Cardiovascular Flashcards
Key lab findings with cholesterol emboli
Eosinophilia, eosinophiluria, and low complement
Skin findings in cholesterol emboli
- Livedo reticularis (reticulated, mottled, discolored skin due to swollen venules from capillary obstruction)
- Blue toe syndrome
Internal organ damage in chiolesterol emboli
- Acute kidney injury
- Pancreatitis
- Mesenteric ischemia
- Embolic stroke, amaurasis fugax
3 potential triggers of vasovagal syncope
Stress, pain, or urination
What, if any, are the warning signs of:
- Syncope 2/2 arrhythmia
- Syncope 2/2/ orthostatic hypotension
- Vasovagal syncope
- Arrhythmia: no warning
- Orthostatic hypotension: lightheadedness when standing up
- VasovagaL; nausea, diaphoresis, pallor in response to stress, pain, or urination
What can be done to abort a vasovagal syncope episode when a person starts feeling nauseous, sweaty, and pale?
Physical counterpressure measures (PCM: squatting, arm-tensing, leg-crossing, and leg-crossing with lower body muscle tensing)
Treatment of primary Raynaud’s syndrome? Secondary?
Primary: Trigger avoidance and CCBs if necessary
Scondary: The same, plus aspirin to patients at risk for digital ischemia
Difference between primary and secondary Raynaud’s in terms of:
- Demographics
- Symmetry
- Risk of tissue injury
Demographics: Primary is younger women (<30), secondary is more older men (>40)
Symmetry: Primary is symmetric, secondary may be asymmetric
Risk of tissue injury and ulceration: only in secondary
Causes of secondary Raynaud’s syndrome (6)
- Connective tissue disease (lupus, scleroderma)
- Occlusive vascular disease
- Hyperviscosity syndromes
- Sympathomimetic drugs
- Birth control pills
- Smoking
An ICU patient on pressures has necrosis of distal fingers and toes. Likely cause?
Norepinephrine-induced vasospasm (can also caused mesenteric ischemia and AKI)
Most common location of cardiac myxoma?
Potential hemodynamic consequence?
Murmur?
Mostly in LA.
Can mimic mitral stenosis by blocking LA outflow, may lead to HF
Early diastolic mumor - “tumor plop”
Complications of cardiac myxoma (3)
- LA outflow obstruction and heart failure
- Invasion leading to arrhythmias or heart block (or effusion)
- Emboli (e.g. stroke)
Murmurs that get louder with standing and valsalva and quieter when squatting
HOCM and MV prolapse
Enlarged “water bottle” cardiac silhouette on CXR
Pericardial effusion (may follow URI)
Signs of pericardial effusion on EKG
- Electrical alternans (in voltage amplitude)
2. Low-voltage QRS complexes
Clinical signs of cardiac tamponade
Beck’s triad: hypotension, elevated JVP, muffled/distant heart sounds
Pulsus paradoxus may also be seen (also seen in constrictive pericarditis, sever asthma/COPD)
What may be seen on CXR in constrictive pericarditis?
Pericardial calcifications
Heart sounds in constrictive pericarditis
Pericardial friction rub: high-pitched grating/squeking sound during systole (most common), diastole, or both
Pericardial knock: high-frequency mid-diastolic sound (due to abrupt cessation of diastolic filling)
JVP increases or stays the same with inspiration. Cause?
Kussmaul’s sign due to constrictive pericarditis
(Normally JVP decreases during inspiration due to blood being drawn into the chest and heart, but here it cannot take the extra volume)
Sharp x and y descents on central venous tracing. Cause?
Constrictive pericarditis
Sharp X descent (systole): RA cannot relax fully because of pericarditis
Sharp Y descent (diastole): RV filling is limited
Causes of constrictive pericarditis (4)
- Idiopathic
- Viral
- Tuberculosis
- Iatrogenic (radiation or heart surgery)
Pain of acute pericarditis
Sharp, pleuritic, and relieved by leaning forward
EKG in acute pericarditis
Diffuse ST elevation and PR depression
First-line treatment for acute pericarditis?
Alternative?
