Cardiovascular conditions, signs, causes and differentials Flashcards
Chest discomfort common differentials?
MI
Angina
Pericarditis
Aortic dissection
Other:
Oesophageal spasm
Pneumothorax
Musculoskeletal pain (costochondritis)
Breathlessness common differentials?
Heart failure
Angina
Pulmonary embolism
Pulmonary hypertension
Other: Respiratory disease Anaemia Obesity Anxiety
Palpitation common differentials?
Tachyarrhythmias
Ectopic beats
Other:
Anxiety
Hyperthyroidism
Drugs
Syncope and dizziness common differentials?
Arrhythmias Postural hypotension Aortic stenosis Hypertrophic cardiomyopathy Atrial myxoma
Other:
Vasovagal syncope
Epilepsy
Anxiety
Oedema common differentials?
Heart failure
Constrictive pericarditis
Venous stasis
Lymphoedema
Other: Nephrotic syndrome Liver disease Drugs Immobility
Which arrhythmia is the only one with gradual onset?
Sinus tachycardia
Which three arrhythmias are regular and fast in character?
Sinus tachycardia
Supraventricular tachycardia
Ventricular tachycardia
What are the five types of arrhythmias? (There are more than 5!)
Sinus tachycardia Extrasystoles Supraventricular tachycardia - two kinds (wolf Parkinson white AVRT, and AVNRT) Atrial fibrillation Ventricular tachycardia
Causes of unilateral leg oedema?
DVT Soft tissue infection Trauma Immobility Lymphoedema (when lymphatic system doesn’t drain lymph properly)
Causes of bilateral leg oedema?
Heart failure
Chronic venous insufficiency
Hypoproteinaemia (e.g. nephrotic syndrome/cirrhosis)
Lymphatic obstruction
Drugs (e.g. NSAIDS, amlodipine, fludrocortisone)
Vitamin B12 deficiency
Immobility
What does xanthelasma represent?
Predictor of cardiovascular disease
Risk of: MI, coronary heart disease and mortality.
Indicates for checking for xanthomata on patellar and Achilles tendons.
(Can occur in normolipidaemic patients)
What is corneal arcus?
Creamy yellow discolouration at the boundary of the iris and cornea due to cholesterol deposition.
(Can occur in normolipidaemic patients)
Causes of an irregular pulse?
Sinus arrhythmia Atrial extrasystoles Ventricular extrasystoles Atrial flutter (some cases) Second degree heart block (some cases)
Common causes of atrial fibrillation?
HTN HF MI Thyrotoxicosis Alcohol-related heart disease Mitral valve disease Infection (most often respiratory or urinary) Surgery (esp. cardiothoracic surgery)
Causes of myocardial ischemia?
CAD Anaemia Cocaine abuse (vasoconstriction- coronary artery spasm) Aortic stenosis (Backflow obstructs blood flow) HOCM (IV septum obstructs blood flow) Thyrotoxicosis Aortic dissection Pericarditis
Which type of murmur is pansystolic?
Mitral regurgitation
As systole happens, blood is forced out of the other end of the ventricle
Which type of murmur is heard early in diastole and is heard best with the patient sat forward?
Aortic regurgitation
Heard best in the left 4th intercostal space
Which murmur is heard in the mid-diastole and is loudest at the apex?
Mitral stenosis
Which type of murmur is the only ejection-systolic murmur?
Aortic stenosis (most common murmur)
Cardiovascular causes of chest pain?
CAD Aortic stenosis HOCM Tachyarrhythmias Cocaine Anaemia Thyrotoxicosis Aortic dissection Pericarditis
GI differentials for chest pain?
GORD
Gallstones
Peptic ulcer
Pancreatitis
Respiratory differentials for chest pain?
PE
Pneumothorax
Pneumonia
Pleurisy
What is typical angina?
Angina=Symptomatic reversible myocardial ischemia.
To distinguish it from atypical angina and non-angina chest pain, must have all three characteristics:
- Constricting discomfort in chest and/or in adj areas (Jaw, shoulder, arm or back)
- Precipitated by physical exertion
- Relieved by rest or GTN within 5 minutes
What is atypical angina?
Chest discomfort with any 2 of the following:
- Constricting discomfort in chest and/or in adj areas (Jaw, shoulder, arm or back)
- Precipitated by physical exertion
- Relieved by rest or GTN within 5 minutes
e. g. stabbing (not constricting) discomfort in chest brought on by running and relieved by gtn qualifies
What is unstable angina?
