Cardiovascular Examination

Question 1

Aetiology of Cardiovascular Disease?

Answer 1

Cardiovascular disease is the leading cause of death world wide (15.2 million deaths in 2016) – (WHO 2018)

Question 2

Steps to Cardiovascular?

Answer 2

1.History taking 2.General Assessment (Sam’s presentation) 3.Work up of patient 4.Differential Diagnosis/Verification of patient history/ Referral for further investigation TREATMENT FOR DENTAL ISSUE

Question 3

Cardiovascular history taking?

Answer 3

History of Chest pain 4 cardinal signs of pain: 1 – Duration (0nset, frequency, time) 2 - Location (localized/generalized/radiating) 3 - Quality (Sharp, Dull, crushing) 4 - Precipitating and aggravating factors (exercise, patient position Dizziness? Sweating? Nausea/vomiting? Dyspnea? If experiencing chest pain at presentation treat as medical emergency

Question 4

Cardiovascular Examination process?

Answer 4

1. Over view of patient 2. is the patient comfortable at rest 3. Malar rash (mitral stenosis) 4. INspect chest for scars or abnormalities 5. Insect legs (harvest, odema) 6. Hands 7. pulses 8. JVP 9. Face 10. Auscultate

Question 5

Pain in the cardiovascular examination?

Answer 5

SOCRATES European Society of Cardiology: Typical angina Meets all three of the following characteristics: 1. Characteristic retrosternal chest discomfort—typical quality and duration 2. Provoked by exertion or emotion 3. Relieved by rest or GTN (glyceryl trinitrate) or both Atypical angina Meets two of the above characteristics Non-cardiac chest pain Meets one or none of the above characteristics

Question 6

Assessing Dysponea?

Answer 6

Visually assess and ask about breathing Change in the compliance of the lungs or increased resistance to lung movement causes conscious awareness of forcibly breathing (usually passive). Types: -Cardiac dyspnoea (Chronic and occurs with exertion) -Orthopnoea (Supine) -Nocturnal dyspnoea (Sudden) Cardiac Dyspnea: Compliance of lungs reduced due to leaking interstitial fluid due to poor left ventricular out put raising end ventricular diastolic pressure and pulmonary artery pressure. Orthopnoea: when supine breathing is difficult, when standing breathing improves due to movement of fluid to bottom of lungs increasing oxygen possibility. Nocturnal dysponea: acute pulmonary oedema or a pulmonary embolus, left ventricle failure causing increase in interstitial fluid. Patient wakes up gasping for breath

Question 7

6 Ps of Dysponea?

Answer 7

1. Pump Failure 2. Pneumonia 3. Pulmonary Embolis 4. Possible Foreign body 5. Pulmonary Bronchial Constriction 6. Pneumo-Thorax

Question 8

What sort of Odema is mostly seen in cardiac issues? What to check?

Answer 8

Ankle odema. Colour and temperature WNL Worst in evening Cause usually biventricular failure or RHS ventricular failure Can be caused by vasodilating drugs

Question 9

What are palpitation?

Answer 9

‘An awareness of the heart beating’

Question 10

What to clarify if patient has palpitations?

Answer 10

Clarify sensation? How often? Does the heart feel fast or slow? Are there other symptoms? Is it in the neck or chest? Have they had a ECG?

Question 11

Why do palpitations occur?

Answer 11

Incorrect stimulation of the sympathetic and parasympathetic, particularly the vagus nerve, (anxiety and stress) Gastrointestinal distress. Sympathetic overdrive (panic disorder, low blood sugar, hypoxia, antihistamines (levocetirizine), low red blood cell count, heart failure, mitral valve prolapse) Hyperdynamic circulation (valvular incompetence, thyrotoxicosis, hypercapnia, high body temperature, low red blood cell count, pregnancy). Abnormal heart rhythms (ectopic beat, premature atrial contraction, junctional escape beat, premature ventricular contraction, atrial fibrillation, supraventricular tachycardia, ventricular tachycardia, ventricular fibrillation, heart block).

Question 12

Syncope verse Presyncope

Answer 12

Syncope: transient loss of consciousness due to acute hypotensive episode Presyncope: transient sensation of weakness without loss of consciousness

Question 13

Types of Syncope?

