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[ECG] Conditions, risk factors, signs, differentials, on ecg and xray > Cardiovascular conditions, signs, causes and differentials > Flashcards

Cardiovascular conditions, signs, causes and differentials Flashcards

1
Q

Chest discomfort common differentials?

A

MI
Angina
Pericarditis
Aortic dissection

Other:
Oesophageal spasm
Pneumothorax
Musculoskeletal pain (costochondritis)

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2
Q

Breathlessness common differentials?

A

Heart failure
Angina
Pulmonary embolism
Pulmonary hypertension

Other:
Respiratory disease 
Anaemia
Obesity
Anxiety
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3
Q

Palpitation common differentials?

A

Tachyarrhythmias
Ectopic beats

Other:
Anxiety
Hyperthyroidism
Drugs

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4
Q

Syncope and dizziness common differentials?

A 
Arrhythmias
Postural hypotension 
Aortic stenosis
Hypertrophic cardiomyopathy 
Atrial myxoma

Other:
Vasovagal syncope
Epilepsy
Anxiety

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5
Q

Oedema common differentials?

A

Heart failure
Constrictive pericarditis
Venous stasis
Lymphoedema

Other:
Nephrotic syndrome
Liver disease
Drugs
Immobility
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6
Q

Which arrhythmia is the only one with gradual onset?

A

Sinus tachycardia

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7
Q

Which three arrhythmias are regular and fast in character?

A

Sinus tachycardia
Supraventricular tachycardia
Ventricular tachycardia

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8
Q

What are the five types of arrhythmias? (There are more than 5!)

A 
Sinus tachycardia 
Extrasystoles
Supraventricular tachycardia - two kinds (wolf Parkinson white AVRT, and AVNRT)
Atrial fibrillation 
Ventricular tachycardia
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9
Q

Causes of unilateral leg oedema?

A 
DVT
Soft tissue infection 
Trauma
Immobility
Lymphoedema (when lymphatic system doesn’t drain lymph properly)
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10
Q

Causes of bilateral leg oedema?

A

Heart failure
Chronic venous insufficiency
Hypoproteinaemia (e.g. nephrotic syndrome/cirrhosis)
Lymphatic obstruction
Drugs (e.g. NSAIDS, amlodipine, fludrocortisone)
Vitamin B12 deficiency
Immobility

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11
Q

What does xanthelasma represent?

A

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)

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12
Q

What is corneal arcus?

A

Creamy yellow discolouration at the boundary of the iris and cornea due to cholesterol deposition.

(Can occur in normolipidaemic patients)

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13
Q

Causes of an irregular pulse?

A 
Sinus arrhythmia
Atrial extrasystoles
Ventricular extrasystoles
Atrial flutter (some cases)
Second degree heart block (some cases)
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14
Q

Common causes of atrial fibrillation?

A 
HTN
HF
MI
Thyrotoxicosis
Alcohol-related heart disease
Mitral valve disease 
Infection (most often respiratory or urinary)
Surgery (esp. cardiothoracic surgery)
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15
Q

Causes of myocardial ischemia?

A 
CAD
Anaemia
Cocaine abuse (vasoconstriction- coronary artery spasm)
Aortic stenosis (Backflow obstructs blood flow)
HOCM (IV septum obstructs blood flow)
Thyrotoxicosis
Aortic dissection
Pericarditis
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16
Q

Which type of murmur is pansystolic?

A

Mitral regurgitation

As systole happens, blood is forced out of the other end of the ventricle

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17
Q

Which type of murmur is heard early in diastole and is heard best with the patient sat forward?

A

Aortic regurgitation

Heard best in the left 4th intercostal space

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18
Q

Which murmur is heard in the mid-diastole and is loudest at the apex?

A

Mitral stenosis

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19
Q

Which type of murmur is the only ejection-systolic murmur?

A

Aortic stenosis (most common murmur)

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20
Q

Cardiovascular causes of chest pain?

A 
CAD
Aortic stenosis
HOCM
Tachyarrhythmias
Cocaine
Anaemia
Thyrotoxicosis 
Aortic dissection 
Pericarditis
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21
Q

GI differentials for chest pain?

A

GORD
Gallstones
Peptic ulcer
Pancreatitis

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22
Q

Respiratory differentials for chest pain?