Angina of increasing frequency or severity.
Occurs at rest or Occurs on exertion.
Associated with increased risk of MI
What is stable angina?
Angina that is induced by exertion and relieved by rest.
Good prognosis, unlike unstable angina.
What is decubitis angina?
Angina (typical or atypical) induced by lying flat.
Causes of Angina?
Atheroma (most common)
Anemia Coronary artery spasm Aortic stenosis Tachyarrhythmias HOCM Arteritis and small vessel disease
What are the associated symptoms of angina? (Beside the discomfort, precipitation and relieving factors)
Dyspnoea
Nausea
Sweatiness
Fainting
In ACS what is the chest pain like?
SOCRATES
Site = Chest, Diffuse, poorly localised (visceral)
Onset = Often during exertion
Character = Heavy, constricting pressure
Radiation = Arm(s), jaw, neck, shoulder, epigastrium
Associated symptoms = Nausea, Sweating(clammy), dyspnoea, syncope or HTN
Timing = Minutes to hours
Exacerbating factor = Eating
Severity = Variable
Causes of ventricular fibrillation?
Signal conduction issue or oxygen deprivation
Due to:
- Irritable ventricular cells (Hyper/Hypokalemia, Hyper/Hypocalcemia, Hyper/Hyponatremia)
- Scarring of myocardium (Previous MI)
- Cardiomyopathy (CAD, myocarditis or
Signs of ventricular fibrillation?
Pulseless And signs of ACS: Constricting chest pain Dyspnoea Cyanosis Nausea Sweating Syncope
Signs of ventricular tachycardia?
Heart rate up to 250bpm
What is focal ventricular tachycardia?
HR >100bpm at rest, lasting for longer than 30 seconds.
Due to irritable myocardial cells due to hormones or ischemia.
Causing ventricular depolarisation to radiate from the scar
(it circles the scar, giving off its own ventricular heart beat causing over-firing of the ventricles)
Seen as wider QRS on ECG
What is re-entrant ventricular tachycardia?
HR >100bpm at rest, lasting for longer than 30 seconds.
Due to myocardial scarring, ventricular depolarisation to radiate from the scar.
(it circles the scar, giving off its own ventricular heart beat, causing over-firing of the ventricles)
Seen as wider QRS on ECG
What is supraventricular tachycardia?
A group of arrhythmias with a heart rate of >100bpm at rest, originating in the SAN or AVN.
Which condition does intermittent claudication indicate?
Peripheral arterial disease
What is a “strong apical impulse felt over the precordium”?
A strong apex beat felt over the thorax immediately in front of the heart.
- a normal heart finding.
What is vasovagal syncope?
Fainting.
Signs: loss of consciousness, pale, clammy, vomiting, slow threads pulse, fast recovery.
You faint when your brain doesn’t get enough blood.
Cause: In short, the heart isn’t well filled, a cerebral process causes the heart to beat forcefully triggering baroreceptors, and causing vasodilation and reduced heart rate while the heart isn’t full. This means reduced blood flow to the brain and loss of consciousness.
The baroreceptors in the left ventricle are not only innervated by stretch but also by vigorous and forceful systolic contraction.
- Decreased venous return
- Decreased left ventricular filling
- Reduced baroreceptor stretch
- Sympathetic drive increases
- Heart beats more rapidly but with reduced blood volume
- Increased baroreceptor stimulation from forceful contractions
- Increased parasympathetic effects: vasodilation and reduced heart rate.
- Brain doesn’t receive high blood flow
- Loss of consciousness ensues
What is carotid sinus hypersensitivity?
A condition where the carotid sinus response to stretch (massage) is particularly strong and induces syncope.
Treatment = pacemaker with electrodes to ventricle and atria
What is the most common type of hypertension?
Essential hypertension is most common (90% of HTN)
Essential hypertension AKA primary hypertension
Which parts of the human anatomy can cause secondary hypertension?
Kidney Lungs Heart Adrenal glands Thyroid gland Parathyroid gland Adipose tissue Blood vessels
Which pathologies can cause secondary hypertension?
Go through body systematically, then exogenous causes
Sleep apnoea syndrome (SAS)
Hypothyroidism and hyperthyroidism
Primary hyperparathyroidism
Pheochromocytoma (Adrenal medulla chromaffin cell adenoma)
Primary aldosteronism (Conn syndrome, adenoma of the adrenal cortex)
Cushing’s syndrome
Renovascular disease
Primary renal disease
Coarctation of the aorta
Which drugs can cause secondary hypertension?