First-line: NSAIDs
Alternative: Colchicine
Treatment for Dressler’s syndrome (post-MI autoimmune pericarditis)
High-dose aspirin
Type of pericarditis that does not affect the myocardium
Uremic pericarditis (no EKG changes)
Treatment for uremic pericarditis
Hemodialysis
Most common predisposing valvular anomaly leading to endocarditis
Mitral valve prolapse (often with MV regurgitation)
Immunologic phenomena in bacterial endocarditis
- Osler nodes (painful fingertip nodules)
- Roth spots (retinal hemorrhage with pale centers)
- Glomerulonephritis
- Rheumatoid factor
(Janeway lesions, splinter hemorrhages, etc are embolic)
Embolic phenomena in bacterial endocarditis
- Septic emboli to brain (stroke), fingers (gangrene),e tc
- Renal or splenic infarcts
- Splinter hemorrhages
- Janeway lesions (painless)
- Conjunctival hemorrahge
(Osler nodes, Roth spots, and glomerulonephritis are immunoloigic)
Difference between Osler’s nodes and Janeway lesions
Osler’s nodes: painful and palpable (on fingertips, immune mediated)
Janeway lesions: painless
What can cause AV block in bacterial endocarditis?
Perivalvular abscess
Effect of inspiration on right-sided murmurs
Increased
Clinical triad of splenic abscess in endocarditis
Fever, leukocytosis, LUQ pain
Modified Duke criteria for bacterial endocarditis
Definite: both major or one major and 3 minor
Possible: one major and one minor or 3 minor
Major:
1. Blood cx with typical organism
2. Valvular vegetation
Minor (6): Predisposing cardiac lesion, IV drug use, fever, embolic phenomena, immunologic phenomena, atypical blood cx organism.
Subacute endocarditis associated with dental procedure or respiratory tract infection
- Strep viridans: mostly S. mutans and S. anguis (others are S. mitis and S. oralis)
- Less commonly, Eikenella corrodens (one of the HACEK)
Endocarditis associated with IBD and colon cancer
Strep gallolyticus (formerly named Strep bovis)
Endocarditis associated with prosthetic valves, implanted devices, and intravascular catheters
Staph epi
Endocarditis associated with nosocomial UTIs
Enterococcus
Right-sided endocarditis associated with IV drug use
Empiric therapy?
Staph aureus most commonly (can also be strep or enterococci)
Empirically treat with vancomycin
Medication for hyperlipidemia that leads to flushing and itching?
What can be given to help?
Niacin
Can give aspirin to reduce flushing (flushing is prostaglandin mediated)
Who should be on a statin?
- All diabetics 40-75
- Hyperlipidemia (e.g. LDL >190)
- Clinically significant atherosclerotic disease (ACS/MI, angina, stroke/TIA, PAD)
- ASCVD risk 7.5% or more
RA and PCWP in cardiogenic shock? Hypovolemic shock? Anaphylactic shock? Tension pneumothorax? Massive PE?
Cardiogenic: Both elevated
Hypovolemic: Both decreased
Anapylactic/septic: Both normal or decreased
Tension pneumothorax: both decreased (decreased venous return)
Massive PE: high RA, decreased PCWP
A ventilated patient has decreased CO and low RA pressure - potential cause?
Pneumothorax due to barotrauma on PEEP (high pressure leads to elevated intrathoracic pressure, kinda like a tension pneumothorax)
Effect of large AV fistula on hemodynamics
- Low diastolic pressure (decreased vascular resistance)
- Wide pulse pressure (high venous return)
- May lead to high-output heart failure
JNC 8 guidelines for target BP
<140/90 for all under 60 years and all with CKD or DM
<150/90 in patients over 60 w/o CKD or DM
JNC guidelines on initial antihypertensive agent in CKD? DM?
CKD or DM: ACEI/ARB
JNC 8 guidelines for initial hypertensive agent in those without CKD or DM, by race
Black: Thiazide or CCB, not ACEI/ARB
Other race: any of thiazide, CCB, or ACEI/ARB
Labs for a new diagnosis of hypertension
- Urinalysis (for occult hematuria and urine protein/creatinine ratio)
- Chemistries
- Lipid panel
- EKG
Most effective lifestyle change in essential hypertension?
Second-most?
