GMED3009- CCF (heart attack) Flashcards
Definition of congestive cardiac failure (CCF)
clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.
- CO = SV x HR-becomes insufficient to meet the metabolic needs of the body.
- SV- determined by preload, afterload and myocardial contractility.
Aetiology of CCF
- Acute causes
o Acute myocardial infarction
o Arrhythmias
o Pulmonary emboli
o Thyrotoxicosis
o Hypertensive crisis
o Papillary muscle rupture
o Ventricular septal defect - Chronic causes
o Anaemia
o Bacteria endocarditis
o Valvular disorder
o Coronary artery disease
o Congenital heart disease
o Cardiomyopathy
o Pulmonary diseases
o Hypertension
o HIV infection
Left sided failure
- Occurs when the left ventricle of the heart is affected
o Common causes include CHD and hypertension
o Cardiac output is reduced due to loss of ventricular functioning
o It is divided into two categories: systolic dysfunction (impaired ventricular contraction and ejection) and diastolic dysfunction (impaired relaxation and ventricular filling)
o Whether or not a patient with HF has systolic or diastolic dysfunction depends on the ejection fraction (EF), which is defined as the amount of blood pumped from the ventricle in one heartbeat. If the EF is <40%, it is systolic dysfunction, and if it is >40%, it is diastolic dysfunction
o 70% of patients with HF have systolic dysfunction compared to 30% with diastolic dysfunction
o Pressures in the left ventricle and atrium increase as the amount of blood remaining in the ventricle after systole increases
o These pressures impair filling, causing congestion and increased pressures in the pulmonary vascular system which consequently result in fluid movement from the blood vessels into interstitial tissues and alveoli
Types of left sided failure
SYSTOLIC FAILURE - reduced contractility
Also known as heart failure with a reduced ejection fraction (HFrEF)
o Occurs when the ventricle fails to contract adequately to eject a sufficient blood volume into the arterial system
o It is affected by loss of myocardial cells due to ischemia and infarction, cardiomyopathy or inflammation
o The result is that although the heart may fill well during diastole, the failing myocardium is unable to eject sufficient blood during systole.
o This leads to dilatation of the heart and stretching of the muscle fibres
o According to Starling’s law, there is an initial increase in the force of contraction that helps to restore cardiac output. Eventually, however, this compensatory mechanism starts to fail and cardiac output falls, with progressive dilatation of the ventricle
o Clinical manifestations are those of decreased cardiac output such as weakness, fatigue, decreased exercise tolerance
DIASTOLIC FAILURE - impaired relaxation & abnormal ventricular filling
- related to chronic hypertension and ischemic heart disease
o Occurs when the heart cannot completely relax in a diastole, disrupting normal filling .
o Passive diastolic filling decreases, increasing the importance of atrial contraction to preload
o Diastolic dysfunction results from decreased ventricular compliance due to hypertrophic and cellular changes and impaired relaxation of the heart muscle
o Manifestations result from increased pressure and congestion behind the ventricle: shortness of breath, tachypnoea, respiratory cackles would result if the left ventricle is affected. While the distended neck veins, liver enlargement , anorexia and nausea would result if right ventricle is affected,
Right sided failure
o In right-sided failure, the right ventricle is impaired
o Increased pressure in the pulmonary vasculature or right ventricular muscle damage, impairs the right ventricle’s ability to pump blood into the pulmonary circulation.