Easier to spot, since date of drug use may correspond to HTN onset
Oral contraceptive pill (progesterone effect on small vessels)
NSAIDS (inhibition of COX in the kidney, reducing the vasodilatory prostaglandin production)
Stimulants (cocaine, amphetamines)
Calcineurin inhibitors (inhibit the activation of T cells by calcineurin; a phosphatase)
Antidepressants
What are the signs of general hypertension?
General hypertension is a type of secondary HTN
Onset is before puberty
No obesity
Severe or resistant HTN
Acute rise (not a slow progression)
What are the signs of coarctation of the aorta?
Mixture of hypotension and hypertension in the body:
Hypertension in the right arm
Hypotension in the lower limbs and left arm
Delayed/diminished femoral and left brachial pulse
What are the signs of hypertensive urgency?
Headache
Dyspnoea
Epistaxis
Severe anxiety
What are the signs of a hypertensive emergency?
AKA malignant hypertension
Chest pain (LV failure)
Back pain
Vision change (Retinopathy)
Difficulty speaking (Encephalopathy - neurological deficit)
Numbness (Encephalopathy - neurological deficit)
Weakness (Encephalopathy - neurological deficit)
What is hypertensive urgency?
A type of hypertensive crisis, a complication of hypertension.
Systolic >180 mmhg or Diastolic >110 mmhg
No target organ damage (kidneys, heart, brain)
What is a hypertensive emergency?
The most severe type of hypertensive crisis, a complication of hypertension.
Systolic >180 mmhg or Diastolic >120 mmhg
Target organ damage: retinopathy, nephropathy, left ventricular failure and encephalopathy
What are the common cardiovascular differentials for syncope (transient LOC)?
ACS
Ventricular arrhythmias
AV block (HB)
Acute AF
CHF
Hypovolaemia
Aortic stenosis
What is dyspnoea?
A subjective symptom where the patient is uncomfortably aware of their breathing.
Associated with increased work of breathing and increased respiratory rate.
Occurs in cardiovascular, respiratory and severe anaemia disease
Pathophysiology:
Blood isn’t flowing through the lungs fast effectively
Gas exchange isn’t happening
Blood lacks the capacity to uptake oxygen
Which physiological mechanisms are orthopnoea caused by?
Pooling of blood in the pulmonary vasculature.
Pulmonary oedema.
Orthopnoea - shortness of breath on lying flat
What is a bruit?
A murmur heard over any vessel other than the heart
e.g. carotid bruit heard in hyperthyroidism or aortic stenosis radiating to the carotid or axilla
What is aortic stenosis?
Pathological narrowing of the aortic valve that obstructs the flow of blood.
Since the left ventricle generates a lot of pressure but the obstruction prevents that from all being relieved the murmur is a crescendo-decrescendo.
It may also have an ejection click as the aortic valve snaps open under the pressure.
Systole:
- M/T valves close - HS 1
- Pressure builds in ventricles
- A valve pops open - Snap
- Crescendo-decrescendo mumur
- A/P valves close - HS2
Why is aortic regurgitation during diastole?
To make an extra sound, blood must pass backwards through the aortic valve.
The aorta and elastic vessels have a lot of blood pumped in to them by systole, their elasticity means that it pumps blood. The aortic valve isn’t completely shut therefore blood is pushed backwards through it.
Fundament: Elasticity of vessels immediately attached to the left ventricle - aorta, large vessels etc
What is heart failure?
AKA Congestive heart failure
Heart failure is a complex syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the heart to function as a pump to support physiological circulation.
(AKA Congestive heart failure since the heart is congested with blood)
A clinical syndrome - not a diagnosis.
Basic types are:
- HF with preserved LV function - EF >45%
- HF with LV dysfunction - EF <45%
Defined by echocardiography estimates of EF.
Heart failure is said to be “decompensated” (or acute exacerbation of HF, or acute HF) in the case of:
Rapid onset or worsening of symptoms and/or signs of heart failure, requiring urgent evaluation and treatment. - acute HF is a clinical syndrome just like HF.
Pathophysiology of HF symptoms:
- Something damages the heart’s contractility (Lesion, hypertrophy, ischemia, clot, scar etc)
- More blood is left in the heart at the end of systole,less blood is pumped out - SV decreases
- THIS IS THE HEART FAILURE- - Body wants more blood: SV must increase
- The body increases blood returned to the heart (Increase preload) and increases the heart’s force of contraction to increase SV.
