG findings for Prinzmetal's angina show?
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ST-elevation
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Stress-tests and angiography for Prinzmetal's angina show?
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normal results
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how is Prinzmetal's angina diagnosed?
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1) ECG w/ST-elevation and 2) normal stress test/angiography
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how is angina induced with a pharmaceutical challenge for Prinzmetal's angina?
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ergonomine
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what is the most common cause of congestive heart failure?
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ischaemia
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what does a displaced apex beat (to 6th ICS) indicate?
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left ventricular hypertrophy
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systolic heart failure is synonymous with?
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decreased LVEF and dilated cardiomyopathy
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what is an S3 gallop caused by?
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left ventricular hypertrophy
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in a patient with left cardiac failure and shortness of breath, what is the next best step in management?
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oxygen, diuretics, nitrates and morphine (90% will improve)
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in a patient with systolic cardiac failure, what is the goal of treatment?
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preload reduction, with diuretics
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what percent of cardiac output is attributed to atrial contraction in a healthy heart?
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10-20%
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under ventricular failure, what percent of cardiac output is attributed to atrial contraction?
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40-50%
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loss of atrial contribution to cardiac output results in what respiratory pathology?
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pulmonary oedema
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how does sputum appear with pulmonary oedema?
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pink (blood filtrate) and frothy
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how does a chest x-ray appear in congestive heart failure?
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prominent pulmonary vessels; kerley B-lines; enlarged cardiac silhouette; diaphragmatic meniscus
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what is the most sensitive position for detecting pulmonary oedema on CXR? What volume of fluid is detected?
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lateral x-ray, which can detect 50-75ml
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how do ABGs appear in congestive heart failure?
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respiratory alkalosis (from hyperventilation): normal/decreased CO2, increased HCO3-
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what is the value in performing an ECG for congestive heart failure?
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detecting any arrhythmias which may be corrected
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how is congestive heart failure managed acutely?
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1) oxygen, 2) diuretics [Lasix], 3) nitrates, 4) morphine, 5) dobutamine [positive inotrope]
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what is the effect of dobutamine on the heart?
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positive inotrope: increased contractatility, decreased afterload
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how is congestive heart failure managed chronically?
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1) diet (low salt), 2) vasodilators [ACEI/ARB first line; hydralazine/nitrates second line], 3) beta-blockers, 4) spironolactone, 5) digoxin, 6) digoxin, 7) surgery
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what is the first line vasodilator for CHF? Second line?
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First: ACE-I or ARB, Second: hydralazine & nitrates (isosorbide)
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what is the only nitrate approved for use in CHF?
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isosorbide
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what is the function of chronic beta-blockers in the treatment of CHF?
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1) anti-ischaemic, 2) anti-arrhythmic
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what positive inotrope is used chronically in the treatment of CHF?
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digoxin
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what is the function of digoxin in the chronic treatment of CHF?
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improve symptoms (does not decrease mortality)
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what surgeries should be considered for CHF?
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valvular replacement, implantable AED, heart transplant
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what is the mechanism of action for digoxin (digitalis)?
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competes with potassium on Na/K ATPase pump, increasing contractility of the heart
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what effect does hyperkalaemia have on digoxin?
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decreased effectiveness
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what is the danger of hypokalaemia when taking digoxin?
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increased activity, allowing increased toxicity
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what drugs are used for chronic management of CHF that protect against digoxin toxicity?
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beta-blockers, ACE-I/ARBs, and spironolactone
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how does digoxin (digitalis) toxicity commonly present?
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GI disturbances (N/V), CNS disturbances, blurred vision (yellow halos), gynaecomastia, arrhythmias
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what severe adverse effect is attributed to digoxin?
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sudden cardiac death
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how is digoxin toxicity managed?
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stop drug, administer potassium if hypokalaemic, lidocaine, phenytoin and digibind (for acute ODs)
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how does one differentiate between systolic and diastolic heart failure?
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echo cardiogram
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what kind of heart failure is an S4 gallop associated with?
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diastolic failure
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how is diastolic heart failure managed differently from systolic?
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do not give a positive inotrope (contraction is normal)
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what valve does rheumatic fever most commonly affect?
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mitral valve
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what valves can rheumatic fever affect?