A

PE
Pneumothorax
Pneumonia
Pleurisy

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23
Q

What is typical angina?

A

Angina=Symptomatic reversible myocardial ischemia.
To distinguish it from atypical angina and non-angina chest pain, must have all three characteristics:

  1. Constricting discomfort in chest and/or in adj areas (Jaw, shoulder, arm or back)
  2. Precipitated by physical exertion
  3. Relieved by rest or GTN within 5 minutes
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24
Q

What is atypical angina?

A

Chest discomfort with any 2 of the following:

  1. Constricting discomfort in chest and/or in adj areas (Jaw, shoulder, arm or back)
  2. Precipitated by physical exertion
  3. 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
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25
Q

What is unstable angina?

A

Angina of increasing frequency or severity.

Occurs at rest or Occurs on exertion.

Associated with increased risk of MI

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26
Q

What is stable angina?

A

Angina that is induced by exertion and relieved by rest.

Good prognosis, unlike unstable angina.

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27
Q

What is decubitis angina?

A

Angina (typical or atypical) induced by lying flat.

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28
Q

Causes of Angina?

A

Atheroma (most common)

Anemia
Coronary artery spasm
Aortic stenosis
Tachyarrhythmias 
HOCM
Arteritis and small vessel disease
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29
Q

What are the associated symptoms of angina? (Beside the discomfort, precipitation and relieving factors)

A

Dyspnoea
Nausea
Sweatiness
Fainting

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30
Q

In ACS what is the chest pain like?

SOCRATES

A

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

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31
Q

Causes of ventricular fibrillation?

A

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
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32
Q

Signs of ventricular fibrillation?

A 
Pulseless
And signs of ACS:
Constricting chest pain
Dyspnoea
Cyanosis
Nausea
Sweating
Syncope
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33
Q

Signs of ventricular tachycardia?

A

Heart rate up to 250bpm

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34
Q

What is focal ventricular tachycardia?

A

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

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35
Q

What is re-entrant ventricular tachycardia?

A

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

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36
Q

What is supraventricular tachycardia?

A

A group of arrhythmias with a heart rate of >100bpm at rest, originating in the SAN or AVN.

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37
Q

Which condition does intermittent claudication indicate?

A

Peripheral arterial disease

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38
Q

What is a “strong apical impulse felt over the precordium”?

A

A strong apex beat felt over the thorax immediately in front of the heart.

  • a normal heart finding.
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39
Q

What is vasovagal syncope?

A

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.

  1. Decreased venous return
  2. Decreased left ventricular filling
  3. Reduced baroreceptor stretch
  4. Sympathetic drive increases
  5. Heart beats more rapidly but with reduced blood volume
  6. Increased baroreceptor stimulation from forceful contractions
  7. Increased parasympathetic effects: vasodilation and reduced heart rate.
  8. Brain doesn’t receive high blood flow
  9. Loss of consciousness ensues
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40
Q

What is carotid sinus hypersensitivity?

A

A condition where the carotid sinus response to stretch (massage) is particularly strong and induces syncope.

Treatment = pacemaker with electrodes to ventricle and atria

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41
Q

What is the most common type of hypertension?

A

Essential hypertension is most common (90% of HTN)

Essential hypertension AKA primary hypertension

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42
Q

Which parts of the human anatomy can cause secondary hypertension?

A 
Kidney 
Lungs
Heart
Adrenal glands
Thyroid gland
Parathyroid gland
Adipose tissue 
Blood vessels
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43
Q

Which pathologies can cause secondary hypertension?

Go through body systematically, then exogenous causes

A

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

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44
Q

Which drugs can cause secondary hypertension?

Easier to spot, since date of drug use may correspond to HTN onset

A

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

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45
Q

What are the signs of general hypertension?

General hypertension is a type of secondary HTN

A

Onset is before puberty

No obesity

Severe or resistant HTN

Acute rise (not a slow progression)

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46
Q

What are the signs of coarctation of the aorta?

A

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

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47
Q

What are the signs of hypertensive urgency?

A

Headache

Dyspnoea

Epistaxis

Severe anxiety

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48
Q

What are the signs of a hypertensive emergency?

