lecture 1 Hx and Ex Flashcards
Hands – Inspection (Dorsum)
- Clubbing
- Splinter haemorrhages
- Quincke’s sign
- Koilonychia
- Tar staining of fingers
- Peripheral cyanosis
- Tendon xanthoma
Hands – Inspection (Palmar)
• Osler’s nodes • Janeway lesion • Palmar xanthoma • Palmar crease pallor (anaemia)
Hands – Palpation
- Temperature
- Sweatiness
- Capillary refill time – normal up to 2 seconds
Examination – Arms
• Radial pulse – rate – rhythm • Radio-radial delay • Collapsing pulse • Blood pressure • (Brachial pulse)
Examination – Face
- Facies (eg marfanoid)
- Conjunctival pallor (anaemia)
- Arcus senilis
- Xanthelasma
- Central cyanosis
- Dentition
Examination – Neck
- Jugular venous pulse (patient’s right only obvs)
* Carotid pulse (both sides)
Examination – JVP
• Internal jugular vein is collapsible, relatively inelastic and in direct continuity with the right atrium • JVP = visible pulsation at meniscus of column of blood in internal jugular vein (transition between collapsed and distended parts of internal jugular vein) • ⇒JVP is useful marker of right atrial pressure • Measured with patient at 45o, vertical height from sternal angle (normal £3 cm)
between the clavicaular and sternal head of the SCM and the mastoid process.
• Causes of raised JVP:
• Causes of raised JVP: – fluid overload – heart failure – valve disease – TR, TS, PR, PS – pericardial disease – tamponade, constriction – pulmonary hypertension – massive PE
Cannon wave JVP
Cannon wave = strikingly large ‘a’ wave (seen in AV
dissociation e.g. complete heart block)
(‘a’ wave coincides with atrial
systole/contraction)
Kussmaul’s sign JVP
Kussmaul’s sign = abnormal rise in JVP during inspiration
seen in cardiac tamponade
Examination – Carotid Pulse
• Assess volume and character
• Carotid pulse volume reflects left ventricular stroke volume:
– increased with exercise, fever and arteriovenous fistula
– decreased with poor cardiac output (heart failure) and during
tachycardia
– variable in AF
– pulsus alternans in heart failure
– pulsus paradoxus in cardiac tamponade
• Carotid pulse character can be: – normal – slow-rising in severe AS – collapsing in severe AR – bisferiens in HOCM
Examination – Precordium Inspection
Inspection • Scars • Pacemaker • Chest wall deformity • Visible apex beat • Other visible pulsations
Examination – Precordium Palpation
Palpation • Apex beat • Left parasternal heave (RVH) • Thrills (palpable murmurs) Examination
Examination – Precordium Apex Beat
Apex Beat
• Assess location and character
• Causes of displaced apex beat:
– cardiomegaly
– dextrocardia
– mediastinal shift
• Causes of absent apex beat: – obesity – emphysema – pleural effusion – pericardial effusion
• Characters of apex beat: – normal – tapping (severe MS) – heaving (LV pressure overload = LVH) – thrusting (LV volume overload, e.g. MR and AR) – diffuse/dyskinetic (endstage heart failure)
Examination – Precordium Auscultation
Auscultation
• Always palpate the carotid pulse at the same time (for timing) • Listen to all 4 areas + axilla + neck + manoeuvres for MS/AR • Identify S1 and S2 first • Assess murmurs: – location and radiation – timing: systolic, diastolic, etc – intensity: grade out of 6
Examination – Precordium Auscultation – A Suggested Sequence
- Mitral area (with diaphragm)
- Axilla (with diaphgram)
- MS manoeuvre (with bell, turned to left, in expiration)
- Tricuspid area (with diaphragm)
- Pulmonary area (with diaphragm)
- Aortic area (with diaphragm)
- Neck, both sides (with bell or diaphragm)
- AR manoeuvre (with diaphragm, sitting forward, in expiration)
Examination – Precordium Heart sounds
- First heart sound (S1) = coincides with carotid upstroke
- Second heart sound (S2) = occurs after carotid upstroke
• Physiological splitting of second heart sound
– = normal splitting of S2 into aortic and pulmonary components
(A2 before P2)
– more split in inspiration and less split in expiration
– more obvious in young people
• Third and fourth heart sounds = diastolic sounds, occur with
raised LV end-diastolic pressure
Examination – Precordium Murmurs
Causes of PSM:
Causes of PSM: MR, TR, VSD
Murmurs Causes of ESM
Causes of ESM: AS, HOCM, PS, ASD
Murmurs Causes of EDM:
Causes of EDM: AR, PR
Murmurs Causes of LDM:
Causes of LDM: MS, TS
Examination – Remainder
• Back of chest
– basal fine inspiratory crackles
– sacral pitting oedema
- Peripheral pitting oedema
- Vein harvest scar(s)
- ± pulsatile liver (if severe TR thought to be present)
• Offer to do – peripheral pulses – BP (if not done already) – fundoscopy – urinalysis
History – Chest Pain Differential diagnoses
• Cardiovascular – coronary artery disease (myocardial ischaemia) – pericarditis – myocarditis – aortic dissection
• Gastrointestinal – oesophageal spasm – gastro-oesophageal reflux – peptic ulcer disease – cholecystitis – pancreatitis
• Pulmonary – pneumothorax – pneumonia – pulmonary embolism – lung cancer
• Musculo-skeletal – myalgia – fibromyalgia – costochondritis (Tietze’s syndrome) – neuropathic pain – bone pain
• Psychiatric