Most: Weight loss
Next: DASH diet (rich in fruits, vegetables, low-fat dairy)
Causes of secondary hypertension (8)
Renal: 1. Renal parenchymal disease 2. Renal artery stenosis Endocrine 3. Primary aldosteronism 4. Pheochromocytoma 5. Cushing syndrome 6. Hypothyroidism and hyperthyroidism 7. Primary hyperthyroidism Vascular: 8. Aortic coarctation
Treatment-refractory systemic hypertension with recurrent flash pulmonary edema
Consider renal artery stenosis
Hypertension patient develops hypokalemia after staring a thiazide diuretic
Primary aldosteronism
Sequence of the work-up for primary aldosteronism
- Aldosterone / renal ratio (will be >20)
- Adrenal suppression test (salt load will not suppress aldosterone level)
- CT of adrenals
4a. If adenoma on CT in a younger patient (<35-40), can go to surgery
4b. But if it is an older patient (>35-40), do adrenal venous sampling to confirm the adenoma is the source
Treatment for primary aldosteronism due to bilateral adrenal production
Aldosterone receptor blockers: spironolactone or eplerenone
Causes of isolated systolic hypertension (ISH) (3)
- Stiff aorta and major arteries
- Aortic regurgitation
- Hyperdynamic states (anemia, hyperthyroid, AV fistula)
Key physical exam finding in malignant hypertension
Papilledema, retinal hemorrhage, or exudates
Hypertensive encephalopathy
Severe hypertension with cerebral edema and non-localizing neurologic signs and symptoms
Possible kinds of end organ damage in hypertensive emergency (10)
Brain: 1. Hypertensive encephalopathy 2. Ischemic or hemorrhagic stroke 3. Subarachnoid hemorrhage 4. Retinopathy Cardiac/Vascular 5. Acute heart failure 6. Acute coronary syndrome 7. Acute pulmonary edema 8. Aortic dissection Other: 9. Acute hypertensive glomerulosclerosis 10. Microangiopathic hemolytic anemia
Definition of pulmonary hypertension
PA pressure >25 mm Hg
Groups of pulmonary hypertension
1: Primary PA HTN (idiopathic, genetic, connective tissue disease)
2. Left heart failure
3. Lung disease / hypoxia
4. Thromboembolic (multiple PEs)
5. Mixed/other (sarcoidosis, vasculitis, PV)
Treatment options for idiopathic pulmonary hypertension
- Endothelin receptor blockers like bosentan
- PDE5 inhibitors like sildenafil
- Prostanoids like epoprostenol
Treatment for pulmonary hypertension due to left heart failure
Loop diuretics and ACEI/ARB
Treatment for pulmonary hypertension due to chronic lung disease
Oxygen and potentially bronchodilators
Treatment for pulmonary hypertension due to chronic thromboembolic occlusion
Long-term anticoagulation
Potential EKG changes in mitral stenosis
- P mitrale: broad notched P wave
- Atrial tachyarrhythmias may be seen
- RV hypertrophy may be seen: tall R in V1, V2
What symptom can mitral stenosis lead to due to compression?
Hoarseness due to compression of the recurrent laryngeal nerve, due to LA hypertrophy
Arrhythmia that may be seen in mitral stenosis
Atrial fibrillation (due to LA dilation) (also seen in mitral regurgitation)
Most common cause of mitral regurgitation in the first world? In the developing world?
First-world: mitral valve prolapse (myxomatous degeneration)
Developing world: rheumatic heart diase
(Other causes: MI, endocarditis, mitral annular calcification)
Holosystolic murmur with accompanying S3
Mitral regurgitation
Low-pitched diastolic rumble with a loud S1 and opening snap after S2
Mitral stenosis
Arrhythmia that may be seen in mitral regurgitation
Atrial fibrillation (due to LA dilation) (also seen in mitral stenosis)
Valve disease following pacemaker placement
Tricuspid regurgitation (damage to valve or inadequate leaf coaptation to the wire)
Diastolic decrescendo murmur
Aortic regurgitation
Most common cause of aortic regurgitation in young adults in developed countries
Congenital bicuspid valve
Other causes: endocarditis, rheumatic heart disease, Marfan syndrome, syphilitic aortitis
Pulsus parvus et tardus
Aortic stenosis
Mid-to-late peaking systolic murmur with soft single S2
Aortic stenosis
LV outflow obstruction with left-right asymmetry of carotid pulses and BP between arms
Supravalvular aortic stenosis: congenital narrowing the ascending aorta
(Often also have coronary artery stenosis)
What is classic angina pectoris?
Atypical angina?
Classic angina has all three of:
- Typical location, quality, and duration
- Provoked by exercise and/or emotional upheaval
- Relieved with nitroglycerin or rest
Atypical angina: two out of three
First-line treatment of stable angina?
Alternate or adjunct?
First-line: Beta-blockers
Alternate/adjunct: CCBs
(May also use sublingual nitroglycerin for acute episodes, and may add long-acting nitrates)
When can you go directly to coronary angiography (e.g. no stress test) in the work-up of suspected stable angina pectoris?
Classic anginal chest pain in a man over 40 or a woman over 60
(Classic angina has all three of:
1. Typical location, quality, and duration
2. Provoked by exercise / emotional upheaval
3. Relieved by nitroglycerin / rest)
When do you not use exercise EKG as the initial stress test?