AKA malignant hypertension

A

Chest pain (LV failure)

Back pain

Vision change (Retinopathy)

Difficulty speaking (Encephalopathy - neurological deficit)

Numbness (Encephalopathy - neurological deficit)

Weakness (Encephalopathy - neurological deficit)

49
Q

What is hypertensive urgency?

A

A type of hypertensive crisis, a complication of hypertension.

Systolic >180 mmhg or Diastolic >110 mmhg

No target organ damage (kidneys, heart, brain)

50
Q

What is a hypertensive emergency?

A

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

51
Q

What are the common cardiovascular differentials for syncope (transient LOC)?

A

ACS

Ventricular arrhythmias

AV block (HB)

Acute AF

CHF

Hypovolaemia

Aortic stenosis

52
Q

What is dyspnoea?

A

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

53
Q

Which physiological mechanisms are orthopnoea caused by?

A

Pooling of blood in the pulmonary vasculature.

Pulmonary oedema.

Orthopnoea - shortness of breath on lying flat

54
Q

What is a bruit?

A

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

55
Q

What is aortic stenosis?

A

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:

  1. M/T valves close - HS 1
  2. Pressure builds in ventricles
  3. A valve pops open - Snap
  4. Crescendo-decrescendo mumur
  5. A/P valves close - HS2
56
Q

Why is aortic regurgitation during diastole?

A

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

57
Q

What is heart failure?

AKA Congestive heart failure

A

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:

  1. HF with preserved LV function - EF >45%
  2. 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:

  1. Something damages the heart’s contractility (Lesion, hypertrophy, ischemia, clot, scar etc)
  2. More blood is left in the heart at the end of systole,less blood is pumped out - SV decreases
    - THIS IS THE HEART FAILURE-
  3. Body wants more blood: SV must increase
  4. The body increases blood returned to the heart (Increase preload) and increases the heart’s force of contraction to increase SV.
    - COMPENSATED HEART FAILURE-
  5. Something happens to the heart to decrease its contractility further (MI, dilation, hypertrophy, scar, lesion etc).
  6. The preload (LV- end diastolic volume/pressure) or the force of contraction can’t be Increased enough to make up for this.
  7. 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-
  8. Pulmonary hypertension occurs = Pulmonary oedema occurs - (cough and fatigue)
  9. This backtracks through the right ventricle and reduces venous return - (ankle/sacral oedema)
58
Q

What are the causes of mitral regurgitation?

A

Rheumatic heart disease (damages leaflets)

Ischemic heart disease (by damage done to papillary muscles)

Valvular vegetations (Endocarditis)

Physiological regurgitation (leaflets grow apart)

59
Q

What is a reentrant arrhythmia?

A

An area of cardiac myocyte that is heterogenous (e.g. lesion or ischemic).

It occurs during the following set of conditions:

  1. 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
  2. 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
  3. 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.

60
Q

What are the signs and symptoms of heart failure?

A

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)

61
Q

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

A

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

62
Q

What are the four most common causes of chronic heart failure?

A

Coronary artery disease

Hypertension

Valvular disease

Myocarditis

Other causes:
1. Infiltrative diseases; amyloidosis, haemochromatosis, sarcoid

  1. Congenital heart diseases
  2. Pericardial disease
  3. Toxin-induced: heroin, alcohol, cocaine, amfetamines, lead, arsenic, cobalt, phosphorus
  4. Infection: bacterial, fungal, viral (HIV), Borrelia burgdorferi (Lyme disease), parasite (e.g., Trypanosoma cruzi [Chagas disease])
  5. Endocrine disorders: diabetes mellitus, thyroid disease, hypoparathyroidism with hypocalcaemia, phaeochromocytoma, acromegaly, growth hormone deficiency
  6. Systemic collagen vascular diseases: lupus, rheumatoid arthritis, systemic sclerosis, polyarteritis nodosa, hypersensitivity vasculitis, Takayasu syndrome, polymyositis, reactive arthritis
  7. Chemotherapy-induced: for example, adriamycin, trastuzumab
  8. Nutritional deficiencies: thiamine, protein, selenium, L-carnitine
  9. Pregnancy: peripartum cardiomyopathy
  10. Familial cardiomyopathy
  11. Tachycardia-induced cardiomyopathy
  12. Pulmonary causes: COPD, pulmonary fibrosis, recurrent pulmonary emboli
63
Q

What is infective endocarditis?

