Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
350 Cards in this Set
- Front
- Back
What do isotropy and lusitropy refer to?
|
Contraction and relaxation of the heart, respectively.
|
|
The definition of cardiac failure is?
|
mechanical failure of the heart to maintain perfusion and meet requirements of tissues
|
|
CCF stands for what? What does it denote?
|
CCF stands for Congestive Cardiac Failure, and denotes combined RHF and LHF
|
|
What is the definition of low output cardiac failure?
|
Inadequate output (<35% ejection fraction), or only adequate with high filling pressures
|
|
Concentric hypertrophy occurs from what stressor?
|
Pressure overload; increased systolic pressure
|
|
Eccentric hypertrophy occurs from what stressor?
|
Volume overload; increased diastolic pressure
|
|
What cardiac drugs can contribute to heart failure?
|
Beta-blockers (inadequate heart rate); anti-arrythmic drugs (negatively inotropic drugs)
|
|
What presenting complaint is common to both low output and congestive heart failure?
|
Sleep disturbances
|
|
The two tests that can rule out heart failure are?
|
ECG combined with BNP (brain/b-type natriuretic peptide)
|
|
On chest x-ray, how will CCF appear?
|
A cardiothoracic ratio of >50% will be seen, bat-wing shadows, prominent upper lobe veins, pleural effusions, Kerley B lines
|
|
What are the three types of natiuretic peptides?
|
atrial natriuretic peptide (ANP, from the atria), brain natriuretic peptide (BNP, from ventricles) and C-type natriuretic peptide (from endothelia)
|
|
What is the function of the natriuretic peptides?
|
They are released by the heart under increased P or V, to reduce BP
|
|
What two hormones do natriuretic peptides suppress?
|
RAAS and Endothelin
|
|
The 6-year prognosis for heart failure patients, upon diagnosis, is?
|
<20%
|
|
What are the basic management strategies for heart failure?
|
Treat medical/iatrogenic causes; cease smoking; reduce weight; proper nutrition (reduce salt)
|
|
what is the most likely cause of chest pain, if no risk factors are known?
|
reflux
|
|
what is the best initial test for a patient presenting with chest pain?
|
ECG
|
|
in a patient presenting with chest pain, which is reproduced with palpation, what is the likely cause?
|
costochondritis
|
|
what can provide relief from chest pain, if it is due to reflux?
|
antacids
|
|
what are the likely causes of chest pain if it is epigastric?
|
Dyspepsia (more common) OR Peptic Ulcer
|
|
If chest pain is localized to the RUQ, with tenderness, what is the likely cause?
|
Gallbladder disease
|
|
what are the characteristic of chest pain that indicate a pulmonary embolism?
|
tachypnoea/dyspnoea, cough, pleuritic pain, haemoptysis
|
|
sudden onset of chest pain and dyspnoea is associated with what pathology?
|
pneumothorax
|
|
what are the distinguishing trademarks of chest pain in a myocardial infarction?
|
severe pain, lasting >20min
|
|
what clinical picture of chest pain is typical of aortic stenosis?
|
angina*, syncope, CHF, systolic ejection murmus
|
|
what is the typical clinical picture of chest pain from myocarditis?
|
vague/mild pain
|
|
sharp chest pain that is worse when supine, and relieved by sitting up is typical of?
|
pericarditis
|
|
sharp chest pain radiating to the back, with a 'tearing' sensation is likely?
|
aortic dissection
|
|
what is the most common risk factor for coronary artery disease?
|
hypertension
|
|
what lifestyle factor can provide the greatest immediate improvement, for coronary artery disease?
|
smoking cessation
|
|
at what age is a parents' myocardial infarction considered a risk factor for an individual?
|
dad < 55; mom < 65
|
|
what is the most common location for myocardial infarction pain to present?
|
substernal
|
|
what drug can be administered for alleviation of pain from myocardial infarction?
|
nitroglycerine
|
|
if a patient is given nitroglycerine for chest pain and it worsens, what is the cause?
|
GORD (relaxes the lower esophogeal sphincter)
|
|
why do some patients get nause/vomiting, diarrhoea & bradycardia with an MI?
|
inflammation of the inferior wall of the heart irritates the diaphragm, which aggrevates the vagus nerve
|
|
what is the most common physical finding for a patient with a myocardial infarction?
|
a normal physical
|
|
does MI pain ever present as positional, pleuritic or tender?
|
no, none of these symptoms
|
|
if one is suffering from an aortic dissection, what is the expected difference in BP between arms?
|
>20mmHg
|
|
what is the only cause of a fixed S2 split?