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all of them (but most common is MV)
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what is the best initial test for valvular heart disease?
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echocardiogram
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what findings on CXR are consistent with valvular heart disease?
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cardiac enlargement, and other signs of CHF
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what finding on ECG are consistent with valvular heart disease?
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cardiac enlargement
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what is the most accurate test for valvular heart disease?
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catheterization
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what complications are common to all forms of valvular heart disease?
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1) TIA/stroke and 2) CHF
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what is the most common cause of mitral valve stenosis?
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rheumatic fever
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what population is most commonly affected by MV stenosis in developed countries?
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(damn) immigrants!
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what is the female:male ratio of MS?
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2:1
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when is the most common time for women to present with mitral stenosis?
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pregnancy
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what is the mechanism behind hoarseness in mitral stenosis?
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enlarged LA presses against the recurrent laryngeal nerve
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why do patients with mitral stenosis sometimes present with dysphagia?
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esophageal compression
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how does mitral stenosis sound on auscultation?
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cardiac - loud S1; opening snap following S2 … pulmonary - rales
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what is the difference between orthopnea and paroxysmal nocturnal dyspnoea?
|
orthopnea is relieved by sitting up, while PND is not
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what major complication are patients with mitral stenosis at risk of?
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TIA/stroke (LA atrial enlargement leads to Afib,which may throw off emboli)
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what ECG findings are consistent with mitral stenosis?
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LA enlargement & RVH. Possible Afib.
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what CXR findings are consistent with mitral stenosis?
|
LA enlargement causes the mainstem bronchus to be pushed up, and the left heart border to be straightened
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what is the clinical presentation of mitral stenosis?
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RHF, dyspnoea, rales, orthopnoea/PND, fatigue, wasting, haemoptysis, hoarseness, dysphagia, decreased pulse pressure, loud S1
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how do mitral valves appear on echocardiogram when they are stenosed?
|
as thickened MV leaflets
|
|
|
what medication can be used to treat mitral stenosis?
|
(trick Q:) no medication for stenosis, per se, just management of complications [reduce preload]
|
|
|
how is mitral valve stenosis managed?
|
medically: diuretics, or surgically: balloon valvuloplasty
|
|
|
what is the best treatment for mitral stenosis?
|
surgical balloon valvuloplasty
|
|
|
why is balloon valvuloplasty used to manage mitral stenosis in pregnant women?
|
as diuretics are contraindicated (teratogenic)
|
|
|
what is the most common cause of aortic stenosis?
|
aging (calcifications)
|
|
|
what clinical feature carries the worst prognosis for patients with aortic stenosis?
|
CHF
|
|
|
what is the most common clinical feature of aortic stenosis?
|
angina
|
|
|
what does pulsus tardus et parvus mean?
|
a pulse which is 'small' and 'late' (seen in aortic stenosis)
|
|
|
what are the clinical features of aortic stenosis?
|
CHF, syncope, angina, pulsus tardus et parvus, carotid thrill, S4 gallop (LVH)
|
|
|
what ECG findings are consistent with aortic stenosis?
|
LVH
|
|
|
what CXR finding are consistent with aortic stenosis?
|
calcifications, cardiomegaly, pulmonary congestion
|
|
|
what echocardiogram findings are consistent with aortic stenosis?
|
thickened aortic leaflets, and LVH
|
|
|
what is the criteria for surgery, in a patient with aortic stenosis?
|
AVA < 0.8 cm2
|
|
|
what is the preferred surgery for aortic stenosis?
|
valve replacement
|
|
|
why is balloon valvuloplasty not effective in management of aortic stenosis?
|
stenosis is usually due to calcification, which is hard to expand
|
|
|
what is the prognosis of a patient with aortic stenosis & ventricular dilation?
|
12-24 months
|
|
|
what is the most common cause of mitral regurgitation?
|
left ventricle dilation
|
|
|
what is the most common cause of left ventricle dilation, in mitral regurgition?
|
infection
|
|
|
on auscultation, what findings are consistent with mitral regurgitation?
|
pansystolic murmur; S3, with soft S1 (S2 split)
|
|
|
what ECG findings are consistent with mitral regurgitation?
|
LVH & LA enlargement
|
|
|
what CXR finding are consistent with mitral regurgitation?
