More cardio review Flashcards
What are the Categories of AF?
Paroxysmal - lasts less than 48 hrs (90% have recurrent episodes
Persistent - lasts greater than 7 days
Permanent - Lasts greater than a year
Lone - no evidence of structural disease
What are the risk factors of AF?
Structural - cardiomyopathy and valvular abs
Conduction - sick sinus syndrome and WPW
Functional - AMI and pericarditis
Stress on the heart - P.E, HTN and Ischaemic heart disease
Physiologic and hyperadrenergic states - stress, fever, drugs and medications, hyperthyroidism
What are symptoms of AF?
Palpitations
SOB
Lightheadness and syncopal episodes
+/- neurological deficit
Ask about PMHx of drugs/alcohol/caffeine/illicit drugs
IHD/HTN/Hyperthyroid/conduction or structural abs
What are examination findings in AF?
Vitals - Irregularly irregular
check BP for decompensation
Fever could be a potential cause
HS - listen for murmurs/valvular abs/
Signs of CCF - elevated JVP, bibasal crackles, Pedal oedema
What are investigation findings in AF?
ECG - absence of p waves and irregular R-R intervals
Echocardiography : TOE - to exclude left atrial appendage thrombus OR TTE (left atrial enlargement/systolic dysfunction)
Bloods - FBE/LFT/UEC/CMP/TFT/Fasting lipids and glucose
CXR - look for CCF
What are the lifestyle modifications you would suggest for someone with hypertension?
a)Exercise - half an hour moderate intensity on most (if not all) days of the week
Daily total can be accumulated during the day
b) Smoking cessation
c)Dietary salt restriction of less than 4g/day
Reccomend low salt and salt reduced foods
d) Alcohol intake limitation - 2/SD a day for men 1/SD a day for women
When do you consider immediate drug therapy in Hypertensive patients?
HIgh absolute CV risk - greater than 15% probability of cardiac event in next 15 years.
Consider in Moderate risk of CV disease and ATSI
How do we grade/classify Hypertension?
Grade 1: 140 - 159 systolic/ 90-99 diastolic (confirm in 2 months
Grade 2: 160 - 179 systolic/ 100 - 109 diastolic (reassess or refer in one month)
Grade 3: Greater than or equal to 180 systolic OR 110 diastolic - Assess or refer within 1-7 days.
Isolated systolic BP increase - manage as per systolic BP for Grade 1/2/3
Isolated systolic BP (with widened pulse pressure) eg. greater than 160 sys but less than 70 dias - refer within 1-7 days (As per grade three htn guideline)
What are treatment targets in people with known HTN?
No co-morboditiies: 140/90
Associated conditions or end organ damage: Less than 130/80
Proteinuria of greater than 1g/day: Less than 125/75
What are first line drug treatments fro HTN?
1) ACE or ARB
2) Dihydropirdine calcium channel blocker
3) Low dose thiazide diuretic (aged 65 or older) - increased risk of new onset T2DM (use with caution in ppl with poor glucose tolerance).
Start at low dose. If target BP is not reached - add another first line agent before increasing dose. If target still not achieved and both drugs well tolerated - then increase dosage.
Use up to 4 types of Anti HTN Drugs to achieve target.
Best pairing is ACE or ARB plus dihydropiridine calcium channel blocker (eg Amlodipine)
Pairings to avoid: ACE/ARB plus NON dihidropyridine calcium channel blocker (eg verapamil/diltiazem)
ACE plus ARB
ACE/ARB plus potassium sparing diuretic ( amiloride or spironlactone) - can cause hyperkalaemia
Which HTN class pairings should be avoided?
Pairings to avoid: ACE/ARB plus NON dihidropyridine calcium channel blocker (eg verapamil/diltiazem)
ACE plus ARB
ACE/ARB plus potassium sparing diuretic ( amiloride or spironlactone) - can cause hyperkalaemia
Do Beta blockers have a role in HTN?
In uncomplicated HTN DONT give because increased risk of diabetes.
Stable patients who are already on a beta blocker dont need to have their meds changed.
What do you do if first line HTN therapy fails?