|
ASD
|
|
hearing an S4 gallop is associated with what pathology? How does it affect treatment?
|
S4 gallop is caused by left-ventricular hypertrophy. It does not change management, as hypertension is the cause and would be addressed regardless!
|
|
what is the cause of an S3 gallop? How does it affect treatment?
|
S3 gallop is caused by fluid overload (CHF), and an ACE-I & diuretic should be given to the patient
|
|
an aortic dissection is associated with the new appearance of what heart sound?
|
Aortic regurgitation
|
|
a new onset of mitral regurgitation, associated with chest pain, if caused by what? How is it managed?
|
Papillary rupture. Management: surgery
|
|
how is an ECG used to tell if a myocardial infarction has occurred?
|
Either 1) ST elevation in 2 leads, or 2) ST depression or T-wave inversion or normal ECG, with positive bloodwork
|
|
how long does it take troponins and CK-MB to elevate after a myocardial infarction? How long until they peak?
|
3-4 hours to rise. 12 hours to peak.
|
|
how long do troponins remain elevated post-MI? How long for CK-MB?
|
troponins: several weeks. CK-MB: 3-4 days. (Hence why CK-MB useful for re-infarction detection)
|
|
what pathology also commonly see raised troponins, besides MI?
|
renal failure, as normal trononin turnover accumulates in the bloodstream
|
|
what are typical physical findings of an aortic dissection?
|
1) loss of pulses, 2) aortic insufficiency, 3) BP difference between R/L
|
|
what is the best initial test for a suspected aortic dissection?
|
chest X-ray (widening of mediastinum)
|
|
after a CXR for a suspected aortic dissection, what tests can be used to confirm diagnosis? Which is the most accurate?
|
Tests: TEE, CT angiogram, MR angiogram. Most accurate: CT angiogram
|
|
with sudden onset of dyspnoea and chest pain (which is worse on exertion) what is the most accurate test for diagnosis of PE?
|
angiogram
|
|
in pregnancy, what test is used to confirm a suspected PE?
|
V/Q scan
|
|
what is specific to ECG readings in a PE?
|
ECG readings are non-specific (trick Q)
|
|
what is the most common cause of pericarditis?
|
viral illness
|
|
on ECG, what is PR-segment depression characteristic of?
|
pericarditis
|
|
what ECG findings are characterisitic of pericarditis?
|
diffuse ST-elevation without Q-waves, and PR-segment depression
|
|
what is first line treatment for pericarditis?
|
NSAIDs
|
|
what is second line treatment for pericarditis?
|
steroids (given if patient re-presents)
|
|
what is the most common cause of viral myocarditis in North America?
|
Coxsackie virus
|
|
how is the pain of myocarditis described?
|
vague and mild
|
|
how do cardiac enzymes appear in myocarditis?
|
CK/CK-MB may be elevated
|
|
how is myocarditis diagnosed?
|
cardiac biopsy
|
|
what test is used to confirm the diagnosis of pneumothorax?
|
CXR
|
|
how does pneumothorax present?
|
abrupt onset of dyspnoea and sharp pleuritic chest pain; breath sounds absent
|
|
what is the first line treatment for pleuritis?
|
NSAIDs
|
|
in clot formation, what compound stabilizes platelets?
|
fibrin
|
|
what compound degrades cross-linked fibrin? What is it's precursor?
|
plasmin (plasminogen)
|
|
what clotting factor is also known as 'platelet stabilizing factor' and prevents their degradation?
|
Factor XIII
|
|
why must tPA be given quickly for an MI?
|
as it must be administered before Factor XIII stabilizes the clot
|
|
what is the most important risk factor for improving mortality in ischaemic heart disease?
|
lowering LDL < 100 (< 70 in diabetics)
|
|
what is the target range for LDL for reducing mortality from IHD?
|
< 100
|
|
what is the relative risk of IHD from smoking?
|
2x
|
|
what is the target range for HDL to reduce the risk of IHD?
|
> 40
|
|
what is the target range for total-cholesterol to minimize the risk of IHD?
|
< 4
|
|
smoking cessation has the greatest impact on what component of serum lipids?
|
HDL
|
|
what is the most common risk factor for IHD?
|
hypertension
|
|
what is the target blood pressure for reducing risk of IHD? (In diabetes or renal failure?)
|
<140/90 (<130/80)
|
|
what is the second line treatment for hypercholesterolaemia, after a statin?
|
another statin!
|
|
what percent of T2DM can be controlled with diet and exercise alone?
|
25%
|
|
what component of serum lipids is improved most from exercise?
