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Jack Misc List > Cardiovascular list conditions (red and orange) > Flashcards

Cardiovascular list conditions (red and orange) Flashcards

1
Q

Aortic stenosis (orange):

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. Obstruction of blood flow across the aortic valve due to aortic calcification. Progressive and long subclinical period. Most prevalent in elderly (rates increasing)
  2. Can be congential (BAV) or acquired (degenerative calcification, RHD). RF: >60, congenital defect.
  3. Active process similar to atherosclerosis leading to deposition of calcium on the valve. There is a pressure gradient and LV hypertrophy to compensate leading to heart failure.
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2
Q

Aortic stenosis (orange):

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. Angina (increased myocardial demand), dyspnoea on exertion, syncope (only valve defect with syncope - heart cannot maintain CO)
  2. Echocardiography (also ECG)
  3. IHD
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3
Q

Atrial stenosis (orange):

  1. Management
  2. Complications
  3. Prognosis
A
  1. Surgical replacement or TAVI if symptomatic, or decreasing EF. If not, surveillance. Vasodilators (ACEi) are contraindicated because they reduce BP which requires heart to increase CO which can be a problem in HF
  2. Acute congestive heart failure, sudden cardiac death
  3. Can become severe over 25yrs but can be less. HF gives poor prognosis (2 years)
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4
Q

Mitral regurgitation (orange):

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. Where the mitral valve refluxes back into the LA. This is common, but prevalence not increasing as less associated with age.
  2. Myxomatous degeneration - too much tissue on the valve, Ischaemic MR. RF = mitral valve prolapse, IE, Hx of cardiac trauma
  3. LV suffers pure volume overlaod cause LVH (leading to progressive heart failure) and LA enlargement (leading to pulmonary hypertension). LVH is more prominent in this condition compared to AS
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5
Q

Mitral regurgitation (orange):

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. Dyspnoea, palpitations, pansystolic murmur, displaced apex beat
  2. Echocardiography (maybe ECG, CXR)
  3. ACS, MS
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6
Q

Mitral regurgitation (orange):

  1. Management
  2. Complications
  3. Prognosis
A
  1. Surgical treatment (replacement or repair), percutaneous approaches emerging (surgery indicated in symptomatic or decreasing EF). If not, serial echo, IE prophylaxis and treat HTN.
  2. AF, pulmonary hypertension and LVH causing CHF
  3. Compensatory phase of 10-15years with LVH. Once patient is symptomatic, mortality rises sharply from HF and progressive dyspnoea.
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7
Q

Chronic coronary syndrome/angina (red):

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. This is a form of ischaemic heart disease where there is inadequate blood supply to the heart. It is progressive, no necrosis. It is very prevalent, particularly at high ages.
  2. Atherosclerosis (arteries clogged with plaques) is the main cause (reduced supply) however increased demand (LVH, anaemia) is also a cause.
  3. Covered. It is progressive but symptoms occur suddenly due to Poiseuille’s law.
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8
Q

Chronic coronary syndrome/angina (red):

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. Chest pain radiating up during exercise that is relieved when exercise stops and breathlessness. Also fluid retention and syncope.
  2. Resting ECG, routine bloods (anaemia), lipid profile, fasting blood glucose
  3. Pericarditis, PE, chest infection
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9
Q

Chronic coronary syndrome/angina (red):

  1. Management
  2. Complications
  3. Prognosis
A
  1. Initially lifestyle education (stop smoking, exercise), antiplatelet therapy to prevent MI, lipid lowering therapy, antihypertensives (B blocker, ACEi) and GTN spray. If angina symptoms persist then revascularisation (PCI or CABG)
  2. Ischaemic heart failure, MI
  3. With lifestyle modification and medications there is a reduction in symptoms and a good prognosis.
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10
Q

Acute coronary syndrome - STEMI (red):

