Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CP1 > cardiology > Flashcards

cardiology Flashcards

1
Q

Describe the characteristic, and contrasting, features of chest pain resulting from myocardial ischaemia

A

Pain similar to angina (retrosternal, crushing, worse with exertion/cold/after food) but more severe and not relieved by GTN spray. Associated with nausea, sweating and vomiting. Patients may experience “angor animi”, a feeling of impending doom.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the characteristic, and contrasting, features of chest pain resulting from aortic dissection

A

Severe tearing pain, felt between shoulder blades. Patient commonly hypertensive or Marfan-oid. Persistent, most severe at onset.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the characteristic, and contrasting, features of chest pain resulting from pleural and respiratory disease

A

Sharp pain, worse on inspiration and coughing. Not relieved by GTN. Not central, may be one sided, no radiation. Often associated with breathlessness or cyanos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the characteristic, and contrasting, features of chest pain resulting from gastro-oesophageal disease

A

GORD will cause a typical “heartburn”, a retrosternal burning sensation after food, relieved by antacids. Oesophageal spasm may be mistaken for MI/angina. It will be relieved with GTN after ~20 minutes, later than the 2 minute relief in angina. The pain will be severe, retrosternal and burning. Often associated with a history of dyspepsia or dysphagia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the characteristic, and contrasting, features of chest pain resulting from musculo-skeletal disease

A

Localised to one location on the chest, tender to palpitation, more sensitive on when moving and respiring.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is a typical history of a patient with acute coronary syndrome?

(symptoms)

A
  • Sever crushing, gripping or heavy chest pain lasting longer than 20 minutes
    • Not relieved by 3x GTN sprays at 5 minute intervals
  • Radiates to the left arm, neck or jaw
  • Associated dyspnoea, nausea, fatigue, sweatiness and palpitations in the elderly or diabetics, who can present later with a variety of symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the clinical features of ACS?

(on examination)

A

Can be variable

  • Sympathetic activation: tachycardia, hypertension, pallor, sweatiness
  • Vagal stimulation: bradycardia, vomiting
  • Myocardial impairment: hypotension, narrow pulse pressure, raised JVP, basal crepitations, 3rd heart sound
  • Tissue damage: low grade pyrexia

Later a pericardial rub and peripheral oedema may develop, or pansystolic murmer due to papillary muscle rupture/ventriculo-septal defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are differential diagnosis of central chest pain from ACS?

(not an objective)

A

Cardiac:

  • Coronary artery spasm
  • Pericarditis/myocarditis
  • Aortic dissection

Non-cardiac:

  • PE
  • Pneumothorax
  • Oesophageal disease
  • Mediastinitis
  • Costochondritis
  • Trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does the spectrum of acute coronary syndromes cover?

A

ST-segment elevation myocardial infarction (STEMI)

Non-ST-segment elevation myocardial infarction (non-STEMI)

Unstable angina (UA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What pathology do all acute coronary syndromes share?

A
  • Atheromatous plaque formation in the coronary arteries
  • Fissuring/ulceration of the plaque leading to platelet aggregation
  • Localised thrombosis, vasocontriction and distal thromboembolism
  • Myocardial ischaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is unstable angina?

A

(aka crescendo angina)

  • Angina occuring at rest, or sudden increased frequency/severity of existing angina
  • Pathologically caused by fissuring of plaques, thus there is a risk of subseuent total vessel occlusion and progression to acute MI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the an acute myocardial infarction?

What are the two different types?

A
  • Occurs followinf full arterial occulsion, with different patterns
  • The diagnosis of MI requires elevations in serum cardiac troponin levels, with additional categorisation based on ECG changes:
    • ST elevation/new left bundle branch block (LBBB) = STEMI
    • No ST elevation/LBBB = NSTEMI (ECG often shows T wave inversion or ST depression)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the time course of an MI?

(not an objective)

0-12 hours

12-24 hours

24-72 hours

3-10 days

10 days - months

A
  • 0-12 hours: infarct not visible, loss of oxidative enzymes
  • 12-24 hours: infarct pale and blotchy , intercellular oedema
  • 24-72 hours: infarcted area excites acute inflammatory response, with dead area soft and yellow with neutophilic infiltration
  • 3-10 days: organisation of infarcted area by vascular granulation tissue
  • 10 days-several months: collagen deposition, infarct replaced by collagenous scar
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does an ECG and serum troponin establish the diagnosis of an ACS?

A

STEMI:

  • ST segment elevation, troponin elevated.
  • Troponin is released at 4-8 hours and peaks at around 24 hours. dectectable for 10 days
  • A release of CK-MB may be an earlier enzyme sign.

NSTEMI:

  • No ST segment elevation, troponin elevated.

Unstable angina:

  • No ST segment elevation, troponin normal.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the management of unstable angina and NSTEMI?

A

(normal A-E)

(asses patient using GRACE score)

BROMANCE

  • Beta-blocker
  • Reassurance
  • Oxygen
  • Morphine
  • Aspirin
  • Nitrates/GTN spray
  • Clopidigrel
  • Exoparin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the management of STEMI?

A

MONA

  • Morphine
  • Oxygen
  • Nitrates (GTN spray)
  • Aspirin

Percutaneous coronary intervention (PCI) is gold standard treatment if available in a timely fashion: door to ballon in 90 minutes, patient transfer advised if intervention can occur within this window

GRACE score as well

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What if PCI are contra-indicated for a STEMI?

What are the conta-indications?

A

Thrombolysis is indicated if PCI not available or there are significant co-morbidities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are contra-indications for thrombolysis?

A
  • haemorrhagic stroke at any time
  • ischaemic stroke within 6 months
  • CNS damage or neoplasm
  • recent trauma (3 weeks)
  • GI bleed within last month
  • known bleeding disorder or aortic dissection.
  • Relative contraindications include pregnancy, liver disease, endocarditis, traumatic CPR, oral anticoagulant therapy, refractory hypertension.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the GRACE score for ACS?

A

Takes into account age, heart rate, blood pressure, class of CHF, renal function, ST segment changes, troponin elevation and whether there was an arrest at admission to give a mortaily risk at various time intervals (usually one for 6 months)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the difference in prognosis between STEMI, non-STEMI and unstable angina with respect to mortality and morbidity

A

6 month mortality in the GRACE registry was 13% for NSTEMI and 8% for UA.

1 month mortality in a community STEMI may be as high as 50%, with 50% of these deaths occurring within 2 hours. Early death may be due to arrhythmia. Of those who reach hospital, 80% survive up to 28 days. Prognosis is worse for anterior infarcts than inferior. Morbidity is likely to be related to the level of ischaemia and myocardial damage sustained.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the potenital short term complications of ACS?

A

Pulmonary oedema:

  • Left heart fails to pump effectively, with poor systolic emptying leading to dilation: ‘a dilated chamber is a failing chamber’
  • The backpressure in the pulmonary veins is reflected into the capillaries, leading to extravasation of low-protein fluid into the alveolar sacs
  • This is a life-threatening emergency, characterised by extreme breathlessness, with sweating and anxiety
  • There may be a cough producing frothy, blood-stained sputum
  • On examination there are signs of acute heart failure with crackles
  • Arterial PO2 falls, and initially PCO2 falls also due to overbreathing, but later the PCO2 rises due to impaired gas exchange

Cardiogenic shock:

  • Carries a high mortality due to the vicious cycle of hypotension causing further reduction in coronary flow, and thus further pump failure ect.