|
HDL
|
|
the impact of 1kg loss of body mass on blood pressure is?
|
a decrease of 1mmHg (linear relationship)
|
|
what lifestyle factor has the greatest impact on BP of all?
|
physical exercise (1mmHg/kg loss!)
|
|
how does stable angina appear on ECG?
|
normal
|
|
what is ST-depression representative of, on ECG?
|
ischaemia
|
|
in an exercise stress test, what is the target HR?
|
85% of maximum (220 - age)
|
|
what are the contraindications to an exercise stress test?
|
1) beta-blockers, 2) digoxin, 3) unstable angina, 4) baseline abnormalities, 5) immobility
|
|
what positive inotropes are used in pharmacological stress tests?
|
adenosine or dobutamine
|
|
what population of patients has a false positive rate in stress tests?
|
females (+/- 2%)
|
|
how is ischaemia differentiated from infarction on radio stress test?
|
thallium is not taken up during stress in either scenario, but upon cessation it is taken up by ischaemic tissue (not infarcted)
|
|
how are angina patients identified as candidates for CABG?
|
1) stress test: positive -> 2) angiogram: 3-vessel disease or left main coronary disease or 2-vessel disease/diabetes
|
|
what is the management of an angina patient with 2-vessel disease?
|
angioplasty/stent
|
|
acute pharmacological treatment for stable angina includes?
|
1) nitroglycerine, 2) oxygen
|
|
what medication is given long-term for stable angina?
|
1) long-acting nitrates or beta-blockers, 2) aspirin, 3) statins
|
|
what two medications have the greatest impact on mortality in stable angina?
|
1) beta-blockers and 2) aspirin
|
|
following PCI angioplasty, what the restenosis rate without a stent? With a stent?
|
without: 1/3. with: 1/5
|
|
acute coronary syndrome encompasses what three disorders?
|
Unstable angina (UA), STEMI and non-STEMI
|
|
all patients presenting with acute coronary syndrome (ACS) are given what treatment?
|
ASA/clopidogrel, heparin, beta-blockers, statin, morphine, ACE-I, oxygen, GPIIb/IIIb inhibitors
|
|
only this type of ACS is a candidate for tPA (or other thrombolytics) for treatment:
|
STEMI
|
|
in ACS, which patients are candidates for CABG?
|
(on angiogram) those with a) 3-vessel disease, b) 2-vessel disease and diabetes, c) left main coronary disease
|
|
what two investigations are used to differentiate acute coronary syndromes?
|
1) ECG, and 2) cardiac enzymes
|
|
what are the ABCDE's for discharging a patient with ACS?
|
aspirin/anti-anginals, beta-blocker/BP drugs, cholesterol(statin)/cigarettes, diet/diabetes, education/exercise
|
|
describe an exercise stress test used for someone with chest pain
|
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)
|
|
after an ACS presenation, how long should one wait before taking a cardiac stress test?
|
5-7 days
|
|
how long must one wait for having sexual intercourse after being discharged from an MI?
|
no waiting; stress test is more demanding of the heart than intercourse
|
|
what is the most common reason for erectile dysfunction after an MI?
|
psychological
|
|
if one is taking Viagra (sidenifil) after an MI, for erectile dysfunction, what medication must be ceased?
|
nitrites
|
|
after ACS, what is the best long-term therapy to avoid VT/VF and sudden cardiac death?
|
beta-blockers
|
|
how do cardiac enzymes and ECG compare between unstable angina and a NSTEMI?
|
ECG - ischaemic changes seen in both (ST-depression); cardiac enzymes - elevated in NSTEMI
|
|
if left unmanaged, how will unstable angina progress with time?
|
with more occlusion it may progress to a NSTEMI
|
|
in Acute Coronary Syndrome, what are the 'high risk factors' used to determine who is a candidate for catheterization? (10)
|
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
|
|
What are the names of some Glycoprotein IIb/IIIa inhibitors?
|
abciximab, eptifibatide, tirofiban
|
|
what form(s) of ACS are treated with thrombolytic therapy?
|
only STEMI (if no contraindications in the patient)
|
|
what is the most common cause of death from MI in the first 24 hours?
|
(ventricular) arryhythmias
|
|
what is the common presentation of someone experiencing an MI (STEMI/NSTEMI)?
|
substernal pain/pressure with radiation (to jaw/arm/etc) lasting 20-30 minutes, experiencing presyncope, N/V, diaphoresis, dyspnoea
|
|
what investigation is used to determine if thrombolytics are used to treat ACS?