- COMPENSATED HEART FAILURE- - Something happens to the heart to decrease its contractility further (MI, dilation, hypertrophy, scar, lesion etc).
- The preload (LV- end diastolic volume/pressure) or the force of contraction can’t be Increased enough to make up for this.
- The blood isn’t being pushed out of the left ventricle very effectively, meaning the left atrium and right ventricle have to work against a greater resistance.
- DECOMPENSATED HEART FAILURE- - Pulmonary hypertension occurs = Pulmonary oedema occurs - (cough and fatigue)
- This backtracks through the right ventricle and reduces venous return - (ankle/sacral oedema)
What are the causes of mitral regurgitation?
Rheumatic heart disease (damages leaflets)
Ischemic heart disease (by damage done to papillary muscles)
Valvular vegetations (Endocarditis)
Physiological regurgitation (leaflets grow apart)
What is a reentrant arrhythmia?
An area of cardiac myocyte that is heterogenous (e.g. lesion or ischemic).
It occurs during the following set of conditions:
- A unidirectional block is in place
- The impulse can’t go through it in one direction
- But as it comes back on the other side it CAN pass through it - Slow conduction (reduced excitability
- as occurs in ischemia or an MI due to release of electrolytes and lack of oxygen
- allows the block to recover and become conducting again - Short action potential
- speeds up the refractory period since less ions move
- makes it easier to repolarise
This all means an impulse that should spread through the heart in one single wave that is generated at the SAN and ends in the ventricles, can turn back on itself and send an impulse back through the heart - reentering.
What are the signs and symptoms of heart failure?
Main symptoms:
Fatigue/tiredness
Light-headedness or syncope
Muscle weakness
Dyspnoea;
- On exertion or at rest
- Orthopnoea
- Paroxysmal nocturnal dyspnoea
Cough (nighttime or daytime)
Chest pain/discomfort
Peripheral oedema: sacral, ascites and lower limb
If severe - central cyanosis and signs of hypoxia
Signs:
Basal crepitations (Rales/crackles)
Tachypnoea
Hepatomegaly (due to congestion of blood in portal system)
S3 gallop (3rd heart sound)
Laterally displaced apex beat
Heart murmurs
Cardiomegaly
Tachycardia (>100)
Raised JVP
ECG changes (arrhythmias, heart block)
What are the causes of acute heart failure? (AKA acute congestive heart failure)
Think of acute conditions too!
Note: “congestive” and “heart failure” make no indication of their aetiology
Decompensation of pre-existing chronic heart failure
Acute coronary syndrome
Hypertensive crisis
Acute arrhythmia
Severe valvular regurgitation
Severe aortic valve stenosis
Acute severe myocarditis
Cardiac tamponade
Aortic dissection
Post-partum cardiomyopathy
Lack of compliance with medical treatment
Volume overload
Infections
Severe brain insult
After major surgery
Reduction of renal function
Drug abuse
Phaeochromocytoma
Septicaemia
Thyrotoxic crisis
Anaemia
Shunt syndromes
What are the four most common causes of chronic heart failure?
Coronary artery disease
Hypertension
Valvular disease
Myocarditis
Other causes:
1. Infiltrative diseases; amyloidosis, haemochromatosis, sarcoid
- Congenital heart diseases
- Pericardial disease
- Toxin-induced: heroin, alcohol, cocaine, amfetamines, lead, arsenic, cobalt, phosphorus
- Infection: bacterial, fungal, viral (HIV), Borrelia burgdorferi (Lyme disease), parasite (e.g., Trypanosoma cruzi [Chagas disease])
- Endocrine disorders: diabetes mellitus, thyroid disease, hypoparathyroidism with hypocalcaemia, phaeochromocytoma, acromegaly, growth hormone deficiency
- Systemic collagen vascular diseases: lupus, rheumatoid arthritis, systemic sclerosis, polyarteritis nodosa, hypersensitivity vasculitis, Takayasu syndrome, polymyositis, reactive arthritis
- Chemotherapy-induced: for example, adriamycin, trastuzumab
- Nutritional deficiencies: thiamine, protein, selenium, L-carnitine
- Pregnancy: peripartum cardiomyopathy
- Familial cardiomyopathy
- Tachycardia-induced cardiomyopathy
- Pulmonary causes: COPD, pulmonary fibrosis, recurrent pulmonary emboli
What is infective endocarditis?
