Systolic Heart Failure, Myocardial Infarction, Pulmonary Embolism and ventricular fibrillation Flashcards

1
Q

Structural abnormalities with systolic heart failure

A

The ventricles may be dilated, thinned or indeed thickened.

-Other structural abnormalities may be present including valve
regurgitation (leaking of blood backwards)
-Mitral or tricuspid valve regurgitation may result from ventricular dilation
due to stretching of the valve ring

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

What are the physiological abnormalities of systolic heart disease?

A
  • The heart loses the ability to pump enough blood to meet the body’s metabolic needs – first in response to vigorous exercise – then to moderat exercise – then to mild exercise – and finally also at rest (no exercise)
  • The heart loses its “pumping reserve”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the prior events to systolic heart failure?

A

-The most common prior event is a myocardial infarction (see earlier “Disease Summary”)
-Viral myocarditis is may lead to systolic heart failure.
-Other causes include the use of chemotherapy drugs which poison heart
muscle as an unwanted side-effect

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

What are the experienced symptoms of systolic heart failure?

A

Tiredness (fatigue), breathlessness (dyspnoea), breathlessness when lying flat (orthopnoea); sudden breathlessness in the night (paroxysmal nocturnal dyspnoea); passing excess urine at night (nocturia); ankle swelling (oedema)

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

What are the clinical signs of systolic heart failure?

A

Rapid respiration (tachypnoea); ankle swelling (oedema); high jugular venous pressure (JVP); tachycardia (fast heart rate); hypotension (low blood pressure); cachexia (loss of skeletal muscle mass); anorexia (loss of appetite)

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

What are the abnormal test results for systolic heart failure?

A
  • Echocardiogram (ultrasound scan of the heart) shows reduced pumping function of heart. Dilatation of ventricle may be seen, and valves can be assessed.
  • A blood test of BNP (Brain Natiuretic Peptide) raised
  • ECG (electrocardiogram) often abnormal due to underlying disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is a medical/ surgical intervention of systolic heart failure?

What drug therapy?
What antagonists?
What diuretics?
What could a pacemaker do?

A

-Daily weight can help detect changes in fluid status.
-Standard drug therapy includes ACE-inhibitor (Angiotensin Converting
Enzyme Inhibitor e.g. ramipril) and beta-blocker e.g. bisoprolol treatment.
-Other drugs such as mineralocorticoid receptor antagonists (e.g.
spironolactone), combination therapy with Angiotensin II Receptor Blocker
and a Neprilysin Inhibitor (ARNI) have prognostic benefit in some groups
-Loop diuretics such as furosemide are used to treat symptoms of fluid
overload but do not have intrinsic prognostic benefit.
-Some patients benefit from a special pacemaker that “resynchronises” the
right and left ventricle systolic contraction.

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

What is the primary and secondary prevention of systolic heart failure?

A
  • Diagnose any underlying disease that might be treated directly (e.g. narrowing of coronary arteries, hypertension)
  • Secondary prevention may involve an implanted cardioverter defibrillator (ICD) to reduce the risk of sudden cardiac death due to ventricular arrhythmia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the structural abnormalities of myocardial infarction (MI)?

A
  • Narrowing of the arteries as a result of coronary atheroma (cholesterol deposits in the wall of the artery – called “plaques” or “stenoses”)
  • Blockage of artery due to blood clot (coronary thrombosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the physiological abnormalities of MI?

A
  • Ischaemia (reduced blood supply) leading eventually to necrosis (death of cells also called infarction) of heart muscle (myocardium)
  • Impaired contraction of myocardium
  • Abnormal electrical activity of heart cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the prior events of MI?

A

-More common in men than women and in the elderly
-Family history of heart disease is often present
-Risk factors (smoking; high blood pressure; high cholesterol; high
blood sugar / diabetes; low exercise; increased weight / obesity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are experienced pains of MI?

A
  • Severe crushing central / generalised chest pain – sudden onset
  • Often pain spreads (radiates) to arm(s) or neck
  • Associated – nausea (sickness); vomiting; sweatiness; breathlessness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the clinical signs of MI?

A

-Patient is clearly distressed due to the pain (unless given morphine)
-Blood pressure may be low and heart rate fast
-Breathlessness may be obvious with fluid heard on lungs during
inspiration due to pulmonary oedema (fluid in alveoli of lungs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the abnormal test results of MI?

A

-The ECG (electrocardiogram) shows “ST segment elevation” if coronary artery is completely blocked
-Blood test demonstrates raised levels of the heart protein “troponin”
-Echocardiogram shows reduced contraction of area affected
-Coronary angiogram (X-ray test of heart arteries) shows an artery
blocked by atheromatous stenosis and by blood clot (thrombosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the medical/ surgical interventions of MI?

A

-This is a major medical emergency: a 999 call should be made ASAP
-Immediate medical treatment includes pain relief with morphine, an
antiemetic; and oral aspirin treatment
-Thrombolytic drugs (dissolve blood clot) have now been largely
replaced by “Primary Percutaneous Intervention” (through a thin tube in arm or leg, clot is removed and a small balloon is used to open the narrowed artery and a metal “stent” placed to hold artery open)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is a primary and secondary prevention of MI?

