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BNKN602 Exam > Week 3 - Heart Failure > Flashcards

Week 3 - Heart Failure Flashcards

1
Q

Define Heart Failure

A

An acute or chronic condition in which the heart doesn’t pump blood as well as it should resulting in congestion (CHF) of blood backing up and unable to meet the demands of the body

  • The heart’s inability to consistently pump enough blood to organs and tissues
  • Cardiac output is insufficient to meet the metabolic demands of the body and accommodate venous return
  • Occurs from either a structural or functional abnormality of the heart
  • The resulting decreased blood supply to body impairs organs and tissue function
  • The dominant feature is inadequate tissue perfusion
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2
Q

What is a structural abnormality of the heart?

A

Valve problem/dysfunction, ventricle thickness, rigidity

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3
Q

What is a Functional abnormality of the heart?

A

Following a MI, cardiomyopathy, CAD (coronary artery disease)

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4
Q

Define Cardiac Output (CO)

A

Stroke Volume x Heart Rate (3.5-5L/min)

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5
Q

Define Stroke Volume (SV)

A

Amount of blood pumped out per heartbeat

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6
Q

Define Preload

A

(Volume) amount of ventricular stretch at the end of diastole. The greater the stretch the stronger the contraction (Starling’s Law)

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7
Q

Define Afterload

A

(Pressure) resistance to the ejection of blood from the ventricle

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8
Q

Define Ejection Fraction, what the normal is and how it is measured

A
  • The ejection fraction (EF) is the amount of blood that is pumped out of the left ventricle (LV) with each heartbeat
  • A decreased EF = decreased amount of blood being pumped out = decreased perfusion
  • It is measured in percentages
  • Normal range is 55-70%
  • An EF of 40% or less indicates HF
  • Calculated from an echocardiogram
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9
Q

What is Systolic Heart Failure?

A
  • Shortened to HFrEF which stands for Heart Failure reduced Ejection Fraction
  • Pumping problem of the heart
  • Inability of the Left ventricle to contract effectively
    ( Ventricles can’t pump hard enough during systole )
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10
Q

What is diastolic heart failure?

A
  • Shortened to HFpEF which stands for Heart failure Preserved ejection fraction
  • It is a relaxing problem
  • Inability of the Left ventricle to relax and fill effectively
    ( Not enough blood fills into ventricles during diastole )
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11
Q

Define systole and diastolic

A

Systole = The ventricles eject blood (pump)
Diastolic = The ventricles fill with blood (relax)

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12
Q

What is Right-Sided Heart Failure?

A
  • The right ventricle cannot eject sufficient amounts of blood - blood backs up in the venous system and may result in:
    • Peripheral Oedema
    • Weight gain but anorexia/nausea may be present
    • Hepatomegaly/Splenomegaly
      • Liver is the last place to send blood back to the heart
    • Ascites
    • Jugular vein distention
  • The blood can back up to the rest of the body via the right atrium and manifest as oedema, legs/ankles/feet, sacrum/penis (dependent areas) around the eyes, organ oedema

(Could experience Anorexia, GI distress, Weight loss, signs related to liver function impairments)

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13
Q

What is Left-Sided Heart Failure?

A
  • The left ventricle cannot pump blood effectively to the systemic circulation. The blood backs up in the pulmonary system so the pulmonary venous pressure increases in:
    • Decrease EF
    • Pulmonary congestion/oedema with dyspnoea
    • Cough
    • Crackles
    • Impaired oxygen exchange
  • LHF is the most common form (from left ventricular dysfunction). Blood cannot get out and around the body, so it backs up in the lungs via the left atrium and pulmonary vein
    • It causes pulmonary congestion and oedema in the lungs

(cough with frothy sputum, Cyanosis and signs of hypoxia, orthopnea)

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14
Q

What is the patho for Heart Failure?

A
  1. MI or cardiac dysfunction/structural abnormality impairs ability of L) ventricle to fill with or eject blood
  2. Poor ventricular function/myocardial damage leads to decreased stroke volume and cardiac output
  3. Leads to a neurohormonal response
  4. Either sympathetic system is activated to increase cardiac workload, or RAAS pathway is activated
  5. Results in vasoconstriction and sodium + fluid retention
  6. Further stress on the ventricular wall and remodelling leads to heart failure
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15
Q

What are some signs and symptoms of heart failure?