|
cardiac enlargement and vascular congestion
|
|
|
what echocardiogram findings are consistent with mitral regurgitation?
|
LA and/or LV dilation; decreased LVEF
|
|
|
what criteria is used to determine if mitral regurgiation should be managed with valve replacement?
|
ejection fraction < 60% OR VESD > 4.5cm OR symptomatic
|
|
|
the most effective medical therapy for mitral regurgitation is?
|
vasodilation: ACE-I (second line: ARB, third line: hydralazine)
|
|
|
what is the first line vasodilator for mitral regurgitation? Second? Third?
|
first: ACE-I, second: ARB, third: hydralazine
|
|
|
medical management of mitral regurgitation includes?
|
vasodilators (ACE-I, ARB, hydralazine), digoxin, diuretics, anticoagulants (if AF present)
|
|
|
what surgical management is used for mitral regurgitation?
|
valve replacement
|
|
|
what is the most common congenital valvular lesion?
|
mitral valve prolapse
|
|
|
mitral valve prolapse causes what pathology?
|
mitral regurgitation
|
|
|
what are the two big risk factors for mitral valve prolapse?
|
1) women, and 2) connective tissue disease
|
|
|
what are the three P's of presentation of mitral valve Prolapse?
|
Pain, Palpitations & Panic attacks
|
|
|
What effect does valsalva maneouvre have on auscultation of mitral valve prolapse?
|
reduces it, as it decreases blood to the heart
|
|
|
how does mitral valve prolapse differ from mitral regurgitation on echo?
|
systolic displacement of mitral leaflets
|
|
|
how is mitral valve prolapse managed?
|
beta-blockers (chest pain/arrhythmias), & endocarditis prophylaxis (if murmur present). Surgery is not neccesary
|
|
|
what are some complications of mitral valve prolapse, if unmanaged?
|
arrythmias & sudden death, CHF, bacterial endocarditis, calcifications of valves, TIA/stroke
|
|
|
what is the most common cause of aortic regurgication?
|
systemic HTN (outweighs all other causes combined)
|
|
|
what auscultation findings does expect with aortic regurgitation?
|
diastolic decrescendo murmur, systolic flow murmur, S3 in early LV decompensation
|
|
|
what ECG findings are consistent with aortic regurgitation?
|
LVH
|
|
|
what CXR finding are consistent with aortic regurgitation?
|
LV or aortic dilation
|
|
|
what echocardiogram findings are consistent with aortic regurgitation?
|
dilation
|
|
|
how is aortic regurgitation managed?
|
1) endocarditis prophylaxis, 2) salt restriction, 3) diurectics/afterload reduction, 4) aortic valve replacement if severe
|
|
|
when is aortic valve replacement indicated for aortic regurg?
|
when a) symptoms are severe or b) ejection fraction < 55%
|
|
|
hypertrophic cardiomyopathy is defined by what ejection fraction?
|
HIGH ejection fraction (can contract, but cannot relax)
|
|
|
in hypertrophic cardiomyopathy, what anatomical findings would one expect on echo?
|
marked hypertrophy of LV (+/- RV), and disproportionate hypertrophy of the septum
|
|
|
a low ejection fraction is characteristic of what type of cardiomyopathy?
|
Dilated cardiomyopathy
|
|
|
in dilated cardiomyopathy, what anatomical finding would one expect on echo?
|
biventricular dilatation
|
|
|
what is the disease hallmark of hypertrophic obstructive cardiomyopathy?
|
unexplained hypertrophy of interventricular septum
|
|
|
what percent of hypertrophic obstructive cardiomyopathies are inherited in an autosomal dominant pattern?
|
over 60%
|
|
|
what drugs worsen obstruction in HOCM?
|
cardiac glycosides, beta-agonists, nitrates, vasodilators
|
|
|
an S4 gallop is indicative of what cardiac pathology?
|
LVH
|
|
|
what is the most common presentation of HOCM?
|
dyspnoea
|
|
|
what two classes of drugs are used to treat HOCM?
|
beta-blockers and CCBs (negative inotropes)
|
|
|
what are the two leading causes of dilated cardiomyopathy?
|
1) ischaemia, 2) alcoholism
|
|
|
what is the most common indication for a heart transplant?
