Cardiovascular Flashcards
Non infectious causes os pericarditis
neoplastic
metabolic
traumatic
post-acute-MI (Dressler Synd)
iatrogenic (Covid vaccines)
Cardiac tamponade triad (Beck’s)
soft heart sounds
elevated jugular venous pressure
hypotension
How to investigate a patient with pericarditis suspicion
ECG
chest X-ray
markers of inflammation (eg CRP, ESR, WCC)
cardiac troponin concentration (marker of myocardial injury)
transthoracic echocardiogram.
Diagnostic criteria for pericarditis
At least 2:
pericarditic chest pain
pericardial rubs
new widespread ST elevation or PR depression on electrocardiogram (ECG)
pericardial effusion (new or worsening)
Acute pericarditis treatment
Colchicine + NSAID (+ cortics if NSAID CI)
Colchicine:
70 kg or more: 500 micrograms orally, twice daily for 3 months
less than 70 kg: 500 micrograms orally, once daily for 3 months
+
aspirin 750 to 1000 mg orally, 8-hourly for 1 to 2 weeks, then decrease the dose by 250 to 500 mg every 1 or 2 weeks to stop
OR
ibuprofen immediate-release 600 mg orally, 8-hourly for 1 to 2 weeks, then decrease the dose by 200 to 400 mg every 1 or 2 weeks to stop
Endocarditis Diagnosis
Duke’s criteria: (2 major and 1 minor criterion OR 1 major and 3 minor OR 5 minor)
MAJOR:
- Positive blood cultures for infective endocarditis typical microorganism from 2 separate blood cultures 12h apart (Viridans streptococci, Streptococcus bovis, HACEK group OR community-acquired S. aureus or enterococci in the absence of a primary focus)
- Evidence of endocardial involvement
(positive echocardiogram for infective endocarditis or regurgitation)
- Single positive blood culture for Coxiella Burnetii or antiphase I IgG antibody titer >1:800
MINOR:
- predisposing heart condition or intravenous drug use
- fever: 38°C
- vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway lesions
- immunologic phenomena: glomerulonephritis, Osler nodes; Roth spots; rheumatoid factor
- microbiologic evidence: positive blood culture but not meeting major criteria or serologic evidence of active infection with organism consistent with infective endocarditis
- echocardiography findings consistent with infective endocarditis but not meeting major criteria
Native valve Endocarditis’ treatment
- Empirical (4-6 weeks):
Benzylpenicillin 1.8 g intravenously, 4-hourly
+
Flucloxacillin 2 g intravenously, 4-hourly
+
gentamicin intravenously over 3 to 5 minutes:
– with septic shock and without kidney impairment: 7 mg/kg, for the first dose
– without septic shock: 4 to 5 mg/kg for first dose
! If MRSA suspected or shock at initial presentation:
– replace benzylpenicillin with vancomycin (adult and child) 25 to 30 mg/kg intravenously
! If hypersensitivity to penicillins:
Cefazoline 2g 8-hourly
+ vancomycin + gentamicin
Therapy for prosthetic valve and cardiac implantable electronic device-associated infective endocarditis
Flucloxacilin + vancomycin + gentamicin
When is prophylaxis for endocarditis indicated?
For patients who meet both of the following criteria:
- Have a cardiac condition associated with an increased risk of developing infective endocarditis and the highest risk of adverse outcomes from endocarditis:
– rheumatic heart disease; prosthetic cardiac valve, including transcatheter-implanted prosthesis; previous infective endocarditis;
congenital heart disease but only if it involves: unrepaired cyanotic defects, including palliative shunts and conduits
repaired defects with residual defects at or adjacent to the site of a prosthetic patch or device (which inhibit endothelialisation)
!! Not patients with cardiac implantable electronic devices. - Are undergoing a procedure associated with a high risk of a bacteraemia that is associated with endocarditis
– Dental procedures; dermatological or musculoskeletal procedures — only those involving infected skin, skin structures or musculoskeletal tissues.
