NEW CARDIO Flashcards

(72 cards)

1
Q

Aortic Dissection - Presenting picture

A
  • Sudden severe midline chest pain – tearing in nature; may be interscapula- Associated PMhx: Aortic valve disease, Hypertension, Pregnancy, Genetics – Marfans, Ehlers-DanlosExamination Findings: - BP (may be high, low or normal)- Asymmetric pulses- Signs of tamponade – hypotension, quiet HS, raised JVP, pulsus paradoxus; pericardial friction rub- Systolic murmur – AR (incompetence)- Ischaemic neurological deficits – hemiplegia, hemiparesis
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2
Q

Aortic Dissection - Ix and Management

A

Investigations- CXR – screening test- TTE or helical CT for diagnosis- ECG findings – may mimic AMI findingsManagement - Surgery

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3
Q

Respiratory causes of Chest Pain

A

• PE• Lung Cancer• Pneumonia• Pleuritis – can be due to infection, pulmonary infarction, tumour, connective tissue disorders

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4
Q

Spontaneous Pneumothorax - when to suspect? Hx/Ex/Ix/Mx?

A
  • Suspect in those with history of – Asthma or COPD and young slender males- O/E – tachycardia, Decreased breath sounds- Diagnosis is made on CXR – expiratory films- Management - <25%, no symptoms – can observe, if symptoms drain, >25%. drain
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5
Q

CP caused by cox-sackie virus (faecal oral route)

A

Epidemic Pleuordynia- Occurs in epidemics and mainly affects children and young adults- Causes chest/upper abdominal pain – often pleuritic in nature, as well as myalgia elsewhere- Diagnosis of exclusion - Management is analgesia

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6
Q

What are features of Chostocondritis?

A
  • Often precedes an URTIOften one sided, sharp and made worse with breathing, physical activity and palpation
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7
Q

Unilateral sharp pleuritic chest pain with a tender, fusiform swelling at the chndrosternal junction?

A

Tietze Syndrome Cause is not well understood – may relate to physical strain or minor injury

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8
Q

Chest pain in Children? Most common causes?

A

Most common cause – idiopathic followed by musculoskeletal, cough related, costochondritis and psychogenic

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9
Q

– low chest pain lasting 30s-3mins after exercise – relieved by standing up right and taking slow deep breaths

A

Precordial Catch aka Texidor twinge or stitch

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10
Q

AF - epidemiology?

A

AF affects 1% of the Australian Population >50% are over 75RR of stroke is increased by 5x and 3x increased risk of CCF

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11
Q

What are the risk factors for Atrial Fibrillation?

A

Structural Abnormalities e.g. valvular abnormalities, cardiomyopathy•

Conduction abnormalities: e.g sick sinus syndrome, WPW•

Functional states: e.g AMI, pericarditis, Heart Failure

Stress on the heart e.g. IHD, hypertension, PE

Physiologic/Hyperadrenergic states – medications and drugs, stress, fever, hyperthyroidism, diabetes mellitus, sepsis, pneumonia, surgery

Acute events like sepsis/pneumonia/surgery can precipitate and then at increased risk of recurrence

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12
Q

What are the categories of Atrial Fibrillation?

A

Paroxysmal (usually <48 hours) - 90% have recurrent episodes but can last up to 7 days (Can be cardioverted)•

Persistent >7 days (can be cardioverted)•

Long standing persistent - continuous AF for >1 year and rhythm control is used.

Permanent AF is continous AF for greater than 1 year but where rhythm control has not been chosen by patient

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13
Q

AF - History?

A

• Palpitations• SOB• Lightheadedness/syncopal episodes• Focal neurological deficit• PMhx• Meds and drugs – e.g. alcohol, caffeine, illicit drugs

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14
Q

AF - Examination findings

A

• Vitals- Pulse irregularly irregular, BP to check for decompensation, fever as potential cause• HS – listen for murmurs – valvular abnormalitites• Chest – if CCF bibasal crackles, peripheral oedema, JVP raised

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15
Q

AF - Investigations

A

• ECG- Absence of p-waves- Irregular RR intervals• Echo- TOE or TTE- TOE used to exclude left atrial appendage thrombusBloods• FBE• UEC• LFT• TSH• Ca/Mg• Fasting glucose• Fasting lipid profile• CXR – check for CCF

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16
Q

AF - Rate control

A

• Beta blocker – e.g. metoprolol 50-200mg/day OR• Non-dihydropyridine calcium channel blocker – e.g. diltiazem or verapamil• Digoxin – indicated for rate control in patients with CCF, LV dysfunction or sedentary individuals• Oral amiodarone – may be indicated when other medical therapies fail• Ablation of AV node or accessory pathways – may be indicated if medical therapies fail

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17
Q

AF - Rhythm control?