Answer 13

• Vasovagal syncope (stress) - Postural Syncope - Micturition Syncope - Tussive Syncope (sneezing) - Arrythmia Syncope (ischaemic heart disease or aortic stenosis) – carotid sinus simultaneous enhancement of parasympathetic nervous system (vagal) tone and withdrawal of sympathetic nervous system tone due to stimulus -cardioinhibitory response (decrease BP, decreased contraction, decreased cardiac output -Vasodepressor response (dilation of blood vessel causing decrease in BP but not HR)

Question 14

Why do cardiovascular patients experience fatigue?

Answer 14

Subjective feeling of tiredness Can be due to: reduced cardiac output Poor blood flow peripherally Poor sleep Anaemia

Question 15

Peripheral vascular disease work up?

Answer 15

Work up : Palpation of the arteries (MGP) Exertional calf pain atrophic skin and loss of hair colour changes of the feet (blue or red) ulcers at the lower end of the tibia Capillary refill

Question 16

What is peripheral vascular disease? what are the 6 Ps of peripheral vascular disease?

Answer 16

Poor blood supply to affected muscles, assessed through distance walked. 6 P’s of peripheral disease P ain - calf P allor – red or blue P ulselessness – Femoral and ankle P araesthesias P erishingly cold - Acute arterial occlusion P aralysed. – indicates Acute arterial occlusion

Question 17

What are the risk factors for Cardiovascular disease?

Answer 17

Previous ischaemic heart disease Hypercholesterolaemia (primary prevention if no coronary heart disease exists, secondary if already does) Smoking (Pack years best predicter of risk. Lubin, J et al. 2016) Hypertension A family history of coronary artery disease Diabetes mellitus (Klamann, A et al. 2000) Chronic kidney disease Chronic inflammatory diseases Erectile dysfunction Dental Caries/Periodontal inflammation Street drug use is relevant. The use of cocaine or amphetamines is an important cause of myocardial infarction in young people.

Question 18

How do you calculate pack years?

Answer 18

Number of cigs a day divided by 20 multiplied by how many years smoking

Question 19

When is family history of cardiovascular disease most significant

Answer 19

IN under 65s. coronary heart disease in first-degree relatives is a risk factor for the disease, the risk is greater in women than in men. (when looking at siblings sister of sister 76% with heart disease vs. brother to sister risk 65. Brother to brother was lower but still 3.5x the risk of the control (S. Pohjola-Sintonen, A. Rissanen, P. Liskola, K. Luomanmäki, Family history as a risk factor of coronary heart disease in patients under 60 years of age, European Heart Journal, Volume 19, Issue 2, 1 February 1998, Pages 235–239, https://doi.org/10.1053/euhj.1997.0543)

Question 20

What is an ectopic beat?

Answer 20

bigeminal rhythm caused by ectopic beats has a characteristic pattern: normal pulse, weak (or absent) pulse, delay, normal pulse and so on. Similarly, every third beat may be ectopic— trigeminy . A pattern of irregularity is also detectable in the Wenckebach phenomenon. Here the AV nodal conduction time increases progressively until a non-conducted atrial systole occurs. Following this, the AV conduction time shortens and the cycle begins again.

Question 21

What causes postural hypotension?

Answer 21

H hypovolaemia (e.g. dehydration, bleeding); hypopituitarism A Addison’s * * Thomas Addison (1793–1860), a London physician. disease (adrenal gland failure) N neuropathy—autonomic (e.g. diabetes mellitus, amyloidosis, Shy–Drager syndrome) D rugs (e.g. vasodilators and other antihypertensives, tricyclic antidepressants, diuretics, antipsychotics) I idiopathic orthostatic hypotension (rare progressive degeneration of the autonomic nervous system, usually in elderly men)

Question 22

Signs of Cardiovascular disease on face - eyes?

Answer 22

Conjunctival pallor – anaemia – ask the patient to gently pull down their lower eyelid Corneal arcus – yellowish/grey ring surrounding the iris – hypercholesterolaemia Xanthelasma – yellow raised lesions around the eyes – hypercholesterolaemia

Question 23

Signs of Cardiovascular disease on face - mouth?

Answer 23

Check for High arched palate – syndromes Notice whether the teeth look diseased, as they can be a source of organisms responsible for infective endocarditis. Look at the tongue and lips for central cyanosis. Inspect the mucosa for petechiae that may indicate infective endocarditis.

Question 24

What is Arterial pulse character?