History – Breathlessness Differential diagnoses
• Cardiovascular – heart failure – valve disease – pericardial disease – pulmonary hypertension – (coronary artery disease) – (arrhythmia)
• Miscellaneous – severe anaemia – obesity – poor cardiovascular fitness – psychiatric
• Pulmonary – obstructive airways disease – interstitial lung disease – pleural disease – pneumothorax – pneumonia / tuberculosis – pulmonary embolism – pulmonary hypertension
questions to ask about presentation of breathlessness
Taking the history
• Onset and duration
• Severity (exercise tolerance in distance or time) and change in
severity
• Relieving factors, e.g. inhalers or GTN spray
• Orthopnoea, PND and swelling
• Associated symptoms
• Previous investigations/diagnoses
• Risk factors (depending on likely diagnosis)
DD for palpitations
The differential diagnosis of palpitations is extensive, and the etiology varies depending upon the population studied. In a study of 190 patients presenting with a chief complaint of palpitations to a university medical center, an etiology was determined in 84 percent [3]. The cause was cardiac in 43 percent, psychiatric in 31 percent, and miscellaneous (eg, medication-induced, thyrotoxicosis, caffeine, cocaine, anemia, amphetamine, mastocytosis) in 10 percent.
Common causes:
Cardiac: Sinus tachycardia Atrial tachycardia Atrial flutter Atrial fibrillation Atrioventricular nodal re-entrant tachycardia Wolff-Parkinson-White syndrome (WPW) Ventricular premature beat Atrial premature beat
Psychiatric:
Anxiety and panic disorder
Infective:
Fever
Endocrine:
Hyperthyroidism
Phaeochromocytoma (probably rare)
Drugs and toxins: Excess alcohol use (binge drinking) Caffeine Medications recreational drugs
what are palpitations
Palpitations are a sensory symptom. They are defined as an unpleasant awareness of the forceful, rapid, or irregular beating of the heart. Patients may at times describe the sensation as a rapid fluttering in the chest, flip-flopping in the chest, or a pounding sensation in the chest or neck, and these descriptions may help elucidate the cause of the palpitations
common first investigations in PT with palpitations
Detailed Hx - many diagnoses are via this e.g. caffeine intake.
12 lead ECG
Ambulatory ECG
TFTs: elevated free T4 and T3, low TSH - hyperthyroidism
Echocardiogram - hypertrophy
what is syncope
Syncope is a transient loss of consciousness, associated with loss of postural tone, with spontaneous return to baseline neurologic function requiring no resuscitative efforts. The underlying mechanism is global hypoperfusion of both the cerebral cortices or focal hypoperfusion of the reticular activating system.
DD of syncope
Syncope is a common complaint in the emergency department (ED). Although most potential causes are benign and self-limited, others are associated with significant morbidity and mortality. the cause of syncope often remains unclear and management must focus on risk stratification to differentiate among patients safe for discharge and those who require emergent investigation and in-hospital management. Near syncope (ie, near loss of consciousness) and true syncope are considered a spectrum of the same symptom, and clinicians should approach them in similar fashion.
Life-threatening conditions — The primary responsibility of the emergency clinician is to assess whether a life-threatening cause of syncope is present, and to provide appropriate management and disposition. The most important causes to consider are: cardiac syncope, blood loss, pulmonary embolism, and subarachnoid hemorrhage. Other conditions, such as seizure, stroke, and head injury, do not meet the technical definition of syncope but should be considered during the initial assessment.
●Cardiac syncope – Cardiac causes are the most common life-threatening conditions associated with syncope. They include arrhythmia, ischemia, structural/valvular abnormalities (eg, aortic stenosis), cardiac tamponade, and pacemaker malfunction. Studies of short term and one year outcomes following syncope found patients with cardiac syncope to be at significant risk for sudden death [2,9]. Patients with syncope and a history of heart failure are at even greater risk .
●Hemorrhage – Large blood loss, particularly acute severe hemorrhage, can manifest as syncope. Important potential causes include: trauma, gastrointestinal bleeding, ruptured aortic aneurysm, ruptured ovarian cyst, ruptured ectopic pregnancy, and ruptured spleen.
●Pulmonary embolism – Hemodynamically significant pulmonary embolism is an uncommon but well documented cause of syncope [11].
●Subarachnoid hemorrhage – Patients presenting with syncope following a headache require evaluation for a possible subarachnoid hemorrhage.
Common conditions
●Neurocardiogenic syncope – Often referred to as vasovagal or vasodepressor syncope, neurocardiogenic syncope is the most common cause of syncope, accounting for 25 to 65 percent of cases [7]. Patients diagnosed with neurocardiogenic syncope have an excellent prognosis with no increase in mortality or morbidity [12].