A

Rate control usually preferred

Rhythm control

DC Cardioversion

Recommended if

  1. rapid ventricular rate, unresponsive to medications and myocardial ischaemia

or

  1. hypotension or heart failure

If <48 hours of known duration of AF can do with immediate anticoagulation and continue post re-version according to VTE risk.

If >48 hours or of unknown duration – either 3/52 anti-coagulation INR 2-3 OR initial anticoagulation, TOE to confirm no atrial thrombus, then cardioversion within 24 hours

Pharmacologic Cardioversion

options include flecainide, amiodarone

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18
Q

How do you decide anti-coagualtion for AF?

A

Determined by the CHA2DS2-VACondition and Points C Congestive heart failure (or Left ventricular systolic dysfunction) 1 H Hypertension: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication) 1 A2 Age ≥75 years 2 D Diabetes Mellitus 1 S2 Prior Stroke or TIA or thromboembolism 2 V Vascular disease (e.g. peripheral artery disease, myocardial infarction, aortic plaque) 1 A Age 65–74 years 10 - low risk - no therapy or low dose aspirin1 - moderate risk – benefit from warfarin/anticoagulation>/= 2 points - high risk and long term oral anticoagulant therapy is strongly recommendedCHADS 2 score Annual stroke rate0 1.9 %2 4%4 8.5%6 18%Other relevant factorsEcho findings - systolic dysfunction and left atrial enlargementVascular factors - previous MI, PVD, complex aortic plaque

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19
Q

What Risk Mitigation strategies are available when prescribing anticoagulation for a patient with AF?

A

Looks at risk of major bleeding whilst on oral anticoagulant treatment

Risk of major bleeding is at least 1-1.5% annually

HAS-BLED• Helps identify correctable RF’s for bleeding and identify patients at high risk• It should not be used to exclude patients from anticoagulant treatment but rather serve to indicate increased monitoring

• Correctable RF’s should be managed

Hypertension (Sytolic BP >160mmHg)

Abnormal renal or liver function

Stroke (history of)Bleeding (Hx of or diathesis

Labile INRS (<6/10 in therapeutic range)

Elderly (>65)

Drugs (antiplatelet agents, NSAIDS, alcohol >/= 8 SD per week)

A high HAS-BLED score (greater than or equal to 3) suggests need for regular review and monitor of risk factors (does not preclude anticoagulation)

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20
Q

Anticoagulation in AF

A

Warfarin or novel anticoagulants (target thrombin directly)

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21
Q

Warfarin in AF

A

Its used in valvular AF - mod/sev mitral STENOSIS or mechanical heart valve. Otherwise use a NOAC

Reduces the incidence of AF related stroke by about 2/3rds

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22
Q

Which novel anticogulants are available? When are they used? What dosage?

A

RivaroxabanDose is 20mg daily – reduce to 15mg OD if CrCl 30-49PBS approved for:• Preventions of stroke and systemic embolism in non-valvular AF and at least one additional risk factor as defined by the CHADS2 score• Prevention of venous thromboembolism after THR or TKR surgery• Treatment of acute PE; DVT or prevention of venous thromboembolism recurrence in people with a history of VTE• Bleeding risk less than or equal to that of warfarin • No antidote - unlike warfarin• Not to be used in patients with hepatic disease, increased INR, severe renal impairmentPradaxa (Dabigatran)150mg BD; Dose reduction to 110mg BD for age >/=75, CrCl 30-50, higher risk of bleedingPBS approved for:• Preventions of stroke and systemic embolism in non-valvular AF and at least one additional risk factor as defined by the CHADS2 score• Prevention of venous thromboembolism after THR or TKR surgery• Treatment of acute PE; DVT or prevention of venous thromboembolism recurrence in people with a history of VTEEliquis (Apixaban) • Requires BD dosing – either 2.5mg BD or 5mg BD• Dose reduction for Age >/= 80; bodyweight = 60kg; Serum Cr >/= 133 • CI – Severe hepatic disease (Child-Pugh C); severe renal impairment CrCl <25; strong clinical risk of bleedingPBS approved for:• Preventions of stroke and systemic embolism in non-valvular AF and at least one additional risk factor as defined by the CHADS2 score• Prevention of venous thromboembolism after THR or TKR surgery*In comparative trials only apixaban was found to have a lower incidence of major bleeds c.f. warfarin

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23
Q

Switching anticoagulants in AF?