|
ECG - must have ST-elevation of >1mm
|
|
which has a greater effect on mortality, in ACS: thrombolytics or angioplasty?
|
angioplasty
|
|
what is the time frame in which reperfusion of ACS must occur?
|
12 hours
|
|
by what time (after presentation) should angioplasty occur with ACS (ie. door-to-balloon)?
|
90 min
|
|
what class of drugs are GPIIb/IIIa inhibitors?
|
antiplatelet
|
|
what drugs have the greatest benefit if given early, before angioplasty?
|
GPIIb/IIIa inhibitors
|
|
in ACS, when are thrombolytics used instead of angioplasty?
|
if facilities are unequipped and there is inadequate time to get patient to closest location that is
|
|
which thrombolytic can only be used once, due to its allogenicity?
|
streptokinase
|
|
upon presentation to hospital, how soon should a patient with ACS be given thrombolytics? (ie. Door-to-needle)
|
30 min
|
|
contraindications to thrombolysis, for ACS, are?
|
recent surgery, active bleeding, head trauma, suspected aortic dissection, prior intracranial haemorrhage, prolonged CPR, poorly controlled HTN (180/100)
|
|
if a patient has stable angina, what is the preferred method of reperfusion therapy?
|
(trick Q:) reperfusion therapy is not indicated for stable angina!
|
|
if reperfusion therapy is deemed unsuccessful and the ACS patient is still unstable, what is the next best step in treatment?
|
emegency CABG
|
|
which tachyarrhythmia is worse: Atrial or Ventrical tachycardia?
|
V-tach, as it can be lethal (SVT just presents with annoying symptoms)
|
|
what is the most common cause of conduction defect between the SA and AV node?
|
ischaemia
|
|
on ECG, what is a prolonged P-R interval (>200ms) indicative of?
|
first-degree heart block
|
|
how is first degree heart block treated?
|
first degree heart block requires no treatment
|
|
on ECG, P-P & R-R intervals that are constant, but out of sync with each other are indicative of?
|
third degree heart block
|
|
what medication can be given for third-degree heart block, if the patient is symptomatic?
|
atropine
|
|
what therapy is given for third-degree heart block, regardless of symptomatology?
|
PPM
|
|
what is the best initial therapy for a symptomatic complete heart block?
|
atropine
|
|
if a QRS complex is >120ms the diagnosis is?
|
Ventricular fibrillation or Ventricular tachycardia
|
|
the next best step in management of ventricular fibrillation is?
|
defibrillation
|
|
the next best step in management of ventricular tachycardia is?
|
(antiarrhythmic drugs:) lidocaine or amiodaone or procainamide
|
|
what is Prinzmetal's angina?
|
angina due to vasospasm, occuring at rest
|
|
angina due to vasospasm (often during sleep) is called?
|
Prinzmetal's angina
|
|
Prinzmetal's angina is common in what patients?
|
migrainers (usually women)
|
|
ECG findings for Prinzmetal's angina show?
|
ST-elevation
|
|
Stress-tests and angiography for Prinzmetal's angina show?
|
normal results
|
|
how is Prinzmetal's angina diagnosed?
|
1) ECG w/ST-elevation and 2) normal stress test/angiography
|
|
how is angina induced with a pharmaceutical challenge for Prinzmetal's angina?
|
ergonomine
|
|
what is the most common cause of congestive heart failure?
|
ischaemia
|
|
what does a displaced apex beat (to 6th ICS) indicate?
|
left ventricular hypertrophy
|
|
systolic heart failure is synonymous with?
|
decreased LVEF and dilated cardiomyopathy
|
|
what is an S3 gallop caused by?
|
left ventricular hypertrophy
|
|
in a patient with left cardiac failure and shortness of breath, what is the next best step in management?
|
oxygen, diuretics, nitrates and morphine (90% will improve)
|
|
in a patient with systolic cardiac failure, what is the goal of treatment?
|
preload reduction, with diuretics
|
|
what percent of cardiac output is attributed to atrial contraction in a healthy heart?
|
10-20%
|
|
under ventricular failure, what percent of cardiac output is attributed to atrial contraction?
|
40-50%
|
|
loss of atrial contribution to cardiac output results in what respiratory pathology?
|
pulmonary oedema
|
|
how does sputum appear with pulmonary oedema?
|
pink (blood filtrate) and frothy
|
|
how does a chest x-ray appear in congestive heart failure?
|
prominent pulmonary vessels; kerley B-lines; enlarged cardiac silhouette; diaphragmatic meniscus
|
|
what is the most sensitive position for detecting pulmonary oedema on CXR? What volume of fluid is detected?