Answer 24

Evaluation of the pulse wave form (the amplitude, shape and volume) is important in the diagnosis of various underlying cardiac diseases and in assessing their severity.

Question 25

What is Jugular venous Pressure?

Answer 25

1. Ensure the patient is positioned at 45° 2. Ask patient to turn their head away from you 3. Observe the neck for the JVP – located inline with the sternocleidomastoid 4. Measure the JVP – number of centimetres from the sternal angle to the upper border of pulsation Raised JVP may indicate – fluid overload / right ventricular failure / tricuspid regurgitation Hepatojugular reflux: Apply pressure to the liver Observe the JVP for a rise In healthy individuals, this should last no longer than 1-2 cardiac cycles (it should then fall) If the rise in JVP is sustained and equal to or greater than 4cm this is a positive result A positive hepatojugular reflux sign is suggestive of right-sided heart failure and/or tricuspid regurgitation This is very uncomfortable to perform correctly – an examiner will often prevent you performing it but remember to mention it!

Question 26

What is a carotid bruit?

Answer 26

A carotid bruit is a vascular sound usually heard with a stethoscope over the carotid artery because of turbulent, non-laminar blood flow through a stenotic area

Question 27

What do we inspect with palms up?

Answer 27

Colour – dusky bluish discolouration (cyanosis) suggests hypoxia Temperature – cool peripheries may suggest poor cardiac output/hypovolaemia Sweaty/Clammy– can be associated with acute coronary syndrome Janeway lesions – non-tender maculopapular erythematous palm pulp lesions – bacterial endocarditis Osler’s nodes – tender red nodules on finger pulps/thenar eminence – infective endocarditis Tar staining – smoker – risk factor for cardiovascular disease Xanthomata – raised yellow lesions – often noted on tendons of the wrist – caused by hyperlipidaemia Capillary refill time – normal is <2 seconds – if prolonged may suggest hypovolaemia

Question 28

What do we inspect with palms facing down?

Answer 28

Splinter haemorrhages – reddish/brown streaks on the nail bed – bacterial endocarditis Finger clubbing: Ask the patient to place the nails of their index fingers back to back In a healthy individual, you should be able to observe a small diamond shaped window (Schamroth’s window) When finger clubbing is present this window is lost Finger clubbing has a number of causes including infective endocarditis and cyanotic congenital heart disease

Question 29

What do we look at for radial pulse?

Answer 29

Radial pulse – assess rate and rhythm Radio-radial delay:,Palpate both radial pulses simultaneously. They should occur at the same time in a healthy adult. Radio-radial delay can be associated with subclavian artery stenosis (e.g. compression by a cervical rib) or aortic dissection

Question 30

What is a collapsing pulse?

Answer 30

Collapsing pulse – associated with aortic regurgitation First, ensure the patient has no shoulder pain. palpate the radial pulse with your hand wrapped around the wrist. Raise the arm above the head briskly. Feel for a tapping impulse through the muscle bulk of the arm as blood empties from the arm very quickly in diastole, resulting in the palpable sensation. This is a water hammer pulse and can occur in normal physiological states (fever/pregnancy), or in cardiac lesions (e.g. AR/PDA) or high output states (e.g. anaemia/AV fistula/thyrotoxicosis)

Question 31

What do we look at for brachial pulse?

Answer 31

assess volume and character

Question 32

What do we assess at the carotid pulse?

Answer 32

Assess character and volume – e.g. slow rising character in aortic stenosis It’s often advised to auscultate the carotid artery for a bruit before palpating, as theoretically palpation may dislodge a plaque which could lead to a stroke However, if you perform carotid auscultation at this point, remember that the ‘bruit’ may actually be a radiating murmur.

Question 33

What is an apex beat?

Answer 33

Located at the 5th intercostal space / midclavicular line Palpate the apex beat with your fingers (placed horizontally across the chest) Lateral displacement suggests cardiomegaly

Question 34

What are heaves?

Answer 34

A parasternal heave is a precordial impulse that can be palpated Parasternal heaves are present in patients with right ventricular hypertrophy Place the heel of your hand parallel to the left sternal edge (fingers vertical) to palpate for heaves If heaves are present you should feel the heel of your hand being lifted with each systole

Question 35

What are thrills?