A

Stop WarfarinCommence new anticoagulant once INR <2

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24
Q

Hypertension assessment/grading

A

Blood pressure Category ActionBP <120/<80 Normal Recheck in 2 yearsBP 120-139/80-89 High Normal Recheck in 1 year or as per CV risk140-159/90-99 Grade 1 Confirm within 2 months160-179/100-109 Grade 2 Reassess or refer within 1 month≥180/110 Grade 3 Reassess or refer within 1-7 daysIsolated systolic - >140/<90 as per systolic aboveIsolated systolic with widened pulse pressure >160/<70 - as for grade 3 hypertension

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25
Who needs Immediate Anti hypertensive treatment?
Those at high absolute CV risk \>15% probability of a CV event in the next 5 years. Can be assumed as high for the following groups:1. Group A - patients 75 years and over2. Group B - patients with existing CV disease including IHD/CCF/Previous Stroke/PVD/LVH/Aortic disease3. Group C - Patients with associated clinical conditions and/or end-organ disease:Associated• Diabetes AND age \>60 or microalbuminuria \>2.5 mg/mmol males \>3.5 females• Dyslipidemia - Total cholesterol \>7.5• Familial hypercholesterolaemia• FHx of premature CV diseaseAND as per group B (also associated)• IHD• CVA • PVD• Aortic diseaseEnd-organ disease• Chronic Kidney disease - eGFR\<60 - Proteinuria defined as urine protein \>300mg/day or Protein/Cr ratio \>/=30 mg/mmol- Microalbuminuria - Alb:Cr ≥ 2mg/mmol males or 2.5 mg/mmol female; 24 hour urinary albumin excretion rate \>20 mcg/min• Vascular disease - atherosclerotic plaque - aorta; carotid; coronary; peripheral vasculature• Hypertensive retinopathyANDGrade 3 hypertension or systolic hypertension with widened pulse pressureFor everyone else consider use of risk charts
26
Hypertension lifestyle risk reduction?
• 30/60 moderate intensity physical cativity on most if not all days of the week - daily total can be accumulated during the day• Smoking cessation• Dietary salt restriction - ?2 or 4g/day - recommend low-salt and salt-reduced foods• Limited alcohol intake = 2 SD per day for men and = 1 SD per day for womenPatient's who need immediate antihypertensive drug treatment include:• Those at high absolute CV risk \>15% probability of a CV event in the next 5 yearsAlso consider drug therapy for• Patients with moderate risk of CV disease as estimated using risk calculator• Aboriginal and Torres Strait Islanders
27
Treatment targets for HTN?
• People with no other co-morbidity \<140/90• People with associated conditions or end organ damage \<130/80People with proteinuria \>1g/day \<125/75
28
First line drugs for HTN therapy?
First line drugs:• ACE-I or ARB• Dihydropyridine Calcium Channel Blockers• Low-dose thiazide diurects (suitable for patients aged 65 years and older - have been associated with increased risk of new-onset diabetesa and should be used with caution in patients with glucose intolerance and/or metabolic syndromeStart dose low, if target BP not reached consider introduction of another first line medication (in addition) before increasing doses. If target is not achieved and both drugs are well tolerated increase doses.Use up to four antihypertensive drugs in combination to achieve targetAvoid these combinations:• Beta-blocker plus verapamil (non dihydropyridine calcium channel blocker)• ACE-I plus ARB• ACE-I or ARB plus potassium sparing diuretics e.g. amiloride, spirinolactoneBased on estimates 50-75% of patients will not achieve satisfactory BP control on monotherapyBased on the best available evidence the most effective combination is ACE-I or ARB plus calcium channel blocker
29
Beta blockers in HTN?
Beta blockers are no longer recommended as first-line therapy in uncomplicated hypertension because of the increased risk of developing diabetes and the recently described trend towards worse outcomes in patient's treated with these compared with other classes of drugs.Stable patients already on a beta-blocker do not need to have their medication changed
30
Follow up and things to consider if inadequate response to first line HTN therapy?
Follow upMedium-low risk check every 6/12High risk check every 3/12Things to consider if inadequate response to treatment• Poor compliance• Lifestyle issues - treatment resistance due to alcohol/recreational drugs; other medications e.g. NSAIDS, high salt intake, volume overload• Undiagnosed secondary hypertension e.g CKD, hyperaldosteronism, renal artery stenosis, phaeochromocytoma, co-arctation of the aorta• Treatment resistance due to sleep apnoea• White coat hypertension
31
Secondary Causes of Hypertension?
