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Phase 2 > Cardiovascular med topics > Flashcards

Cardiovascular med topics Flashcards

1
Q

What are intrinsic cardiac causes of AF?

A
  1. CAD
  2. valvular disease
  3. CHF
  4. pre-excitation tachycardia
  5. cardiomyopathy
  6. pericarditis
  7. tamponade
  8. congenital channelopathies
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2
Q

What are non-cardiac causes of AF?

A
  1. Pulmonary disease → COPD, PE, Pneumonia
  2. hyperthyroidism
  3. increased sympathetic activity/state
    • sepsis, hypovolemia
    • cocaine or amphetamines
    • fever of any cause
  4. electrolyte imbalances
    • hypomagnesemia
    • hypokalaemia
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3
Q

How can you categorise AF?

A
  1. Paroxysmal
    • episodes last > 30 seconds but < 7 days and are self terminating but recurrent
  2. Persistent
    • episodes last more seven days and require cardioversion
  3. Permanent
    • episodes fail to terminate with cardioversion
    • long-standing AF > 1 year that is treatment resistant.
  4. new onset or chronic
  5. haemodynamically stable or unstable
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4
Q

What are suggested mechanisms for AF pathogenesis?

A
  1. Volume overload or haemodynamic stress → atrial hypertrophy or dilation
  2. Atrial ischaemia
  3. inflammation of the atrial myocardium
  4. altered ion conduction by the atrial myocardium
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5
Q

Explain the pathogenesis of AF

A
  1. Afib triggered by:
    1. an automatic foci near pulmonary veins or in diseased, fibrotic atrial tissue
    2. pre-excitiation of the atria as a result of an aberrant pathway (WPW)
  2. Afib sustained by re-entry pathways → more likely to occur in dilated or hypertrophied tissue
  3. Atrial remodelling occurs:
    1. Electrical remodelling within a few hours on new onset Afib
    2. Structural remodelling occurs if AF persists → atrial fibrosis and dilation occurs within a few months
  4. Electrical and structural remodelling increases susceptability to AF → vicious cycle
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6
Q

Explain how AF affects heart physiology

A
  1. atria contract rapidly but ineffectively and uncoordinated → causes stasis of blood within atria → risk of thromboembolism and stroke
  2. Irregular activation of the ventricles by conduction through AV node → tachycardia
  3. can progress to LV dysfunction, heart failure and myocardial ischaemia
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7
Q

What are typical symptoms of AF?

A
  • Breathlessness
  • chest discomfort
  • palpitations
  • light-headedness
  • reduced exercise tolerance
  • syncope
    • due to bradycardia
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8
Q

What are the different ways in which AF can present?

A
  1. asymptomatically on routine ECG or via patient-initiated monitoring (apple watch)
  2. Stroke or TIA
  3. Syncopal episode
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9
Q

what are some manifestations of AF complications?

A
  • Left Heart failure
    • pulmonary oedema
  • thromboembolism
    • Stroke/TIA
    • renal infarct
    • splenic infarct
    • other ischaemic event
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10
Q

what are typical clinical findings on exam in AF

A
  1. irregularly irregular pulse
  2. radial - apical deficit
  3. co-exisiting heart failure
    • raised JVP
    • added heart sounds
    • crackles on auscultation
    • peripheral oedema
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11
Q

What are Cardiogenic causes of syncope?

A
  • Arrythmias
  • obstructive cardimyopathy
  • Acute MI
  • Aortic, mitral or pulmonary stenosis
  • aortic dissection
  • cardiac tamponade
  • pulmonary hypertension
  • saddle PE
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12
Q

What are neurally mediated causes of syncope? (reflex syncope)

A
  1. Carotid sinus syndrome or hypersensitivity
    • from head rotation or pressure on carotid sinus → shaving or tight collar
    • ventricular pause of decreased systolic pressure after carotid sinus massage
  2. situational
    • coughing, defecation, gastrointestinal stimulation or urination
    • abscence of heart disease, history of similar situational fainting
  3. vasovagal
    • mediated by fear, heat exposure, noxious stimuli, pain or stress
    • usually have prodromal symptoms → diaphoresis, dizziness, nausea
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13
Q

what are orthostatic causes of syncope?