|
dilated cardiomyopathy
|
|
|
what chemotherapy drugs can cause dilated cardiomyopathy?
|
vincristine, cyclophosphamide, doxorubicin
|
|
|
how is dilated cardiomyopathy managed medically?
|
ACE-I, beta-blockers, spironlactone, ASA
|
|
|
what clinical features are typical of dilated cardiomyopathy?
|
dyspnoea and PND
|
|
|
ventricular walls that are found to be noncompliant and rigid are characteristic of what cardiomyopathy?
|
restrictive
|
|
|
what are examples of infiltrative diseases that cause cardiomyopathy?
|
sarcoidosis, amyloidosis, haemochromotosis, neoplasia
|
|
|
what are the causes of restrictive cardiomyopathy?
|
a) infiltrative diseases, b) scleroderma, c) radiation
|
|
|
how is restrictive cardiomyopathy managed?
|
(no good treatments:) diuretics, and treat underlying cause
|
|
|
what are the causes of pericarditis/pericardial effusion/tamponade?
|
idiopathic, infections, vasculities, CT disorders (SLE), neoplasms, chest wall trauma
|
|
|
what clinical presentation of chest pain points to pericarditis?
|
pain which is positional and pleuritic in nature
|
|
|
how does pericarditis appear on ECG?
|
P-R segment depression, +/- ST-elevation
|
|
|
what is first line treatment for pericarditis?
|
NSAIDs
|
|
|
if NSAIDs are not successful in managing pain from pericarditis, what treatment should be commenced?
|
steroids
|
|
|
what is the difference in the aetiology between pericardial effusion and cardiac tamponade?
|
fluid accumulation is slow in pericardial effusion, allowing pericardium time to stretch and adapt; tamponade is a rapid development of pericardial fluid
|
|
|
if one presents with chest pain, and the CXR shows clear lung fields, what physical finding helps differentiate pericardial effusion from a PE?
|
pericardial effusion will also have a raised JVP
|
|
|
what is the definition of pulsus paradoxis?
|
a change in systolic pressure of >10mmHg on inhalation
|
|
|
how can one quickly determine if a patient has pulsus paradoxis?
|
taking radial pulse, beat disappears when patient inhales
|
|
|
what ECG finding is used to diagnose pericardial effusion?
|
electrical alternans (caused by respiratory alteration)
|
|
|
what echocardiogram findings are consistent with a pericardial effusion/tamponade?
|
diastolic collapse of the LV; enlarge pericardial space; heart may swing freely
|
|
|
how is pericardial effusion managed?
|
emergency pericardiocentesis
|
|
|
why is cardiac tamponade a medical emergency?
|
due the compression of the heart, heart failure can develop rapidly
|
|
|
how is cardiac tamponade managed acutely?
|
pericardiocentesis, with subxiphoid surgical drain
|
|
|
how does one prevent recurrence of cardiac tamponade?
|
surgical removal of a window of the pericardium
|
|
|
what findings are characteristic of a pericardial effusion and tamponade on auscultation?
|
muffled heart sounds
|
|
|
pulsus paradoxis is characteristic of what major cardiac pathologies?
|
pericardial effusion and cardiac tamponade
|
|
|
what are the non-idiopathic causes of constrictive pericarditis?
|
a) open heart surgery, b) thoracic radiation, c) post-viral infection
|
|
|
hearing a pericardial knock on auscultation is characteristic of what pathology?
|
constrictive pericarditis
|
|
|
what is Kussmaul's sign?
|
rising of the neck veins on inspiration
|
|
|
Kussmaul's sign is seen in which two cardiac pathologies?
|
restrictive cardiomyopathy, and constrictive pericarditis
|
|
|
how is a clinical diagnosis of constrictive pericarditis made?
|
both 1) raised JVP and 2) pericardial knock
|
|
|
what is the most accurate test for diagnosis of constrictive pericarditis?
|
CT, or MRI
|
|
|
how is mild constrictive pericarditis managed? Severe?
|
Mild - sodium restriction & diuretics; Severe - pericardiectomy
|
|
|
what prophylaxis is used against endocarditis?
|
penicillins (penicillin, amoxycillin, etc)
|
|
|
what effect does leg-raising or squatting have on blood flow in the heart?