Thromboembolism:

  • Mural thrombus formation over the inflamed area of endocardium can cause emboli to the brain, kidney, gut, lower limbs ect. causing infection

Venticulo-septal defect:

  • Intracardiac rupture may occur through the septum, causing left-right shunt and development of severe LVF if severe

Ruptured chordae tendiae:

  • Leads to mitral valve incompetence

Rupture of ventricular wall:

  • Usually occurs 2-10 days after the infarct, due to re-organisation and softening of the wall
  • This leads to haemopericardium (blood in pericardial sac), cardiac tamponade (compression of the heart due to fluid in pericardium) and rapid death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the potential long term complications of ACS?

A

Heart failure:

  • IHD is the most common cause of left heart failure
  • Often leads to right heart failure

Dressler’s syndrome

  • Immune-mediated pericarditis, associated with a high ESR and sometimes anti-myocardial antibodies
  • Rare, develops 2-10 months after infarction
  • Pericarditis gives a sharp chest pain, exacerbated by movement and lying down - relieved by sitting forward
  • May be a pericardial effusion, leading to dyspnoea if it compresses adjacent bronchi

Ventricular aneurysm formation:

  • Gradual distension of the infarcted part of the ventricular wall, which has been replaced by a collagen scar
  • Aneurysmal rupture will lead to cardiac tamponade and death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe the pathway of care developed within the hospital for STEMI/non-STEMI and unstable angina

A
  • Aspirin 300mg + Clopidogrel 300mg.
  • Sublingual GTN.
  • Oxygen (*if <94%, check NICE guideline).
  • Brief history.
  • IV access and bloods (troponin, FBC, lipids, biochemistry, glucose).
  • 12-lead ECG.
  • IV opiate and antiemetic.
  • Beta-blocker if not contraindicated.
  • GPIIb/IIIa inhibitor if PCI available.

STEMI - “MONA” = Morphine, Oxygen, Nitrates, Aspirin NSTEMI/UA - “BROMANCE” = Beta-blocker, Reassurance, Oxygen, Morphine, Aspirin, Nitrates (GTN), Clopidogrel and Enoxoparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the TIMI scoring system?

A

In patients with UA/NSTEMI, the TIMI risk score is a simple prognostication scheme that categorizes a patient’s risk of death and ischemic events and provides a basis for therapeutic decision making.

  • age>65
  • >3 Cornary artery disease risk factors
  • known CAD (stenosis>50%)
  • aspirin use in last 7 days
  • severe angina
  • ST deviation
  • elevated cardiac markers.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Define stable angina

A

Episodic pain that takes place when there is increased myocardial demand, usually upon exercise, in the presence of impaired perfusion by blood. relieved by rest. Usually fades within minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe the typical history of a patient with stable angina

A
  • Ischaemic pain of the myocardium, varying from a mild ache to a severe pain that provokes sweating and fear
  • The pain is provoked by exercise, especially after meals, in the cold, and if the patient is angry/excited
  • It fades quickly with rest, and in some patients the pain occurs predictably at certain levels of exertion
  • There may be associated breathlessness

Usually no abnormal findings on examination, occasionally a 4th heart sound

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the potenial underlying causes of angina?

A
  • Coronary artery disease
    • causes a decrease in blood flow reaching areas of myocardium
  • Valvular heart disease
    • increases cardiac workload
  • Cardiomyopathy
    • interferes with cardiac contractility
  • Anaemia
    • reduces oxygenation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the causes myocardial ichaemia?

A
  • Reduced perfusion:
    • Atheroma
    • Embolus
    • Thrombosis
    • Spasm or inflammation of coronary arteries
    • Generalised hypotension
  • Reduced blood oxygenation
    • Anaemia
    • Carboxyhaemoglobinaemia
  • Increased tissue demands
    • Increased CO
    • Cardiac hypertrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What clinical signs may be present in chronic stable angina pectoris?

A
  1. Xanthelasmata (cholesterol deposits around the eyes)
  2. tendon xanthoma (cholesterol deposits in the hands/skin)
  3. hypertension
  4. anaemic signs
  5. hyperthyroidism signs
  6. aortic stenosis (ejection systolic murmur radiating into neck)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

List recognised risk factors for coronary artery disease

A
  • Increasing age
  • Male gender
  • Family history
  • Smoking
  • Diet: high fat, low fruit and veg
  • Obesity
  • Hypertension
  • Hyperlipidaemia
  • Diabetes Mellitus
  • type A personality
  • haemostatic factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is coronary heart disease?

A

Also known as ischemic heart disease (IHD), is a group of diseases that includes: stable angina, unstable angina, myocardial infarction, and sudden cardiac death. It is within the group of cardiovascular diseases of which it is the most common type.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Define arteriosclerosis?

A
  • Non-specific thickening and hardening of the walls of arteries causing a loss of contractility and elasticity, and decreased blood flow
  • Often due to prolonged hypertension in smaller arteries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is atheroma?

A
  • Specific degenerative disease affecting large/medium sized arteries
  • When this leads to thickening and hardening of the arterial wall, it is termed atherosclerosis: most common cause of arteriosclerosis affecting large/medium arteries
  • Atherosclerosis reduces tissue perfusion, as well as predisposing to thrombus and aneurysm formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Describe the pathology of atheroma formation

A
  • Damage to the endothelium due to a variety of risk factors allows entry of LDLs into the intima
  • This lipid is taken up by macrophages in the intima, and accumulates excessively as it is able to bypass normal receptor mediated uptake, forming a ‘fatty streak’
  • As the macrophages take up more and more lipid, they release free lipid into the intima
  • The macrophages also stimulate cytokines, which leads to collagen deposition by inflammatory cells, and the intimal lipid plaques becomes fibrotic
  • At this stage it appears raised and yellow, and leads to pressure atrophy of the media and disruption of the elastic lamina
  • Increased secretion of collagen forms a dense fibrous cap to the plaque, which is now hard and white
  • Advanced places also show free lipid as well as lipid in macrophages
  • The endothelium is fragile and often ulcerates, allowing platelet aggregation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What investigations would you do on a patient with suspected angina?

A

Clinical assessment alone can be sufficient to confirm stable angina

  • Exclude other causes: FBC, glucose, lipids, thyroid function test
  • Resting 12-lead ECG: usually normal, may be signs of previous MI (consider aortic stenosis if LVH/LBBB)
  • Then use clinical assessment and ECG findings to estimate the likelihood of CAD using NICE tool:
    • If >90% treat as stable angina
    • If 61-90%, coronary angiography is indicated
    • If 31-60% functional imaging is indicated
      • SPECT myocardial perfusion scan, exercise echo, stress MRI
    • If 10-30% CT calcium scoring is used
      • If <10% investigate for another cause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What drugs are used to treat angina?

A

Symptomatic treatment:

  • GTN spray + B-blocker or calcium inhibitor as first line
  • Combination therapy, or nicorandil for refractory disease

Secondary prevention:

  • Statin
  • Low dose aspirin
  • ACE inhibitor if co-morbid diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What combination therapy is used for refractory disease (doesn’t respond to the 1st line treatment - in this case of GTN spray and b-blocker or calcium channel blocker) of angina?