Chronic kidney disease • Underlying cause not able to be treated• May be both a cause and consequence of hypertension• Defined as 3 months or more of an eGFR\<60 or other markers e.g. albuminuria \>30 mcg/mg creatinine in a first morning voided urine sample• ACE-I should be part of regimenGood screening tests:UEC/First morning voided urine for alb:cr ratioPrimary hyperaldosteronism • Causes: 60% bilateral adrenal hyperplasia; 35% aldosterone-productng adenomas; remainder due to adrenal cardinoma, unilateral adrenal hyperplasia etc• Often associated with raised BMI; sleep apnoea and hypokalemia (not always present)• These patients are at risk of LVH; AMI; AF; stroke and the metabolic syndromeGood screening test:• Aldosterone/renin ratio - if high \>20-40 confirmatory tests may be done which include 2 L n/saline or captopril and remeasurement of ratio if there is supression then treatment is best done with an agent such as spirinolactone. • If there is no suppression HRCT of the adrenals/adrenal venous sampling +/- surgery may occurRenal artery stenosis • Up to a 1/3 of cardiac patients requiring stenting also have renal artery stenosis• Medical management of this has been shown in studies to be just as effective as stenting there the only times where you would consider stenting would be in a patient who cannot tolerate and CAI or ARB or in patients with ongoing poor control despite maximum medical therapyGood screening test:Renal doppler U/S - other options HR CTA or MRACushing syndrome Good screening test - Urinary free cortisol \>100mcg/day; midnight serum cortisol; high dose dexamethasone suppression testsPheochromocytoma Good screening test - plasma metanephrines/cathecholamines; 24 hour urine for VMA and metanephrines/catecholaminesIf the above are positive search for an adrenal lesion should be done via CT or MRI abdomenCoarctation of the aorta Key is blood pressure differences across the limbs; systolic murmur may also be heardGood scrrening test Echo Sleep apnoea
32
Acute Pulmonary Oedema precipitating causes?
Cardiac• AMI• Arrhythmias • Uncontrolled hypertension• Significant valvular disease (stenosis and regurgitation)Pulmonary• PE• Infection Others• Anaemia• Hyperthyroidism• Medications• Excessive alcohol and salt intake
33
APO investigations?
ECG - check for AF, AMI, LVHCXR• Enlargement of Cardiothoracic ratio \>50• Pulmonary congestion (Bat wing oedema)• Fluid in the fissures• Kerley B lines (interstitial oedema - usually seen at the lung bases)• Prominent upper lobe vessels• Blunting of costophrenic anglesBloods• FBE• UEC• LFT• TSH• CK and Tn• BNP - may be done in larger centres
34
APO acute management?
• Sit patient upright• Oxygen• ECG• Pulse oximetry• IV access - can do bloods at the same timesMedicationsCPAP
35
APO medications?
MedicationsGTN • Sublingual or topical• To be given if BP systolic \>90 mmHg• Given IV in some major hospitals (ensuring that BP is \>100mmHg)Lasix • Usual daily dose or 1-1.5mg/kg• Beneficial effect is accelerated by pre-treatment with a vasodilatorMorphine• No longer recommended• Emerging data links it use with increased intubation and mortality rates• No studies have ever shown benefit
36
CPAP in APO?
CPAP• Effective in pre-load and afterload reduction• Associated with decreased intubation and mortalityPatient with the following conditions may benefit from early CPAP listed in order of evidence:• Acute exacerbations of COPD• Acute cardiogenic pulmonary oedema• Pneumonia - patients with COPD and immunocompromised seem to benefit• COPD or APO where a decision has been made not to intubate - prevent deterioration• COPD or APO where extubation has failed after a brief course of intubation - CPAP might ease the transision\*CPAP is not recommended in asthma, ARDS, other causes of respiratory failure
37
Complications of CPAP?
• Pain or ulcer over nasal bridge• Mucosal dryness• Eye irritation - if the mask seal is not complete• Gastric insufflation (air blowing) or aspiration
38
ICU therapies for APO (aside from CPAP?)
• Adrenaline infusion• Vasodilators (sodium nitroprusside)• Inotropes (for cardiogenic shock or hypoperfused state with systolic BP \<90mmg Hg) (aramine eg)• Mechanical support e.g. intra-aortic balloon pump)
39
In regards to treatment for peripheral arterial disease, which of the following treatments can improve walking distance? Choose one (1) option.Rampiril 10mg orally daily Smoking cessation Simvastatin 40mg orally daily A graduated walking program All of the above
All of the abovehttps://www.racgp.org.au/afp/2013/june/peripheral-arterial-disease-diagnosis/
40
Patricia is a 65 year old female patient who you have been seeing for several years for management of her diet-controlled type 2 diabetes. She reports a healthy diet which is low in salt and she has recently lost 10% of her body weight. Over the past six months she has started walking for 60 minutes each day with a friend. Patricia is a non-smoker and non-drinker. Six months ago you diagnosed her with hypertension and prescribed perindopril arginine 5mg daily which she has been taking regularly with no side effects. During Patricia’s last consultation three months ago you noted that her blood pressure was still168/95. She had some blood pressure readings performed at the local pharmacy since then which show similar readings. You recheck her blood again today and it is 170/90. How do you manage Patricia’s blood pressure now? Advise Patricia that no change to her anti-hypertensive medication is required at this stage and encourage continued lifestyle change Add amlodipine 5mg daily Add metoprolol 50mg daily Increase Perindopril arginine to 10mg daily Add Irbesartan 150mg daily