o The right ventricle and atrium become distended and blood accumulates in the systemic venous system
o Increased venous pressures cause abdominal organs to become congested and peripheral tissue oedema to develop
o Signs and symptoms include: ascites, peripheral oedema, and enlarged liver
Underlying causes of systolic heart failure include
- Diabetes mellitus
- Hypertension
- Valvular heart disease (stenosis or regurgitant lesions)
- Arrhythmia (supraventricular or ventricular)
- Infections and inflammation (myocarditis)
- Peripartum cardiomyopathy
- Congenital heart disease
- Drugs (either recreational, such as alcohol and cocaine, or therapeutic drugs with cardiac side effects, such as doxorubicin)
- Idiopathic cardiomyopathy
- Rare conditions (endocrine abnormalities, rheumatologic disease, neuromuscular conditions)
Underlying causes of diastolic heart failure include
- Coronary artery disease
- Diabetes mellitus
- Hypertension
- Valvular heart disease (aortic stenosis)
- Hypertrophic cardiomyopathy
- Restrictive cardiomyopathy (amyloidosis, sarcoidosis)
Pathophysiology of CCF
1) excessive blood or fluid in the lungs or body tissues caused by the failure of ventricles to pump blood effectively. CCF occurs when the left ventricle cannot pump out the amount of blood entering the ventricle, or when the ventricle is damaged and cannot effectively pump enough blood to meet the body’s requirements. It may also occur due to a build up of excess fluid in the body due to renal failure or dysfunction due to disease. Blood begins to congest in the lungs (pulmonary oedema).
2)
2) The alveoli are unable to exchange gases effectively creating severe dyspnoea in patients. As the condition progresses, this congestion will eventually cause the right ventricle to fail. When this occurs, valuable blood supply (containing oxygen and nutrients) to the systemic cells is seriously disrupted, and the by-products of metabolism (such as CO2) are no longer eliminated effectively causing toxins to accumulate and ultimately causing cell death
Stages of CCF
AT RISK
Stage A = At high risk for heart failure, but without structural disease or symptoms of heart failure
Stage B= Structural heart disease, such as left ventricular hypertrophy/dysfunction, but without signs or symptoms of heart failure
HEART FAILURE
Stage C=Structural heart disease with prior or current symptoms of heart failure
Stage D= Treatment-resistant heart failure requiring specialized intervention
NYHA functional classification of heart disease -developed functional guidelines for classifying people with heart disease based on tolerance to physical activity.
Class I
No limitation of physical activity.
Ordinary physical activity does not cause fatigue, dyspnoea, palpitations or anginal pain.
Class II
Slight limitation of physical activity. No symptoms at rest.
Ordinary physical activity results in fatigue, dyspnoea, palpitations or anginal pain.
Class III
Marked limitation of physical activity but usually comfortable at rest.
Less than ordinary physical activity causes fatigue, dyspnoea, palpitations or anginal pain.
Class IV
Inability to carry on any physical activity without discomfort. Symptoms of cardiac insufficiency or of angina may be present even at rest.
If any physical activity is undertaken, discomfort is increased.
Clinical manifestations of CCF
fluid overload and pulmonary congestion, including dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. Others, however, do not have congestive symptoms but have signs and symptoms of low cardiac output, including fatigue, effort intolerance, cachexia, and renal hypoperfusion.
Discuss the routine medical and nursing care of a patient with a CCF.
Daily weights: Performed on the same scale, the same time of day, and in clothing of the same/similar weight
Capillary refill: Press down on nail bed. Delayed if > 3 seconds for color to return
Standard vitals signs: Oxygen saturation, blood pressure, pulse, and temperature
Pain assessment: Use numerical scale (0-10); assess location, onset, quality, and characteristics
Respirations: Assess respiratory rate/depth, use of accessory muscles, labored breathing, and other signs of respiratory distress auscultate
Lung sounds: Auscultate for the presence of crackles and other adventitious lung sounds consistent to pulmonary edema
Heart sounds: Auscultate heart rate, rhythm, or character (example: thready or bounding pulse). Note: In patients with any kind of cardiovascular disease, it’s important to auscultate for an apical pulse to obtain the heart rate, rather than relying upon the radial pulse or digital methods
Labs: CBC/CMP, especially electrolytes and renal values such as BUN and creatine (the kidneys are the often the first organ system after the heart to show signs of decreased profusion). Arterial blood gases (ABG’s) are particularly important if the patient is at risk for shock
Intake and output ration (I/O’s): Anuria/oliguria may be indicative of renal insufficiency (again, (the kidneys are the often the first organ system after the heart to show signs of decreased profusion)
Skin turgor: Usually assessed by gently tugging the skin on the patient’s chest or hand
Skin/extremities: Assess for peripheral edema, documented as none, trace, or 1+ through 4+
Cardiac output: Elevate legs when in sitting position and edematous extremities when at rest. Observe for changes in skin including temperature, moisture, color, and capillary refill time. Assess for chest pain. Monitor hourly urine output
Tissue perfusion: Administer medications and position the patient to enhance oxygenation. Rationale: Positioning will promote oxygenation.