An infection of the endocardial (innermost- in contact with blood) surface of the heart; surface, valves, chordates tendiniae.
Caused by a select group of microorganisms, normally staph. A
Classification:
Acute = develops over days-weeks with a fever present
Subacute = develops over weeks-months, apyrexial with vague symptoms
Type - depending on area colonised:
- Native valve
- Prosthetic valve
- Device-related
- Right-sided (often IVDU)
MOA:
- Typically endothelial damage occurs within the heart due to turbulent blood flow.
- Platelets and fibrin adhere to the exposed collagen matrix and create a prothrombotic area
- INFECTION SOURCE INTRODUCED TO BODY- - Bacteraemia causes colonisation of this area
- Fibrin deposition and platelet adhesion continues
- A mature infected vegetation has grown
- Pieces break off and cause stroke or DVT
What are the signs and symptoms of infective endocarditis?
Note: since it’s an intravascular infection, we may expect the infection to be carried elsewhere in the body
Can be a variable presentation: acute, subacute or chronic with low grade fever
In 90% of cases:
Dyspnoea
Fever/chills
Murmurs
Other systemic symptoms: Fatigue Weakness Weight loss/anorexia Myalgia Arthralgia Night sweats
Peripheral signs:
RETINA - Roth spots (haemorrhages with small clear centres, an immunological phenomena)
MOUTH - Petechiae (circular, non-raised spots on skin/mucosa)
PALMS/FINGERS/SOLES/TOES - Janeway lesions (non-raised erythematous flat lesions, vascular phenomena)
FINGERS - Osler nodes (tender subcutaneous nodes on distal finger)
NAILS - Subungual haemorrhages (dark red lines in nailbeds)
Signs of emboli:
Chest pain
Stroke - focal neurological signs
Meningism - photophobia, neck stiffness, headache
What are the differentials for signs of heart failure?
Dyspnoea, cough, fatigue and tiredness
COPD
Pulmonary fibrosis
Pneumonia
PE
Cirrhosis
Nephrotic syndrome
Pericardial disease
Venous stasis
DVT
What is paroxysmal atrial fibrillation?
Episodes of AF lasting:
- Between 30 seconds and 7 days duration
- Self terminating
- Recurrent
What is atrial fibrillation?
A chaotic and irregular atrial contraction that is a type of supraventricular arrhythmia.
Types: paroxysmal, persistent and permanent
MOA:
- Insult to the atria occurs- HTN, MI, Aortic stenosis, LV dysfunction, atrial tachycardia,atrial flutter etc
- Atria pressure goes up and they dilate, inflame and fibrose
- Dilation;
- Fractionates mother wave (more re-entrance)
- Slows conduction (synchronicity decreases)
- Shortens refractory period (more re-entrance) - Fibrosis slows conduction and increases chances of reentrance
- Atria now fire randomly causing twitching instead of proper contractions - fibrillation
What are the possible signs and symptoms of atrial fibrillation?
Often asymptomatic
Dizziness/syncope
Palpitations - most common
Tachycardia
Dyspnoea - most common
Irregularly irregular pulse on palpation (sometimes the atria trigger a ventricular beat randomly)
Chest discomfort - most common
Fatigue
Reduced exercise tolerance (due to HF or tachycardia)
Malaise
Polyuria (due to increased release of ANP)
May present as complication:
Stroke
TIA
Heart failure
What is persistent atrial fibrillation?
Episodes of AF that last longer than 7 days duration
What is permanent atrial fibrillation?
AF that:
- Fails to terminate using cardioversion therapy
- Or is terminated but recurs within 24 hours
What is fast atrial fibrillation?
Atrial fibrillation with a fast ventricular rate.
This is due to the ventricles trying to compensate for their poor filling when the atria don’t squeeze blood in to them.
What is atrial tachycardia?
Rapid atrial activation caused by a region of the atria that is not caused by the sinus node, causing a HR of 100-250 bpm.
This is not a form of AF
What is atrial flutter?
An extreme version of atrial tachycardia, where macro-reentrance causes rapid depolarisation of the entire heart, and a HR of 250-320bpm.
ECG shows multiple sawtooth P waves between
QRS complexes and rate of >250bpm.