The correct response is: Add amlodipine 5mg daily. Current guidelines recommend the use of either an angiotensin-converting enzyme inhibitor (ACE i) or angiotensin receptor blocker (ARB) first line for treatment of hypertension in patients with type 2 diabetes. This is a superior choice to other anti-hypertensives in this group of patients because these drugs have been found to reduce progression to microalbuminuria and reduce the risk of renal impairmen.If monotherapy with an ACEi or ARB does not sufficiently reduce blood pressure the next step is to add one of either a calcium channel blocker or a low dose thiazide or thiazide like diuretic. Combination therapy, defined by the use of at least two antihypertensive drugs, is required in up to 50–70% of patients to reach blood pressure targets. It is widely accepted that combining two classes of antihypertensive drug lowers blood pressure more than doubling the dose of one drug. The Royal Australian College of General Practitioners. General practice management of type 2 diabetes: 2016 – 2018. East Melbourne, Victoria. https://www.racgp.org.au/download/Documents/Guidelines/Diabetes/2015diabetesmanagement.pdf
41
You are seeing a 62 year old female patient who consistently has high blood pressure readings in the clinic. Today her blood pressure is 162/97mmHg. She reassures you she just has “white coat hypertension” and that she is not concerned about her blood pressure.You convince her that you need to obtain some normal blood pressure readings outside of the clinic in order to agree with her diagnosis of “white coat hypertension”. Although she will not agree to a 24 hour ambulatory blood pressure recording, she will agree to home blood pressure monitoring. She borrows the automated blood pressure device the clinic loans out to patients. Which of the following statements about home blood pressure readings is correct? Choose one (1) option. Blood pressure should be monitored at different times in the morning and evening Blood pressure should be checked after eating and vigorous exercise Blood pressure should be checked before taking regular daily medications Blood pressure should be taken three times daily for four consecutive days Caffeine and cigarettes should be avoided for at least 15 minutes before measuring blood pressure
The correct response is: Blood pressure should be checked before taking regular daily medicationsPatients should be given advice on how to correctly take home blood pressure readings. They should be advised to take the readings before medication, food and vigorous exercise for seven consecutive days. The readings should be taken at the same time each morning and night. Cigarettes and caffeine need to be avoided for at least 30 minutes before taking a reading.Reference:Sharman, J. et al. How to measure home blood pressure: recommendations for healthcare professionals and patients. Australian Family Physician, 2016; 45(1-2):31-34. https://www.racgp.org.au/afp/2016/januaryfebruary/how-to-measure-home-blood-pressure-recommendations-for-healthcare-professionals-and-patients/
42
A 45 year old male presents with episodes of a racing heart, sweating and headaches. He states that these symptoms have increased in the last 6 months and are now a daily occurrence. On examination he appears well, is afebrile and has a blood pressure of 170/110. He has lost 5kg since his last clinic appointment 2 months ago. Which of the following investigations would be a suitable screening test for his most likely diagnosis? Choose one (1) option.Plasma aldosterone to plasma renin activity ratio Early morning cortisol level 24 hour urinary catecholamines and metanephrines Short synacthen test 1mg overnight dexamethasone suppression test
The correct response is: 24 hour urinary catecholamines and metanephrinesThis case is describing a patient with symptoms and signs consistent with a pheochromocytoma. 24 hour urinary catecholamines and metanephrines have a sensitivity of 90% and specificity of 98% for this condition. Reference:Gendy R, Rashid P. Incidental adrenal masses - A primary care approach. Australian Family Physician 2017; 46(6): 385-390.https://www.racgp.org.au/afp/2017/june/incidental-adrenal-masses-a-primary-care-approach/
43
A 76 year old male presents with fatigue, intermittent palpitations and shortness of breath at rest. He is currently on Perindopril for his hypertension but has no other regular medications. He has a past history of peripheral arterial disease and a transient ischaemic attack (TIA) 2 years ago.On examination you note that he has an irregularly irregular heart rate. You suspect the patient has atrial fibrillation and order an ECG which confirms this diagnosis. You base your decision for anticoagulation for stroke prevention on this patient’s CHA2DS2-VA score.What is this patient’s score? Choose one (1) option. 8 7 6 5 4
The 2018 Australian Clinical Guidelines for the Diagnosis and Management of Atrial Fibrillation recommends the use of the CHA2 DS2-VA score to assess stroke risk. This patient’s score is 6:History of hypertension: 1 pointAge ≥75 years: 2 pointsHistory of prior TIA: 2 pointsVascular disease (peripheral arterial disease: 1 pointReferenceNational Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand. Australian Guidelines for the Diagnosis and Management of Atrial Fibrillation 2018. https://www.heartlungcirc.org/article/S1443-9506(18)31778-5/fulltext (Accessed November 2019)