Consider lifestyle issues:
Treatment resistance due to ETOH or recreational drugs?/Other meds like NSAIDS?/
High salt intake?
Volume overload?(too much fluid intake)
Undiagnosed secondary HTN: Chronic kidney disease Hyperaldosteronism Renal artery stenosis Phaeochromocytoma Coarcatation of the aorta
Treatment resistance due to sleep apnoea? White coat hypertension.
What are the presenting symptoms in pericarditis?
Chest pain - three types
Pleuritic (most common) worse with lying flat
Pain mimicking heart attack (central left sided crushing)
Pain synchronous with heart beat and radiating to left shoulder
Examination findings in pericarditis?
Possibly signs of tamonade
Fever
What is your probability diagnosis in chest pain? (According to probability only)
Psychogenic
Muscular
Angina
What is your protocol for AF rate control?
Beta-blockers: Eg metoprolol 50 -200mg/day
OR
Non-dihydropyridine calcium channel blocker: Diltiazem or Verapamil
Digoxin is indicated for rate control IF patient has CCF, LV dysfunction or sedentary.
Oral amiodarone - where other medical therapies fail
Ablation of AV node or other pathways - where other medical therapies have failed.
Whats your protocol for rhythm control in AF?
Rate control is preferred.
Only if rate control has failed.
DC cardioversion - Rapid ventricular rate thats unresponsive to medications AND/OR myocardial ischaemia, HTN or CCF.
If its less than 48 hours that the patient has been in AF - you can perform DC cardioversion without anticoagulation
If its greater than 48 hours or unknown duration: 3 weeks of anticoagulation and get INR to 2-3 OR Initial anticoagulation - then TOE to confirm there’s no atrial thrombus and then cardiovert within 24 hours.
Pharmacological cardioversion is another option: Amiodarone or Fleicanide
Acute managment of AF?
In patients without CCF and without pre-excitation:
IV Metoprolol or Verapamil
Metoprolol: 2.5-5mg IV over 2 minutes (up to 3 doses)
Verapamil: 0.075mg/kg - 0.15mg/kg IV over 2 minutes
In patients with CCF and WITHOUT pre-excitation:
IV Digoxin or IV amiodarone
In patients WITH pre-excitation:
Can only give IV amiodarone
When do you anti-coagulate in AF?
CHA2DS2VA score: CCF - 1 point HTN - 1 point AGE: 2 points Diabetes: 1 point Previous stroke or TIA: 2 points Vascular disease - 1 point
If your score is ZERO: Low Risk - no need for therapy or low dose aspirin
ONE: moderate risk - benefit from warfarin or anticoagulation
Greater than or equal to 2 points: High risk - Long term anti coagulation therapy is recommended
Stroke rate increases with more points
Other relevant factors: ECHO findings: systolic dysfunction and left atrial enlargement
Vascular factors: previous AMI, peripheral vascular disease and complex aortic plaques
How can you mitigate risk of bleeding on Anticoagulation therapy for AF?
Risk of major bleeding whilst on oral anticoagulation: 1-1.5 % annually
HASBLED: Risk mitigation framework (help identify correctable risk factors for bleeding and high risk patients) (NOT to exclude patients from therapy but indicate patients who need more monitoring - manage correctable risk factors)
Hypertension (Systolic BP greater than 160)
Abnormal Renal or Liver function
Stroke (history)
Bleeding (history or a bleeding diathesis)
Labile INRs (less than 6/10 in therapeutic range)
Elderly (Greater than 65)
Drugs (antiplatelet agents/NSAIDS/ETOH greater than or equal to 8 SD a week)
Warfarin reduces risk of AF related stroke by 2/3
whilst novel anticoagulants target thrombin directly.
What does the framingham risk equation a marker of?
Absolute CVD event risk over next 5 years.
Less than 10% low risk (review every 2 years)
10 - 15% moderate (review every 6 to 12 months)
Greater than 15% high (Review according to clinical context)
What is Framingham risk equation useful for? Any populations that need special consideration?
PRIMARY cardiac prevention. Not secondary (as these patients are already at high risk).