A
  • Primary (before the MI) and secondary (after MI) prevention focuses on treatment or avoidance of “risk factors” (see above)
  • Key drugs used are (a) Aspirin (antiplatelet action to prevent blood clot) (b) Ticagrelor or Clopidogrel (antiplatelet action to prevent blood clot especially when a coronary stent present) (c) Beta-blockers (lower heart rate and blood pressure through blocking effects of adrenaline and noradrenaline) (d) Statins (HMG-CoA reductase inhibitors that lower blood cholesterol) (e) ACE-inhibitors (block angiotensin converting enzyme to prevent production of angiotensin II)
17
Q

What are the structural abnormalities of Pulmonary Embolism (PE)?

A
  • Blockage of part of the pulmonary arterial tree as a result of embolism (movement from one place in body to another) of blood clot (occasionally fat embolus, air embolus or amniotic fluid embolus)
  • Blockage of deep veins of the leg or abdomen by blood clot
18
Q

What are the physiological abnormalities of PE?

A

Impaired perfusion (blood flow) of alveoli / lungs resulting in low oxygen levels in the blood

19
Q

What are the prior events to PE?

A
  • Usually the source of the thrombus (blood clot) that moves to the lungs – is in the deep veins of the legs
  • Causes of deep vein thrombosis (DVT) are described in another “Disease Summary Sheet”
  • Hospital admission for surgery (e.g. hip replacement) and immobility may predispose.
20
Q

What are the experienced symptoms of PE?

A
  • Symptoms of PE are sudden-onset dyspnoea (shortness of breath), tachypnoea (rapid breathing), chest pain of a “pleuritic” nature (worsened by breathing), cough and haemoptysis (coughing up blood)
  • About 15% of all cases of sudden death are attributable to PE
21
Q

What are the clinical signs of PE?

A

-Sinus tachycardia is common.
-Collapse, and circulatory instability due to decreased blood flow
through the lungs and into the left side of the heart may be initial
presentation in severe cases
-Approximately 90% of cases of PE are secondary to DVT, therefore
patients must be assessed for possible DVT if PE suspected.
-Occasionally, a pleural friction rub (noise like an object being
rubbed) may be heard over the affected area
-Strain on the right ventricle may be detected (felt on chest wall)
-Raised jugular venous pressure (seen in neck)

22
Q

What are the medical/ surgical intervention of PE?

A

-Usual treatment starts with oxygen given at a high flow rate
-Thrombolytic drugs may given by intravenous infusion to dissolve
the blood clot in life-threatening cases

23
Q

What is the primary and secondary prevention of PE?

A

Anticoagulants are used immediately and for some months (initially low molecular weight heparin by injection and later oral anticoagulant e.g. Apixaban/ Warfarin)

24
Q

What are the structural abnormalities of Ventricular Fibrillation (VF)?

A
  • The heart may appear to have an entirely normal structure (e.g. genetic condition of “Long-QT Syndrome”)
  • Ventricles may be hypertrophied (more muscle) due to high blood pressure or genetic disease (e.g. Hypertrophic Cardiomyopathy)
  • Most frequently the ventricles are dilated and scarred (e.g. after a myocardial infarction or viral myocarditis )
25
Q

What are the physiological abnormalities of VF?

A

-If the heart goes into ventricular fibrillation – all electrical activity becomes disorganised and chaotic
-The heart “quivers” or “fibrillates” but does not “beat”
-No blood is pumped to the lungs or the body causing rapid loss of
consciousness

26
Q

What are prior events to VF?

A
  • Often there is no warning of this condition with the result being sudden cardiac death
  • It commonly occurs after myocardial infarction (coronary thrombosis leading to heart attack) and also when heart failure (chronic weak pumping of heart – see separate disease summary sheet) is present
27
Q

What are the experienced symptoms of VF?

A
  • There may have been some prior warning symptoms of palpitations; light-headedness; chest pain
  • The patient loses consciousness within seconds of the start of ventricular fibrillation
28
Q

What are the clinical signs of VF?

A
  • Patient is motionless, unresponsive to verbal command or shaking, has slow / deep snoring or no signs of breathing
  • No pulse can be detected
  • Collapse is sudden and dramatic
29
Q

What are medical and surgical interventions of VF?

A

As with all medical emergencies the ABC strategy should be followed

  • A – Airway (this need to be protected by extending the neck)
  • B – Breathing can be supported using oxygen and “bag and mask”
  • C- Circulation can be supported by external cardiac massage
  • The definitive treatment is DC electrical shock (defibrillation) and should b attempted as soon as possible once rhythm determined.
30
Q

What are the primary and secondary preventions of VF?

A

-Detection of the risk of VF in young adults requires knowledge of the family history – particularly any cases of sudden cardiac death or unexplained collapse
-Beta-blockers are sometimes used to reduce the risk of ventricular rhythm
abnormalities
-Implanted Cardioverter Defibrillators (ICD) can be implanted like a pacemaker
for patients who survive or who are at high risk of a first event