Cardio Flashcards
The main cause of Coronary artery disease
Atherosclerosis
What is the cause of vasospastic angina
Cigarette smoking, use of stimulants (e.g., cocaine, amphetamines) or sumatriptan, alcohol, stress, hyperventilation, exposure to cold
There is an association with other disorders involving vasospasms (e.g., Raynaud phenomenon, migraine headaches)
Outline in one sentence treatment approach for
- mild CHD
- moderate CHD
- severe CHD
All patients: risk factor reduction and antiplatelet drugs
Mild CHD: pharmacologic therapy
Moderate CHD: consider coronary angiography and percutaneous transluminal coronary angioplasty (PTCA)/percutaneous coronary intervention (PCI)
Severe CHD: coronary angiography and revascularization or coronary artery bypass grafting
What are the 1st line anti-anginal treatment
First-line
1) Beta-blockers (except in vasospastic angina): can reduce the frequency of coronary events
2) Nitrates
Can prevent exertional angina
Suitable for relief of acute angina or for long-term treatment
What are the 2nd line anti-anginal treatment
CCB
What are the indications for revascularization and what are the 2 techniques
Indications
1) In stable angina: activity-limiting symptoms despite optimal medical treatment, contraindications to medical therapy, stenosis of critical (e.g., LCA) or multiple coronary arteries
2) Acute coronary syndrome
Techniques
1) Percutaneous coronary intervention
2) Coronary artery bypass grafting
ACS includes 3 conditions which are
1) Unstable angina
2) NSTEMI
3) STEMI
Acute coronary syndrome: suspicion or confirmed presence of acute myocardial ischemia and/or myocardial infarction
Further classified as unstable angina, NSTEMI, and STEMI
What is the difference between occlusions in the 3 difference ACS
Unstable angina–> Partial occlusion of coronary vessel → decreased blood supply → ischemic symptoms (also during rest)
NSTEMI–>Classically due to partial occlusion of a coronary artery
Affects the inner layer of the heart (subendocardial infarction)
STEMI–>Classically due to complete occlusion of a coronary artery
Affects full thickness of the myocardium (transmural infarction)
Cardiac biomarkers are seen positive in
NSTEMI and STEMI
NOT IN UNSTABLE ANGINA
ECG changes in NSTEMI
Normal or nonspecific (e.g., ST depression, loss of R wave, or T-wave inversion)
No ST elevations
ECG changes in STEMI
ST elevations (in two contiguous leads) or new left bundle branch block
ECG changes in NSTEMI/unstable angina
No ST elevations present Nonspecific changes may be present. ST depression Inverted T wave Loss of R wave
To remember the ECG leads with maximal ST elevation in anterior MI, think “SAL”
SAL”: “Septal (V1–2), Apical (V3–4), Lateral (V5–6).
Troponin which is most sensitive is
Troponin T
What is the best test for definitive diagnosis of acute coronary occlusion
Coronary angiography
Which artery is the most –> least likely to get occluded(3)
left the anterior descending artery
right coronary artery
circumflex artery.
What risk stratification score can be used for unstable angina/NSTEMI
TIMI score for unstable angina/NSTEMI
State some cardiac causes of chest pain
Pericarditis Myocarditis Takotsubo cardiomyopathy Aortic dissection Valvular anomaly (e.g., acute mitral regurgitation, aortic regurgitation, aortic stenosis) Vasospastic angina
State some resp causes of chest pain
Pulmonary embolism Pneumonia pleuritis Pneumothorax Asthma COPD
State some GIT causes of chest pain
Gastroesophageal reflux disease, esophagitis
Boerhaave syndrome, esophageal perforation
Acute gastritis
Mallory‑Weiss syndrome
Dyspepsia, peptic ulcer disease
Acute pancreatitis
Cholelithiasis, cholecystitis, biliary colic
State derm and MSK causes of chest pain
costochondritis and herpes zoster
State some psych causes of chest pain
Anxiety
Depression
Stimulant drug use (e.g., cocaine)
MONA for ACS, but can we give all of these drugs to all the patients
Primary interventions of MI treatment include “MONA”: Morphine, Oxygen, Nitroglycerin, and Aspirin. But remember: Morphine, oxygen, and nitroglycerine are not necessarily indicated for every patient
GTN–>Contraindications: inferior wall infarct (due to risk for hypotension), hypotension, and/or PDE 5 inhibitor (e.g., sildenafil) taken within last 24 hours
What is the immediate 1st step of STEMI
REVASCULARIZATION
Tell me about emergency coronary angiography
Emergent coronary angiography: with percutaneous coronary intervention (PCI)
Preferred method of revascularization
Balloon dilatation with stent implantation (see cardiac catheterization)
Ideally, door-to-PCI time should be < 90 minutes. It should not exceed 120 minutes.