Answer 35

A thrill is a palpable vibration caused by turbulent blood flow through a heart valve (the thrill is a palpable murmur) You should assess for a thrill across each of the heart valves in turn To do this place your hand horizontally across the chest wall, with the flats of your fingers and palm over the valve to be assessed

Question 36

What do we listen to when we auscultate the lungs?

Answer 36

Crackles may suggest pulmonary oedema (e.g. secondary to left ventricular failure) Consider chronic lung diseases if the patient has no other signs of fluid overload (e.g. pulmonary fibrosis) Sacral oedema/pedal oedema – may indicate right ventricular failure

Question 37

How do we auscultate?

Answer 37

1. Palpate the carotid pulse to determine the first heart sound. 2. Auscultate ‘upwards’ through the valve areas using the diaphragm of the stethoscope: Mitral valve – 5th intercostal space – midclavicular line (apex beat) Tricuspid valve – 4th or 5th intercostal space – lower left sternal edge Pulmonary valve – 2nd intercostal space – left sternal edge Aortic valve – 2nd intercostal space – right sternal edge 3. Repeat auscultation across the four valves with the bell of the stethoscope. 4. Auscultate the carotid arteries with the patient holding their breath to check for radiation of an aortic stenosis murmur (this is known as an accentuation manoeuvre). 5. Sit the patient forwards and auscultate over the aortic area during expiration to listen for the murmur of aortic regurgitation (this is known as an accentuation manoeuvre). 6. Roll the patient onto their left side and listen over the mitral area with the bell during expiration for mitral murmurs (regurgitation/stenosis)

Question 38

What extra tests can we order to check heart function?

Answer 38

Urine analysis (infective endocarditis)

Fundi – retinal changes

Temperature

Chest X-ray (exposes patient to radiation)

ECG Echocardiography – M wave, 2D, Doppler, colour flow mapping

Exercise stress testing FBC (with lipid testing/chair side lipid testing)

Thyroid function tests

Glucose screening for DM Homocysteine level determination

CRP assay (ELISA), - troponin if pain

Question 39

What is a murmur?

Answer 39

Murmurs - flow velocities of 4 metres per second or more across narrowed aortic valves and even higher velocities when the mitral valve leaks—lead to more prominent murmurs. Innocent murmur below this. Murmurs diagnosed from where sound can be heard, loudness and pitch. Murmur heard should be referred as needs dynamic testing for diagnosis.

Question 40

What are the main drugs’ associated with cardiac disease?

Answer 40

Cholesterol-lowering drugs Potassium or magnesium Proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitors Vasodilators Warfarin NOACs

Question 41

How do Diuretics work?

• side effects?
• interactions?

Answer 41

Work at distal conveluted tubule to increase urine output by increasing the amount of Na+ excreted by blocking the reabsorption. Works to decrease odema in CVS, decreases blood volume decreasing preload (and output) = decrease in venous pressure. also possible vasodilation.

Used in: HF, HT

1-Thiazine based inibit NA+ trasporter

2-Loop diretics inibit trapsorter in ascending limb

• Prolonged use of NSAIDS (+10 days) can decrease efficiency
• Use with corticosteroids increased risk of hypokalemia
• Postural Hypotension risk
• lichenoid reactions reported
• xerostomia

eg Lasix 80mg daily (2x 40mg) 60 min onset, 8 hour duration

Question 42

What is an ACE-I?

• who takes them?
• Side effects?
• interactions?

Answer 42

Angiotensin Converting Enzyme Inhibitor (HF and HT)

• Works at site of ACE production in lung to stop convertion of angiotension 1 to 2 to increase vasodilation. Blocking the breakdown of bradykinin, increase bradykinin levels, which can contribute to the vasodilator action of ACE inhibitors ‘prils’
• peroral burning, postural hypotension,
• possible contribution to neutropenia (delayed wound healing, increase in bleeding times)

NSAID interaction decreases ACEI mechanism

• can produce cough
  e. g. ramipril 2.5mg per day (depends on what for)

Question 43

What are ARBS?

• side effects
• Interactions

Answer 43

Angiotenson recepter blockers

Decreases blood pressure by acting on receptor antagonists that block type 1 angiotensin II (AT1) receptors on bloods vessels (smooth muscle contraction) and other tissues such as the heart. “Startins”

-as with ACEI

Question 44

What are Nitrates used for?