Autonomic activation causes neurocardiogenic syncope. Three types of responses are seen: a cardioinhibitory response, a vasodepressor response, and a mixed response with features of both. Significant bradycardia and/or hypotension accompany the acute loss of consciousness. Potential triggers are numerous and often determination of the underlying cause is made in the outpatient setting. (See “Reflex syncope”.)
Most patients with neurocardiogenic syncope experience a prodrome, which may include dizziness or lightheadedness, a sense of warmth, pallor, nausea/vomiting, abdominal pain, and diaphoresis, prior to their loss of consciousness. Examples include micturition or defecation syncope, situational syncope (eg, while having blood drawn), or cough-mediated syncope.
●Carotid sinus hypersensitivity – Carotid sinus hypersensitivity is a variant of neurocardiogenic syncope, resulting from pressure at the carotid sinus. External pressure to the neck can induce this reflex response. Common causes include shaving, a tight collar, and turning of the head.
●Orthostasis – Orthostatic syncope comprises between 5 and 24 percent of syncope cases and can be defined by a drop in blood pressure of more than 20 mmHg, or a reflex tachycardia of more than 20 beats per minute. Orthostasis is most often caused by a loss of intravascular volume, from any number of causes, or by failure or instability of the autonomic nervous system. Nevertheless, clinicians should remain cautious because orthostasis can occur with cardiac syncope. Syncope from orthostatic hypotension is a diagnosis of exclusion in the emergency department, reserved for low risk patients who have symptoms consistent with the diagnosis.
Orthostatic vital signs are neither sensitive nor specific in assessing volume status or diagnosing syncope [13-15]. Many patients become symptomatic if their systolic blood pressure drops below 90 mmHg, but a large portion of the population who meets the definition of orthostasis do not have syncope. Elders, pregnant women, and patients taking drugs with vasodilating effects are predisposed to develop symptomatic orthostasis.
●Medications – The effects of medications account for 5 to 15 percent of syncopal events. The mechanism can be orthostasis or cardiotoxicity. Medications often implicated include calcium channel blockers, beta blockers, alpha blockers, nitrates, antiarrhythmics, diuretics (affecting volume status and electrolyte concentrations), and medications affecting the QTc interval (eg, antipsychotics and antiemetics).
Other conditions
●Neurologic syncope – True syncope is defined by an immediate, spontaneous return to baseline function following loss of consciousness, without new focal neurologic findings. Therefore, true neurologic causes, representing underlying neurovascular disease and not transient autonomic dysfunction, are rare.
Examples of neurologic syncope include: subarachnoid hemorrhage, transient ischemic attack, subclavian steal syndrome, and complex migraine headache. Stroke and transient ischemic attacks generally cause focal neurologic deficits that do not recover rapidly or completely. Often, patients with cerebrovascular disease convey a history of nonsyncopal episodes featuring neurologic deficits. Syncope may be misconstrued as seizure because many patients with transient loss of consciousness have brief convulsive episodes, particularly if bystanders or objects keep them upright. Syncope can usually be differentiated from seizure by the brevity of the convulsions and the lack a true postictal phase.
●Psychiatric syncope – Anxiety and panic disorders can cause situational syncope. Emergency clinicians must be cautious when attributing syncope to psychiatric causes. Patients with hypoxia, inadequate cerebral perfusion, or other medical conditions may appear confused or anxious. Patients with psychiatric syncope are generally young, without cardiac disease, and complain of multiple episodes.
●Drug induced loss of consciousness – Drugs of abuse and alcohol may cause a transient loss of consciousness, but generally these patients manifest signs of toxicity, and do not spontaneously return to normal neurologic function immediately after regaining consciousness. Alcohol can also cause symptomatic orthostasis by impairing vasoconstriction [18].
●Metabolic – Metabolic causes of syncope include hypoglycemia and hypoxia.
first investigations in syncope
full Hx
physical examination inc BP
Electrocardiogram — An ECG should be obtained in all patients with syncope. The ECG is suggestive of an arrhythmic cause of syncope if any of the following abnormalities is present (table 5) [1]:
The initial clinical evaluation, including carotid sinus massage, electrocardiogram (ECG), and basic laboratory testing, established a suspected cause of syncope in 69 percent. Neck movements can precipitate carotid sinus syncope, a type of reflex syncope caused by hypersensitivity of the carotid sinus.
Hx for syncope or pre-syncope
1 - when did this occur
2 - what situation was the pt in
3 - how did they feel before they collapsed
4 - did they actually lose consciousness and for how long
5 - did anyone witness this and ask them to describe it
6 - incontinence or bite tongue?
7 - did they hit their head or sustain other injuries
8 - how did they feel when they came round
9 - how do they feel now? any problems with speech, vision or movement.
10 - have they ever experienced a similar episode
11 - any hx of cardiac disease
12 - do they ever feel dizzy or weak standing up
13 - young female - any possibility of pregnancy? any abdominal pain or vaginal bleeding
14 - are they diabetic and when did they last eat
15 - have they ever had a severe head injury
16 - on any medications
17 - any non-prescription drugs or alcohol
18 - do they drive a motor vehicle.