|
lateral x-ray, which can detect 50-75ml
|
|
how do ABGs appear in congestive heart failure?
|
respiratory alkalosis (from hyperventilation): normal/decreased CO2, increased HCO3-
|
|
what is the value in performing an ECG for congestive heart failure?
|
detecting any arrhythmias which may be corrected
|
|
how is congestive heart failure managed acutely?
|
1) oxygen, 2) diuretics [Lasix], 3) nitrates, 4) morphine, 5) dobutamine [positive inotrope]
|
|
what is the effect of dobutamine on the heart?
|
positive inotrope: increased contractatility, decreased afterload
|
|
how is congestive heart failure managed chronically?
|
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
|
|
what is the first line vasodilator for CHF? Second line?
|
First: ACE-I or ARB, Second: hydralazine & nitrates (isosorbide)
|
|
what is the only nitrate approved for use in CHF?
|
isosorbide
|
|
what is the function of chronic beta-blockers in the treatment of CHF?
|
1) anti-ischaemic, 2) anti-arrhythmic
|
|
what positive inotrope is used chronically in the treatment of CHF?
|
digoxin
|
|
what is the function of digoxin in the chronic treatment of CHF?
|
improve symptoms (does not decrease mortality)
|
|
what surgeries should be considered for CHF?
|
valvular replacement, implantable AED, heart transplant
|
|
what is the mechanism of action for digoxin (digitalis)?
|
competes with potassium on Na/K ATPase pump, increasing contractility of the heart
|
|
what effect does hyperkalaemia have on digoxin?
|
decreased effectiveness
|
|
what is the danger of hypokalaemia when taking digoxin?
|
increased activity, allowing increased toxicity
|
|
what drugs are used for chronic management of CHF that protect against digoxin toxicity?
|
beta-blockers, ACE-I/ARBs, and spironolactone
|
|
how does digoxin (digitalis) toxicity commonly present?
|
GI disturbances (N/V), CNS disturbances, blurred vision (yellow halos), gynaecomastia, arrhythmias
|
|
what severe adverse effect is attributed to digoxin?
|
sudden cardiac death
|
|
how is digoxin toxicity managed?
|
stop drug, administer potassium if hypokalaemic, lidocaine, phenytoin and digibind (for acute ODs)
|
|
how does one differentiate between systolic and diastolic heart failure?
|
echo cardiogram
|
|
what kind of heart failure is an S4 gallop associated with?
|
diastolic failure
|
|
how is diastolic heart failure managed differently from systolic?
|
do not give a positive inotrope (contraction is normal)
|
|
what valve does rheumatic fever most commonly affect?
|
mitral valve
|
|
what valves can rheumatic fever affect?
|
all of them (but most common is MV)
|
|
what is the best initial test for valvular heart disease?
|
echocardiogram
|
|
what findings on CXR are consistent with valvular heart disease?
|
cardiac enlargement, and other signs of CHF
|
|
what finding on ECG are consistent with valvular heart disease?
|
cardiac enlargement
|
|
what is the most accurate test for valvular heart disease?
|
catheterization
|
|
what complications are common to all forms of valvular heart disease?
|
1) TIA/stroke and 2) CHF
|
|
what is the most common cause of mitral valve stenosis?
|
rheumatic fever
|
|
what population is most commonly affected by MV stenosis in developed countries?
|
(damn) immigrants!
|
|
what is the female:male ratio of MS?
|
2:1
|
|
when is the most common time for women to present with mitral stenosis?
|
pregnancy
|
|
what is the mechanism behind hoarseness in mitral stenosis?
|
enlarged LA presses against the recurrent laryngeal nerve
|
|
why do patients with mitral stenosis sometimes present with dysphagia?
|
esophageal compression
|
|
how does mitral stenosis sound on auscultation?
|
cardiac - loud S1; opening snap following S2 … pulmonary - rales
|
|
what is the difference between orthopnea and paroxysmal nocturnal dyspnoea?
|
orthopnea is relieved by sitting up, while PND is not
|
|
what major complication are patients with mitral stenosis at risk of?
|
TIA/stroke (LA atrial enlargement leads to Afib,which may throw off emboli)
|
|
what ECG findings are consistent with mitral stenosis?
|
LA enlargement & RVH. Possible Afib.
|
|
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
|
|
what is the clinical presentation of mitral stenosis?
|
RHF, dyspnoea, rales, orthopnoea/PND, fatigue, wasting, haemoptysis, hoarseness, dysphagia, decreased pulse pressure, loud S1
|
|
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
|