A
  1. Drug induced
    • alcohol, antihypertensives, antiparkinsonian drugs, diuretics, diabetic drugs
  2. Postural tachycardia syndrome
  3. primary autonomic failure
    • MS
    • Parkinsons
    • wernicke encephalopathy
  4. secondary autonomic failure
    • demyelinating disease
    • polyneuropathy
    • diabetes mellitus
    • SCI
  5. volume depletion
    • Acute blood loss
    • GI loss (d and V)
    • inadequate fluid intake
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14
Q

what investigations to order for suspected AF?

A
  1. ECG
    • irregularly irregular rate without visible p waves
    • tachycardia
    • narrow QRS complex
  2. Biochemisty
    1. UECs
    2. TFTs
    3. LFTs
    4. Troponins, BNP, D-dimer, Toxicology
  3. Imaging
    1. TTE → assess cardiac function and rule out structual disease
    2. CXR → pulmonary disease or HF
  4. further
    1. holter monitor for paroxysmal AF investigations
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15
Q

What are important principles of treatment for any patient with AF?

A
  1. correct reversible or treatable causes
  2. encourage lifestyle modifications
  3. consider if anticoagulation is appropriate (CHA2DS2VASc)
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16
Q

What is the treatment for haemodynamically unstable patients with AF

A
  • emergency electrical cardioversion to restore stable pulse

- uses defibrillator

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17
Q

what are clinical features that suggest instability of a patient with AF?

A
  1. decreased level of consciousness
  2. chest pain
  3. Dyspnoea
  4. systolic of less than 90
  5. diaphoresis
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18
Q

what are choices of anticoagulants and when are they indicated?

A
  1. NOACS
    • rivaroxaban, apixiban, dabigatran
      • preferred long term management in nonvalvular AF
  2. Warfarin
    • valvular AF, CKD or severe liver disease
  3. Heparin
    • preferred in pregnancy
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19
Q

What are the treatment options for patients who are stable and have AF?

A
  1. Rhythm Control
    • Pharmacological cardioversion
      • Amiodarone
      • Flecainide
    • electrical DC cardioversion
  2. Rate ControlPharmacological
    • Beta blocker
      • Metoprolol
      • atenolol
    • CCB
      • verapamil
      • diltiazem
    • Digoxin
      • in those with poor LF ejection fraction/HF or sepsis
    Surgical
    • AV nodal Ablation
    • implantation of permanent pacemaker
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20
Q

What are the criteria of the CHA2DS2VASc ?

A
  1. Congestive Heart failure +1
  2. Hypertension +1
  3. Age older than 75 +2
  4. Diabetes Mellitus +1
  5. Stroke, TIA or TE + 2
  6. Vascular disease (prior MI, PAD etc) +1
  7. Age 65-74 +1
  8. Sex Category female +1
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21
Q

Complications of AF?

A
  • thromboembolic events
    • stroke, TIA
    • Specific organ infarcts
    • acute limb ischaemia
  • Left heart failure
  • pulmonary oedema
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22
Q

what is sinus arrhythmia

A
  • variation in the P-P interval corresponding with the respiratory cycle
  • occurs as a normal physiological variation in young, healthy people
  • due to changes in vagal tone throughout breathing
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23
Q

what increases and decreases HR in sinus arrhythmia?

A
  • inspiration increases Hr by decreasing vagal tone

- Expiration decreases HR by increasing vagal tone

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24
Q

what are pharmacological causes of sinus tachy?

A
  • beta agonists
  • sympathomimetics
  • antimuscarinics
  • caffeine
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25
Q

what are non-pharm causes of sinus tachy?

A
  • exercise
  • pain
  • anxiety
  • hypoxia/hypercabia
  • hypovolaemia
  • fever
  • anaemia
  • sepsis
  • PE
  • tamponade
  • hyperthyroidism
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26
Q

What are the ecg findings in sinus tachy?

A
  • p waves can be hidden behind t waves

- gives camel hump appearence

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27
Q

what are pharmacological causes of sinus brady?

A
  1. beta blockers
  2. CCBs
  3. digoxin
  4. opiates
  5. amiodarone
  6. GABAergic agents
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28
Q

what are non-pharm causes of sinus brady?