Answer 44

Nitric Oxide are vasodilators. naturally produced by vascular endothelial cells. When used synthetically for angina mimics action. elaxing vascular smooth muscle (vasodilation), inhibiting platelet aggregation (anti-thrombotic), and inhibiting leukocyte-endothelial interactions (anti-inflammatory). HF, HT, Angina and MI.

commonly: nitroglycerin
- headache (caused by cerebral vasodilation) and cutaneous flushing. Other side effects include postural hypotension and reflex tachycardia
- Viagra profound vasodilation

Dose: nystat 0.3-0.6mg up to 3 times 5mins apart

Question 45

What are Aldosterone Antagonists?

Answer 45

K-sparring Diuretic. Used for severe HF (spironolactone)

Antagonize the actions of aldosterone (aldosterone receptor antagonists) at the distal segment of the distal tubule. This causes more sodium (and water) to pass into the collecting duct and be excreted in the urine. They are called K+-sparing diuretics because they do not produce hypokalemia like the loop and thiazide diuretics.

Often used with loop diretics.

• ACE inhibitors: potentiate hyperkalemia
• non-steroidal anti-inflammatory drugs: reduced diuretic efficacy

Dosage aldactone, spironolactone, 2 days duration, 2 hr onset, range: 25-200 mg PO qDay

Question 46

What are Beta Blockers?

Answer 46

Cardioinhibitory drug class. block the binding of norepinephrine and epinephrine to receptors inhibiting the sympathetic pathway(partial agonists). If non selective also leads to vasorelaxtion due to cAMP release. ‘olols’

hypertension, angina, myocardial infarction, arrhythmias and heart failure.

-Bronchoconstriction in non selective,bradycardia, reduced exercise capacity, heart failure, hypotension, and atrioventicular (AV) nodal conduction block

Dosage: 50-100mg daily

Question 47

What are CCBs?

Answer 47

Calcium Channel Blockers.

bind to L-type calcium channels located on the vascular smooth muscle, cardiac myocytes, and cardiac nodal tissue (sinoatrial and atrioventricular nodes). Decreasing influx of Ca into muscle.

HT, Angina, Arrythmias

‘Pines’

Side effects: flushing, headache, excessive hypotension, edema and reflex tachycardia. Baroreceptor reflex activation of sympathetic nerves and lack of direct negative cardiac effects can make dihydropyridines a less desirable choice for stable angina than diltiazem, verapamil or beta-blockers.

Dosages: 60mg 20min onset, 8hrs

interacts with microlides, hypotension

Question 48

Adrenergic Agonists? a1 and a2

Answer 48

binding to alpha-adrenoceptors located on the vascular smooth muscle. Most of these drugs act as competitive antagonists to the binding of norepinephrine that is released by sympathetic nerves synapsing on smooth muscle.

HT

Side effect: Dry Mouth, taste change

dizziness, orthostatic hypotension (due to loss of reflex vasoconstriction upon standing), nasal congestion (due to dilation of nasal mucosal arterioles), headache, and reflex tachycardia (especially with non-selective alpha-blockers). Fluid retention

Dosage:

Question 49

Digoxin?

Answer 49

Used for AF, Aflutter, HF

de effects may include loss of appetite, nausea, trouble seeing, confusion, and an irregular heartbeat. kidney function sesensitive.

used in triple therapy for HF.

mechanism of action involves inhibition of the sodium potassium adenosine triphosphatase (Na+/K+ ATPase), mainly in the myocardium.

125-250mg daily, 2 day half life

Question 50

What risks are associated with HF patients?

Answer 50

▪Sudden elevation of BP

▪Adverse outcome ACS, MI or stroke

▪Release of endogenous catecholamines as response to stress/anxiety

▪From exogenous catecholamines in form of vasoconstrictors in LA

▪Potential drug reactions

▪Oral adverse effects of medication

Question 51

Surgical Risk Calculator?

Answer 51

Question 52

When do we delay treatment for HF patients?

Answer 52

▪BP – 180 systolic 120 diastolic is hypertensive crisis – consider anxiety and LA use will cause increase in most patients

▪Elective non-cardiac surgery should be deferred for at least 6 weeks and ideally 3 months following Percutaneous coronary intervention with bare metal stenting

▪Elective non-cardiac surgery should be deferred for 12 months following drug eluting stent placement

▪5% mortality rate if interrupted

▪Warfarinsed patient INR over 4, correspond with treating physician

▪Delay non elective dental procedures for 6 months post MI

▪Higher frequency of reoccurrence in diabetics, women within 18 months

Question 53

Do we modify medications?

