Multiple choice Flashcards
Typical signs and symptoms of a cardiac arrhythmia
Signs:
Hypotension
Tachypnea
Signs of diminished perfusion
High jugular venous pressure
Cannon a waves
Variation in intensity of first heart sound, caused by loss of atrioventricular (AV)
synchrony
Symptoms:
Palpitation
Light-headedness
Syncope (faint)
Chest pain
Anxiety
Fatigue
Sinus rhythm (60-100
Sinus arrythmia
Five steps to identify this heart rhythm:
60-100 beats per minute
Irregular (varies more than 0.08 sec)
Is there a P wave before each QRS? Are P waves upright and uniform?
What is the length of the PR interval? 0.12-0.20 seconds (3-5 small squares)
Do all QRS complexes look alike? What is the length of the QRS complexes?
0.06-0.12 seconds (1½ to 3 small squares)
Sinus Tachycardia
Asystole (0bpm)
Atrial fibrillation
Five steps to identify this heart rhythm:
What is the rate?
Atrial: 350-400 bpm; ventricular: variable
What is the rhythm? Irregularly irregular
Is there a P wave before each QRS? Are P waves upright and uniform? Normal P waves are absent
What is the length of the PR interval? Not discernable
Do all QRS complexes look alike? What is the length of the QRS complexes? Yes; 0.06-0.12 seconds (1½ to 3 small squares)
Sinus bradycardia
Sinus pause
VF
Rhythm in which three or more PVCs arise in sequence at a rate greater than 100 beats per minute. V-tach can occur in short bursts lasting less than 30 seconds, causing few or no symptoms. Sustained v-tach lasts for more than 30 seconds and requires immediate treatment to prevent death. V-tach can quickly deteriorate into ventricular fibrillation.
Atrial flutter
Five steps to identify this heart rhythm:
What is the rate? Atrial: 250-400 bpm; ventricular: variable
What is the rhythm? Atrial: regular; ventricular: may be irregular
Is there a P wave before each QRS? Are P waves upright and uniform? Normal P waves are absent; flutter waves (f waves) (sawtooth pattern) are present
What is the length of the PR interval? Not measurable
Do all QRS complexes look alike? What is the length of the QRS complexes?
Yes; 0.06-0.12 seconds (1½ to 3 small squares)
Torsades de pointes
Associated with a prolonged QT interval. Torsades appears in short bursts that terminate spontaneously but frequently recur and degenerate into ventricular fibrillation. The hallmark of this rhythm is the upward and downward deflection of the QRS complexes around the baseline. The term ‘Torsades de Pointes’ means ‘twisting about the points.’
Idioventricular rhythm
Indicate a dying heart with slowing rates. Common fatal rhythm in elderly patients. SA and AV nodes completely fail to fire, and impulses arise from the ventricular tissues in an attempt to prevent cardiac standstill. Very distorted QRS in every beat and no P wave. Idioventricular rates can be accelerated (> 100 bpm) or agonal (< 20 bpm).
Agonal rhythm (last of the heart before death)
What is the treatment for acute coronary syndrome (ST elevation)
Oxygen
May limit ischemic injury
New trends/guidelines <95% O2
Aspirin - 300 mg (PO)
Blocks platelet aggregation (clumping) to keep clot from getting bigger
Dissolved breaks medication down faster & allows for quicker absorption
Hold if patient allergic or for a reliable patient that states they have taken aspirin within last 24 hours
Nitroglycerin - 0.4 mg SL every 5 minutes
Dilates coronary vessels to relieve vasospams
Increases collateral blood flow
Dilates veins to reduce preload to reduce workload of heart
Morphine – Intravenous Push
Decreases pain & apprehension
Mild venodilator & arterial dilator
Reduces preload and afterload
Given if pain level not changed after the 2nd dose of nitroglycerin
Give 2.5mg slow IVP repeated every 2-5 minutes as needed
Treatment for Atrial Fibrillation (AF)
- Preventing blood clots, so warfarin, dabigatran and aspirin
- Slowing the heart rate down, beta blocker (metoprolol), calcium channel blockers (verapamil) and digitalis (digoxin).
- control heart rhythm so amiodarone, sotalol and flecainide
- Others include catheter ablation and electrical cardioversion
Explain the initial treatment for irregular heart rhythms
- Treat patient not the monitor
- Obtain baseline vitals before and/or during ECG monitoring
- transcutaneous pacing (pacing the heart for the patient)
- Tachycardias can be well tolerated rhythms
treatment and nursing care for a patient in VT
Depends if they are pulse OR no pulse
NO PULSE:
Immediate CPR
Defib
ARC flowchart = follow
Pulse:
Amiodarone (anti-arrhythmic)
Infusion of sotalol (Beta blocker)
Synchronised cardioversion
what is flaccid paralysis
Flaccid paralysis is a neurological condition characterized by weakness or paralysis and reduced muscle tone without other obvious cause (e.g., trauma).
Diagnostic investigations for CCF
Almost always Echocardiography: two-dimensional and doppler used to determine systolic and diastolic LV performance
ALSO USED: CT, ECG, X-ray, Angiography, ABG, FBC, U&E, BUN and LVT’s
Pathophysiology of heart failure (CCF)
1.) Left Ventricular Failure:
Systolic dysfunction: Reduced cardiac contractility → decreased ejection fraction.
Diastolic dysfunction: Impaired relaxation → increased filling pressures and pulmonary congestion.
