Cardiology 4 Flashcards

1
Q

What is dilated cardiomyopathy?

A
Most common cardiomyopathy in young people, most of the time its idiopathic 
In some cases there's a history of myocarditis or chemotherapy agents 
Shortness of breath- murmur 
Enlarged ventricular shadow 
S3 gallop 
Caused by ischaemia and hypertension 
Other causes:
Alcohol
Beriberi (Vitamin B1 deficiency)
Coxsackie
Chagas disease
Cocaine
Doxorubicin
Haemachromatosis 
Thiamine deficiency 
Causes biventricular heart failure, mitral and tricuspid regurgitation
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2
Q

What is restrictive cardiomyopathy?

A

Causes decreased ventricular compliance and diastolic dysfunction, it is most commonly caused by myocardial fibrosis after open heart surgery, and radiation
Caused by: amyloidosis, sarcoidosis, endocardial fibroelastosis
Low amplitude QRS

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3
Q

What is constrictive pericarditis?

A

A condition characterized by incomplete filling of the cardiac chambers due to thickening of the parietal pericardium.
Fatigue, hepatomegaly, dyspnea- pericardium can not accommodate changes in cardiac volume.

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4
Q

What is pulmonary insufficiency (regurgitation)?

A

Characterized by an incompetent pulmonary valve that leads to a backflow from the pulmonary artery to the right ventricle.
Pulmonary hypertension and a decrescendo diastolic murmur in the pulmonic area
Most common causes are pulmonary hypertension, IE, rheumatic heart disease

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5
Q

What is cardiac tamponade characterised by?

A

Sudden drop in blood pressure, altered mental status, jugular venous distention, pulsus paradoxus, and distant heart sounds
Results from pericardial effusion where blood or fluid accumulates in the pericardial space.
Cardiac tamponade is differentiated from other types of pericardial effusion by the accumulation of pericardial fluid under pressure, which compresses the heart chambers and decreases cardiac output.

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6
Q

What causes myocarditis?

A

Trypanosoma cruzi, a protozoan endemic to Central and South America.
Adenovirus, coxsackie B, parvovirus B19 (developed world)
Patients typically have a prodrome of fever, myalgia, and malaise several days prior to the onset of cardiac symptoms
S3 or S4 gallops
Respiratory distress
Shock (hypotension, hypoperfusion, altered mental status).

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7
Q

What is pericardial tamponade?

A

Often after trauma
Presents with jugular venous distension, hypotension and distant heart sounds (Becks triad)
This fluid exerts an increasing amount of pressure on the heart thus compromising its ability to fill and decreasing cardiac output

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8
Q

What is the TIMI score?

A

Age ≥65 years
At least three risk factors for coronary heart disease (these include hypertension, diabetes, dyslipidemia, smoking, or family history of early MI)
Prior coronary stenosis of ≥50%
ST-segment deviation on admission EKG
At least two anginal episodes in prior 24 hours
Elevated serum cardiac biomarkers
Use of aspirin over past seven days

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9
Q

What is a myocardial rupture?

A

Characterized by a laceration or tearing of the wall of the ventricles or atria of the heart.
Acute hemodynamic deterioration and sudden death

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10
Q

What are pulmonary embolisms?

A

Life threatening
A massive embolism obstructs the right ventricular outflow tract and therefore suddenly increases pulmonary vascular resistance, causing acute right heart failure
Rise in troponin due to ventricular ischaemia

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11
Q

How do PEs present?

A

Small/medium- breathlessness, pleuritic chest pain, haemoptysis, tachypnoeic, pleural rub
Massive- severe central chest pain, shocked, sweaty, pale, tachypnoea, tachycardia, syncope, raised JVP, right ventricular heave
Occurs more frequently in pregnancy, leading cause of maternal death

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12
Q

What is Kussmaul’s sign?

A

JVP rises paradoxically with inspiration

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13
Q

What are AAA?

A
Can be asymptomatic
US offered to men 65-74
Epigastric or back pain 
Rupture- epigastric pain radiating to the back, hypovolaemic shock 
Surgery for symptomatic or >5.5cm
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14
Q

What is a thoracic aneurysm?

A

caused by cystic medial necrosis and atherosclerosis
Asymptomatic
Cause pressure on local structures- back pain, dysphagia, cough
Aortic regurgitation

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15
Q

What are the types of aneurysm (structurally)?