A

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:

  1. Native valve
  2. Prosthetic valve
  3. Device-related
  4. Right-sided (often IVDU)

MOA:

  1. Typically endothelial damage occurs within the heart due to turbulent blood flow.
  2. Platelets and fibrin adhere to the exposed collagen matrix and create a prothrombotic area
    - INFECTION SOURCE INTRODUCED TO BODY-
  3. Bacteraemia causes colonisation of this area
  4. Fibrin deposition and platelet adhesion continues
  5. A mature infected vegetation has grown
  6. Pieces break off and cause stroke or DVT
64
Q

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

A

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

65
Q

What are the differentials for signs of heart failure?

Dyspnoea, cough, fatigue and tiredness

A

COPD

Pulmonary fibrosis

Pneumonia

PE

Cirrhosis

Nephrotic syndrome

Pericardial disease

Venous stasis

DVT

66
Q

What is paroxysmal atrial fibrillation?

A

Episodes of AF lasting:

  • Between 30 seconds and 7 days duration
  • Self terminating
  • Recurrent
67
Q

What is atrial fibrillation?

A

A chaotic and irregular atrial contraction that is a type of supraventricular arrhythmia.

Types: paroxysmal, persistent and permanent

MOA:

  1. Insult to the atria occurs- HTN, MI, Aortic stenosis, LV dysfunction, atrial tachycardia,atrial flutter etc
  2. Atria pressure goes up and they dilate, inflame and fibrose
  3. Dilation;
    - Fractionates mother wave (more re-entrance)
    - Slows conduction (synchronicity decreases)
    - Shortens refractory period (more re-entrance)
  4. Fibrosis slows conduction and increases chances of reentrance
  5. Atria now fire randomly causing twitching instead of proper contractions - fibrillation
68
Q

What are the possible signs and symptoms of atrial fibrillation?

A

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

69
Q

What is persistent atrial fibrillation?

A

Episodes of AF that last longer than 7 days duration

70
Q

What is permanent atrial fibrillation?

A

AF that:

  • Fails to terminate using cardioversion therapy
  • Or is terminated but recurs within 24 hours
71
Q

What is fast atrial fibrillation?

A

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.

72
Q

What is atrial tachycardia?

A

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

73
Q

What is atrial flutter?

A

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.

74
Q

What are the differentials for atrial fibrillation?

i.e. an irregular pulse has been found

A

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

75
Q

What are the causes of atrial fibrillation?

A

Hypertension

HF with/without reduced ejection fraction

Polygenic

Monogenic - cardiomyopathies

Post-operative

Mitral stenosis

Exercise-induced

76
Q

In the case of post-MI regurgitation, which part of the heart is damaged: leaflet, chordae tendineae or papillary muscles?

A

Papillary muscles

77
Q

What are the signs and symptoms of life-threatening haemorrhage?

A

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)

78
Q

What is peripheral vascular disease?

A

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.

79
Q

What are the acute pathological processes of peripheral vascular disease?

A

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

80
Q

What are the chronic pathological processes of peripheral vascular disease?

A

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

81
Q

What are the signs/symptoms of acute limb ischemia in PVD?

A

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

82
Q

If a limb is hot, swollen and tender, could this be an ischemia due to peripheral arterial disease?

A

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

83
Q

What is claudication?

A

Aching muscles during effort:

  • predictable,
  • worse on hills or with loads or at speed
  • settles quickly on rest
84
Q

In peripheral vascular disease, what is rest pain?

A

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.

85
Q

In peripheral vascular disease, a person with Fontaine classification 4 limb ischemia has tissue loss, what constitutes tissue loss?

A

Ulcers

Necrosis

Gangrene

86
Q

What is cerebrovascular disease?

A

Atheroma of the carotid artery (the main supply of the cerebrum).

May present with carotid bruit.

87
Q

How does cerebrovascular disease present?Which conditions will occur?

A

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)

88
Q

What is an aneurysm?

A

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.

89
Q

What is ectasia?

A

Abnormal dilation of an artery that is less than 50% of its normal diameter. (Pre-aneurysm)

90
Q

What is arteriomegaly?

A

Generalised dilation of an artery, unlike an aneurysm which is only in a specific place on the artery.

91
Q

What are the types of cause of aneurysm?