|
increases blood flow (exagerates most murmurs)
|
|
|
on ECG, normally shaped complexes with regular pacing, but < 60bpm is called?
|
sinus bradycardia
|
|
|
what drugs are known to cause sinus bradycardia?
|
a) beta-blockers, b) CCBs, c) digoxin, d) phenothiazines
|
|
|
are there circumstances in which sinus bradycardia is normal?
|
yes. Elite athletes have heart rates below 60BPM often
|
|
|
what are some causes of excess vagas tone, which can cause sinus bradycardia?
|
acute MI, carotid sinus pressure, vomiting, valsalva manoeuvre, phenothiozines, digitalis
|
|
|
how is sinus bradycardia managed if asymptomatic?
|
sinus bradycardia requires no treatment
|
|
|
what is first line treatment for managing acute sinus bradycardia, if symptomatic? Second line?
|
first line: atropine. Second line: transcutaneous pacemaker
|
|
|
how is chronic sinus bradycardia, which is symptomatic, managed?
|
transvenous pacemaker
|
|
|
on ECG, a prolonged PR interval > 0.20s is known as?
|
heart block - first degree
|
|
|
what drug can produce a first-degree heart block?
|
digitalis (digoxin)
|
|
|
what is the leading cause of first-degree heart block?
|
aging
|
|
|
what is the treatment for first-degree heart block?
|
nothing; first-degree heart blocks require no treatment
|
|
|
on ECG, PR intervals which progressively lengthen until a QRS complex is 'dropped' is known as?
|
heart block - second degree (Mobitz I)
|
|
|
on ECG, dropped QRS complexes with consistent PR intervals of normal duration is known as?
|
heart block - second degree (Mobitz II)
|
|
|
what is the most common cause of a Mobitz I heart block?
|
aging
|
|
|
which type of heart block is a Wenckebach?
|
Mobitz I (second degree, type I)
|
|
|
How is a Mobitz I heart block treated?
|
atropine, only if symptomatic
|
|
|
How is a Mobitz II heart block treated?
|
PPM, as it has the potential to progress to a third degree heart block
|
|
|
which requires intervention: Mobitz I or II?
|
Mobitz II, as it has the potential to progress to a complete heart block (third degree)
|
|
|
on ECG, regular P-P and R-R intervals, which are out of sync with each other is called?
|
Heart block - third degree (complete heart block)
|
|
|
which patients with a third degree heart block should get a PPM?
|
all of them
|
|
|
is atropine useful for complete heart blocks?
|
for acutely symptomatic patients
|
|
|
Adam-Stokes attacks are characterized by a sudden loss of consciousness, with or without CHF. What type of heart block are they associated with?
|
Third degree (complete) heart block
|
|
|
all cardioversions should be synchronized, except for what arrhythmia?
|
Ventricular Fibrillation
|
|
|
synchronized cardioversion refers to synchronization with which part of the cardiac cycle?
|
Synchronized with the R-wave of the QRS complex
|
|
|
sudden onset of ectopic tachyarrhythmia followed by abrupt cessation is known as?
|
paroxysmal supraventricular tachycardia
|
|
|
how long of a P-R interval is required for classification as first-degree heart block?
|
>200ms
|
|
|
what is the majority of paroxysmal supraventricular tachycardia caused by?
|
re-entry from the AV node (80%)
|
|
|
how does paroxysmal supraventricular tachycardia appear on ECG?
|
as sinus tachycardia (130-200bpm), but with a 'sense' of a P-wave prior to QRS complexes
|
|
|
how is paroxysmal supreventricular tachycardia managed?
|
increasing vagal tone: 1) carotid sinus massage, 2) IV verapamil/diltiazem or adenosine [cures 90%], 3) IV propanolol/esmolol, 4) digoxin, 5) unstable: cardioversion
|
|
|
what are the only calcium channel blockers shown to work in SVT?
|
verapamil/diltiazem
|
|
|
a patient with a cardiac arrhythmia is considered 'unstable' when displaying what symptoms?
|
chest pain, hypotension, shortness of breath, confusion
|
|
|
what is the only arrhythmia that adenosine is used for?
|
SVT
|
|
|
an ECG displaying tachycardia with 3+ variations in P-wave morphology and PR interval is called?