- Unable to exercise to target heart rate (85% of maximum, which is 220-age)
- Pacemaker or LBBB (difficult to interpret)
When does revascularization improve outcomes in chronic stable angina? (4)
- Angina refractory to medical therapy
- Involvement of a large area of myocardium on stress testing
- Left-main and 3-vessel disease
- Significant CAD w/ reduced LV systolic function
What does a fixed perfusion defect represent on technetium-99 myocardial perfusion imaging stress testing?
Variable?
Fixed: scar tissue
Reversible: ischemia due to CAD
Which of these do you hold and which do you continue prior to cardiac stress testing?
- ACEI/ARB
- Beta blockers
- CCBs
- Digoxin
- Diuretics
- Nitrates
- Statins
Hold beta-blockers, CCBs, and nitrates (these all immediately impact cardiac dynamics)
Continue others (ACEI/ARB, digoxin, diuretic, statins)
Treatment for vasospastic angina
CCBs (e.g. diltiazem)
Medications to avoid / be cautious with in vasospastic angina
Non-selective beta-blockers (e.g. propanolol): loss of beta2 vasodilation can worsen vasospasm
Aspirin: Inhibiting prostacyclin production can worsen vasospasm
Medical treatment for acute STEMI
MONABASH + dual antiplatelet: Morphine prn for pain Oxygen prn (sat >92%) Nitroglycerin prn for pain Aspirin (chewed) + plavix Beta blocker ACEI Statin Heparin
When are beta-blockers CI in acute MI
Decompensated HF or bradycardia
Treatment of patients with MI who have decompensated HF but normal/high BP?
If they have hypotension?
Normal BP: Supplemental O2 and a loop diuretic
Hypotension: Supplemental O2 and a vasopressor (e.g. NE), +/- loop diuretic
What does S4 indicate?
Stiff LV wall (can be seen with MI, hypertension)
Treatment of unstable sinus bradycardia during an acute MI
IV atropine
Most common arrhythmias within 10 minutes of occlusion in MI?
10-60 minutes after?
First 10 minutes: re-entrant ventricular arrhythmias
10-60 minutes: Abnormal automaticity
Location and vessel of MI with ST elevation in V1-V4
Anterior MI: LAD
Location and vessel of MI with ST elevation in I, aVL, V5, and V6, and ST depression in II, III, and aVF
Lateral: LCX or diagonal artery
Location and vessel of MI with ST depression in V1-V3
Posterior: RCA (if right-dominant, 70%) or L circumflex (if left-dominant, 20%)
(Other 10% are co-dominant)
Location and vessel of MI with ST elevation in II, III, and aVF
Inferior MI: usually RCA (80%), sometimes L circumflex
Location and vessel of MI with ST elevation in V1 > V2 and III > II
Right ventricle: RCA occlusion
What vessel occlusion(s) can lead to SA node block?
RCA (60%) or L circumflex (40%)
What vessel occlusion(s) can lead to AV node block?
RCA (80%), L circumflex 20%
Treatment for MI with JVD but clear lungs?
What should not be given?
This is an RV MI:
- Give IV saline to increase preload
- Avoid vasodilators like nitrates (reduce preload)
Treatment of pericarditis shortly after MI
Aspirin and/or colchicine
Avoid other NSAIDs
Acute mitral regurgitation during MI: Cause? Murmur? Complication?
Cause: papillary muscle rupture in inferior MI
Murmur: may be MR murmur, but may be little or no murmur due to early equalization of LA and LV pressures
Complication: acute pulmonary edema
MI complicated by chest pain, shock, a new holocystolic murmur, and left and right heart failure?
Type of MI seen in?
Intraventricular septum rupture. May be seen with LAD or RCA MI
MI complicated by chest pain, shock, and distant heart sounds?
Free wall rupture. May be seen with LAD MI (the “widowmaker”)
Late complication of MI leading to HF, arrhtyhmia, mitral regurgitation, or mural thrombus
Ventricular aneurysm
Persistent ST elevation well after MI
Ventricular aneurysm
Medications shown to improve morbidity and mortality in CAD patients
- Dual antiplatelet therapy
- Beta-blockers
- ACEIs/ARBs
- Statins
- Aldosterone antagonists (e.g. spironolactone) w/ EF <40% and symptomatic HF or DM)
How is treatment of cocaine-induced MI different than a regular MI?
- Give benzodiazepenes
- Beta-blockers are CI (loss of beta2) - can give CCB instead
- No fibrinolytics (increased risk of intracerebral hemorrhage)
- Otherwise similar: aspirin, O2, nitrates, can do PCI
Medication that can help prevent pathologic remodeling if started within 24 hours of an MI
ACEI/ARB
Molecular target of clopidogrel
P2Y12 receptor on platelets