What are the indications for thrombolytic therapy and what are the drugs that can be used
Thrombolytic therapy: tPA, reteplase, or streptokinase
Indications:
If PCI cannot be performed < 120 minutes after onset of STEMI
If PCI was unsuccessful
No contraindications to thrombolysis
State some contraindications for thrombolysis
Any prior intracranial bleeding Recent large GI bleeding Recent major trauma, head injury, and/or surgery Ischemic stroke within the past 3 months Hypertension (> 180/110 mm Hg) Known coagulopathy
Walk me through the STEMI management(eTG)
- A- Intubate?, B- Ventilate? , C- IV acces/fluids?
- MONA
- Investigations eg. ECG, Trops
- Admit under coronary care unit
- MedicateDual antiplatelet therapy- Aspirin + Clopidogrel (Dose of clopidogrel dependant on means of reperfusion therapy used- i.e. lower dose if doing fibrinolytic therapy)
- Reperfusion - 2 methods, one must be started within 12 hours post-presentation, because post 12 hours infarction may already be complete. May be considered after 12 hours if there is - 1) Viable myocardium (R wave progression in infarcted leads) 2) Continued ischaemia (Persisting chest pain) 3) Major complications (shock)
1) PCI- within 90 minutes of presentationPre procedure- Dual Anti-platelet, Anti-coagulation - Unfractionated heparin/ Enoxaparin (LWMH)
2) Fibrinolytic therapy - tTPA Alteplase - If known that PCI cannot be performed within 90 mins, start this witin 30 mins.Pre procedure- Dual Anti-platelet, Anti-coagulation - Unfractionated heparin/ Enoxaparin (LWMH)
What is the priority in STEMI and what is the priority in NSTEMI
The priority for a STEMI is re-establishing blood flow in the occluded coronary artery (reperfusion), which is achieved with percutaneous coronary intervention or fibrinolytic therapy.
The priority for a NSTEMI is plaque stabilisation and the prevention of coronary occlusion with medical therapy, and, if appropriate (TIMI score >3 –> revascularisation PCI, preferably within 72 hours)
What is the most common causes of IE
Staphylococcus aureus (45–65%)
Acute IE is caused by
Staphylococcus aureus (45–65%)
Subacute IE is caused by
Viridans streptococci
Most common cause of subacute IE, especially in predamaged native valves (mainly the mitral valve
Common cause of IE following dental procedures
Produce dextrans that facilitate binding fibrin-platelet aggregates on damaged heart valves
What is the criteria used for IE
Duke’s criteria
Most common cause of IE
Staphylococcus aureus (45–65%)
Most common cause of acute IE for all groups (including IV drug users and patients with prosthetic valves or pacemakers/ICDs)
FROM JANE
FROM JANE - Fever Roth's spots Osler nodes Murmur Janeway lesions Anemia Nail bed hemorrhage Emboli
Extra-cardiac symptoms of IE
- what are the reasons for extracardiac symptoms
- state as many as you can
These manifestations are mainly caused by bacterial microemboli and/or the precipitation of immune complexes
1) Petechiae; especially splinter hemorrhages (hemorrhages underneath fingernails)
2) Janeway lesions: non-tender, erythematous macules on palms and soles (due to microemboli and microabscesses with neutrophilic capillary infiltration)
3) Osler nodes: painful nodules on pads of the fingers and toes
4) Roth spots: retinal hemorrhages with pale centres
Signs of acute renal injury, including hematuria and anuria
Splenomegaly and possible LUQ pain
Neurological manifestations (e.g., seizures, paresis)
Signs of pulmonary embolism (e.g., dyspnea)
Possible arthritis
In IE, which nodules are painful and which are not
Osler nodes are painful–>OOOOO
Janeway lesions are not
What are the clinical consequences of IE systemically(like you know the pathophysiology, what will happen because of it)
Bacterial thromboemboli from bacterial vegetation → vessel occlusion with infarctions
Formation of immune complexes and antibodies against tissue antigens → glomerulonephritis, Osler nodes
What are the clinical consequences of IE systemically(like you know the pathophysiology, what will happen because of it)
Bacterial thromboembolic from bacterial vegetation → vessel occlusion with infarctions
Formation of immune complexes and antibodies against tissue antigens → glomerulonephritis, Osler nodes
Outline the Duke criteria(Modified)
The Duke criteria help to diagnose infective endocarditis.
To confirm the diagnosis, one of the following requirements must be met:
- Two major criteria
- One major and three minor criteria
- Five minor criteria
Major diagnostic criteria
1) Two separate blood cultures positive for typical pathogens
2) Evidence of endocardial involvement in echocardiography
3) A new valvular regurgitation (worsening of a pre-existing murmur is not sufficient)
Minor diagnostic criteria
Predisposition: underlying heart disease or IV drug abuse
Fever ≥ 38°C (100.4F)
Vascular abnormalities
Immunologic disorder
Microbiology
Outline the Duke criteria(Modified)
The Duke criteria help to diagnose infective endocarditis.