Respiratory tract or ear, nose and throat procedures; Genitourinary and gastrointestinal tract procedures—only if surgical antibiotic prophylaxis is required or for patients with an established infection
Prophylatic treatment for infective endocarditis:
amoxicillin 2 g (child: 50 mg/kg up to 2 g) orally, 60 minutes before the procedure.
What’s the more usual sign find on EKG in WPW disease?
Delta wave
What’s the finding on EKG in pericarditis?
Wide spread concave ST elevations
What are the drug most commonly associated with EKG findings?
Digoxin and anti-convulsivants/antipsychotics
What’s the finding on EKG in digoxin toxicity?
infra-desnivelamento “curvo” do segmento ST
Whats’ the EKG finding in hipocalcemia?
ST segment and QT interval shortening
What’s the EKG findings in hipokalemia?
- U wave
- Long PR interval
- Depressed ST segment
- Inverted and shallow T waves
Most common cause of pericarditis
Viral
Coxsackie B, influenza and Epstein-Barr viruses.
What’s the first line treatmente for HAS in patients 65>?
Low-dose thiazide diuretic
!!!They are not recommended for younger patients due to the risk of diabetes associated with long-term use.
What’s the long term use risk associated with thiazide diuretics?
DM
What’s the findings in the physical exam of aortic valve stenosis?
Ejection systolic murmur heard best at the upper right sternal border and a slow-rising pulse. Decreases with valsalva manoeuvre.
What’s the findings in the physical exam of Hypertrophic obstructive cardiomyopathy (HOCM)
Ejection systolic murmur that increases with valsalva manoeuvre
What’s Dressler’s syndrome?
An autoimmune pericarditis that occurs up to six weeks post-AMI.
What’s Kussmaul’s sign?
An increase in the jugular venous pulse during an inspiration. A sign of right ventricular insuficiency. Also common in pericarditis.
Electrical alternans in ECG indicates…?
Pleural effusion or Cardiac Tamponade
Alternating QRS amplitudes in any or all leads on an electrocardiogram (ECG) with no additional evident changes in conduction pathways of the heart.
What is Pulsus paradoxus and what it indicates?
Pulsus paradoxus is defined as a fall of systolic blood pressure of >10 mmHg during the inspiratory phase
Cardiac tamponade
MI shown in ST elevation in leads I, aVL, V5, V6 is caused by which artery impairment?
Circumflex coronary artery
A lateral STEMI.
Usually occurs in combination with an anterior STEMI.
ST segment elevation in leads II, lll and aVF. Which coronary artery is most likely to be involved in this event?
Right coronary artery
When to hear a functional murmur?
When there’s hyperdynamic circulation, such as anaemia or thyrotoxicosis
How’s a mitral valve regurgitation murmur?
Pan-systolic, loudest over the apex.
How’s a aortic sclerosis murmur?
Mid-systolic ejection murmur loudest at the second right intercostal space. S1 and S2 are both normal. There is no radiation to the axilla or carotids. Performing the Valsalva maneuver does not increase murmur intensity.
ECG findings on WPW
Wide QRS, Narrow PR and delta wave
Where are the aortic aneurysm more common?
Descending aorta
What’s the most common aortic aneurysms?
Abdominal aortic aneurysms are by far the most common. Thoracoabdominal aortic aneurysms comprise approximately 10% of all aortic aneurysms.
What are the risck factors for aortic aneurysms?
Female
Advanced age
Smoking - most important
HAS
Family history
What’s the other finding in someone carrying a poplyteal aneurysm?
An abdominal aortic aneurysm
A triad of intense abdominal pain radiating through to the back, profound hypotension, and a pulsatile abdominal mass is related to?
Rupturing aortic aneurysm
When to consider CT with contrast for aortic aneurysm?
For aneurysms greater than 5cm in which repair is being considered or planned.
In patients presenting with acute rupture, imaging via CT is recommended for patients who are haemodynamically stable. If unstable, imaging is not absolutely required prior to intervention.
!Remember: Angiography is not reliable for determining aneurysm diameter as the possible presence of thrombus obscures the outer limit of the aneurysm
Initial management for ruptured aortic aneurysm?
- resuscitation in preparation for surgery
- Pain control
- Systolic blood pressure should be maintained between 80 – 100mmHg to minimize further damage to the aorta and limit blood loss.
