Heart disease and failure Flashcards

1
Q

Risk factors of CVD

A
High cholesterol
High blood pressure
Smoking
Obesity
Diabetes
Age
Family history
Previous heart attack
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2
Q

Clinical manifestations of IHD

A

Development of atherosclerosis - fatty streak, lipid deposition, intimal fibrosis
Atherosclerotic plaque leads to an imbalance between myocardial oxygen supply and demand

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3
Q

Signs/symptoms

A

Asymptomatic
Stable angina
Acute coronary syndromes - unstable angina, NSTEMI, STEMI
Long term: HF, arrhythmias, sudden death

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4
Q

Typical angina

A

Substernal chest discomfort
Provoked by exertion
Relieved by rest/nitrates within minutes

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5
Q

What is an acute coronary syndrome

A

Unstable angina
Acute MIs
- you can tell if its MI by rise in troponin on blood test (not elevated in unstable angina)
Characterised by development of a thrombosis at the site of acute disruption

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6
Q

STEMI

A

ST elevation on ECG
Complete coronary occlusion
Need timely diagnosis

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7
Q

NSTEMI

A

ST depression, variable T wave

Incomplete coronary occlusion

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8
Q

ACS symptoms

A

Discomfort that lasts and radiates
Occurs with exertion and at rest
Not relieved by GTN
Breathlessness, nausea/vomiting, sweating/clamminess

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9
Q

Immediate assessment

A

Patient history
ECG
Physical exam
Then risk stratification and blood test (troponin)

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10
Q

Management of ACS

A

Antiplatelet therapy (aspirin, clopidogrel)
Anti-ischaemic therapy (nitrates)
Thrombolysis (if STEMI)
Secondary prevention (statin, ACE inhibitor, beta blocker, lifestyle)

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11
Q

Other causes of raised NSTEMI

A

Pneumonia, PE
Pericarditis, sepsis
Heart failure, uncontrolled tachyarrhythmias

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12
Q

High risk ACS patients

A
Elevated troponin
Renal impairment
Recurrent chest pain
Changes on ECG
Haemodynamic instability
Major arrhythmias, HF
Elderly
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13
Q

Cardiac output equation

A

CO = HR x SV
At rest: 70ml/kg/min
Stroke volume affected by contractility, preload and afterload

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14
Q

Low output heart failure

A

Systolic (iscahemic injury, pressure/volume overload)

Diastolic (hypertrophy, infiltrative disorders, constrictive pericarditis, restrictive cardiomyopathy)

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15
Q

High output heart failure

A

Caused by increased demand on CO
High demand for blood
Causes: anaemia, pregnancy, Pagets disease, sepsis, acromegaly, thyrotoxicosis

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16
Q

Cardiomyopathy

A

Dilated: 50% familial, or toxins, or systemic disease
Hypertrophic: familial
Restrictive - amyloid

17
Q

Pathophysiology of heart failure

A

Reduced SV and CO -> compensatory mechanisms
Vasoconstriction, increased venous return -> enhanced contractility (starling law)
Results in augmented muscle mass
Activation of neurohormonal system (noradrenaline = increased heart rate; vasoconstriction, ANP, RAAS)

18
Q

RAAS/compensation in heart failure

A

Vasoconstriction
Na and water retention
Excessive tachycardia

19
Q

What does Left ventricular failure do to the kidneys

A

Decreased CO
Reduction in renal perfusion
Activation of RAAS
Increased blood volume

20
Q

What does left ventricular failure do to the brain

A
Hypoxic encephalopathy
Irritability
Loss of attention
Restlessness
Stupor and coma
21
Q

Effects of right sided heart failure

A

Liver and portal system (hepatomegaly, centrilobular necrosis, cardiac cirrhosis)
Spleen
Abdomen
Subcutaneous tissue (oedema
Pleural and pericardial space (effusions)

22
Q

Biventricular failure

A

Due to same pathological process on each side of heart

Or left heart failure leads to volume overload and then right heart failure

23
Q

Side effects of left ventricular failure

A

Pulmonary congestion and oedema

Heavy wet lungs - breathlessness, orthopnoea, paroxysmal nocturnal dyspnoea