To confirm the diagnosis, one of the following requirements must be met:
- Two major criteria
- One major and three minor criteria
- Five minor criteria
Major diagnostic criteria
1) Two separate blood cultures positive for typical pathogens
2) Evidence of endocardial involvement in echocardiography
3) A new valvular regurgitation (worsening of a pre-existing murmur is not sufficient)
Minor diagnostic criteria
1) Predisposition: underlying heart disease or IV drug abuse
2) Fever ≥ 38°C (100.4F)
3) Vascular abnormalities
4) Immunologic disorder
5) Microbiology
Which diagnostic test is the most sensitive for IE
Only negative findings on transesophageal echocardiography (TEE) can reliably rule out endocarditis, as transthoracic echocardiography (TTE) is not sensitive enough!
How many cultures are needed for IE
Blood Cultures- 3 sets from separate venepuncture sites
IE treatment for-Prosthetic valve
vancomycin+flucloxacillin+gentamicin
IE treatment for-Native valves
benzylpenicillin+flucloxacillin+gentamicin(triple therapy)
Life-threatening condition of chest pain-4
Myocardial infarction
pulmonary embolism
aortic dissection
pneumothorax
ECG right ventricular strain pattern is
S1Q3T3 pattern, right bundle branch block.
RHD includes 2 conditions what are the (or 2 clinical sequelae)
Acute pancarditis as a sequela of GAS infection
Chronic cardiac valvular changes as a complication of acute rheumatic fever
Is rheumatic fever associated with strep skin infection
Rheumatic fever is not associated with streptococcal skin infections (e.g., erysipelas, impetigo, cellulitis).
JONES criteria and CAFEPAL
Major criteria
Arthritis (migratory polyarthritis involving primarily the large joints)
Carditis (pancarditis, including valvulitis)
Sydenham chorea (CNS involvement)
Subcutaneous nodules
Erythema marginatum
Minor criteria Arthralgia Fever ↑ Acute phase reactants (ESR, CRP) Prolonged PR interval on the electrocardiogram
What must be met in JONES criterion
Interpretation: two major OR one major plus two minor criteria are required for diagnosis.
Confirmation of GAS infection
↑ Antistreptolysin O titer (ASO): antibodies against metabolites of GAS
Confirmation of GAS infection can be done through what kind of tests
-what will be an FBC show?
↑ Antistreptolysin O titer (ASO): antibodies against metabolites of GAS
Positive rapid streptococcal antigen test or throat culture for GAS
FBC:Normochromic, normocytic anemia of chronic inflammation
Leukocytosis
Echocardiogram (may show mitral or aortic regurgitation)
What is the treatment for Acute ARF(eTG)
- IM- Benzathine benzylpenicillin IM, single-dose, then followed by
- Oral- Phenoxymethylpenicillin for 10 days (need to ensure adherence)
What is the treatment for arthritis and fever
- NSAIDs
- Aspirin
Stop NSAID after the patient has been symptoms free for 1-2 weeks
What is the treatment for chorea
- Carbamazepine / sodium valporate
How to prevention measure should be taken for ARF
Prevention - Antibiotic prophylaxis against GAS infection to prevent recurrence of acute rheumatic fever and development or progression of rheumatic heart disease
- IM- Benzathine benzylpenicillin IM, every 28 days
Erysipelas is caused by
Erysipelas is almost always caused by Streptococcus pyogenes (group A streptococcus).
Acute pericarditis vs constrictive pericarditis-definition
Acute pericarditis is inflammation of the pericardium that either occurs as an isolated process or with concurrent myocarditis.
Constrictive pericarditis is characterized by compromised cardiac function caused by a thickened, rigid, and fibrous pericardium secondary to acute pericarditis.
The most common cause of pericarditis
Viral
Can MI give you pericarditis
Yes
Myocardial infarction: pericarditis may occur either within 1–3 days as an immediate reaction (i.e., post-infarction fibrinous pericarditis),
or weeks to months following an acute myocardial infarction (Dressler syndrome).
State some of the features of constrictive pericarditis
Symptoms of fluid overload (backward failure)
Jugular vein distention, ↑ jugular venous pressure
Kussmaul sign
Hepatic vein congestion → hepatomegaly, painful liver capsule distention, hepatojugular reflux
Peripheral edema or anasarca, ascites with abdominal discomfort
Symptoms of reduced cardiac output (forward failure)
Fatigue, dyspnea on exertion
Tachycardia
Pericardial knock: sudden cessation of the ventricular filling during early diastole that is heard best at the left sternal border
Pulsus paradoxus: ↓ blood pressure amplitude during deep inspiration
Pericarditis-ECG-initial stage
Stage 1: initial diffuse ST elevations, but ST depression in aVR and V1; PR segment depression
Treatment for
1) Acute pericarditis
2) Constrictive pericarditis
Acute pericarditis is often self-limiting and resolves within approx. 2–6 weeks.