What shouldn’t never be used?

A

B-blockers and dihydropyridines such as amlodipine are the combination used

NEVER combine a rate-limiting calcium channel blocker and a B-blocker, this can cause asystole (heart stops beating)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How should nitrates be used to treat angina?

Mechanism of action?

Side effects?

A
  • Sub-lingual spray is first line for symptom relief
  • spray under tongue, wait 5 minutes and spray again. If pain after 10 minutes call 999
  • Can be used prior to performing activities that provoke angina
  • They cause marked venorelaxation, thus reducing pre-load on the heart
  • This can cause venous pooling on standing, thus can cause postural hypotension and dizziness
  • They also affect large muscular arteries, reducing aaortic pressure and cardiac afterload, as well as dilating coronary vessels
  • Decreased pre-load and after-load decreases the oxygen requirement of the myocardium and coronary vasodilation leads to increased oxygen delivery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How do B-blockers treat angina? - mechanism of action

Side effects?

A
  • ß1 adrenoceptors are found mainly on the heart, acting to increase heart rate and stroke volume
  • ß2 adrenoceptors act to cause smooth muscle relaxation in many organs, e.g. the trachea
  • In ischaemic heart disease, ß1 selective ß-blockers are used to reduce cardiac rate and force (reduce myocardial oxygen consumption) with little broncho-constrictive effect as possible
  • They also have an anti-hypertensive effect by reducing cardiac output, and decrease renin release from juxta-glomerular cells
  • They also have class two anti-arrhythmic effects

Side effects:

  • Bronchoconstriction: contradiction in asthma, caution in COPD
    Cardiac depression/bradycardia: can be critical if combined with other rate limiting agents
  • Hypoglycaemia: impair the sympathetic warning signs of hypo’s
  • Fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are types of calcium channel blockers? -examples

How do they work?

Side effects?

A
  • Dihydropyridines (amlodipine/nifeipine) or rate-limiting agents (verapamil/diltiazem)
  • All work to prevent smooth muscle contraction, reducing afterload and causing coronary vasodilation
  • The rate-limiting agents also act on cardiac calcium channels in the AV node to control heart rate, exhibiting class IV anti-arrhythmic effects
  • Side effects are:
    • flushing
    • headache
    • Ankle swelling
    • Constipation (GI smooth muscle inhibition)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is Nicorandil and how does it work?

A
  • Causes marked vasodilation
  • It is combinded NO donor and also an activator of ATP-sensitive K-channels on vascular smooth muscle cells, leading to hyperpolarisation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the framingham risk score?

A

The Framingham Risk Score is a gender-specific algorithm used to estimate the 10-year cardiovascular risk of an individual.

Assessment for primary prevention of CHD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is QRISK 2?

A

QRISK2 (the most recent version of QRISK) is a prediction algorithm for cardiovascular disease (CVD) that uses traditional risk factors (age, systolic blood pressure, smoking status and ratio of total serum cholesterol to high-density lipoprotein cholesterol) together with body mass index, ethnicity, measures of deprivation, family history, chronic kidney disease, rheumatoid arthritis, atrial fibrillation, diabetes mellitus, and antihypertensive treatment.

(better than framingham)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What ECG changes may develop during an exercise stress test for patient with angina?

A

Down sloping ST segment depression, T wave inversion. False positives and false negatives are common (20%), though these patients will have good prognosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Describe the typical history of pulmonary oedema

Give symptoms for acute pulmonary oedema as well

A
  • Dysponea (SOB)
  • Paraxysmal noctural dysponea
  • Orthopnea (SOB when lying down): due to increased venous return on lying down, and can be measured objectively by number of pillows required to sleep
  • Cough: producing frothy, blood stained sputum

Acute presentation:

  • Severe dyspnoea
  • Productive cough
  • Anxiety and perspiration
  • Cheyne-Stokes respiration in LVF: cycling apnoea/hyperventilation due to impaired response of respiratory centre to CO2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Describe the pathophysiolgy of pulmonary oedema

(not an objective)

A
  • Pulmonary oedea is due to an increase in fluid in the alveolar wall (pulmonary interstitium), which then affects the interstitial spaces
  • The most common cause is left ventricular failure, which causes increased pressure in the alveolar capillaries and leakage of fluid into the interstitium
  • This leads to subjective dyspnoea, but can remain stable for some time
  • Severe LVF causes leakage of fluid from the interstitium into the alveolar spaces, leading to a severe acute impairment of respiratory function
  • Capillary rupture can lead to leakage of red cells also, which are up taken by macrophages and broken down: macrophages containing iron pigment in the alveoli/interstitium are thus termed ‘heart failure cells’
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the common causes of pulmonary oedema?

A
  • Increased capillary pressure:
    • Cardiogenic: LVF, valve disease, arrhythmias, ventricular septal defect, cardiomyopathy, negatively inotropic drugs
    • Pulmonary venous obstruction
    • Iatrogenic fluid overload
  • Increased capillary permeability
    • Acute respiratory distress syndrome (ARDS)
    • Infection: pneumonia/sepsis
    • Disseminated intravascular coagulation
    • Inhaled toxins
  • Reduced plasma oncotic failure
    • Renal/liver failure: hypoalbuminaemia
  • Lympathic obstruction:
    • Tumour/parasitic infection
  • Others:
    • Neurogenic: raised ICP/head injury
    • PE
    • Altitude
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the clinical feature on examination of pulmonary oedema?

A
  • Tachypnoea
  • Tachycardia, with gallop rhythm
  • Raised venous pressure
  • Peripheral shutdown
  • Widespread crackles/wheezes on auscultation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are differiential diagnosis for pulmonary oedema?

A
  • If no cardiac cause for pulmonary oedema is present, Acute respiratory distress syndrome should be suspected
  • Chest infection may similarly produce a cough but is less likely to give pink frothy sputum and breathlessness
  • Pulmonary embolism typically presents with pleuritic chest pain, cough and shortness of breath
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Outline the general principles of management of pulmonary oedema due to acute/decompensated heart failure

A
  • Sit patient upright, administer 100% oxygen
  • IV diamorphine 1.25-5mg
  • IV furosemide 40mg-80mg
  • GTN spray 2 puffs sublingual (unless systolic BP <90)
  • Continue necessary investigations and history as above
  • If SBP >100, start an IV infusion of nitrate
    • Consider non-invasive ventilation (e.g. CPAP) if not improving
  • If SBP <100, treat as cardiogenic shock, alert ICU
    • May require invasive ventilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What investigations would you do in a patient with acute pulmonary oedema?

What would you expect to find?

A
  • ABG:
    • Initial type 1 respiratory failure due to hyperventilation, with later type 2 respiratory failure due to impaired gas exchange
  • Bloods:
    • FBC, U&E, glucose, D-dimer, CRP
  • CXR:
    • diffuse haziness (‘bat wing oedema’) with Kerley B lines and upper zone vessel enlargement, cardiomegaly pleural effusions
  • ECG:
    • tachycardia, arrhythmia, signs of a cardiac cause
  • Echocardiography:
    • to demonstrate a cardiac cause, e.g. MI/valvular disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

In a cardiac examination of a patient with pulmonary oedema what might you find?