A
  1. sleep
  2. increased vagal tone or stimulation
  3. hypothyroidism
  4. hypothermia
  5. anorexia nervosa
  6. electrolyte abnormalities
29
Q

What are normal heart rates for a newborn?

A

110-150BPM

30
Q

What are normal heart rates for 2 years?

A

85-125bpm

31
Q

what are normal heart rates for 4 years?

A

75-115bpm

32
Q

What are normal heart rates for 6+ year olds?

A

60-100bpm

33
Q

What are the cardiac causes of Chest pain?

A
  1. ACS
  2. Tamponade
  3. Pericarditis
  4. Myocarditis
  5. Endocarditis
  6. Cardiomyopathy
  7. aortic dissection
  8. valvular disease
  9. HF exacerbation
  10. Arrhythmias
34
Q

What are pulmonary causes of chest pain?

A
  • PE
  • tension pneumothorax
  • pneumonia
  • bronchitis
  • asthma/copd exacerbation
  • pulmonary oedema
  • pleural effusion
  • pleurisy
  • lung cancer
  • infarction
35
Q

what are MSK causes of chest pain?

A
  • costochondritis
  • trauma
  • rib fracture
  • oestoarthritis
  • fibromyalgia
36
Q

what are gastrointestinal causes of chest pain?

A
  • Oesophageal perf
  • mallory weiss tears
  • GORD
  • gastritis
  • Oesphagitis
  • PUD
  • achalasia
  • Hiatus herna
  • biliary disease
  • pancreatitis
  • hepatitis
37
Q

what are other causes of chest pain?

A
  • renal infarction
  • Shingles or neuralgia
  • RA or SLE
  • pscyhiatric cause
38
Q

What are the 7 Life Threatening Causes of chest pain? (4-2-1 rule)

A
  1. heart related causes
  • ACS
  • Aortic dissection
  • Myocarditis/ pericarditis
  • pericardial effusion /Tamponade
  1. Lung causes
  • PE
  • Tension pneumothorax
    1. GI causes
    • Perforated Oesphagus
39
Q

what are the 4 pillars of treatment for angina?

A
  1. Beta blockers → reduce myocardial O2 demand
  2. CCBs or nitrates → reduced myocardial O2 demand/ vasodilate coronary vessels
  3. long term antiplatelets → aspirin, clopidogrel, dual antiplatelet therapy
  4. comorbidity management → HTN, DM, Hypercholesterolaemia
40
Q

Describe the pathophysiology behind a hypertensive crisis?

A
  1. severe, rapid increase in BP → vessels wall shear stress
  2. releases humeral factors and local activation of coagulation cascade → small vessel fibrinoid necrosis → release of vasoconstrictive agents
  3. ongoing cycle of damage → more vascular damage, tissue ichaemia + vasoconstrictor release
  4. Pressure natriuresis → volume depletion → RAAS activation further worsens hypertensive crisis
41
Q

Which organ systems are most commonly affected in a hypertensive crisis and what are the symptoms?

A
  1. Neurological
    • headache
    • altered level of consciousness
    • focal neurological signs
    • retinopathy → arteriolar changes, haemorrhage, exudate, papilloedema
  2. cardiovascular
    • angina
    • Acute MI
    • Acute LV failure
    • arrhythmias
  3. renal
    • acute kidney injury
    • oliguria +/- haematuria
  4. Vascular
    • aortic dissection
42
Q

what are some aetiological causes for secondary HTN? (RECENT) -> can also cause hypertensice emergency

A
  1. Renal
    • renal artery stenosis, ADPKD, renal failure, glomerulonephritis, lupus nephritis
  2. Endocrine
    • cushing syndrome, primary aldosteronism (Conn’s), hyperthyroidism, phaeochromocytoma, acromegaly, congenital adrenal hyperplasia
  3. Coarctation of the aorta
  4. Estrogen → OCP
  5. neurological
    • raised ICP, use of stimulant drugs, intercranial haemorrhage etc
  6. Treatment
    • medications → glucocorticoids, NSAIDS, Sympathomimetics
43
Q

what are the principles for choice and number of antihypertensives?

