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Cardiology Flashcards

1
Q

What is hypotension?

A

A drop in BP >20 systolic (>30 when HTN), and/or drop in >10 diastolic upon standing.

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2
Q

What are the causes of hypotension?

A

Hypovolaemia
Alcohol
Autonomic dysfunction: diabetes, Parkinson’s
Medication - ASDA –> anti HTN, sedatives, diuretics, alpha blockers

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3
Q

What is the typical presentation and investigations for hypotension?

A
  • BP as above
  • Pre syncope/syncope –> light headedness, tunnel vision
  • Often worse in morning
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4
Q

What are the management options for hypotension?

A

Initial conservative

  • Advise fluid intake
  • Get up slowly
  • If pre prandial then small meals little and often
  • ? referral to possible falls service

Not worked

  • Consider referral for drug Tx
  • 1st line –> mineralocorticord –> fludrocortisone –> increase retention Na and water.
  • 2nd line –> sympathomimetic –> midodrine
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5
Q

What is peripheral vascular disease?

What are the two major RF?

What are the main groups?

A
  • Reduction in blood supply to the lower limbs due to narrowing and occlusion of the arteries supplying the lower limbs.
  • Most commonly causes by atherosclerosis.
  • Smoking and diabetes
  1. Chronic limb ischaemia –> intermittent claudication, critical limb ischaemia
  2. Acute limb ischaemia
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6
Q

What is intermittent claudication and it’s typical presentation?

A

-Narrowing of the peripheral arteries means that upon exertion e.g walking that demand for extra O2 and blood cannot be met due to increased demand. ANGINA OF THE LEGS

  • Presents w pain/achey/burning of muscles after exertion.
  • Pain relieved by rest w/i minutes of stopping
  • Can walk predictable distance before stopping and symptoms
  • May have non healing wounds on leg
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7
Q

What is critical limb ischaemia?

A
  • Inadequate perfusion of tissue even at rest.
  • Progression of intermittent claudication.
  • Presents w continuous pain even when at rest.
  • Patient might report hanging legs out of bed at night to relieve symptoms
  • Possible ulcers and gangrene
  • SIGN OF IMMINENT RISK OF LIMB LOSS IF NOT TREATED.
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8
Q

What is acute limb ischaemia?

A

Sudden occlusion of a peripheral artery as a result of a thrombus e.g plaque rupture and therefore sudden decrease in limb perfusion that threatens limb viability.
Sudden onset of leg pain- can be w a background on claudication etc or present suddenly w/o history
-RISK OF LIMB LOSS
-6 Ps –> pallor, paralysis, pulseless, paraaetheisa, perishingly cold

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9
Q

How are peripheral vascular diseases diagnosed?

What is buergers angle?

A

PVD examination –> absent pulses
-1ST line –> duplex colour US –> visualise arteries and stenosis
-Ankle brachial pressure index
1 = normal. 06-0.9 = claudication 0.3-0.6 = rest pain
<0.3 = impending

Buergers angle –> patient supine, raise legs to 45 degrees, observe colour after 1-2 mins, pallor indicates ischaemia.

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10
Q

What is the management of intermittent claudication?

A
  • Smoking cessation key.
  • Supervised exercise programme
  • Established CVD then atorvastatin 80mg
  • Antiplatelet w clopidogrel 1st line not aspirin?
  • If neither of above work, consider referral to vascular for sugery e.g bypass or angioplasty
  • Don’t want to be referred for surgery –> vasodilator –> naftidrofuryl oxalate.
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11
Q

What is the management of critical limb ischamia?

A
  • Urgent referral to vascular
  • As above
  • Surgery
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12
Q

What is the management of acute limb ischaemia?

A

EMERGENCY ASSESSMENT BY SPECIALIST
-Systemic anticoag –> heparin?

Non viable limb –> amputation
Viable –> revascularisation –> endovascular often preferred, other options percuatneous catheter directed thrombolysis, surgical thromboectomy

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13
Q

What is giant cell arteritis?

Who are those most at risk?

What condition is connected to GCA?

A
  • Systemic vasculitis of the medium and large arteries.
  • Most effects temporal arteries –> temporal arteritis.
  • Females >50
  • Polymyalgia rheumatica –> 40% with GCA have
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14
Q

What is the presentation of GCA?

A
  • Sudden onset unilateral throbbing headache in temporal arteries
  • Pulseless temporal arteries or other e.g thickening, nodularity, tender.
  • Scalp tenderness
  • Intermittent jaw claudication –> pain on eating
  • Visual loss –> can be sudden. e.g amarosis fugax.
  • Other visual symptoms –> visual field defects, tunnel vision
  • Polymyalgia rheumatica –> bilat upper arm stiffness.
  • Irreversible painless vision loss can occur suddenly.
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15
Q

What are the investigations for GCA?