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. This is where there is myocardial cell death due to a lack of blood supply, so severe there is ST segment elevation in 2 leads. This is very common, but incidence is dropping.
  2. Mainly atherothrombotic occlusion of a coronary artery. CHD is leading cause/atherosclerosis. Plaque ruptures causing blood clot. RF: Age, smoking, HTN, DM, FH, hyperlipidaemia
  3. If occulsion is severe and persistent, myocardial cell necrosis follows causing LV failure.
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11
Q

Acute coronary syndrome - STEMI (red):

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. Chest pain radiating up to neck, distress, anxiety, dyspnoea, Pansystolic murmur.
  2. ECG - STEMI occurs within hours. Also classify by (non-)Q wave. Serum troponin distinguishes unstable angina.
  3. NSTEMI, unstable angina, pericarditis
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12
Q

Acute coronary syndrome - STEMI (red):

  1. Management
  2. Complications
  3. Prognosis
A
  1. Aspirin + Ticagrelor (P2Y2i), morphine, GTN, oxygen, anticoagulants and PCI/thrombolysis.
    Secondary prevention - modify RF and medication (statins, antihypertensives, antiplatelet therapy etc.)
  2. Cardiac arrest, cardiogenic shock, valve defects
  3. Not good, many die.
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13
Q

Acute coronary syndrome - NSTEMI (red):

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. Same as MI but with no ST elevation. About 50% of MI are STEMI
  2. CHD is the leading cause. Same RF as STEMI
  3. Same as STEMI really, however for a NSTEMI, there is usually partial or near-complete occlusion of a coronary artery resulting in compromised blood flow to myocardium with subsequent injury/infraction demonstrated by elevated troponin.
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14
Q

Acute coronary syndrome - NSTEMI (red):

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. Chest pain radiating up to the neck, distress, sweatiness, dyspnoea (same as STEMI).
  2. ECG - check for ST elevation, serum troponin confirms either STEMI or NSTEMI
  3. Stable angina, pericarditis, STEMI, PE
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15
Q

Acute coronary syndrome - NSTEMI (red):

  1. Management
  2. Complications
  3. Prognosis
A
  1. For acute presentation: Antiplatelet therapy, O2 adjunct, GTN + morphine, beta blocker, CCB. Assess need for PCI. Post stabilisation give cardiac rehab, antiplatelet therapy, Bblockers, statins, ACEi, ARB
  2. Cardiac arrhythmias. Other complications like CHF, cardiogenic shock are lower risk than in STEMI
  3. High risk of morbidity and mortality from future event.
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16
Q

Unstable angina (red):

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. Same as NSTEMI but there is no necrosis. Characterised by chest pain at rest with crescendo pattern or new onset angina. Very common.
  2. CAD is the cause in nearly all cases. RF = F, PH/FH of CAD, increased age.
  3. There is a rupture of a plaque stimulating platelet activation and thrombus formation but the thrombus is not usually completely occlusive.
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17
Q

Unstable angina (red):

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. Same as STEMI/NSTEMI - increasing frequency/severity of chest pain or dyspnoea.
  2. ECG - rarely changes, serum troponin should not have risen.
  3. Stable angina, NSTEMI, STEMI
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18
Q

Unstable angina (red):

  1. Management
  2. Complications
  3. Prognosis
A
  1. First line - similar to STEMI/NSTEMI: oxygen, nitrates, morphine for pain, beta blocker + dual antiplatelet therapy (aspirin + clopidogrel/ticagrelor). Secondary prevention - statin, ACEi, CCB. Assess need for PCI/CABG.
  2. Iatrogenic bleeding, CHF, ventricular arrhythmias
  3. Still bad, mortality almost equal to ST elevation.
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19
Q

Pericarditis (orange):

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. Pericarditis is an inflammation of the pericardium, acute is <4-6weeks. Diagnosis depends on chest pain, friction rub, ECG changes, pericardial effusion. Constrictive/chronic pericarditisis a late complication of acute where the heart is encased in a rigid, fibrotic sac that prevents adequate diastolic filling. Makes up 5% of chest pain A&E admissions.
  2. 80-90% idiopathic (viruses). Other causes - MI, malignancy or surgery. RF: Male, 20-50yrs, recovery from MI/other trauma, AIDs.
  3. Pericardium can expand to accomodate over time. Pericarditis (Acu or Chr) rarely causes Cardiac tamponade
20
Q