44
Your patient, 73 year old Rohan Balci, is concerned about a new small pigmented skin lesion on his forearm. Your examination confirms a 4mm pigmented lesion with some border irregularity. You plan to perform an excisional biopsy but are concerned about bleeding risks as Rohan is on aspirin and prasugrel which was commenced nine months ago following his ST elevation myocardial infarction. This was treated with percutaneous coronary intervention and a single coronary artery stent.What is the most appropriate way in which to manage Rohan’s skin lesion? Choose one (1) option.Excise under local anaesthetic; cease aspirin and prasugrel the day prior to the procedure and resume the next day following the excision. Excise under local anaesthetic; cease aspirin and prasugrel for 10 days prior to the procedure and resume the next day following the excision. Wait for three months until the planned cessation of prasugrel while continuing aspirin; then excise under local anaesthetic. Continue his current medications and excise under local anaesthetic. Continue his current medications and treat the skin lesion with cryotherapy.
The correct response is: Continue his current medications and excise under local anaesthetic.A new pigmented skin lesion with border irregularity requires a histological diagnosis to exclude melanoma. It is not appropriate to wait three months or to treat with cryotherapy. Any cessation of dual anticoagulant therapy in this patient would carry a significant risk of stent thrombosis and recurrent myocardial infarction. There is likely to be increased bleeding at excision when on dual anticoagulation therapy but an excision on the forearm might be managed with additional local measures such as extra local pressure and additional sutures.References:Jayasinghe R, Markham R, Adsett G. Dual antiplatelet therapy: Management in general practice. Australian Family Physician 2013; 42 (10): 702-705. https://www.racgp.org.au/afp/2013/october/dual-antiplatelet-therapy/ (Accessed January 2020).
45
You are seeing a 62 year old female patient who consistently has high blood pressure readings in the clinic. Today her blood pressure is 162/97 mmHg. She reassures you she just has “white coat hypertension” and is not concerned about her blood pressure. You convince her that you need to obtain some normal blood pressure readings outside of the clinic in order to agree with her diagnosis of “white coat hypertension”. Although she will not agree to a 24 hour ambulatory blood pressure recording, she will agree to home blood pressure monitoring. She borrows the automated blood pressure device the clinic loans out to patients. Which of the following statements about home blood pressure readings is correct? Choose one (1) option.Patients should be advised to sit quietly for 1 minute before taking their blood pressure at home Home blood pressure readings are less reliable than clinic readings in terms of determining the true underlying blood pressure Patients should be advised to take one blood pressure measurement morning and evening for seven consecutive days Average home blood pressure readings of 135/85 mmHg or more is the threshold for diagnosing hypertension Patients should be advised to take three blood pressure readings daily over a four week period
The correct response is: Average home blood pressure readings of 135/85 mmHg or more is the threshold for diagnosing hypertensionTwo measurements of home blood pressure should be taken, one minute apart, after 5 minutes of sitting quietly, morning and evening, for 7 consecutive days.Reference:Sharman, J. et al. How to measure home blood pressure: recommendations for healthcare professionals and patients. Australian Family Physician 2016; 45(1-2): 31-34.https://www.racgp.org.au/afp/2016/januaryfebruary/how-to-measure-home-blood-pressure-recommendations-for-healthcare-professionals-and-patients/
46
Fred is a seven year old boy is brought to you by his parents who say that he has has been complaining of trouble with his vision at school. On examination his blood pressure is 145/90mmHg. You take further history and perform further examination to determine is Fred is likely to be suffering with secondary or essential hypertension. Which feature in this list is MOST likely to fit with essential hypertension?Abdominal bruit Ambiguous genitalia Delayed femoral pulses Diastolic hypertension History of umbilical artery catheterisation History of urinary tract infections Malignant hypertension Nocturnal hypertension Family history of hypertension Oedema Prepubertal child Resistant hypertension despite the concurrent use of 3 anti-hypertensives at adequate doses from different classes Tachycardia, sweating, headache and flushing
Obesity and a family history of hypertension make essential rather than secondary hypertension more likely.Gupta-Malhotra M et al. Essential Hypertension vs. Secondary Hypertension Among Children. Am J Hypertens. 2015 Jan; 28(1): 73–80.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4318949/ (Accessed Dec 2018)
47
Pathophysiology of Heart Failure?
Myocardial injury↓LV dysfunction (EF\<40%)↓Activiation of renin-angiotensin-aldosterone system and the sympathetic nervous system↓In turn detrimental to ventricular structure and function