Population requiring special considerations:
These populations are Underestimated by FRE): ATSI Pacific islanders Socioeconomic deprivation Obesity/Overweight Individuals over 70 years AF Chronic kidney disease
These populations dont need risk calculation (Already high risk)
History of CVD, Diabetes with age over 60 or Microalbuminuria, Moderate or severe chronic kidney disease, Familial hypercholesterolaemia, total chol > 7.5, BP > 180/110
When do we initiate lipid modifying therapy?
- CVD event - IHD/Previous Stroke/PVD/
- T2DM with LDL > 2.5 (after lifestyle - statin), Triglycerides > 2 (after lifestyle - fibrate)
- Familial HC - statin therapy
- ATSI - screen from 18 (consider if LDL is greater than 2.5 after lifestyle)
- CKD - Strong RF for cardiac event- risk of myopathy from statin is greater - higher doses should not be used.
- Those with a calculated absolute risk of greater than or equal to 15%
- Those with absolute risk of 10-15% where other risk factors are present:
a) FHX of premature CHD (First degree developed CHD<60)
b) Chronic kidney disease
c) Metabolic syndrome
What is metabolic syndrome?
Central obesity, increased waist circumference (>/94 cm in caucasian men, >/80cm Caucasian women) PLUS any TWO of:
Reduced HDL: or on treatment for this < 1 in men, < 1.3 in women.
Raised TG (or on treatment for this) >/ 1.7
Raised BP > 130/85
Raised FG > 5.5 or T2DM
What advice around smoking should be given to people about CVD?
- Smoking- dose dependent relationship.
Current Smokers have 70% increased risk of death due to CVD.
On cessation - risk reduces rapidly
50% risk reduction 1year after cessation
After 15 years of abstinence - risk of coronary artery disease related death is approx same as those that have never smoked.
There are pharmacological choices available to help cease smoking.
What are first line pharmacological choices for smoking cessation?
- Nicotine replacement
- Varenicline/Champix - shown to be most effective
- Buproprion
Use of the above has been shown to double the rate of long term smoking abstinence.
What is the relationship between blood pressure and CVD?
Systolic BP is a stronger/more consistent predictor of CV events than diastolic BP,
What is relationship between obesity and CVD?
LDL decreases and HDL increases with weight loss.
Even more accurate than BMI is waist circumference
In Caucasians should be < 94cm in men
< 80cm in women
Studies have shown that approx 10% reduction in weight yields significant improvements in BP/Lipids/HBA1c
Margaret Banks is a 49-year-old woman well known to your practice. She presents for her regular prescriptions. She is currently on telmisartan, hydrochlorothiazide and amlodipine. Her blood pressure today is 150/100mmHg. You note that she has had similar blood pressure readings on three recent separate occasions.
Which of the following criteria is consistent with the current screening recommendations for primary aldosteronism as a cause for Margaret’s hypertension? Choose one (1) option.
Hypertension with spontaneous or diuretic-induced hyperkalaemia
Hypertension (BP >140/90mmHg) resistant to three conventional anti-hypertensive drugs (including a diuretic)
Hypertension and a family history of hypertension or cerebrovascular accident at less than 60 years of age
Hypertension presenting with a single systolic blood pressure reading above 180mmHg
Hypertension (BP >170/100mmHg) with proteinuria
The correct answer is: “Hypertension (BP >140/90mmHg) resistant to three conventional anti-hypertensive drugs (including a diuretic).”
While primary aldosteronism accounts for 5% - 10% of hypertension in general practice and up to 30% of those with refractory hypertension, the Bettering the Evaluation and Care of Health (BEACH) program revealed that aldosterone measurement was only ordered on 66 occasions in over 1,500,000 GP-patient encounters. Screening for cases of secondary hypertension is low relative to the number of patients with hypertension who fulfil current screening recommendations.