|
Multifocal Atrial Tachycardia (MAT)
|
|
|
how is multifocal atrial tachycardia managed?
|
calcium channel blockers
|
|
|
an ECG displaying tachycardia with a regular sawtooth pattern of P-waves is called?
|
atrial flutter (AFL)
|
|
|
how is atrial flutter managed if the patient is unstable?
|
cardioversion
|
|
|
what medical management of atrial flutter is available?
|
digoxin, verapimil or diltiazem, beta-blockers
|
|
|
what is the most common arrhythmia?
|
atrial fibrillation (AF)
|
|
|
what is the most common cause of atrial fibrillation?
|
hypertension, which dilates the left atrium
|
|
|
an ECG which displays tachycardia with irregular R-R intervals and fibrillatory P-waves is typical of?
|
atrial fibrillation (AF)
|
|
|
what is the goal of treatment for atrial fibrillation?
|
rate control and chronic anticoagulation
|
|
|
if a patient presents with their first episode of atrial fibrillation and they are unstable, how should they be managed?
|
1) anticoagulation [warfarin], 2) cardioversion
|
|
|
what is the target therapeutic range for warfarin?
|
INR of 2-3
|
|
|
in asymptomatic patients with atrial fibrillation, what drugs are used to managed rate? Which is first line?
|
beta-blockers, digoxin and CCBs can all be used and are equally effective.
|
|
|
if a patient with Afib is being electively cardioverted, what medication should be given beforehand?
|
an anticoagulant
|
|
|
which is more effective: electrical or pharmacological cardioversion?
|
electrical
|
|
|
which patients with AF should be considered for cardioversion?
|
those that are symptomatic or unstable
|
|
|
what drugs can be used for pharmacological cardioversion of AF?
|
amiodorone, dofetilide, flecainide, ibutilide, propafenone and quinidine
|
|
|
what drugs can be used to *maintain* sinus rhythm after cardioversion of AF?
|
amiodorone, disopyramide, dofetilide, felcainide, propafenone and sotalol
|
|
|
what is a Maze procedure?
|
treatment of AF, which involves catheter ablation of abherrent foci (usually pulmonary veins)
|
|
|
what management can be used to obtain permenant control over AF?
|
catheter ablation (Maze procedure)
|
|
|
if a patient presents with SOB, hypotension, JVD & bilateral crackles and AF is found on ECG, what is the next best step?
|
electric cardioversion
|
|
|
an ECG with tachycardia, wide QRS complexes, shortened PR-intervals (<120ms) and delta waves is characteristic of what cardiac arrhythmia?
|
Wolff-Parkinson-White (WPW) syndrome
|
|
|
what is the cause of Wolff-Parkinson-White Syndrome?
|
an abherrent conduction track around the AV node
|
|
|
how is chronic WPW syndrome managed?
|
ablation therapy
|
|
|
how is WPW syndrome managed acutely?
|
unstable - cardioversion; stable - procainamide
|
|
|
what is the first line treatment for Wolff-Parkinson-White patients if they are stable?
|
procainamide
|
|
|
are digoxin, beta-blockers, and calcium channels antagonists useful in WPW syndrome?
|
No, they are contraindicated, as they promote abherrent conduction around the AV node (by blocking normal AV firing)
|
|
|
an ECG displaying tachycardia with wide (>140ms), regular QRS complexes is characteristic of?
|
ventricular tachycardia
|
|
|
what cardiac drug has ventricular tachycardia as a toxic side-effect?
|
digoxin
|
|
|
what is the most common cause of V-tach?
|
ischaemic heart disease, especially post-MI
|
|
|
when is V-tach considered 'sustained'?
|
when it lasts >30s
|
|
|
how is sustained V-tach managed?
|
emergency cardioversion
|
|
|
what is first line medication to manage stable patients with V-tach? Second line?
|
1) lignocaine, 2) amiodorone or sotalol
|
|
|
how is a stable patient with V-tach managed?
|
oxygen, medication (lignocaine > amiodorone > procainamide), cardioversion (last resort)
|
|
|
Torsades de Pointes is often self limiting, but if the patient is unstable how should it be managed?
|
First line: transvenous pacing (90-100bpm), second: magnesium sulfate
|