- Temperature control of the patient is an important element as patients quickly become hypothermic from shock and may precipitate a diffuse coagulopathy.
- Haemodynamically stable patients may undergo CT to evaluate whether endovascular repair is feasible if facilities are present for endovascular intervention.
- Haemodynamically unstable patients should be transferred to the operating theatre immediately to control haemorrhage with concurrent resuscitation
Treatment of asymtomatic aortic aneurysm
Elective repair is the most effect treatment in preventing rupture. But should not undertaken until the risk of rupture exceeds the risks associated with repair.
If >5,5cm in diameter, repair, if no CI.
Asymptomatic patients with inflammatory type abdominal aortic aneurysm or with complications such as distal embolisation, or bowel obstruction require urgent repair regardless of aneurysm size.
Survaillance of asynptomatic aortic aneurysms
Clinical assesment + USG in every 6 months if <4,5cm
If 4,5-5cm, USG 3 moths
When the aneurysm is deemed to require intervention, the patient will undergo planning for repair via contrast enhanced CT
Smoke cessation
Drug interaction: Warfarin + Amiodarone
Increased bleeding risk - Haematoma formation
(Amiodarone decreases the hepatic metabolisation of warfarin)
Drug interaction: Amiodarone + estatins
Amiodarone inhibit the chromossome P450, enhancing estatin activity and raising the likelihood of estatin-related adverse effects:
Muscular pain,
Myopathy
Rhabdomyolisis - ^^^ K (and risk of cardiac arrest) + renal failure due to myoglobin deposit
What’s the most useful marker of myocardial re-infarction in a patient who already has myocardial infarction 12 hours ago?
The CK-MB elevation is the best indicator of myocardial re-infarction because of its short half-life of 12 hours
Serum troponin levels should be assayed at the time of initial assessment and then at 3–6 hours. Troponin levels reach their peak at 12 hours and remain elevated for 7 to 10 days, making troponin a uniquely useful test for patients with delayed presentations.
Chest pain duration and intensity similar to the first event may happen in other conditions like pericarditis etc. So it is not very specific for re-infarction.
anti-mitochondrial antibody
primary biliary cholangitis (PBC, previously termed primary biliary cirrhosis)
primary biliary cholangitis - overview (cf, epidemiology)
PBC is a chronic liver disease characterized by autoimmune destruction of the intrahepatic bile ducts with resulting cholestasis. It presents most commonly in middle-aged women and is insidious in onset. As the disease progresses, jaundice, hepatomegaly, steatorrhea, and portal hypertension may develop. Additional complications can include severe hyperlipidemia (with xanthelasma) and metabolic bone disease. PBC is often associated with other autoimmune disorders (eg, autoimmune thyroid disease).
primary biliary cholangitis VS autoimmune hepatitis
Autoimmune hepatitis is associated with elevated titers of antinuclear antibodies and anti-smooth muscle antibodies. It is characterized by fluctuating hepatocellular injury (ie, elevated transaminases) rather than cholestasis. First-line treatment includes oral glucocorticoids.
Aortic Stenosis and its Clinical Features
This patient likely has congestive heart failure due to aortic stenosis.
The classic description of the murmur associated with aortic stenosis includes a harsh systolic, crescendo-decrescendo murmur at the right upper sternal border that radiates to the carotid arteries.
The S4 heart sound is also present and occurs due to left atrial kick against a stiff left ventricle, which is a result of the high resistance generated by the stenosed aortic valve. 🩺❤️
What are the three most common causes of aortic stenosis in the general population?
The three most common causes of aortic stenosis in the general population are senile calcific aortic stenosis, bicuspid aortic valve, and rheumatic heart disease.
Notably, a bicuspid aortic valve is the cause of aortic stenosis in the majority of patients under the age of 70. 🧬🏥
How can the murmur of aortic stenosis be distinguished from that of hypertrophic cardiomyopathy?
The murmur of hypertrophic cardiomyopathy can be easily confused with that of aortic stenosis.
Both conditions can cause a systolic crescendo-decrescendo murmur and an S4 heart sound.