What are the differentials for atrial fibrillation?
i.e. an irregular pulse has been found
Atrial flutter - Refular sawtoothed p-waves on ECG
Atrial extrasystoles - common
Ventricular ectopic beats
Sinus tachycardia (HR >100)
Atrial tachycardia (HR 100-250)
Atrioventricular nodal re-entry tachycardia
Wolff-Parkinson-White syndrome (Developmental disorder: extra routes for impulses to run from ipsilateral atria-ventricle, bypasses the AV node and the conduction delay)
Multifocal atrial tachycardia
What are the causes of atrial fibrillation?
Hypertension
HF with/without reduced ejection fraction
Polygenic
Monogenic - cardiomyopathies
Post-operative
Mitral stenosis
Exercise-induced
In the case of post-MI regurgitation, which part of the heart is damaged: leaflet, chordae tendineae or papillary muscles?
Papillary muscles
What are the signs and symptoms of life-threatening haemorrhage?
Look significantly unwell
Low blood pressure and tachycardia - signs of shock
To begin the major haemorrhage pathway they must be losing >150ml per minute but blood loss may be hidden (e.g. AAA)
What is peripheral vascular disease?
Essentially arterial sclerosis - an inevitable, degenerative, generalised condition
MOA = Senescence, stress, and toxin exposure cause damage to the endothelium, then platelets, immune cells, lipid deposition and SMC proliferation, in combination with inflammation.
Pathophysiology:
The actual disease itself is often only symptomatic when embolism, thrombosis, dissection or trauma occur to the blood vessel and its impaired function comes to light.
Prognosis:
Occlusion can occur anywhere, the more proximal the occlusion, the worse the prognosis.
Prognosis also depends on collateralisation and if the tissue has had time to acclimatise to ischemia (e.g. chronic PVD has had time to prepare), and if caught early or late.
What are the acute pathological processes of peripheral vascular disease?
Mild:
Small vessel thrombosis
Transient claudication
Critical:
Emboli - cardiac or leading to aneurysm
Dissection
(Aetiology of PVD is atherosclerosis, but the pathophysiology is the result of these processes)
Large vessel thrombosis - thrombophilia, graft occlusion or leading to aneurysm
What are the chronic pathological processes of peripheral vascular disease?
Mild:
Collateralised peripheral arterial occlusive disease (PAOD) - major cause of claudication
Fontaine classification 2 - intermittent claudication (after walking 200M)
Critical:
Decompensated PAOD
Fontaine classification 3 - rest pain (from claudication)
Fontaine classification 4 - ischemic ulcers or gangrene
What are the signs/symptoms of acute limb ischemia in PVD?
The six P’s:
Pale Perishing cold Pulseless Painful Paraesthetic Paralysed (numb or mottled)
The first four symptoms:cold, pulseless and painful limb occur within first four hours and are reversible. (Intervention from the vascular surgeon is possible to reperfuse the limb).
Once the limb is paraesthetic the limb is threatened.
Finally, when the limb is paralysed it is now non-viable and must be removed.
Ischemic means no blood SUPPLY, so it is arterial in nature - an ischemic limb is not like a venous issue, it is cold
If a limb is hot, swollen and tender, could this be an ischemia due to peripheral arterial disease?
No
An ischemic limb is cold, pulseless and pale - because blood supply is impaired.
A hot, swollen, tender limb is most often an acute venous issue e.g. DVT
What is claudication?
Aching muscles during effort:
- predictable,
- worse on hills or with loads or at speed
- settles quickly on rest
In peripheral vascular disease, what is rest pain?
The deterioration of claudication, it is an icy, burning, constant aching pain in the foot:
- worse on elevation or at night (perfusion pressure is lower on the limbs in the evening)
- requires opiates (a severe pain)
For diagnosis of Fontaine classification 3 (rest pain), you need to have had 2 weeks of rest pain.
If left untreated it WILL develop in to ulcers, necrosis and gangrene.
In peripheral vascular disease, a person with Fontaine classification 4 limb ischemia has tissue loss, what constitutes tissue loss?
Ulcers
Necrosis
Gangrene
What is cerebrovascular disease?
Atheroma of the carotid artery (the main supply of the cerebrum).
May present with carotid bruit.
How does cerebrovascular disease present?Which conditions will occur?
Disease is asymptomatic until event occurs (embolisation from a plaque in carotid artery):
Stroke (cause of one in six strokes)
TIA (recovery within 24 hours)
Amaurosis (transient vision loss in the ipsilateral eye)
What is an aneurysm?
An abnormal dilation of an artery that is >50% of its normal transverse diameter.