48
Clinical features of Heart Failure?
Clinical features• Exertional dyspnoea and fatigue• PND• Orthopnoea• Ankle oedema
49
What are the NYHA classification stages of heart failure?
Class 1 - asymptomatic LV dysfunctionClass 2 - symptoms with normal activitiesClass 3 - symptoms with less than normal activitiesClass 4 - symptoms at rest
50
What are the causes of heart failure?
• IHD – accounts for 50% of patients with CCF in Australia• Hypertension• Valvular heart diseaseLess common:• Congenital• Diabetes• Thyroid related• Connective tissue diseases• Myocarditis• Peripartum• Drug induced e.g. alcohol or chemotherapy
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Heart failure examination findings?
Raised JVPVentricular strain - gallop rhythm; tachycardiaBibasal crepsPulsatile hepatomegalyAscitesPeripheral oedema
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Investigations in heart failure?
Bloods• FBE/UEC/LFT/TFT/Fe studies/auto-immune screen• CK and Tn may be relevant• BNP - if \<100 pg/ml - make CCF very unlikely; can be elevated in renal failure; CCF, PE, other severe illnesses – useful if an echo cannot be organised in a timely fashion• CXR - bibasal opacity; enlarged cardiothoracic ratio; pleural effusions• ECG – look for ischaemic changes – Q waves, ST changes, LBBB, AFTransthoracic Echo• All patients with suspected CCF should undergo a transthoracic echo to assess LV systolic function • Up to a 1/3 of CHF patients have normal LV systolic function (often termed diastolic failure – failure of ventricular relaxation) – in these patients no specific pharmacologic therapy has been shown to improve mortality• In patients with abnormal diastolic function - diastolic CCF may be considered - often occurs in elderly females with hypertension, can also occur in those with diabetes, obesity, IHDUses• Can help find causes - e.g. valvular heart disease; LV hypertrophy; pulmonary hypertension; regional wall motion abnormalities• Can be used to assess response of LV function to therapy - serial measurement of EFNormal LVEF 40-70%; reduced is \<40%As a routine – annual is recommended
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What vital signs should you aim for in heart failure?
Should aim for a systolic BP 105-11 and HR 55-60
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Non pharmacological management in heart failure?
• Fluid restriction - \<1.5L; less than 1L in severe (\<2L when exacerbations are not present)• Na restriction \<2g per day• Daily weighing at home with an action plan• Alcohol cessation in alcohol related cardiomyopathy, o/wise limiting alcoholic and caffeinated beverages to = 2sd/day• Smoking cessation• Regular physical activity but bed rest during acute exacerbations• Vaccination - influenza and pneumococcal
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ACE and ARBs in heart failure?
• Improve morbidity and mortality• Should be started immediately at low doses and titrated up over 3-4 weeks (do not double dose at less than 2 weekly) – aim to have patient on maximal doses• UEC should be checked within 2 weeks of starting and discontinued with K+ \>5.5 or Cr\>20% increase from baselineARBs - shown to have similar improvements in mortality and morbidity• Considered in those who cannot tolerate ACE-I's• Can be combined with ACE-I in those who remain symptomatic – some evidence on decreased hospitalisations but no clear mortality benefit – combination should be left to use by specialists
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Beta blockers in heart failure?
• Are indicated in all patients with CHF• Improve mortality and morbidity• Beta blockers with proven mortality benefit include - carvedilol, bisoprolol and extended release metoprolol (recently a fourth has been approved nevibolol)• Should be commenced at small doses when a patient is euvolemic and titrated up over 1-2 months – start low and go slowMay initially worsen heart failure symptoms and therefore patients should be stable prior to commencement• Euvolemic• No pulmonary crackles• Minimal peripheral oedema• Systolic BP \>85 w/out symptomatic postural dropStart at low dose and aim for HR 55-60 - should be reduced if HR\<55
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Side Effects of beta blockers (in heart failure)?
• Hypotension• Fatigue• Bronchoconstriction in patients with reversible obstructive airways disease – should not be withheld for patients with COPD; should be used with caution in patients with mild to moderate asthma• Mild worsening of CCF symptoms initially - important to warn patients of this initially
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Aldosterone antagonists in heart failure?
Australian guidelines recommend use in those on both an ace-I and beta-blocker and are still symptomatic with severe symptoms• Shown to have a mortality benefit in Class III/IV CCF• Eplenerone (selective aldosterone antagonist)– shown to improve mortality in patients with LV dysfunction post MI • Careful monitoring of electrolytes and renal function is important - can cause hyperkalemia – 1/52 after commencing or changing dose; 1/12 for 6/12 then 6/12 once stable dosing• CI in significant renal impairment Cr cl \<30mL/min OR if K .5.5• Should not be used in those on an ace-I and ARB (or only under guidance of a specialist)
