Systolic Heart Failure, Myocardial Infarction, Pulmonary Embolism and ventricular fibrillation Flashcards
Structural abnormalities with systolic heart failure
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
What are the physiological abnormalities of systolic heart disease?
- 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”
What are the prior events to systolic heart failure?
-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
What are the experienced symptoms of systolic heart failure?
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)
What are the clinical signs of systolic heart failure?
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)
What are the abnormal test results for systolic heart failure?
- 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
What is a medical/ surgical intervention of systolic heart failure?
What drug therapy?
What antagonists?
What diuretics?
What could a pacemaker do?
-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.
What is the primary and secondary prevention of systolic heart failure?
- 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
What are the structural abnormalities of myocardial infarction (MI)?
- 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)
What are the physiological abnormalities of MI?
- 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
What are the prior events of MI?
-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)
What are experienced pains of MI?
- Severe crushing central / generalised chest pain – sudden onset
- Often pain spreads (radiates) to arm(s) or neck
- Associated – nausea (sickness); vomiting; sweatiness; breathlessness
What are the clinical signs of MI?
-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)
What are the abnormal test results of MI?
-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)
What are the medical/ surgical interventions of MI?
-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)
What is a primary and secondary prevention of MI?
- 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)
What are the structural abnormalities of Pulmonary Embolism (PE)?
- 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
What are the physiological abnormalities of PE?
Impaired perfusion (blood flow) of alveoli / lungs resulting in low oxygen levels in the blood
What are the prior events to PE?
- 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.
What are the experienced symptoms of PE?
- 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
What are the clinical signs of PE?
-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)
What are the medical/ surgical intervention of PE?
-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
What is the primary and secondary prevention of PE?
Anticoagulants are used immediately and for some months (initially low molecular weight heparin by injection and later oral anticoagulant e.g. Apixaban/ Warfarin)
What are the structural abnormalities of Ventricular Fibrillation (VF)?
- 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 )
What are the physiological abnormalities of VF?
-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
What are prior events to VF?
- 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
What are the experienced symptoms of VF?
- 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
What are the clinical signs of VF?
- 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
What are medical and surgical interventions of VF?
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.
What are the primary and secondary preventions of VF?
-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