A
  1. begin with one antihypertensive if mild or two if moderate HTN
  2. reassess within one month, then 3-6 months, then annually
  3. if treatment goal is not reached with one drug, increase dose or add a second
  4. if treatment goal is not reached with two drugs, add a third but consider the potential for secondary causes.
44
Q

what are the 4 classes of first line antihypertensives? give examples

A
  1. ACEis
    • captopril
    • enalapril
    • lisinopril
    • perindopril
  2. ARBs
    • valsartan
    • losartan
  3. thiazide diuretics
    • hydrochlorothiazide
  4. Peripheral/dihydropyridine CCBs
    • amlodipine
    • nifedipine
45
Q

what are the 5 classes of second line antihypertensives? give examples

A
  1. beta blockers
    • metoprolol, propranolol
    • first line in patients with other cardiac comorbidities or thyroid disease
  2. loop diuretics
    • frusemide
    • symptomatic heart failure and ckd
  3. aldosterone antagonists
    • spironolactone
  4. direct renin inhibitors
    • aliskiren
    • not to be combined with ACEis or ARBs
  5. alpha-1 blockers
    • prazosin, doxazosin
    • used as an adjunct in patients wth BPH
46
Q

What can cause heart block?

A
  1. Structural heart disease
    • Ischaemic heart disease, congenital heart disease, post cardiac surgery, inflammatory cardiac conditions etc
  2. neurocardiogenic
    • increased vagal tone
      • physiological in athletes
      • pathological in OSA or during vomiting, suctioning, intubation
  3. toxic/metabolic
    • electrolyte disturbances → hyperkalaemia
    • acid-base disorders
    • cardiotoxic drugs → BB, CCBs, Dig, CO, cyanide
  4. Infections
    • Infective endocarditis, lyme disease, acute rheumatic fever
  5. endocrine
    • thyroid disease, adrenal disease
47
Q

what is the appearance/criteria on ECG of prolonged QTc for men and women?

A
  • prolonged QT interval corrected for heart rate
  • QTC > 440ms in men (11 small boxes or ~ 2 large boxes)
  • QTc > 460ms in women
  • QTc above 500ms → increased risk of TdP
48
Q

Why is a prolonged QT dangerous?

A

Can turn into torsades de pointes

49
Q

What are the shockable cardiac arrest rhythms?

A
  1. Ventricular fibrillation
  2. Pulseless VT
  3. Polymorphic VT
50
Q

What are non-shockable Cardiac arrest rhythms?

A
  1. Pulseless electrical activity (PEA) -> any rhythm without a pulse that is not one of the shockable rhythms
  2. Asystole
51
Q

What are examples of intrinsic causes of normocytic anaemia?

A
  1. haemoglobinopathies
    • sickle cell disease, inherited Hb disorders that decrease RBC lifespan
  2. Enzyme deficiencies
    • Pruvate kinase def
    • G6PD deficiency
  3. inherited membrane defects
    • hereditary spherocytosis
52
Q

What are the two categories of macrocytic anaemia and examples of conditions that cause this

A
  1. megaloblastic → presence of megaloblastics and hypersegmented neutrophils
    • B12 or folate deficiency
      • both are essential for erythropoiesis
    • medications
      • phenytoin, trimethoprim, sulfonimides
  2. Non-megaloblastic
    • liver disease
    • AUD
    • multiple myeloma
    • hypothyroidism
53
Q

Describe pernicious anaemia → cause of B12 deficiency

A
  • chronic autoimmune condition that causes atrophic gastritis
  • autoantibodies against the gastric parietal cells damages then and reduces the amount of IF they produce
  • associated with thyroid conditions and achlorhydria (HCL def.)
54
Q

what are risks associated with blood transfusion?

A
  1. fever -> febrile, non-haemolytic transfusion reaction
  2. urticaria
  3. anaphylaxis
  4. acute haemolysis from ABO incompatibility -> acute haemolytic transfusion reaction
  5. bacterial contamination of blood products
  6. Transfusion related lung injury (TRALI) and Transfusion associated circulatory overload (TACO → pulmonary oedema
55
Q

what are the 4 main pathophysiological mechanisms behind causes of ischaemic stroke?

A
  1. Large artery atherosclerosis
    • carotid, verebral or major cerebral arteries → plaque or thrombus breaks off and occuldes cerebral vessels
  2. small vessel or lacunar stroke
    • thrombotic occlusion of small penetrating arteries
  3. cardioembolism
    • thrombus in the left heart (eg due to AF) → embolism and occlusion
  4. rarer causes
    • dissection
    • vasculitis
    • venous sinus thrombosis
    • hypercoagulability
56
Q

What are the 4 main causes behind haemorrhagic stroke?