A

Pale, grey, SOBOE, orthopnea (unable to lie flat and breathe), nocturia (increased urination overnight due to lying flat and kidneys being well perfused), oedema, confusion, tachycardia, hypotensive, dry cough, dyspnoea, weak pulse, tachypnoea, fatigue, anxiety, ECG abnormalities, palpitations, restlessness, hypoxaemia, moist cough, diaphoresis, cyanosis, dizzy, light-headed, nausea, weight-gain, SOB, crackles on auscultation, ascites, exercise intolerance

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16
Q

What are some risk factors/aetiology for Heart Failure?

A
  • Ischaemia - Myocardial infarction (elevated Troponin)
  • Valve disease
  • Cardiomyopathy
  • Pericarditis
  • Fluid overload (renal failure, Intravenous fluid (IVF))
  • Hypertension
  • Smoking
  • Type 2 Diabetes
17
Q

What are some nursing interventions for HF?

A
  • Ensure daily weigh to indicate fluid retention or cardiac overload
  • Start a FBC and fluid restriction to monitor fluid retention and ensure pt is hydrated but not exceeding fluid restriction to avoid overload and improve oedema
  • Educate on healthy eating and exercise
18
Q

What are some clinical manifestations of Left-Sided Heart Failure?

A
  • Dyspnoea (difficulty breathing)
    • Orthopnoea (difficulty breathing when lying flat)
    • Paroxysmal Nocturnal Dyspnoea
    • Pulmonary congestion - cough, crackle, wheeze
19
Q

What are some clinical manifestations of Right-Sided Heart failure?

A
  • Renal Failure
    • Peripheral Oedema
    • Ascites (fluid collection in spaces within the abdomen)
    • Enlarged Liver and spleen
    • Distended JVP (jugular venous pressure)
    • Fluid weight gain
20
Q

What are compensatory mechanisms the body uses for HF?

A
  • Baroreceptors (pressure sensors) in the aortic and carotid arteries sense a drop in the BP
  • The Sympathetic nervous system (SNS) releases adrenalin and noradrenaline
    • Short-lived response - the aim is to increase BP by increasing HR and thus circulating blood volume
  • Low cardiac output and vasoconstriction result in decreased renal perfusion - renin is related to the kidneys
  • This initiates the renin-angiotensin-aldosterone system (RAAS)
21
Q

How is the SNS involved in compensatory mechanisms for HF?

A

SNS Activation = Body says, “I’ve had this damage, BP is low, I need to increase BP by vasoconstriction and make the heart go faster and pump harder and stronger.” Initially protective factor but over time it damages the ventricles and it becomes decompensated HF and the person is in trouble

  • Results in:
    • Increased heart rate and contractility which increases blood pressure
22
Q

How is the renin-angiotensin-aldosterone system (RAAS) involved with compensatory mechanisms for HF?

A

Neuro-hormonal Activation = Body aims to increase circulating blood volume by using RAAS. Aldosterone increases sodium and water reabsorption at the renal tubules. ADH increases water reabsorption and urine output decreases

  • Results in:
    • Increased blood volume (related to aldosterone and Anti-Diuretic Hormone (ADH) secretion) which increases preload angiotensin II and decreases vascular capacity which decreases afterload
23
Q

What are the pathophysiology consequences of HF?

A

Decreased blood and O2 supply to body (pump failing)

24
Q

Are puffy ankles a left or right sided heart failure?

A

Right as the Right ventricle is failing to pump the blood forward to the lungs, backing up in the body via the right atrium

25
Q

Someone has crackles/fluid in their lungs. Is it right or left heart failure?

A

Left as Left Ventricle is failing to pump the blood forward to the body, is backing up in the lungs via the Left Atrium

26
Q

What is chronic heart failure?