The walls of the blood vessel are calcified, occluded and thinned.
Normal aorta is 2.5cm diameter, an aortic aneurysm is 1.5 times its normal size
Often surgeons use this term to refer specifically to an atherosclerotic infrarenal abdominal aortic aneurysm
Aneurysms are a generalised arterial disease:
Aneurysms originate from CAD, just like many other diseases, so you should expect comorbidities like; IHD, cerebrovascular disease, poor mesenteric and renal circulation etc
These in turn affect the outcome of an aneurysm.
What is ectasia?
Abnormal dilation of an artery that is less than 50% of its normal diameter. (Pre-aneurysm)
What is arteriomegaly?
Generalised dilation of an artery, unlike an aneurysm which is only in a specific place on the artery.
What are the types of cause of aneurysm?
True aneurysms (pathology arises from all layers of arterial wall): Atherosclerotic - most common cause
Mycotic - infection of the arterial wall
Inflammatory - 10% of all aneurysms
Connective tissue disorder - ehlers danlos or other
False aneurysms (only one layer of artery wall is affected): puncture of artery
Which locations in the body do aneurysms occur within?
Intracerebral
Aortic - aortic is most common, thoracic is second most common
Visceral
Iliac
Popliteal
What is the difference between a fusiform and a saccular aneurysm?
Fusiform - general dilatation (uniform) of entire artery
Saccular - asymmetrical dilatation
What are the symptoms of an abdominal aortic aneurysm?
Asymptomatic
Back pain
Tenderness (over aneurysm)
In the case of rupture:
Limb ischemia
Hypotension
(Warning: Any woman age 10-50 could be pregnant)
What are the risk factors for abdominal aortic aneurysms?
What are the risk factors for abdominal aortic aneurysms?
Male
Over 60 (1 in 25 over 65’s have an AAA)
Hypertension and smoking together
Family history of AAA
What is an aortic dissection?
Note: the aorta is the main vessel of the body, it sits closely to the spine as it travels inferiority.
The separation of the layers of the aortic blood vessel wall.
Anatomy: tunica intima, media and adventitia
MOA: Tear In the intima allows blood to enter between the intima and media. This is pumped down this false lumen and propagated along this new space, this makes the media/adventitia bulge outward and downward.
Propagation can move forwards or back along the aorta.
What are the causes of aortic dissection?
Hypertension (present in 67%, most common cause, they cause stress and degenerative changes to the wall)
Connective tissue disease: Marfan’s syndrome and ehlers danlos (both weaken the wall because the dna codes for low fibre content)
Aneurysm
Trauma
What is a type A Aaortic dissection?
Stanford system:
Type A = dissection in the ascending aorta; before the origin of the left subclavian artery
Most common site is in the first 10cm of the arch of the aorta because it is the area of highest sheer stress and turbulence is highest here.
What is a type B Aaortic dissection?
Stanford system:
Type B = a dissection on the descending aorta; from the origin of the left subclavian artery onwards/downwards
e.g. abdominal dissection
What are the signs/symptoms of an aortic dissection?
Sudden, severe, tearing central chest pain (can radiate up the neck/jaw/back)
Sweating
Nause
Dyspnoea
Weakness
Syncope
Early diastolic murmur (acute aortic regurgitation)
Difference in BP between the arms
CARDIAC TAMPONADE - hypotension, raised JVP, muffled heart sounds
Why is a young patient particularly worrying if they are pale, tachycardic and hypotensive?
Because a young patient has good ability to peripherally constrict therefore preserving their BP, the point at which they present like that is where they are close to 60% blood loss.
In short: the body can compensate in BP for up to 60% blood loss (at the expense of cardiac output and tissue perfusion) but then the BP dives rapidly
They require urgent medical attention at this point.
What is shock?
An acute state of tissue under-perfusion, it causes a generalised cellular hypoxia.
Shock = cardiovascular!
- The supply of oxygen is inadequate to meet the demand.
- Oxygen utilisation may be abnormal, particularly by the mitochondria.
- It comes with haemodynamic abnormalities but it ISN’T just the haemodynamic abnormalities.
Which physiological parameters can change to give a drop in blood pressure, such as in shock?
Change in cardiac output:
1. Reduced heart rate (bradycardia)
- Fall in stroke volume
- Reduction in vascular tone (vasodilation)
What are the four types of shock?