What does the diagnostic investigation show?

What would you see on duplex US?

A
  • Bloods –> CRP and ESR increased
  • Diagnosis –> temporal artery biopsy –> multinucleated giant cells
  • Duplex US of arteries –> hyperechoic halo sign
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16
Q

What is the management for GCA?

A
  • Referral via local GCA pathway and immediate Tx w high dose prednisolone.
  • Visual symptoms –> urgent same day referral to rheumatology and opthalmology. 60-100mg prednisolone.
  • Not visual –> urgent referral ideally same day but can be w/i 3. 40-60mg prednisolone, often can cause rapid improvement in symptoms.
  • On predisolone for 2 years.
  • Offer PPI for gastric protection.
  • Bisphosphantes, calcium, vit d, osteoporosis as steroids
  • Aspirin 75mg –> decreases risk visual loss and strokes
17
Q

What is tetralogy of fallot?
What are the components?

What are the RF?

A
  • The most common cause of cyanotic congenital heart disease.
  • It typically presents at around 1-2 months, although may not be picked up until the baby is 6 months old
  • RF –> rubella infection, mother >40 years, alcohol consumption in pregnancy, diabetic mother.

Tetralogy of Fallot –> four coexisting pathologies

  • Ventricular septal defect (VSD)  allows blood to flow between ventricles.
  • Overriding aorta  entrance to aortic (aortic valve) further to R than normal above VSD  when RV contracts and sends blood upwards  aorta in direction of travel of blood, greater % deoxy blood enters aorta from R side heart.
  • Pulmonary valve stenosis  great resistance to flow blood in RV  encourages blood to flow through VSD rather than pul vessels. Overriding and stenosis  encourage blood to shunt from R side heart to L  cyanosis.
  • Right ventricular hypertrophy  increase strain on RV as attempts to pump blood against resistance LV and pul stenosis  RVH.

-These abnormalities cause  R to L shunt  blood bypasses the child’s lungs  therefore not oxygenated. Deoxygenated blood enters systemic circulation causeing cyanosis.

18
Q

What is the typical presentation of TOF?

A
  • Common –> collapse or cyanosis in 1st month life, hypercyanotic spells w increasing episodic cyanosis which typically occurs when baby crying and breathing deeply/rapidly. Typical TOF murmur can disappear during spell.
  • Cyanosis, Clubbing, Poor feeding, Poor weight gain
  • Ejection systolic murmur due to pulmonary stenosis –> heard loudest in the pulmonary area (second intercostal space, left sternal border/edge)
  • “Tet spells” –> These episodes may be precipitated by waking, physical exertion or crying. The child will become irritable, cyanotic and short of breath. Severe spells can lead to reduced consciousness, seizures and potentially death.
  • Right-sided aortic arch is seen in 25% of patients

When mild –> can present in childhood when older.
-Depends on degree of RV obstruction

19
Q

What are Tet spells?

When is an example of when they an occur?

A
  • Intermittent symptomatic periods where the right to left shunt becomes temporarily worsened, precipitating a cyanotic episode.
  • Occurs when pulmonary vascular resistance increases or the systemic resistance decreases.
  • e.g if the child is physically exerting themselves they are generating a lot of carbon dioxide –> a vasodilator that causes systemic vasodilation and therefore reduces the systemic vascular resistance. Blood flow will choose the path of least resistance.
20
Q

What is the difference between presentation of TOF and TGA?

A
  • TGA (transposition of great arteries)
  • Cyanotic heart disease presenting w/I first days life whereas TOF at 1-2 months.
  • TGA  no murmur, loud single S2 audible and prominent RV impulse palpable.
21
Q

What are the investigations for TOF?

What do you see on chest x ray?

A

ECHO –> DIAGNOSTIC –> Doppler flow studies –> produce pictures that show direction of blood flow. Can assess severity and abnormality of shunt.

  • CXR –> “boot shaped” heart due to right ventricular thickening. Most cases are picked up before the child is born during the antenatal scans. Additionally, an ejection systolic murmur caused by the pulmonary stenosis may be heard on the newborn baby check.
  • ECG –> RVH
22
Q

What is the management for tetraology of fallot?

A
  • In neonates –> a prostaglandin infusion can be used to maintain the ductus arteriosus. This allows blood to flow from the aorta back to the pulmonary arteries.
  • Cyanotic episodes may be helped by beta-blockers to reduce infundibular spasm. Relax RV and improve flow into pulmonary vessels.
  • Total surgical repair by open heart surgery is the definitive treatment (surgery often in two parts), however mortality from surgery is around 5%.
  • Prognosis depends on the severity, however it is poor without treatment. With corrective surgery 90% of patients will live into adulthood.

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