A
  1. long standing hypertension → primary cause
    • induces cerebrovascular changes and damages vessel walls
  2. malignancy
  3. illict drug use
  4. AV malfrmations (eg aneurysm)
57
Q

What type of stroke causes contralateral hemiparesis of face, arm and leg? and what type of gait does this produce?

A
  1. Hemiplegic gait

2. Posterior limb of the internal capsule

58
Q

Summary of Symptoms in MCA stroke?

A
  1. contralateral upper limb sensory and motor loss or weakness (may have some LL involvement
  2. Wernicke and Broca’s aphasia may be seen
  3. contralateral hemiparesis of face, arm and leg → causing hemiplegic gait
  4. Homonymous hemianopia without macula sparing, or quandrantanopias.
59
Q

What is the medial and lateral arterial supply to the Midbrain?

A
  • Medial = basilar branches

- Lateral = PCA and SCA

60
Q

what is the medial and lateral supply to the Pons?

A
  • medial = basilar branches

- Lateral = AICA

61
Q

what is the medial and lateral arterial supply to the medulla?

A
  • medial = Vertebral and anterior spinal arteries

- Lateral = PICA

62
Q

What region of the brain and what is the clinical presentation in a ACA stroke?

A

Region

  • M1 and S1 in the medial, interior portion → therefore affects LL
  • Prefrontal cortex

Features

  1. contralateral lower limb sensory losses and weakness
  2. disinhibition, personality changes
  3. urinary incontinence
63
Q

What region of the brain and what is the clinical presentation in a PCA stroke?

A

Region

  1. thalamus
  2. Midbrain
  3. occipital lobe
  4. hippocampus

Features

  1. sensory loss, aphasia, visual loss, personality changes, agitation
  2. midbrain syndromes
  3. contralateral homonymous hemianopia with macular sparing
  4. Memory deficits
64
Q

What are the 4 M structures in a medial brainstem stroke? what symptoms does this produce?

A
  1. Motor Pathway (CST) → contralateral arm and leg weakness
  2. Medial Longitudinal fasiculus (MLF) → ipsilateral INO (loss of adduction)
  3. Motor nucleus and nerve → ipsilateral loss of affected cranial nerve
  4. Medial lemniscus → Contralateral loss of vibration and proprioception in the arm and leg
65
Q

What are the 4 S structures in a lateral brainstem stroke? what symptoms does this produce

A
  1. Spinocerebellar tract → ipsilateral ataxia
  2. sympathetic fibres → ipsilateral horners
  3. Sensory nucleus of CNV → ipsilateral loss of pain and temp to face
  4. Spinothalamic tract → contralateral loss of pain and temp in arm and leg
66
Q

Which 4 CNs are in the midline?

A
  • CNIII - Oculomotor
  • CNIV - trochlear
  • CNVI - abducens
  • CNXII - hypoglossal
67
Q

Which cranial nerves are affected and the symptoms in a stroke affecting the Midbrain?

A

Basiler arteries medially and superior cerebellar and posterior cerebral laterally

1. CNIII oculomotor → ipsilateral eye is turned down and out + mydriasis
2. CNIV trochlear → contralateral eye depression impaired when adducted
68
Q

Which cranial nerves are affected and the symptoms in a stroke affecting the Pons?

A

Basilar arteries medially and AICA laterally

  1. CNV → ipsilateral loss of sensation to face
  2. CNVI → ipsilateral weakness of abduction of eye
  3. CNVII → ipsilateral facial weakness
  4. CNVIII → vestibulocochlear → ipsilateral sensorineural hearing loss
69
Q

Which cranial nerves are affected and the symptoms in a stroke affecting the Medulla?

A

Vertebral artery and anterior spinal artery medial, PICA lateral

  1. CNIX → glossopharyngeal → ipsilateral loss of gag reflex and pharyngeal sensation
  2. CNX vagus → ipsilateral palatal weakness → deviates away
  3. CNXI → accessory → ipsilateral weakness of trapezius and SCM
  4. CNXII → hypoglossal → ipsilateral weakness of tongue → deivates towards

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