Hypovolaemic - reduced intravascular volume
Cardiogenic - pump failure
Distributive - vasodilation and malperfusion
Obstructive - failure of circulatory flow
Often two or more exist but one will be primary
What are the causes of hypovolaemic shock?
Haemorrhage
Burns
GI loss: vomiting - diarrhoea - fistula
Dehydration: heat exposure - Polyuria
What are the causes of distributive shock?
Infection: Sepsis - Pancreatitis
Trauma
Burns
Spinal cord injury
Anaphylaxis
What are the causes of cardiogenic shock?
MI and myocardial ischemia
Arrhythmia
Acute valve pathology
What are the causes of obstructive shock?
Tension pneumothorax
Pericardial tamponade
Pulmonary embolism
- All preventing the heart filling/emptying and the aorta transporting blood
Which physiological systems are activated in shock?
Sympathetic system and Adrenal catecholamine release (vasoconstriction in peripheries- skin/gut/kidneys, Increased HR, tachypnoeic)
RAAS - Sodium and water retention
Coagulation system
Cortisol - stress response system
Which physiological processes cause the symptoms/signs of hypovolaemic shock?
- Loss of serum volume = loss of preload
- Decreased stroke volume = loss of cardiac output
- Heart rate increases and systemic vascular resistance increases to compensate for loss of BP
- This causes tachycardia and blood diversion away from peripheries - “heart racing and pale/clammy”
- As soon as it can’t compensate, the systolic BP falls - hypotension
- RAAS activation prevents urine production - Oliguria
- Once decompensated = tissue hypoperfusion - cognitive changes and metabolic acidosis occur
In treatment of major haemorrhage, what are the risks of ischemia and ischaemic toxins released on individual organs of the body?
LUNGS: Acute lung injury (ALI) - toxins inflame the lungs
KIDNEYS: Renal failure - due to underperfusion and resultant AKI
GUT: Gut failure and gut sepsis - The gut breaks down during ischemia and can’t contain the toxins and bacteria it normally has within it
Blood: Disseminated intravascular coagulation (DIC) and Acute coagulopathy of trauma shock (AcoT)
What is disseminated intravascular coagulation?
Lots of cells present tissue factor to the circulation system, this activates lots of thrombin and fibrin generation, particularly in the microvascular areas.
MOA- These form lots of clots, causing lots of small areas of microvascular ischemia. This then diffusely activates the fibrinolytic system which causes release of fibrin degradation products, and prevents clot formation in more useful places.
This causes:
- Hypoperfusion
- Factor consumption
- Hyperfibrinolysis (Clot inhibition)
- Activated factor C upregulation (more thrombin causes more activation of thrombinmodulase)
- High serum FDP level (e.g. D-dimer)
- Kinin and plasmin release, which causes vasodilation and the consumptive shock profile.
What are the differentials for acute chest pain?
Cardiovascular: ACS Aortic dissection Pericarditis Myocarditis Stable angina Tamponade Mitral valve prolapse Pulmonary hypertension Aortic stenosis Arrythmias
Respiratory: PE Pneumonia Pneumothorax Pleurisy Lung cancer
Musculoskeletal- trauma, costochondritis
GI:
GORD
Gastritis
Gastroduodenal ulcer
Pancreatic/biliary:
Acute cholecystitis
Pancreatitis
Anxiety/panic attack
Oesophageal spasm
Fibromyalgia
What are the symptoms of shock?
Palpitations
Tachypnoea
Muscle weakness
Cool extremities
Agitation (early shock)
Cognitive decline (late shock or hypoglycaemia)
Cyanosis
How are murmurs graded?
1-6: Barely audible Faint but immediately heard on auscultation Easily heard Very easily heard with palpable thrill Very loud Heard without stethoscope
What are the general characteristics of a murmur?
- Timing - systolic,diastolic or continuous
- Location - Heard best at RICS, LSE, Apex (generally)
- Radiation - carotid or axilla
- Shape - crescendo/decrescendo, decrescendo, uniform, decrescendo/crescendo
- Intensity
- Pitch
- Quality
- Response to manoeuvres
Three areas to auscultate aortic and mitral murmurs:
2nd Right ICS, left lower sterna edge and apex
2nd Right ICS = Aortic stenosis
Apex = Mitral stenosis and mitral regurgitation
Left lower sternal edge = Aortic regurgitation
Where is aortic regurgitation best heard?
Left lower sternal edge
Where is mitral regurgitation best heard?
Apex - same as mitral stenosis
Apex is the MITRAL area