Answer 53

Recent Literature:

DAPT does have increased post-opertative bleeding risk and incident of post operative cardiac complications still showed an incidence of 20% (Syed S 2019, BJA

Systematic review: Continuing anticoagulation during dental procedures did not increase the risk of bleeding in most trials, questioned follow up periods. Heparin bridging was associated with an increased bleeding incidence (Chahine J et al 2019)

Meta analysis: postoperative haemorrhage is exacerbated with DAPT, but it could be controlled by enhancing haemostasis methods. Recommend continuing long-term DAPT before tooth extraction (no statically significance between surgery types found) (Li L et al. 2019).

Patients can and should be maintained on their antiplatelet/anticoagulant regimen when undergoing dental procedures, including dental extractions. Prolonged or increased bleeding in these patients, especially those on single or dual antiplatelet therapy, is generally a manageable challenge or inconvenience but rarely life-threatening. (Hanna I 2019)

CANZ guidelines 2009

If possible, continuation of antiplatelet therapy is recommended in patients with prior coronary artery stenting undergoing non-cardiac surgery

In selected cases, in patients receiving DAP prior to surgery, consider bridging therapy with heparin/tirofiban or heparin/eptifibitide (limited data in support of such treatments

Question 54

What are local hemostatic measures?

Answer 54

Local Haemostatic Measures:

• Sit up right, place gauze, apply pressure (10-15 mins) (usually sufficient to stop bleed even in AntiCOAG patients.
• If not resolved; use suction and light to identify site of bleed (mucosa near FOM, subgingival region, socket wall, apical region).
• Infiltrate site with LA with adrenaline
• Absorbable hemostatic agent – Gelatamp (colloidal silver gelatin sponge – decreased post op complication rates Cai YH 2009), Surgicel (Absorbable Hemostat (oxidized regenerated cellulose), gelfoam (cellulose sponge, mechanical not chemical help).
• Transexamic acid – as topical solution with additional pressure (stabilises existing clot).
• Suture if required, ligate if vessel, diathermy, if hasn’t resolved transport to ED.

Warfarin: 9a, 7a, 10a, 2

NOACs: 10a

Question 55

Medical Emergency

General Heart issues (mostly alive - Mostly dead)

Answer 55

▪Cease treatment

▪remove stressors to reduce anxiety

▪Call for assistance

▪(ambulance services, advance life support team), monitor vital stats BP, HR, BR, oxygen saturation

▪Assess level of consciousness

▪Position for comfort, or supine if poor perfusion

▪Administer nitroglycerine (GTN) sublingual tablet (0.3-0.6mg) or spray (0.4-0.8mmg) every 5min if pain persists, max three doses

▪Monitor vitals, beware of hypotension

▪contraindications (hypotension, sildenafil, hypersensitivity)

▪If new or severe pain persists past 10min, suspected ACS

▪Administer aspirin 300mg orally if no contraindications (hypersensitivity)

▪Monitor vital signs till help arrives

▪If oxygen saturation levels <93%, administer supplemental O2 via Hudson mask

▪O2 admin in non hypoxic patients may increase size of infarct1

▪If patient loses consciousness à Basic Life Support till help arrives

▪Start CPR, use automated external defibrillator if shockable rhythm

Question 56

Cardiac Arrest Medical Emergency?

Answer 56

DRSABCD - mostly dead

▪Not conscious, no pulse, not breathing

▪Stop treatment

▪Call 000

▪CPR with Defib (only give O2 if below SpO2 of 93%)

▪Bag valve mask (guedels or LMA)

▪30 comp 2 breaths

▪Continue until pulse returns or help arrives

▪If available: IV adrenaline 1ml after second shock or 88mg 2% lidocaine. Saline 30ml pushed.

Question 57

medical Emergency - Syncope

Answer 57

Mostly Alive ABCDE

▪Patient feels faint

▪Stop treatment

▪Tilt chair back/lay down

▪Raise legs

▪Give O2

▪Measure HR

▪Assess consciousness

▪Loss of consciousness

▪Stop treatment

▪Raise legs higher than head

▪Measure HR/BP

▪Atropine can be given (600mcg)

▪Should regain consciousness rapidly, monitor recovery, measure standing BP, refer for MGP assessment