Pericarditis (orange):

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. Sharp, retrosternal, pleuritc chest pain (radiating to arm) which is characteristically relieved by leaning forwards. Pericardial friction rub (stethoscope) is pathognomonic sign. Chronic pericarditis resembles right sided HF with jugular distension, oedema, ascites and Kussmaul’s sign/Pulsus paradoxus.
  2. ECG - concave upwards ST elevation across all leads (in MI St elevation is convex and in only local leads). Also bloods, CXR, echo.
  3. MI.
21
Q

Pericarditis (orange):

  1. Management
  2. Complications
  3. Prognosis
A
  1. High doses of NSAIDs (aspirin), rest, Colchicine. If cardiac tamponade - pericardiocentensis/pericardiectomy. Chronic constrictive pericarditis also treated by excision of pericardium, NSAIDs (PPI), Colchicine.
  2. Cardiac tamponade, chronic constrictive pericarditis.
  3. Most patients with pericarditis have a good prognosis. Cardiac tamponade rarely occurs, constrictive pericarditis occurs in 1% of patients, however high risk for bacterial aetiologies.
22
Q

Heart failure (red):

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. An inability of the heart to deliver blood at a rate commensurate with metabolising tissues despite normal or increased cardiac filling pressures. It is very common in the elderly (HFREF more common than HFPEF)
  2. Most common cause is IHD, then HTN. Other causes are cardiomyopathy, myocarditis, valvular disease, endocardial and pericardial causes. RF: MI, DM, old age.
  3. When CO is insufficient, compensatory mechanisms (SNS, RAAS, ANP, hypertrophy) are pathological and not helpful. HFREF means problems with systole (usually caused by IHD). HFPEF is other one - problems with diastole (LVH, common in elderly HTN patients).
23
Q

Heart failure (red):

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. Breathlessness, fatigue, leg swelling/peripheral oedema, , cold peripheries, tachycardia and cardiomegaly.
  2. Echo, serum NTproBNP
  3. Ageing, physical inactivity, COPD/PE.
24
Q

Heart failure (red):

  1. Management
  2. Complications
  3. Prognosis
A
  1. Consider acute complications. Give ACEi (ARBs if intolerant) + beta blockers - counter compensation. Also consider spironolactone, diuretics. ICDs/transplantation.
  2. Pleural effusion, acute decompensation of chronic heart failure leading to pulmonary oedema/cardiogenic shock
  3. 50% fatality in 5 years.
25
Q

Aortic aneurysm (orange):

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. A localised permanent dilatation of an artery. Common in white males age 50-79.
  2. Can be abdominal, thoracic. They largely arise from atherosclerotic disease. RF: cigarette smoking, FH, increased age, males.
  3. Cause symptoms by either pressure on adjacent structures, in AAA epigastric/back pain, or rupturing - hypovolaemic shock.
26
Q

Aortic aneurysm (orange):

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. Usually asymptomatic (incidental), back/epigastric pain.
  2. Ultrasonography/CT
  3. Diverticulits, appendicitis, IBS
27
Q

Aortic aneurysm (orange):

  1. Management
  2. Complications
  3. Prognosis
A
  1. Monitor, aggressive cardiovascular risk management. If large/symptomatic consider surgical repair.
  2. Ruptruing (death), abdominal compartment syndrome, intestinal ischaemia (pressure) and AKI
  3. Most patients with rupture die before theatre, however surgical repair has high risk of mortality.
28
Q

Aortic dissection (orange)

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. Aortic dissection results from tear in intima. Blood under high pressure creates a false lumen in the deceased media. Usually results in men >50.
  2. Medial degeneration predisposes the condition. Aneurysms can cause this, caused by atherosclerosis. Some inherited conditions like Marfan syndrome increase likelihood.
  3. Intimal tear is initial event, blood passes through the media and can occlude branches of aorta (renal etc.)
29
Q