A
  • Heart failure is commonly caused by IHD
  • Common in the elderly, one to the main reasons for admission to hospital
  • The pathological processes that underpin heart failure result in decreased contraction, decreased filling or both
  • The ongoing inability of the heart to pump enough blood through the body to ensure a sufficient supply of oxygen
27
Q

What is the difference between ACUTE and CHRONIC HF?

A
  • Acute (I.e. post-surgery overload) - is common in the elderly and can correct the cause
    with diuretics and it goes away
    • Chronic (I.e related to myocardial dysfunction caused by IHD, cardiomyopathy,
      Hypertension or valvular disease/disorders
28
Q

If someone had an MI, why might they get HF?

A

Damage to the myocardium, especially Left Ventricle (ineffective pumping). Depending on the extent of the infarction that would affect the severity of the HF

29
Q

How do you know if someone has HF?

A
  • Indigestion
  • SOB
  • SOBOE
  • Increased HR (to pump more oxygen around body)
  • Low BP
  • Oedema
  • Dyspnoea
  • Agitation/confusion
30
Q

What assessments would you use for a patient with HF?

A
  • Rapid assessment
  • Posterior chest assessment
  • Peripheral vascular assessment (COWSCAMP)
  • Apical pulse
31
Q

What are some diagnostic interventions you would use?

A
  • Chest X-Ray -> Cardiomegaly (enlarged heart)
  • ECG -> arrhythmias, ST changes (Slow conduction through the ventricles, seen in the QRS complexes)
  • Echocardiogram -> Left Ventricle Dysfunction, Ejection fraction %
  • JVP (jugular venous pressure)
  • Neurohormones -> Increased Brain Natriuretic Peptide (Protein released from heart in response to ventricular wall stretch and is elevated in HF)
  • Exercise tolerance test
  • Cardiac catheterisation
32
Q

What is the management of HF?

A

Firstly: Treat the underlying cause if possible (I.e. MI, Valve dysfunction, ischaemia)

  • Aim to increase cardiac function and decrease myocardial workload with beta blockers etc.
  • Prevent harmful neuroendocrine responses, e.g. SNS, RAAS, ventricular remodelling -> ACE inhibitors
  • Manage with medication, daily weight, O2 if required, fluid restriction, low sodium diet and other lifestyle modifications
  • The nurse has a role in providing education and management of symptoms
33
Q

What is the patho of an MI?

A

In a heart attack there is a sudden blockage of a coronary artery by a blood clot. Coronary arteries are blood vessels that supply the heart muscle with blood and oxygen. Blockage of a coronary artery deprives the heart muscle of blood and oxygen, causing injury to the muscle. Injury to the chest muscle causes chest pain and the sensation of chest pressure. If blood flow is not returned to the heart muscle within 20-40 minutes, irreversible death to the heart muscle will begin to occur. Muscle will continue to die for 6-8 hours, at which time the heart attack is usually ‘complete.’ The dead heart muscle is eventually replaced by scar tissue.

34
Q

What is the aetiology of an MI?

A
  • The development over many years of fatty plaques in the walls of the arteries
  • A clot forming on one of the plaques

Fatty plaque can start building up on the inside walls of the coronary arteries (atherosclerosis) at an early age. Over the years, the build up of plaque increases and they become larger which as a result, the arteries gradually become narrower and less elastic. As the arteries narrow, there is less room for the blood to flow through. If a clot forms on the plaque, the artery can become blocked, cutting off the blood supply to part of the heart muscle = heart attack.

35
Q

What are some signs and symptoms of an MI?

A
  • Chest pain
  • Pain on L) arm
  • Pain can go into your neck, back, jaw, stomach, and abdomen
  • The pain can be squeezing, pressing, tightness,
  • Sweating
  • Feeling faint
  • Vomiting
    Being short of breath
36
Q

What are some nursing interventions with someone who has had an MI?

A
  • 02 supplementation as required to maintain tissue perfusion
  • Administer GTN spray for vasodilation to open up the arteries to allow for blood flow
  • Administer asprin antiplatelet to prevent further thrombus formation
  • Fluid restriction to reduce risk of excess fluid due to decreased organ perfusion

BNKN602 Exam (17 decks)

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