However, the murmur of hypertrophic cardiomyopathy is typically best appreciated in the lower left sternal border and does not typically radiate to the carotids. 🩺📈
What is the recommended endoscopic surveillance protocol for patients with CLE without intestinal metaplasia?
In patients with long-segment (≥3 cm) CLE without intestinal metaplasia or dysplasia, endoscopic surveillance should follow the protocol for long-segment Barrett’s esophagus (BE), occurring every 2–3 years.
For individuals with 1 to <3 cm of CLE without intestinal metaplasia or dysplasia, a repeat endoscopy in 3–5 years is suggested, with consideration for discharge from surveillance if the repeat endoscopy with Seattle protocol biopsies again shows no intestinal metaplasia or dysplasia.
Patients with CLE less than 1 cm without intestinal metaplasia or dysplasia on biopsies should not undergo endoscopic surveillance. 📅🔍
what factors influence the decision for acute rhythm control in hemodynamically stable patients with atrial fibrillation, and which drugs are used for acute pharmacological cardioversion?
In hemodynamically stable patients, acute rhythm control may be considered if they are symptomatic or if it is their first episode with an onset of less than 48 hours 🩺📊
Flecainide and amiodarone are the two drugs available for acute pharmacological cardioversion 🩹
What is the recommended approach for patients with hemodynamically stable atrial fibrillation lasting more than 48 hours or of unknown duration, and when can acute rhythm control be attempted?
For patients with hemodynamically stable atrial fibrillation lasting more than 48 hours or of unknown duration, acute rhythm control should ideally be attempted only after anticoagulation for three weeks 📅
Anticoagulation should be continued for at least four weeks after cardioversion 🩸
It is reasonable to attempt acute cardioversion after a transesophageal echocardiogram has excluded a left atrial thrombus 📸
What are the treatment options for acute rate control in atrial fibrillation?
Treatment options for acute rate control include beta blockers, non-dihydropyridine calcium channel antagonists, and amiodarone 🩺
Amiodarone is typically reserved for highly symptomatic patients with known left ventricular dysfunction when other drugs could be contraindicated 🚑
What are the first-line therapies for long-term rate control in patients without left ventricular dysfunction?
First-line therapies for long-term rate control in patients without left ventricular dysfunction are beta blockers (e.g., metoprolol), non-dihydropyridine calcium channel blockers (e.g., verapamil), or digoxin, with monitoring of serum concentrations 📊📈
What is the recommended first-line rate control therapy for patients with left ventricular dysfunction, and which drugs are contraindicated in this context?
In patients with left ventricular dysfunction who are not being considered for rhythm control or who have failed rhythm control, first-line rate control therapy should be with beta blockers (e.g., bisoprolol, carvedilol, controlled-release metoprolol, or nebivolol), or digoxin 🫁
Non-dihydropyridine calcium channel blockers are contraindicated in patients with left ventricular dysfunction 🚫
How does aortic valve regurgitation (AR) result in different murmurs, and where are these murmurs best heard?
Aortic valve regurgitation (AR) causes three different murmurs due to the backflow of blood from the aorta into the left ventricle during diastole 🫁
The diastolic crescendo murmur is best heard over the left sternal border 🩺
The increased end-diastolic left ventricular volume results in a functional flow murmur during systole, often best heard between the apex and the left sternal border 📊
In severe AR, a rumbling mid-diastolic jet murmur (Austin-Flint murmur) may be heard. The jet flow strikes the anterior leaflet of the mitral valve and closes it prematurely 🌬️
How can you differentiate Aortic stenosis from other valvular lesions based on murmur characteristics and auscultation locations?
Aortic stenosis is associated with an ejection murmur in the aortic area, often associated with thrills. It has a harsh quality and may radiate to the carotids 🌬️
How does Mitral valve regurgitation result in different murmurs, and where are these murmurs best heard?
Mitral valve regurgitation causes a holosystolic systolic murmur radiating to the axilla and best heard over the apex 🫁
How does Mitral valve stenosis result in different murmurs, and where are these murmurs best heard?
Mitral valve stenosis is characterized by an opening snap after the S2 and a diastolic rumbling murmur, best heard at the apex 🩺