The Endocrine Society’s current screening recommendations for primary aldosteronism include:
Sustained blood pressure (BP) above 150/100 mmHg on each of three measurements obtained on different days, or
Hypertension (BP >140/90 mmHg) resistant to three conventional antihypertensive drugs (including a diuretic), or
Controlled BP (<140/90 mmHg) on four or more antihypertensive medications
Hypertension and spontaneous or diuretic-induced hypokalaemia
Hypertension and adrenal incidentaloma
Hypertension and sleep apnoea
Hypertension and a family history of early-onset hypertension or cerebrovascular accident at a young age (<40 years)
All hypertensive first-degree relatives of a patient with primary aldosteronism
Frank Buongiorno is a 72 year old man admitted to your rural hospital with an infective exacerbation of chronic obstructive pulmonary disease. He deteriorates quickly following admission. Initially he required oxygen via nasal prongs and then 6 litres of oxygen via Hudson mask. Frank is starting to appear very fatigued. He has an advanced care plan that states “not for cardiopulmonary resuscitation, intubation or ventilation”, but he does wish to have non-invasive ventilation if required. His advanced care plan also indicates that he does not want to be retrieved for intensive care.
His initial venous blood gas (VBG) shows a pH of 7.29 and pCO2 of 55. You prepare for non-invasive ventilation. However, you are aware that due to staffing issues, you will not be able to keep Frank on non-invasive ventilation overnight. Despite ongoing input from the intensive care consultant over the phone to optimise the settings, Frank appears to be getting drowsier over the next few hours. You check his arterial blood gas (ABG) four hours after starting non-invasive ventilation:
pH
7.21 (7.35 – 7.45)
paCO2
88 (35 - 45)
pO2
60 (80 - 100)
HCO3
36 (22 – 26)
BE
+4 (-2 to +2)
Other values are within normal range.
What is your interpretation of Frank’s arterial blood gas (ABG)? Choose one (1) option.
Type II respiratory failure with respiratory acidosis and acute metabolic compensation
Type I respiratory failure with respiratory acidosis with acute metabolic compensation
Type II respiratory failure with mixed acidosis
Type II respiratory failure with respiratory acidosis and acute-on-chronic metabolic compensation
Type I respiratory failure with respiratory acidosis and chronic metabolic compensation
The correct response is: Type II respiratory failure with respiratory acidosis and acute-on-chronic metabolic compensation
You interpret the ABG as showing Type II respiratory failure with respiratory acidosis and acute-on-chronic metabolic compensation, and with this result go back to Frank and explain that unfortunately the treatment does not appear working and he is likely to die over the next few hours or days without invasive ventilation or intensive care support which he has previously indicated that he did not want. He requests that his family be notified and that he be kept comfortable.
Type I respiratory failure results in hypoxia with normal carbon dioxide, indicating failure of oxygenation.
Type II respiratory failure leads to hypoxia and hypercapnia, indicating failure of oxygenation and ventilation.
It is possible to calculate whether metabolic compensation for hypercapnia is acute or chronic using the simple formula:
HCO3
(Baseline 24 mmol/L)
Every 10 mmHg change in PaCO2 from baseline 40 mmHg
ACUTE
CHRONIC
↑ PaCO2
1
4
↓ PaCO2
2
5
Using this formula, his PaCO2 has gone up by 50mmHg (i.e. 5 points) from baseline 40mmHg, so if his metabolic compensation was acute, you would expect his HCO3 to be 29 (baseline 24mmol/L + 5 x 1). If his metabolic compensation was chronic, you would expect his HCO3 to be 44 (baseline 24mmol/L + 5 x 4) and his pH to be closer to normal if the chronic compensation was effective. His bicarbonate was 36 and he was inadequately compensated for his hypercapnia, suggesting acute-on-chronic compensation.
A VBG is a good substitute for an ABG in many circumstances, and it is much easier and less invasive to obtain, however the normal reference ranges are slightly different. Correlation between VBGs and ABGs is poor in some clinical situations, including marked hypercapnia.
References:
Cadogan M. Acid Base Disorders. Life in the Fast Lane blog 2019.
Nickson C. VBG versus ABG. Life in the Fast Lane blog 2019.
What specific advice do you give to patients about how to take home blood pressure readings?
Two measurements of home blood pressure should be taken, one minute apart, after 5 minutes of sitting quietly, morning and evening, for 7 consecutive days.