A
  • Tachycardia
  • gallop rhythm
  • bilateral basal crackles
  • shortness of breath
  • cough
  • raised JVP
  • peripheral oedema
  • hepatomegaly may be present
53
Q

What clinical features of common heart murmers may underlie an episode of acute pulmonary oedema?

A

Valvular heart disease may lead to acute heart failure, and thus give pulmonary oedema.

Patients with hypertension may experience episodes of “flash” pulmonary oedema.

54
Q

What would you find on a CXR for a patient with pulmonary oedema?

A
  • Hazy hila
  • prominent vasculature (especially superiorly)
  • fluid in the fissures
  • Kerley B-lines.
55
Q

Define cogestive cardiac failure

A

Congestive cardiac failure is a failure of both sides of the heart, failure being defined as an inability of the heart to act as a pump to sufficient levels to perfuse metabolic tissues adequately.

56
Q

What are the common causes of congestive cardiac failure?

A

The main causes include:

  • Ischaemic heart disease (35-40%)
  • Dilated cardiomyopathy (30%)
  • hypertension (20%)

Rarer causes include infection, valvular heart disease (poor ventricular filling (AV stenosis) or ventricular overload (regurgitation)), congenital heart disease (septal defect → overload), alcohol and drugs, arrhythmias (AF, tachymyopathy, CHB), pericardial disease and hyperdynamic circulation (anaemia, hyperthyroid, haemochromatosis).

57
Q

Cardiac output is a function of ……

A

Cardiac output is a function of the pre-load (is pressure ont the ventricular wall prior to wall contraction/end of diastole), afterload (the pressure in the wall of the left ventricle during ejection/contraction - end of sytole) and myocardial contractility, which interact in a complex way as described by Starling’s law

58
Q

Describe a typical history of a patient with cogestive cardiac failure

(4 stages)

A

New York Heart Association (NYHA) classification:

  • Stage 1: Disease present, no undue dyspnoea from normal activity
  • Stage 2: Dysponea present on ordinary activities
  • Stage 3: :Less then ordinary activity causes dysponea, which is limiting
  • Stage 4: Dysponea present at rest, any activity causes discomfort

Typical symptoms include exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea and fatigue. It may be associated with weight loss (cardiac cachexia) caused by a combination of anorexia, poor tissue perfusion and reduced exercise tolerance (wasting of disuse)

59
Q

What are the typical clinical fndings for a patient with congestive heart failure?

A
  • Jugular venous distension (raised JVP)
  • Hepatomegaly/ascites
  • Dependent pitting oedema
  • Pleural effusions
  • Cardiomegaly
  • gallop rhythm
  • 3rd heart sound
  • Bibasal course crackles
60
Q

Why can congestive heart failure cause the syndrome of ‘cardiac cachexia’?

A
  • Life-threatening weight loss due to a combination of heatomegaly (nausea and decreased appetite) and increased metabolic demands
61
Q

What is the recommened long-term management of congestive heart failure?

A

Confirmed diagnosis of LV dysfunction:

  • Lifestyle advice
  • ACEi + ß-blocker as first line
  • Diuretic if symptomatic oedema
  • Spironolactone/ARTA/hydralazine plus nitrate second line
  • Dioxin thrid line
62
Q

First line treatment for congestive cardiac failure is an ACE inhibitor and beta-blocker.

How should it be given?

Examples?

Mechanism of action?

Contracindications?

Side effects?

A

ACEi usually introduced first, with b-blockers added when stable

ACE inhibitors: -pril

  • E.g. ramipril, captopril, lisinopril
  • Low dose should be used and titrated upwards
  • Work to reverse the neurohormal adaption (RAAS) in CCF (angiotensin converting enzyme inhibitor)
  • Not to be used with NSAIDs (renal risk)
  • Not to be used with patients with low bp - systolic below 100 (risk of severe hypotension)
  • Side effects:
    • Renal - monitor urea, creatinine and K+ before and during treatment
    • Risk of first dose hypotension
    • 10% of pts develop dry cough

Beta-blockers: -olol

  • E.g. metoprolol, bisoprolol, nebivolol
  • Ued to block the sympathetic activity that causes maladaptation - also has antiarrhythmic effects
  • By reducing sympathetic drive symptoms initally become worse so use low dose and titrate up
  • Contra-indicated in asthma - caution with COPD
63
Q

Why are diuretics used for CCF?

what ones are used?

A
  • For symptomatic relief of oedema, but also ventilate
  • Thiazides (bendoflumethiazide) are used in failure or in elderly patients
  • Loop diuretics (furosemide) are used especially in pulmonary oedema
64
Q

What investigations should be done in a patient with suspected congestive heart failure?

A
  • Bloods:
    • FBC, LFT, U&Es, Thyroid functions tests, cardiac enzymes in acute failure
  • B-type natriuretic peptide (BNP): a normal level will exclude heart failure, so a good screen for breathlessness in general practice
  • CXR:
    • cardiomegaly and pulmonary oedema
  • ECG:
    • signs of ischaemia, hypertension or arrhytmias
  • Echo:
    • if ECG or BNP are abnormal
    • Gold standard for diagnosis
    • Ejection fraction <45% diagnostic
65
Q

On examination of a patient with CCF what might you find?

A
  • Hepato- and cardio-megaly may be present
  • bilateral basal crackles
  • SOB
  • gallop rhythm
  • S3 (3rd heart sound)
  • elevated JVP
  • peripheral oedema
  • ascites
  • tachycardia.
66
Q

Outline the importance of daily monitoring of weight in assessing response to diuretic treatment

A

It is important that patients do not lose weight too rapidly. A weight loss of around 0.5-1kg per day may be optimal, and weight loss may be an indicator of decongestion. It is important not to drop a patient’s weight too quickly as that may push them into kidney failure. Simultaneously electrolyte balance should be monitored.

67
Q

Classify the causes of valvular heart disease

A

Infective:

  • Inflammation of the endocardium of heart valves (valvulitis) can result from immune mediated damage (e.g. in acute rheumatic fever) or direct infection (e.g. bacterial/fungal endocarditis)
  • Valvular inflammation has two important consequences:
    • Collagen exposure and thrombus development in the short-term
    • Post-inflammatory scarring, leading to long-term functional impairment
  • Left sided heart valves are more freuently the site of endocarditis, thus emboli from valve thrombosis classically produces infarcts in systemic organs
  • Most common cause of chronic heart valve scarring is rheumatic fever - immune disorder

Congenital:

  • Aortic stenosis is commonly due to calcification of a congenital bicuspid aortic valve

Ischaemic:

  • Mitral regurgitation is often caused by papillary muscle dysfunction post-infarction
68
Q

The most common cause of chronic heart valve scarring is rheumatic fever. What is rheumatic fever and how does it cause heart valve scarring?

A

It is an immune disorder that occurs in children, usually following tonsillitis/pharyngitis caused by group A ß-haemolytic streptococci (GAS)

  • There is antibody production to GAS, yet these antibodies cross-reat with cardiac antigens to cause a self-limiting myocarditis/pericarditis
  • Although this is self-limiting, there is damage to heart valves that heals by progressive fibrosis of the valve leaflets and chordae tendinae
  • This leads to shrunken, fibrotic valve leaflets, often secondary calcification
  • If there is no convincing history of rheumatic fever, the term ‘post inflammatory scarring’ is used instead
69
Q

List the different types of murmers you can get

Are they systolic or diastolic?