Treat underlying cause
Restricted physical activity
NSAIDs plus colchicine (alleviates symptoms, reduces rate of recurrence)
Glucocorticoids if NSAIDs are ineffective
Constrictive pericarditis
Treat underlying condition
Symptomatic therapy (manage fluid overload with diuretic therapy)
Pericardiectomy (complete removal of the pericardium)
Complication if pericarditis is not treated
Constrictive pericarditis(as a complication of acute pericarditis) Cardiac tamponade
Most common causes of myocarditis
- viral
- bacterial
Coxsackie B1-B5 (picornavirus), parvovirus B19,
β-hemolytic Streptococcus group A (acute rheumatic fever) Corynebacterium diphtheriae (diphtheria, diphtheria toxin)
Clinical features of myocarditis
- Often asymptomatic
- Preceding (1–2 weeks) flulike symptoms
- Fatigue, weakness, dyspnea
- Cardiac arrhythmias: often sinus tachycardia; palpitations or syncope
- Chest pain: indicates pericardial involvement (perimyocarditis)
- Acute decompensated congestive heart failure with dilated cardiomyopathy
- Cardiogenic shock in fulminant cases
Auscultation findings
1) systolic murmurs
2) Heart failure → S3 (and S4) gallops
3) Pericarditis → pericardial friction rub
Complications of myocarditis
1) Progression to dilated cardiomyopathy
2) Heart failure or sudden cardiac death
3) Acute and/or persistent arrhythmias
Pericardial effusion
Pericardial effusion is the acute or chronic accumulation of fluid in the pericardial space (between the parietal and the visceral pericardium) and is often associated with a variety of underlying disorders.
Pericardial effusion and cardiac tamponade symptoms and signs
- Usually initially asymptomatic
- Shortness of breath, especially while lying down (orthopnea)
- Beck’s triad
1) Hypotension
2) Muffled heart sounds
3) Distended neck veins - Tachycardia, pulsus paradoxus
- Retrosternal chest pain
- Apical impulse difficult to locate or nonpalpable
- Pallor, cold sweats
- Symptoms of left heart failure and symptoms of right heart failure
- Cardiogenic shock, asystole
Beck’s triad
- Beck’s triad
1) Hypotension
2) Muffled heart sounds
3) Distended neck veins–>Due to elevated jugular venous pressure.
CXR in pericardial effusion shows
CXR: enlarged cardiac silhouette, clear lungs, in severe cases a globular “water bottle-shaped” heart contour (water bottle sign)
Treatment for pericardial effusion and cardiac tamponade
1) Depends on
2) What is the treatment for those approaches
Unstable –> Pericardial fluid drainage: ultrasound-guided pericardiocentesis or surgical drainage
Stable–> underlying cause
What are the causes of pericardial effusion and cardiac tamponade
Hemopericardium
- Cardiac wall rupture (e.g., the complication of myocardial infarction)
- Chest trauma
- Aortic dissection
- Cardiac surgery (e.g., heart valve surgery, coronary bypass surgery)
Serous pericardial effusion
- Idiopathic
- Acute pericarditis (especially viral, but also fungal, tuberculous or bacterial)
- Malignancy
- Poststernotomy syndrome
- Uremic
- Autoimmune disorders
- Hypothyroidism
Most common cause of syncope
Vasovagal
State the types of syncope
1) Cardiac–>Arrhythmogenic syncope and CVD syncope
2) Reflex/vasovagal
3) Orthostatic syncope (postural hypotension)
Which two investigations do all syncope patients get
ECG (for all patients!)
CBC (↓ serum Hb)
What are the life-threatening conditions you should rule out in syncope
It is important to rule out life-threatening causes of syncope such as pulmonary embolism, hemorrhage, or serious cardiac conditions!
DDx for syncope
Seizure Vertebrobasilar insufficiency Craniocerebral injury--> TBI Heatstroke Panic attacks(Hyperventilation)
State some common causes of syncope
Vasovagal Arrhythmias Dehydration Drugs--> new drug started? Intoxication Hypoglycemia
Bilateral edema of the leg mainly points to a diagnosis of
Cardiac failure
Generalized peripheral pitting edema with swelling of the eyelids indicates
Hypoalbuminemia (e.g., in nephrotic syndrome)
Non-pitting edema suggests
lymphatic disorders and thyroid conditions.
What are the 4 internal edema
Interstitial pulmonary edema
Cerebral edema
Ascites
Pleural effusion
Cause of edema in the CHF
↑ Pc due to venous congestion (e.g., congestive heart failure)