2.) Right Ventricular Failure:
Caused by increased pressure from the lungs (pulmonary hypertension) → systemic fluid retention (e.g., oedema, ascites).
3.) Fluid Buildup:
Pulmonary congestion → dyspnoea (difficulty breathing).
Systemic congestion → peripheral oedema, ascites.
4.) Renal Dysfunction:
Reduced kidney perfusion → fluid retention → worsens heart failure.
Types of heart failure
1.) Left-Sided Heart Failure (HF)
Normal Function: The left ventricle pumps oxygen-rich blood from the lungs to the body. The left ventricle is the main pumping chamber, larger and stronger than the others.
In Left-Sided HF: The left side of the heart works harder to pump the same amount of blood, leading to decreased efficiency.
Two Types:
Systolic HF: Left ventricle loses ability to contract normally → reduced ejection fraction.
Diastolic HF: Left ventricle loses ability to relax and fill properly → increased filling pressures.
2.) Right-Sided Heart Failure (HF)
Normal Function: The right side pumps used (oxygen-poor) blood back to the lungs for oxygenation.
In Right-Sided HF: Often caused by left-sided HF. Increased pressure in the lungs is transferred back to the right side, causing fluid buildup in the body (edema).
3.) Congestive Heart Failure (CHF)
Mechanism: As blood flow out of the heart slows, blood returning to the heart backs up through veins → congestion in body tissues, leading to edema (swelling).
Pathophysiology of ARDS
- Injury/Exudative Phase (1-7 days post-injury)
Key Features:
- Increased alveolar-capillary permeability → fluid leaks into alveoli.
- Intrapulmonary shunts: Blood passes through fluid-filled alveoli → impaired oxygenation.
- Alveolar collapse and atelectasis: Reduced lung compliance.
Symptoms:
Severe hypoxemia due to fluid-filled alveoli and reduced oxygen exchange. - Proliferative Phase (1-2 weeks post-injury)
Key Features:
- Influx of inflammatory cells: Neutrophils, monocytes, fibroblasts, lymphocytes.
- Pulmonary vasculature damage: Destruction of lung capillaries.
- Fibroblast proliferation: Connective tissue forms in response to injury.
- “Stiff lung”: Microscopic appearance of dense cellular tissue.
- Changes in lung tissue: Enlarged air spaces and fibrotic tissue (scarring) develop (2-4 weeks after injury).
Outcome:
If the phase resolves, inflammation and cellularity decrease. - Fibrosis/Repair Phase (2-3 weeks post-injury)
Key Features:
- Healing and recovery: Inflammation decreases, fibrosis settles.
- Improved oxygenation: Patient can be weaned off mechanical ventilation.
- Long-term recovery: Can take up to 12 months depending on severity.
Outcome:
Lung tissue repairs, but in severe cases, fibrosis may persist and cause long-term lung dysfunction.
Summary:
- Injury/Exudative Phase: Alveolar fluid buildup, intrapulmonary shunting, atelectasis → severe hypoxemia.
- Proliferative Phase: Inflammation and fibrosis, “stiff lung”, tissue damage → lung scarring.
- Fibrosis/Repair Phase: Lung healing, reduced inflammation, improved oxygenation → recovery, but fibrosis may persist.
Treatment for ARDS
Key Components of Management:
1.) Identify and Treat Underlying Cause:
Quick identification of the cause (e.g., infection, trauma) and early aggressive treatment are critical for reducing mortality.
2.) Fluid Management:
Avoid fluid overload!
Fluid management is controversial, but restriction is key to prevent worsening pulmonary edema.
3.) Surfactant Administration:
Neonates with infant respiratory distress syndrome (IRDS) benefit from surfactant, improving survival.
Adults: Surfactant does not improve oxygenation, ventilation duration, or mortality in ARDS.
4.) Steroids:
Use of steroids is controversial but may be considered in the late fibrotic phase of ARDS to reduce inflammation.
5.) Mechanical Ventilation:
Low tidal volumes and limiting ventilation pressure reduce mortality by preventing ventilator-induced lung injury (VILI).
6.) Prone Positioning:
Placing patients in the prone position can improve oxygenation.
Likely works by reducing oedema and atelectasis in the posterior lung, improving ventilation-perfusion matching.
Summary:
Early cause identification and treatment are essential.
Avoid fluid overload and use prone positioning for oxygenation improvements.
Low tidal volume ventilation and consider steroids in late stages.
Surfactant only improves survival in neonates, not adults.
Routine nursing care for respiratory patient / ARDS
Main Goals of Care for Respiratory Failure:
1.) Ensure Adequate Oxygenation & Ventilation:
Use appropriate oxygen delivery devices for supplemental oxygen administration.
Consider humidification to loosen secretions if they are thick and hard to expel.
2.) Hydration:
Encourage adequate fluid intake to maintain hydration and thin secretions, making them easier to remove.
3.) Chest Physiotherapy:
Assist with secretion removal and improve oxygenation through chest physiotherapy and positioning.
Postural drainage can also aid in secretion clearance.
4.) Airway Suctioning:
Use if the patient is unable to expel secretions on their own.
5.) Nutritional Support:
The hypermetabolic state in critical illness increases energy requirements, so ensure nutritional support to maintain body weight and muscle mass.
6.) Breathing Exercises:
Encourage deep breathing and coughing to prevent airway obstruction from secretions.
Positioning:
Position the patient to optimize oxygenation and secretion clearance.