A

Left hand side (oxygenated side_:

  • Aortic stenosis - systolic murmer
  • Mitral regurgitation - systolic murmer
  • Aortic regurgitation - diastolic murmer
  • Mitral stenosis - diastolic murmer

Right hand side:

  • Tricuspid regurgitation - systolic murmer
  • Pulmonary stenosis - systolic murmer
  • Tricuspid stenosis - diastolic murmer
  • Pulmonary regurgitation - diastolic murmer
70
Q

Mitral stenosis - diastolic murmer

What is it?

Where is it best heard?

Causes?

Pathophysiology?

A

Mitral stenosis is a valvular heart disease characterized by the narrowing of the orifice of the mitral valve of the heart.

Mitral valve murmers are best heard with the patient on their left hand side

Causes:

  • Post inflammatory scarring: history of rheumatic fever

Pathophysiology:

  • The LA is unable to empty, leading to pulmonary hypertension
  • The LA becomes dilated and hypertrophies
  • Pulmonary hypertension leads to RHF (cor pulmonale - an alteration in the structure and function of the right ventricle)
71
Q

Mitral stenosis - diastolic murmer

Symptoms and sign?

A

Symptoms:

  • Dysponea & haemoptysis: pulmonary hypertension
  • Fatigue, weakness and abdominal/lower limb oedema: Right heart failure
  • Palpitations: secondary AF

Signs:

  • Malar flush: dusky discolouration in malar distribution, due to vascular stasis
  • Small volume regular pulse, or irregular irregular (AF)
  • Jugular vein distension (RHF)
  • Left parasternal heave, due to RV hypertrophy (aka right ventricular heave)
  • Ausculation: ‘Rumbling’ mid-diastolic murmer heart loudest at apex, just prior to systole (also a loud first heart sound and ‘opening snap’
72
Q

Mitral regurgitation - systolic murmer

What is it?

Where is it best heard?

Causes?

A

Mitral regurgitation a disorder of the heart in which the mitral valve does not close properly when the heart pumps out blood.

Best heard with the patient on their left hand side

Causes:

  • ​Post-inflammatory scarring: commonly rheumatic
  • Post-infarction papillary muscle dysfunction
  • LV dilation: i.e. in LVF hypertrophic cardiomyopathy
  • Mitral prolapse: floppy mitral valve syndrome
73
Q

Mitral regurgitation - systolic murmer

Signs and symptoms?

A

Symptoms:

  • Palpitations: increased stroke volume/AF
  • Dyspnoea/orthopnoea: pulmonary hypertension
  • Fatigue: reduced cardiac output
  • Features of RHF/CCF

Signs:

  • ​Laterally displaced apex beat with a systolic thrill
  • Auscultation: Pansystolic murmer at apex radiating into the axilla
    • Alo a soft first heart sound and prominent third heart sound (due to sudden rush of blood into dilated LV in diastole if decompensated)
  • Signs of CCF develop in later disease
  • AF can develop but is less common than in mitral stenosis
74
Q

Aortic stenosis - systolic murmer

What is it?

Causes?

Pathophysiology?

A

Aortic stenosis is a narrowing of the aortic valve in the heart.

Causes:

  • Calcification of congential bicuspid valve: most common
  • Post-inflammatory scarring: rheumatic fever
  • Senile calcific degeneration: no known cause

Pathophysiology:

  • Progressive outflow obstruction leads to left ventricular hypertrophy, which may lead to angina
  • There is a risk of sudden cardiac death due to arrhythmias, and without surgical intervention prognosis is poor with death in 2-3 years
75
Q

Aortic regurgitation - diastolic murmer

What is it?

Causes?

A

Aortic regurgitation is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during ventricular diastole, from the aorta into the left ventricle.

Causes:

  • Post-inflammatory scarring
  • Infective endocarditis
  • Age-related calcification
  • Dilation of the aortic root to inflammatory diseae (syphilis, aortic stenosis)
76
Q

Aortic regurgitation - diastolic murmer

Signs and symptoms?

A

Symptoms:

  • Usually asymptomatic until acute left ventricular failure
  • Symptoms may include angina pectoris (due to low diastolic BP) and dyspnoea if present

Signs:

  • Bounding/collapsing pulse
  • Wide pulse pressure (e.g. 140/40)
  • Auscultation: early diastolic murmer with a ‘decresendo’ quality
  • Signs of LVF

Certain other signs may be present in very severe disease:

  • Quinke’s sign: capillary pulsation in nail beds
  • De Musset’s sign: head nodding with each heartbeat
  • Duroziez’s sign: murmer on the femoral arteries if pressure applied distally
  • Pistol sht femorals: sharp bang in time with the heartbeat if femorals auscultated
77
Q

Are pulmonary/tricuspid disease more rare than mitral/aortic disease?

What is pulmonary/tricuspid disease most commonly due to?

A

Yes

Most commonly caused by post-infalmmatory scarring in rheumatic disease, endocarditis associated with IV drug users, or carnoid syndrome can lead to pulmonary stenosis. Right-sided murmers are all louder on inspiration

78
Q

What would you find on examination including auscultation of patients with heart valve disease?

A

Mitral stenosis

  • mitral facies/flush, small volume pulse (possibly AF), raised JVP, thrill and heave, mid-diastolic rumble murmur.

Mitral regurgitation:

  • laterally displaced, diffuse apex beat, pansystolic murmur, prominent 3 rd heart sound, signs of right sided heart failure and pulmonary congestion, AF.

Aortic stenosis:

  • small volume, slow rising pulse, sustained/thrusting apex beat, aortic thrill, ejection systolic murmur radiating to carotids (crescendo/decrescendo). 

Aortic regurgitation:

  • Bounding or collapsing pulse. Quincke’s sign (pulsatile nailbeds), De Musset’s sign (head nodding), Duroziez’s sign (pistol shot femorals), Mueller’s sign (pulsatile uvula), Corrigan’s sign (prominent carotids), Hill’s sign (higher BP in legs), laterally displaced, forceful apex beat, and high pitched diastolic murmur.
79
Q

How can you differentiate between systolic and diastolic murmurs?

A

Systolic murmur occurs between first and second heart sounds, Diastolic occurs after second heart sound. Feeling the pulse will allow to establish which sound is S1.

80
Q

How can you diagnose common mitral and aortic murmurs and their common causes

A
  • Aortic Stenosis: Ejection systolic murmur radiating to the carotids (age-related calcification)
  • Aortic Regurgitation: Early diastolic decrescendo murmur
  • Mitral Stenosis: Mid-diastolic murmur (Rheumatic fever)
  • Mitral Regurgitation: Pan-systolic murmur
81
Q

Define infective endocarditis

What are the two broads groups of cases?