Fluid balance: Administer medications to reduce cardiac workload and diuretics as ordered, obtain daily weights, and monitor ABG’s and electrolyte values. Rationale: A weight gain of 3 kg in a period of three days or less is a sign of fluid retention; lab values are predicative of the patient’s status
Activity intolerance: Improve oxygenation to enable to the patient to tolerate activity at an optimal level. Rationale: Tolerance of activity is an indicator of the patient’s overall status and ability to be safely discharged.
Anxiety: Promote oxygenation to slow breathing, lower heart rate, and provide relief of anxiety. Rationale: Anxiety is a symptom that presents secondary to hypoxia. Relief is one of the indicating factors is assessing oxygenation status
Knowledge deficit: Provide education to prepare the patient for discharge and promote continuity of care. Rationale: Hospitals have a responsibility in taking proactive actions to minimize risks of preventable future visits. Nurses play a vital role in providing education to prepare patients for discharge
Cardiac output: Assess for adventitious lung sounds, abnormal heart sounds along with rate and rhythm, presence of chest pain
Oxygenation: Raise the head of the bed by 30 degrees/place the patient in a Semi-Fowler’s position. Administer supplemental oxygen to promote cardiac function by increasing available oxygen and reducing the heart’s oxygen consumption. Monitor oxygen saturation to evaluate trends in the patient’s progress
Fluid overload: Monitor weight daily on the same scale at the same time each morning in similar clothing
Surgical management of CCF
- Heart transplant
- Ablation
- Cardiac angiography bypass graphing (CABG)
- Angiography
- Internal Defibrillator
Pharmological treatment
ACE inhibitors
Beta blockers
Calcium channel blockers
Diuretics
Cardiac glycosides
Digoxin
- increases the strength and efficiency of heart contractions, and is useful in the treatment of heart failure and control the rate and rhythm of the heart.
* Digoxin increases the force of contraction of the muscle of the heart by inhibiting the activity of an enzyme (ATPase) that controls movement of calcium, sodium, and potassium into heart muscle.
* Digoxin also slows electrical conduction between the atria and the ventricles of the heart and is useful in treating abnormally rapid atrial rates.
Quinapril
* ACE inhibitors such as quinapril lower blood pressure by inhibiting the formation of angiotensin II, thereby relaxing the arterial muscles and enlarging the arteries.
* This increases the flow of blood and oxygen to the heart so that it can pump blood more efficiently.
* The enlargement of the arteries elsewhere in the body also makes it easier for the heart to pump blood.
* This is particularly beneficial when there is heart failure. In the kidneys ACE inhibitors increase blood flow and reduce the filtration pressure in the kidneys.
Frusimide
* Frusemide is a potent diuretic.
* It inhibits sodium and chloride absorption in the ascending limb of Henle’s loop and in both the proximal and distal tubules.
* The action on the distal tubule is independent of any inhibitory effect on carbonic anhydrase or aldosterone.
* Frusemide has no significant pharmacological effects other than on renal function.
What is a CPAP
. The PEEP helps keep the alveoli open during exhalation, and inspiratory pressure helps to open additional alveoli, relieving the work of breathing;
2. The pressure generated by CPAP helps move fluid back into the vascular system.
To facilitate this second action, it’s critical that the underlying myocardial dysfunction be corrected. The best method to reduce the elevated pressure in the pulmonary vasculature is the administration of nitrates. Once the pressure in the pulmonary arteries and veins is decreased, CPAP will be better able to move the fluid out of the lungs and into the circulatory system.
Even in the absence of nitrate administration, CPAP can move fluid out of the lungs. Combined with the decrease in work of breathing, this can lower the sympathetic tone of the patient and encourage diuresis.
Therefore, by reducing the work of breathing and relieving pulmonary congestion, CPAP buys time for other treatments, such as nitrates and diuretics, to work.