A 
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

92
Q

Which locations in the body do aneurysms occur within?

A

Intracerebral

Aortic - aortic is most common, thoracic is second most common

Visceral

Iliac

Popliteal

93
Q

What is the difference between a fusiform and a saccular aneurysm?

A

Fusiform - general dilatation (uniform) of entire artery

Saccular - asymmetrical dilatation

94
Q

What are the symptoms of an abdominal aortic aneurysm?

A

Asymptomatic

Back pain

Tenderness (over aneurysm)

In the case of rupture:
Limb ischemia

Hypotension

(Warning: Any woman age 10-50 could be pregnant)

95
Q

What are the risk factors for abdominal aortic aneurysms?

A

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

96
Q

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.

A

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.

97
Q

What are the causes of aortic dissection?

A

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

98
Q

What is a type A Aaortic dissection?

A

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.

99
Q

What is a type B Aaortic dissection?

A

Stanford system:

Type B = a dissection on the descending aorta; from the origin of the left subclavian artery onwards/downwards

e.g. abdominal dissection

100
Q

What are the signs/symptoms of an aortic dissection?

A

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

101
Q

Why is a young patient particularly worrying if they are pale, tachycardic and hypotensive?

A

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.

102
Q

What is shock?

A

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.
103
Q

Which physiological parameters can change to give a drop in blood pressure, such as in shock?

A

Change in cardiac output:
1. Reduced heart rate (bradycardia)

  1. Fall in stroke volume
  2. Reduction in vascular tone (vasodilation)
104
Q

What are the four types of shock?

A

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

105
Q

What are the causes of hypovolaemic shock?

A

Haemorrhage

Burns

GI loss: vomiting - diarrhoea - fistula

Dehydration: heat exposure - Polyuria

106
Q

What are the causes of distributive shock?

A

Infection: Sepsis - Pancreatitis

Trauma

Burns

Spinal cord injury

Anaphylaxis

107
Q

What are the causes of cardiogenic shock?

A

MI and myocardial ischemia

Arrhythmia

Acute valve pathology

108
Q

What are the causes of obstructive shock?

A

Tension pneumothorax

Pericardial tamponade

Pulmonary embolism

  • All preventing the heart filling/emptying and the aorta transporting blood
109
Q

Which physiological systems are activated in shock?

A

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

110
Q

Which physiological processes cause the symptoms/signs of hypovolaemic shock?

A
  1. Loss of serum volume = loss of preload
  2. Decreased stroke volume = loss of cardiac output
  3. Heart rate increases and systemic vascular resistance increases to compensate for loss of BP
  4. This causes tachycardia and blood diversion away from peripheries - “heart racing and pale/clammy”
  5. As soon as it can’t compensate, the systolic BP falls - hypotension
  6. RAAS activation prevents urine production - Oliguria
  7. Once decompensated = tissue hypoperfusion - cognitive changes and metabolic acidosis occur
111
Q

In treatment of major haemorrhage, what are the risks of ischemia and ischaemic toxins released on individual organs of the body?

A

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)

112
Q

What is disseminated intravascular coagulation?

A

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.
113
Q

What are the differentials for acute chest pain?

A 
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

114
Q

What are the symptoms of shock?

A

Palpitations

Tachypnoea

Muscle weakness

Cool extremities

Agitation (early shock)

Cognitive decline (late shock or hypoglycaemia)

Cyanosis

115
Q

How are murmurs graded?

A 
1-6:
Barely audible
Faint but immediately heard on auscultation 
Easily heard
Very easily heard with palpable thrill
Very loud
Heard without stethoscope
116
Q

What are the general characteristics of a murmur?

A
  1. Timing - systolic,diastolic or continuous
  2. Location - Heard best at RICS, LSE, Apex (generally)
  3. Radiation - carotid or axilla
  4. Shape - crescendo/decrescendo, decrescendo, uniform, decrescendo/crescendo
  5. Intensity
  6. Pitch
  7. Quality
  8. 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

117
Q

Where is aortic regurgitation best heard?

A

Left lower sternal edge

118
Q

Where is mitral regurgitation best heard?

A

Apex - same as mitral stenosis

Apex is the MITRAL area

[ECG] Conditions, risk factors, signs, differentials, on ecg and xray (39 decks)

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