A

Infective endocarditis is an infection of the endocardial surface of the heart

A fever and new murmer is infective endocarditis until proven otherwise

There are 2 broad groups of cases:

  • Patients with a structural abnormality of the heart e.g. valve disease, valve replacements or congenital cardiac defects
    • Insidious onset, caused by normal GI/skin commensals that enter the blood in trivial episodes of bacteraemia, then become emeshed in platelet aggregates on abnormal endcardium and proliferate
  • Patients with strucurally normal heart valves
    • Acute, fulminating presentation with pathogenic organisms that directly invade the valve, seen in IV drug addicts, after open heart surgery or following septicaemia

Most common bacteria is streptoccus viridans, with staph aureus and strep epidermis also seen

82
Q

Describe the classical presentation of a patient with infective endocarditis

A

Acute febrile plus a new murmer

May present with insidiou illnes (malaise, lethargy, anorexia, arthralgia)

Other presentations may be with distal infarctions or AKI due to immune complex deposition

83
Q

What clinical features would there be on examination of a patient with infective endocarditis?

A
  • Fever + changing/new heart murmer
  • Microscopic haematuria (70%)
  • Splenomegaly (40%)
  • Osler’s nodes (15%)
    • Tender red nodules in the finger due to immune complex deposition
  • Clubbing (10%)
  • Splinter haemorrhages (10%)
  • Roth spots (5%)
    • pale areas with surrounding haemorrhage on the retina
  • Janeway lesions
    • Painless plamar/plantar macules
  • Petechial rash
  • Digital infarcts
84
Q

What are the common infecting organisms for infective endocarditis?

A
  • Streptococcus viridans (most common)
  • Staph aureus
  • Strep epidermis
85
Q

What morphological changes would be seen on an affected heart valve with infective endocarditis?

What complications may there be?

Describe for acute infective endocarditis and subacute infective endocarditis

A

Acute infective endocarditis:

  • Bacterial proliferation in the valve leads to necrosis of the valve tissue, with rapid perforation of the valves, leading to acute cardiac failure

Subacute infective endocarditis:

  • As the infective organisms are poorly virulent, there is very gradual onset destruction of the valves
  • Stimulation of thrombus formation leads to systemic and the persistant low grade inflammation leads to immunological phenomena

Complications:

  • Systemic emboli (or pulmonary abscesses in right sided disease)
  • Valvular incompetence and congestive cardiac failure
  • Glomerulonephritis
86
Q

What investigations need to be done for a patient with suspected infective endocarditis?

Why?

A
  • Bloods:
    • FBC (may show a mild normochromic normocytic anaemia and polymorphonuclear luecocytes)
    • U&Es (commonly show renal dysfunction, urine frequently shows protein and blood content)
    • CRP/ESR (raised in any infection, but may be useful to show reponse to therapy)
  • Cultures:
    • key diagnostic investigation in infective endocarditis​
    • take 3 sets at different times and sites
  • Urinalysis:
    • Look for proteinuria and microscopic haematuria
  • ECG:
    • at regular intervals, may be MI due to emboli or conduction defects
  • Transthoracic echocardiography:
    • can elicit vegetations and abscesses​
    • In all patients, but negative echo does not rule out endocarditis
87
Q

How is the diagnosis infective endocarditis made?

A

Duke major criteria:

  • Positive culture (typical organism in two cultures)
  • Endocardial involvement on echo (vegetations, abscess, new regurgitation)

Duke minor criteria

  • Predisposition
  • Fever >38
  • Vascular immunological signs
  • Culture/echo positivity not sufficient for ‘major’ criteria

Diagnosis can be made if there are two major, or one major and three minor criteria

88
Q

Outline the antibiotic regimen used to treat endocarditis

A
  • The location of infection means long courses of antibiotics (4-6weeks) are required.
  • Empirical therapy is with benzypenicillin, gentamicin and flucoxacillin if acute, IV for 4 weeks
  • Most patients should respond within 48 hours of appropriate antibiotic therapy, signalled by a reduction in fever and decreases in inflammatory markers CRP and ESR.
  • If relief does not occur, certain prospects need to be considered: PE, Abscess/extensive infection, drug reaction, other nosocomial infection.
89
Q

Describe the indications for surgery

A

Factors balancing the scales against and for surgery include:

  • age
  • co-morbidities
  • presence of prosthetic material
  • cardiac failure
  • organism
  • vegetation size
  • valvular obstruction
  • perivalvular infection
  • worsening disease
  • systemic embolization
90
Q

How would you interpret an ECG?

The steps

A
  1. Determine rate
    • 300/no. of large squares
  2. Determine rhythm
    • Sinus rhythm = each P wave followed by QRS, constant PR interval
  3. Determine cardiac axis
    • Normal = I & II postive
    • Right axis deviation = I negative, III positive
    • Left axis deviation = II & III negative
  4. Assess P waves
    • Peak/tall in right atrial hypertrophy
    • Notched/broad in left atrial hypertrophy
  5. Assess PR interval
    • Time from beginning of the P wave to the beginning of QRS
    • The normal range in 0.12-0.2 sec (3-5 small squares)
    • If longer than 0.22s; first degree heart block
  6. Assess the QRS complex
    • QRS width: wider than 120ms = ventricular origin/bundle branch block
    • QRS height: tall R waves in V1 = Right ventricular hypertrophy, tall R waves in V6 = left ventricular hypertrophy
  7. Assess the ST segment
    • Elevation in MI/pericarditis
    • Depression in ischaemia/digoxin
  8. Assess for pathological T wave inversion
    • T wave inversion in aVR, III and V1/2 can be normal
  9. Assess for Q waves
    • Q waves indicate old infarction - normal in LV leads: I, VL, V5/6
  10. Assess the QT interval
    • From beginning of QRS to end of the T wave
    • Normal is <0.45s, approx. 2 large squares
91
Q

How should you correctly set up an ECG machine?

A
  • Skin must be clean and dry
  • V1/2 are positioned in the 4th intercostal space either side of the sternum
    • Palpate the angle of Louis, and the 2nd intercostal space is adjacent
  • V4 is positioned in the 5th intercostal space, mid-clavicular line
  • V3 is placed between V2 and V4
  • aVR and aVL go on right and left arms respectively
  • aVF goes on the left ankle
  • There is a neutral lead that is placed on the right ankle
92
Q

Why is the ECG trace pattern the way it is?

Why are the waves where they are?

How does it work?

A
  • Myocardial contraction causes fibre depolarisation, which is detected by electrodes on the body
  • The ECG trace should represent the normal electrical activity of the heart;
    • SAN ⇒ atrial depolarisation ⇒ AVN delay ⇒ septal depolarisation ⇒ ventricular depolarisation via bundle of His
  • If the electrical activity starts at the SAN, the heart is described as being ‘sinus rhythm’ i.e. a ‘P wave’ is present, representing atrial depolarisation
  • Depolarisation of the larger mass of the ventricles causes the much larger ‘QRS complex
  • The T wave then represents the repolarisation of the ventricular mass back to its resting state
93
Q

Describe the QRS complex

Abnormalities?

A
  • If the first deflection is downward, then it is a ‘Q’ wave
  • The first upward deflection is always the’R’ wave (regardless of if there has been a Q wave)
  • Any deflection below baseline following the R wave is the S wave
  • QRS is usually <120ms, and if this is prolonged it represents bundle branch block or depolarisation from a ventricular focus
94
Q

How should the T wave be seen on an ECG?

What are T wave abnormalities and causes?

A
  • The T wave is normally inverted in aVR, III and V1/2
    • Sometimes V3 in black people
  • Otherwise, T wave inversion may represent several pathologies:
    • Ischaemia
      • Occurs in both STEMI and NSTEMI
      • T waves become inverted over 24-48h, often permanent
    • Ventricular hypertrophy
      • In leads looking at the involved ventricles
    • Bilateral bundle branch block
    • Digoxin treatment
      • Also causes classical sloped ST segments
95
Q

What ST abnormalities in an ECG tracing can occur?