Aortic dissection (orange)

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. Abrupt, severe onset of tearing central chest pain radiating to back. Maybe syncope (shock), heart/renal failure.
  2. ECG, CXR, CT angiography
  3. ACS, pericarditis, AAA
30
Q

Aortic dissection (orange)

  1. Management
  2. Complications
  3. Prognosis
A
  1. Urgent control of BP and surgical repair (TEVAR). Oxygen/advanced life support also started.
  2. End-organ malperfusion pericardial tamponade and aortic incompetence.
  3. Natural history, usually fatal in 24hrs. 10yr survival after survival is around 52%.
31
Q

Hypertension (red):

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. Elevated blood pressure. Primary/essential means no identifiable cause. Very common, african americans have greater risk.
  2. 90% are primary/essential. Secondary causes include CKD, adrenal gland problems (Conn’s syndrome), thyroid dysfunction etc. RF: DM, diet, sedentary, alcohol, tobacco, genetics/FH
  3. Increase BP can cause structural changes, remodelling and hypertrophy of resistance arterioles.
32
Q

Hypertension (red):

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. None, malignant HTN = headache, visual disturbance, N/V, chest pain.
  2. BP (ABPM, fundoscopy, blood test (lipid, haematocrit, HbA1c, Conn’s). Also ECG and urinalysis for end-organ damage.
  3. Renal artery stenosis
33
Q

Hypertension (red):

  1. Management
  2. Complications
  3. Prognosis
A
  1. See separate brainscape (lifestyle and ACEi generally first line)
  2. CAD/MI, stroke, LVH, CHF, retinopathy, CKD
  3. Uncontrolled gives significant cardiac, vscular, renal and cerebro risk. Modest reductions in BP can have big effects.
34
Q

Peripheral vascular disease (orange)

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. PVD includes a range of vascular syndromes of the blood vessels (narrowing, blocking or spasms can cause PVD). Prevalence increases with age (1% of 40-50, 20% of >80).
  2. The most common cause of PAD is atheroslcerosis. RF: smoking, DM, HTN, age >40 etc.
  3. Pathophysiology is diverse, but it centres on damage, inflammation and structural defects of blood vessels.
35
Q

Peripheral vascular disease (orange)

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. Most are asymptomatic. Symptoms are intermittent claudication (thigh pain relieved with rest). Diminished pulse, cool skin/numbness, pain worse in one leg.
  2. Ankle-brachial index <0.9.
  3. Arthritis
36
Q

Peripheral vascular disease (orange)

  1. Management
  2. Complications
  3. Prognosis
A
  1. Antiplatelet therapy + exercise + risk factor modifiaction. Cilostazol for symptom relief. CABG for critical limb ischaemia, if fails then amputation.
  2. Leg/foot ulcers, gangrene, permanent limb/weakness/numbness
  3. Similar to other types of atherosclerotic disease. Claudication generally remains stable. Chronic limb ischaemia is a bad prognoses - 25% annual mortality.
37
Q

Atrial fibrillation/atrial flutter (red).

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. AF is supraventricular tacharrhythmia, atria beat irregularly. Usually minor symtpoms and can be chronic. Atrial flutter is associated, there is macro-reentrant atrial tachycardia (bpm 250-320). AF is commonest arrhythmia occuring in 15% of patients >75.
  2. CAD, HTN, CHF, valvular disease, DM etc. are risk factors for AF. Also heavy alcohol intake.
  3. Either automaticity or accessory pathways. Damage/remodelling can cause this. AVN lets some signals through cause irregularly irregular ventricular pulse. Blood stagnates and clots.
38
Q

Atrial fibrillation/atrial flutter (red).

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. Can be incidental. Symptoms range from palpitations, irregular pulse, fatigue, chest pain and syncope.
  2. ECG
  3. WPW, atrial tachycardia
39
Q

Atrial fibrillation/atrial flutter (red).