A

True- all layers bulge. fusiform: symmetrical. saccular (berry): asymmetrical
False (pseudoanerysm)- blood pools outside the vessel
Mycotic- infection

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16
Q

What causes aneurysms?

A
Hypertension (atrophy of tunica media)
Male 
>60
Smoking
Tertiary syphillis (inflammation of vasa vasorum)
Bacteroides fragilis
Pseudomonas aeruginosa 
Salmonella
IE
Aspergillus
Candida 
Marfan's/Ehlers-danlos
17
Q

What occurs when the papillary muscles are damaged?

A

Occurs commonly in the left ventricle and causes mitral regurgitation

18
Q

What can hypovolaemia lead to?

A

Tachycardia, hypotension, sunken eyes and dry mucous membranes
Prerenal AKI- oliguria/anuria

19
Q

What is the wells criteria for PE?

A

Symptoms of DVT, including leg swelling, redness, and tenderness to palpation (3 pts),
Tachycardia >100bpm (1.5 pts),
Recent surgery/immobilization >3 days (1.5 pts),
DVT/PE history (1.5 pts),
hemoptysis (1 pt), and
Malignancy (1 pt).

20
Q

What murmur is heard in hypertrophic obstructive cardiomyopathy?

A
Crescendo-decrescendo murmur
Softer if squats/handgrip 
Louder if stands/valsalva
Bifid pulse
S4 sound
21
Q

What is seen in investigation of myocarditis?

A

Rise in troponin and creatine kinase
ECG- sinus tachycardia, T wave inversions, saddle shaped ST elevations
Enlarged heart on chest x-ray
Echo- inflamed heart muscle walls

22
Q

Describe the different patterns of acute MI?

A
Regional MI (90%): infarct of 1 segment of ventricular wall (thrombus formation on an atheromatous plaque)
Regional subendocardial infarction: lysis of thrombus/strong collateral supply limits infarct to subendocardial zone 
Circumferential subendocardial infarction (10%): general hypoperfusion of coronary arteries (hypotensive episode) in artherosclerotic arteries - no Q wave
23
Q

Diagnosis of MI

A

Elevation in serum cardiac troponin levels
ST elevation/new LBBB = STEMI (generally full thickness myocardial infarct)
No ST elevation/LBBB, no Q waves = NSTEMI (partial thickness lesion)

24
Q

Changes to a necrotic area post-MI

A

0-12h: loss of oxidative enzymes
12-24h: infarct pale & blotchy, intercellular oedema
24-72h: infarct area excites acute inflammatory response - soft and yellow with neutrophilic infiltration
3-10d: vascular granulation tissue organisation
10d-months: collagen deposition, infarct replaced by collagenous scar

25
Q

Acute coronary syndrome symptoms

A

Severe crushing chest pain >20mins
Not relieved by 3x GTN at 5min intervals
Radiates to left arm, neck, jaw
Dyspnoea, nausea, fatigue, perspiration, palpitations, angor animi
Silent infarct: presents without chest pain (elderly and diabetic)

26
Q

Acute coronary syndrome on examination:

A

Sympathetic activation: tachy, HTN, pallor, sweating
Vagal stimulation: brady, vomiting
Myocardial impairment: hypotension, narrow pulse pressure, raised JVP, basal creps, 3rd heart sound (blood hitting ventricle wall)
Tissue damage, low grade pyrexia
Later: pericardial rub & peripheral oedema, pansystolic murmur (papillary muscle rupture/ventriculo-septal defect)

27
Q

Changes in troponin in acute coronary syndrome

A

rise 4-8h after onset of symptoms
24h = peak
detectable for 10d
Raised in critically unwell patients with non-cardiac causes

28
Q

ST changes in a non-reperfused STEMI

A

5mins: tall pointed T waves
30mins: ST elevation
2+h: T wave inversion, Q waves develop
Days: ST returns to normal
Weeks: T wave may return to normal, Q wave remains

29
Q

Causes of myocardial ischaemia

A

Reduced perfusion: atheroma, embolus, thrombosis, spasm, inflammation of coronary arteries, hypotension
Reduced blood oxygenation: anaemia, carboxyhaemoglobinaemia
Increased tissue demands: Increased CO, cardiac hypertrophy