What do they mean?

A
  • The ST segment should be ‘isoelectric’, i.e. at the same level as the part between the T wave and the next P wave
  • ST elevation indicates acute myocardial injury; either a recent infection or due to pericarditis
    • Pericarditis is not localised and thus it causes ST elevation in most leads
  • ST depression is usually a sign of ischaemia rather than MI
96
Q

What is a branch block?

How is it seen on an ECG trace?

A
  • The depolarization waves reaches the septum normally, so PR interval is normal, yet there is abnormal conduction through left/right bundle branches (of His)
  • Delayed depolarization of the ventricles thus leads to a wide QRS (>120ms)
97
Q

What happens in a Right bundle branch block?

How is it seen on an ECG trace?

A
  • The septum is depolarized from the left side as normal, causing an R wave in V1 and a small Q wave in V6
  • Excitation on the left ventricle causes an S wave in V1 and R wave in V6
  • As it takes longer for excitation to reach the right ventricle, this depolarises after the left, causing a second R wave (R1) in V1, and a deep S wave in V6
  • RBBB is best seen in V1 (RSR1)
    • Ma_rr_oW: ‘M’ shape in V1, ‘W’ shape in V6

https://lifeinthefastlane.com/ecg-library/basics/right-bundle-branch-block/

98
Q

What happens in a left bundle branch block?

How is shown on an ECG trace?

A
  • The septum will depolarize from right to left, causing Q wave in V1 and an R wave in V6
  • The right ventricle is depolarised before the left ventricle, so there will be a small R wave in V1 and an S wave in V6 (although this often will appear only as a notch)
  • Subsequent depolarization of the left ventricle causes an S wave in V1 and another R wave in V6
  • LBBB is associated with T wave inversion in the lateral leads (I, VI and V5/6 altough not necessarily in all of these)
  • LBBB is best seen in V6 (‘broad ‘M’ complex), and the ‘W’ pattern in V1 is often not fully developed
    • ‘WilliaM’: ‘W’ shape in V1, ‘M’ shape in V6

https://lifeinthefastlane.com/ecg-library/basics/left-bundle-branch-block/

99
Q

What does the PR interval show?

What if it is shorter in length?

A
  • Time from the start of P to the start of the QRS complex
  • Represents the time taken for excitation to spread from the SAN to the ventricular muscle
    • Time is mostly made up of AVN delay
  • If <220ms, this indicated there may be heart block
100
Q

Where is the ST segment?

What may changes show?

How big must these changes be?

A
  • Interval between the end of the S wave and the beginning of the T wave
    • Changes may represent myocardial ischaemia
  • ST elevation must be >2mm in a chest lead, >1mm in a limb lead, on two leads to be significant
101
Q

Where is the QT interval?

What can cause a prolonged QT interval?

What may this cause?

A
  • Time from the start of Q to the end of T
  • Varies with heart rate but can be prolonged by drugs/electrolyte abnormalities
  • A prolonged QT interval may lead to ventricular tachycardia
102
Q

The ECG is made up of 12 characteristic ‘leads’ that view the heart from different directions. What are the directions of each lead?

A
  • The six limb leads (I, II, III, VR, VL, VF) look at the heart in a vertical plane
    • aVR: right ventricle
    • aVL, I: left heart surface
    • II, III & aVF: inferior surface
  • The six V (chest leads - V1-6) look in a horizontal plane
    • V1/2: right ventricle
    • V3/4: septal area
    • V5/6: left ventricle
103
Q

What are signs of normal axis, right and left axis deviation?

A

Normal = I & II positive

RAD = I negative, III positive

LAD = II & III negative

104
Q

What may cardiac axis deviations be a sign of?

A

Axis deviations are not significant in themselves, yet their presence should alert to look for other signs of left or right ventricular hypertropy or other causes such as pulmonary embolus (right axis deviation) or conduction defects (left axis deviation)

105
Q

What is heart block?

A

Abnormal conduction from the SAN to the ventricles

106
Q

What is first degree heart block?

How is it seen on an ECG?

What can it indicate?

A
  • First-degree atrioventricular block is a disease of the electrical conduction system of the heart in which the PR interval is lengthened beyond 0.22 seconds.
  • PR interval >0.22 seconds
  • First degree heart block is not patholigical in itself but can indicate:
    • Coronary artery disease
    • Acute rheumatic fever
    • Electrolyte disturbances
    • Digoxin toxicity
107
Q

What is first degree heart block?

What are the variations of it?

How is it seen on an ECG?

What can it indicate?

A
  • Second-degree atrioventricular block is a conduction block between the atria and ventricles. Excitation intermittently fails to pass through the AVN or bundle of His
  • There are 3 variations:
    • ‘Mobitz type 2’ phenomenon: constant PR interval yet sometimes there is atrial contraction without ventricular contraction
    • ‘Wenckebach’ phenomenon: progressive PR lengthening until an atrial beat is not concluted, and then this cycle repeats
      • Also known as Mobitz type 1
    • 2:1/3:1 conduction: twice as many P waves as QRS complexes

https: //lifeinthefastlane.com/ecg-library/basics/mobitz-2/
https: //lifeinthefastlane.com/ecg-library/basics/wenckebach/

108
Q

What is complete/third degree heart block?

How is it seen on an ECG trace?

What happens to ventricle contraction?

What can cause 3rd degree heart block?

A
  • Atrial contraction is normal but no beats are conducted to the ventricles
  • P waves will be dissociated from the QRS complexes
  • The ventricles are excited by a ‘slow escape mechanism’ from a depolarising focus within the ventricles, giving a wide QRS
  • Can occur acutely following MI or be a chronic state (the chronic state indicates conducting tissue disease)
109
Q

How is sinus bradycardia defined?

How is sinus tachycardia defined?

A

Sinus bradycardia <60 beats per min

Sinus tachycardia >100 beats per min

110
Q

Non-sinus rhythms:

Where can they occur in heart from?

How do they differ on an ECG?

A
  • Abnormal rhythms begin in one of 3 places: atrail muscle, ventricular msucle or AVN (nodal or junctional rhythm)
  • Sinus artial and junctional rhythms are know as ‘superventricular’ and in these the QRS complex is normal as the depolarization spreads to the ventricles in the usual way via the bundles
    • Sinus rhythms give a normal P wave
    • Atrial rhythms give an abnormal P wave
    • Junctional rhythms will not show P waves
  • Ventricular rhythms on the other hand give wide (slower spread of depolarization throigh the ventricles) and abnormal QRS complexes
111
Q

What is an extrasystole?

A
  • If any part of the heart depolarizes quicker than it sound, and this is accompanied by an extra heart beat, this is termed an extrasystole
112
Q

What is supraventricular tachycardia?

4 main types?

Symptoms?

A
  • Supraventricular tachycardia is an abnormally fast heart rhythm (>100) arising from improper electrical activity in the upper part of the heart
  • There are four main types:
    • atrial fibrillation
    • paroxysmal supraventricular tachycardia (PSVT)
    • atrial flutter
    • Wolff-Parkinson-White syndrome
  • Symptoms may include palpitations, feeling faint, sweating, shortness of breath, or chest pain
113
Q

Describe atrial fibrilation?