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Diuretics in heart failure?
• Not appropriate as monotherapy• Used to treat symptoms • Do not have a long term mortality benefit• Once patients are euvolemic diuretics should be reduced or weaned – with other medications uptitrated
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Digoxin in heart failure?
• In patients with persistent symptoms despite the above - digoxin has been shown to improve symptoms and reduce hospitalisations but have no effect on mortality• Of use when a patient also has AF
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When is ivabradine indicated? contraindicated in heart failure?
Specific sinus node inhibitor – leading to decreased HRElevated resting HR is a predictor of death and hospitalisation in CCFImproves outcomes and available on the PBS (authority) where:- Baseline HR \>/= 77- LVEF =35%- NYHA class II or III- In combination with optimal standard CCF treatmentCI if:- BP \<90/50- HR \< 60 (in the untreated state)- Severe hepatic impairment- SA node is not in the cardiac pacemaker
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Other pharmacotherapies in heart failure?
Nitrates - useful in reducing nocturnal dyspnoea, pulmonary hypertension, myocardial ischaemiaIsosorbid mononitrate may be commenced at 30mg noctePatients with ischaemic cardiomyopathy should receive aspirinThose with AF or cardiac thrombus should receive warfarinThere is no strong evidence of the use of aspirin/warfarin in patients with non-ischaemic cardiomyopathy
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When should we refer in heart failure?
Specialist referral should be done for all heart failure patient as referral has been shown to improve symptoms, outcomes and decrease hospital admissionsAs a minimum should be done for:• Diagnostic uncertainty• Age \<65• Questions re: management• Patient has consideration for revascularisation, cardiac device or transplant
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Device therapies in heart failure?
ICD – Decreases mortality in symptomatic CCF patients with LV EF= 35% and in patients with a prior AMI and LVEF = 30%Biventricular pacingCardiac dyssonchrony seen in 1/3 of CCF patients - cardiac resynchronisation therapy/pacing - shown to improve symptoms, mortality and decrease hospitalisations - current criteria for this is:- Class III/IV – severe symptoms- EF\<35% and a broad QRS (greatest benefit in LBBB with QRS \>150ms)- Dysynchrony
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Medications that worsen heart failure?
• NSAIDS• GCS• Thiazolidenidiones – rosiglitazone; pioglitazone• Non-dihydropyridine calcium channel blockers – verapamil or diltiazem• Anti-arrhythmic medicines except for heart failure specific beta blockers and amiodarone• TCA’s
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Assessing fitness to drive in CCF?
Non commercial• Conditional if satisfactory response to treatment AND• There are minimal symptoms relevant to driving• Not fit if symptoms arise on moderate exertionCommercialA conditional may be considered with advice from a treating specialist if:• There is satisfactory response to treatment AND• Exercise tolerance of \>/= 90% of the age/sex predicted capacity according to Bruce protocol AND• EF \>40% AND• The underlying cause has been considered• There are minimal symptoms related to driving
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GP management of heart failure?
Potential KFP question• Call for help/call an ambulance• Commence oxygen• History – focussed PC/PMhx/medications Examination• Vitals – Temp; BP; HR; Sa02; RR• Chest/JVP/HS/Oedema• Monitoring• BP• ECG• Oxygen saturation• Defibrillator on standbyInvestigations• ECG• CXR- Interstitial oedema (often ‘bats wing’)- Fluid in the fissures- Kerley B lines (oedematous septal lines)- Pleural effusions (usually bilateral, frequently R\>L, if unilateral more often on the right)- Peribronchial cuffing – visualisation of small-doughnut shaped rings representing fluid in thickened bronchial walls- The heart may or may not be enlarged• FBE/UEC/LFT/CK and Tn/BNP/ABGManagement• Position – upright – if tolerated• Oxygen – high flow 8-10 L• Vitals including pulse oximetry if available• ECG• IV accessMedications• Lasix IV – Usual daily dose or up to 1-1.5 mg/Kg – consider repeating after 30-60 minutes• Nitrate 10-20 mcg/min IV – adjusting rate to response and ensuring BP is \>100 mmHg (not feasible in GP setting – better to use SL GTN) – augments effect of lasix \* Morphine is no longer recommended due to data revealing links with increased intubation and mortality ratesCPAP• Reduces preload and afterload• Associated with decreased intubation and mortality ratesConditions which may benefit from early CPAP in order of evidence are:• Acute exacerbations of COPD• Acute cardiogenic pulmonary oedema• Pneumonia – in patients with COPD and immunocompromised patientsNOT currently recommended for:• Asthma• ARDS – little benefit has been reported
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