  1. Management
  2. Complications
  3. Prognosis
A
  1. Treat underlying cause (alcohol, thyroid disease, valve disease etc.) Give heparin, DC shock if unstable. Then, either heart rate control (B blockers/CCBs), heart rhythm control (DC cardioversion with B blockers), can give other agents. Catheter ablation techniques (pulmonary vein isolation) useful if resistant to antiarrhythmics. Also Warfarin/Dabigatran if CAHDS2 score >1.
  2. Stroke, CHF, myocardial infarction
  3. Depends on event. In young /alcohol good, if MI then poor. Paroxysmal often develops into sustained. Flutter when treated gives normal prognosis.
40
Q

Heart blocks (red)

  1. Define/epidemiology (define each type).
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. Impaired (delayed/absent) conduction in the heart. First degree - delayed AV conduction (PR interval >0.22s). Second degree some atrial impulses fail to reach the ventricles (M1 = PR elongation until wave absent, repeats)(M2 consistent loss of QRS (half, third etc.)). Third degree is complete heart block (desynchronised). BBB gives wide QRS. All relatively common in Males >50.
  2. CAD, cardiomyopathy fibrosis of conduction tissue (in elderly), drugs
  3. Described in 1.
41
Q

Heart blocks (red)

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. Syncope, HR <40bpm. Fatigue, dyspnoea, chest pain, palpitations
  2. 12 lead ECG, troponin/electrolyte
  3. SVT, AF
42
Q

Heart blocks (red)

  1. Management
  2. Complications
  3. Prognosis
A
  1. First/Second M1 monitr for syncope/symptoms and stop AV nodal blocking agents. Second M2/third - above and specific management (cardiac resynchronisation +/- ICD placement
  2. Fainting, low BP and cardiac arrest (3rd degree can be fatal).
  3. Asymptomatic with first/second are at low risk of worse degrees. 3rd degree means high risk of sudden cardiac death but ok with permanent pacemaker.
43
Q

WPW (orange)

  1. Describe (path/aeti)
  2. Manifestation/ investigations
  3. Complications
  4. Treatment/prognosis
A
  1. This is a type of SVT, specifically an atrioventricular junctional tachycardia (AVRT). It is caused by an accessory pathway (bundle of kent) connecting atria and ventricles. This cause part of the ventricles to be pre-excited.
  2. palpitations, asymptomatic, generic cardiac symptoms. Do ECG.
  3. Prone to AF and VF leading to sudden cardiac death.
  4. Cardioversion, give adenosone. Long term = ablation of accessory pathways.
44
Q

Long QT syndrome (orange)

  1. Describe (path/aeti)
  2. Manifestation/ investigations
  3. Complications
  4. Treatment/prognosis
A
  1. Ventricular repolarisation (QT interval) is greatly prolonged. Causes can be congential (ion channel mutations), electroylyte disturbances (hypokalaemia etc.), drugs (tricylcic antidepressants).
  2. Palpitations and syncope. Other non-specific cardiac symptoms. ECG, gene tests.
  3. Can degenerate into VF causing cardiac arrest and death, also torsades de pointes.
  4. Treat underlying cause, give B blockers/IV isoprenaline. Asymptomatic = normal life expectancy, symptomatic = worse prognosis.
45
Q

Tachycardias (orange)

  1. Describe (path/aeti)
  2. Manifestation/ investigations
  3. Complications
  4. Treatment/prognosis
A
  1. HR >100bpm, beats so fast ventricles do not fill reducing CO. Signals can be; SVT (before ventricles - sinus tachycardia, atrioventricular junctional tachycardias) or ventricular tachycardia (VT) - wide QRS. Assume VT until proven otherwise. Generally caused by faulty connections or automaticity. Myocardial scarring increases likelihood.
  2. Regular palpitations, generic cardiac symptoms (dizziness, dyspnoea, chest pain, syncope). ECG.
  3. Blood clots, HF, sudden death.
  4. SVT - less caffiene. VT - ablation and B blockers. Prognosis is good.
46
Q

Also make sure you know shock - its orange and wouldn’t fit in this format. Know treatment etc.

A

:)

Jack Misc List (9 decks)

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