What is seen on an ECG?

Symptoms of AF?

A
  • Irregular baseline with no P waves
  • The AVN is bombarded and thus will depolarize irregularly, leading to ventricular contraction at an irregular rate;
    • Usually 450-600 atrial contractions per minute
    • Normal QRS as conduction from the AVN is not abnormal
  • Can be asymptomatic, or present with dyspnoea, palpitations, syncope, chest pain or stroke/TIA
114
Q

Describe atrial flutter?

What is seen on an ECG?

Similarities and differences with atrial fibrilation?

A
  • If the atrial rate is above 250/min and no flat rate baseline between P waves exists, atrial flutter is present
    • Normally 300-450 contractions per minute
    • Classic ‘saw-toothed’ baseline
  • It can be thought of similar to atrial fib. in that the normal co-ordination of the atria is lost, however some element of synchronicity still exists
115
Q

Compare atrial fibrilation and atrial flutter on an ECG

A
116
Q

What is Wolff-Parkinson-White (WPW) syndrome?

What is seen on an ECG?

A
  • Wolff–Parkinson–White syndrome (WPW) is a disorder due to a specific type of problem with the electrical system of the heart which has resulted in symptoms.
  • Some people have an accessory conducting bundle alongside the bundle of His, usually in the left hand side of the heart, and unconnected to the AVN
  • As there is no AVN delay, ‘pre-excitation’ occurs with a short PR interval and the QRS shows an early, alurred upstroke called a ‘delta wave’
  • The second part of QRS is normal as the bundle of His conduction catches up
  • The ECG rhythm is sinus, but there is right axis deviation, short PR interval and widened QRS with ‘delta wave’ of pre-excitation
  • The obnly clinical significance of this is that it can cause paroxysmal supraventricular tachycardia
117
Q

What is ventricular tachycardia?

How is it seen on an ECG?

A
  • Ventricular tachycardia is a type of regular and fast heart rate that arises from improper electrical activity in the ventricles of the heart

ECG:

  • Wide, abnormal QRS seen in all 12 leads
  • Potential to transform to VF
118
Q

What is ventricular fibrillation?

How is it seen on an ECG?

A
  • Ventricular fibrillation is when the heart quivers instead of pumping due to disorganized electrical activity in the ventricles
  • It is a type of cardiac arrhythmia Ventricular fibrillation results in cardiac arrest with loss of consciousness and no pulse

ECG:

  • No QRS can be identified and the ECG is totally disorganised
  • The patient will have lost consciousness
119
Q

Describe the ECG features of STEMI and the changes over time

A

ST elevation, then Q wave and T wave inversion begin to develop, Q wave grows larger then stays large, T wave inverts a long way and then reverts a slight way (to be less inverted).

120
Q

Where are the common anatomic locations of deep venous thrombosis?

A
  • Occur in the deep veins of the leg, orginating around the valves
  • The most common veins to thrombose are the:
    • anterior tibial
    • posterior tibial
    • perineal
    • superficial femoral
    • popliteal vein
121
Q

What are risk factors for venous thrombosis?

A

Venous thrombosis often occurs in normal vessels, thus statsis and hypercoagulability factors are the main risk factors:

  • Age/immobility
  • Pregnancy/OCP
  • Malignancy
  • Obesity
  • Surgery
  • Previous DVT
122
Q

What is the Well’s score?

A

The Well’s score can refer to either:

  • DVT probability scoring for diagnosing deep vein thrombosis OR
  • Pulmonary embolism probability scoring for diagnosing pulmonary embolism

Wells criteria include the major risk factors and symptoms associated, and ask if another diagnosis is likely, to sort patients into high and low risk groups. Criteria include: active cancer, bedridden >3 days/major surgery, calf swelling >3cm compared to other leg, visible collateral veins, entire leg swollen, localised tenderness, pitting oedema (greater in symptomatic leg); paralysis/paresis/recent cast and previously documented DVT.

The maximum score is 9. A Wells’ score higher than one should raise clinical suspicion of DVT.

123
Q

What are the clinical features of a deep vein thrombosis?

A

Most DVTs are silent.

Classical clinical features:

  • Calf tenderness & firmness
  • Oedema
  • Erythema & Calor
  • Distension of superficial veins
  • Superficial thrombophlebitis (tender, erythematous, palpable superficial vein)
  • Homan’s sign (pain on dorsiflexion of the ankle, however this is unreliable and should not be tested for as it may dislodge the thrombus)

Some atypical presentations: ilio-femoral thrombosis can prevent severe pain, complete occlusion of a large vein can lead to cyanotic discolouration

124
Q

What investigations would you do for a patient with a suspected DVT?

What do they show?

A
  • D-dimer:
    • D-Dimers are breakdown products of fibrin – and therefore formed by the process of fibrinolysis.
    • Highly sensitive - 80% (although not specific for DVT - increased in infection, pregnancy, malignancy and post-op)
    • Used to rule out DVT if negative combined with a low pretest clinical probability
  • Compression USS
    • Non-collapsing veins indicate presence of DVTs
  • Thrombophilia screen
    • Do prior to commencing anticoagulant therapy if there are no predisposing factors
125
Q

How can acute arterial ischaemia be differentiated from chronic venous insufficiency?

How can they both be differentiated from cellulitis?

A

Acute arterial ischaemia

  • may be identified by the 6 Ps (pain, pallor, parasthesia, paralysis, pulseless, cold)

Chronic venous insufficiency

  • will show VVV LAPS (varicose veins, venous ulcers, venous stars, lipodermatosclerosis, atrophy blanche, pitting oedema, scars).

Cellulitis

  • an infection of the skin and underlying soft tissue, presenting with the four signs of inflammation: pain, heat, swelling, redness.

However, all should be considered in the patient presenting with the acute limb.

126
Q

What is a pulmomary embolism?

How are pulmonary emboli caused?

A
  • A pulmonary embolism is a blockage in the pulmonary artery, the blood vessel that carries blood from the heart to the lungs
  • Generally caused by DVTs in the legs
127
Q

How do PEs classically present?

What can they lead to?

When do they commonly occur?

A
  • Present with
    • Sudden onset breathlessness
    • Pleuritic pain
    • Haemoptysis
    • (however should be included in almost any respiratory differential as they are so common and variable in presentation)
  • They lead to increased pulmonary artery pressure (right heart strain) and ischaemia of the lung, with a ventilation/perfusion mismatch
  • They often occur 10 days post-surgery
128
Q

How are pulmonary embolisms classified?

A

Massive PE (5%)

  • >60% of the pulmonary circulation is blocked, leading to rapid cardiovascular collapse

Major PE (10%)

  • middle-sized pulmonary arteries are blocked leading to breathlessness, pleuritic chest pain and haemoptysis

Minor PE (85%)

  • small peripheral vessels are blocked, and patients may be aysmptomatic, or present as above (haemoptysis rare)
  • Massive PE may ensure following a minor PE, which is known as the ‘premonitory embolus’
129
Q

What clinical signs would you see for a patient with a PE?

A
  • Evidence of DVT
  • Raised JVP
  • Cyanosis if the embolus is large

CP1 (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions