SEM 2 LAB 1: Exercises Vignette 2 Flashcards
What are some types of pacemaker function-related failures?
battery failure, pacemaker-medicated tachycardia
Patients with pacemakers generally face problems that can be grouped into the following categories
1) Failure to pace the appropriate cardiac chamber
Output failure
Capture failure
2) Problem with detecting intracardiac signals
Undersensing
Oversensing
3) Pseudomalfunction
Crosstalk with resultant safety pacing
Pacemaker-mediated tachycardia
Sensor-induced tachycardia
Runaway pacemaker
Lead-displacement dysrhythmia
Twiddler syndrome
What is the result of placing a magnet over a implanted pacemaker?
Pacemaker will be placed in “magnet mode”, which in most devices is asynchronous pacing (AOO, VOO, or DOO).
What is Magnet Mode?
Magnet mode
Applying a magnet to a pacemaker will initiate the magnet mode.
This mode varies with pacemaker set-up and manufacturer.
Usually initiates an asynchronous pacing mode – AOO, VOO, or DOO.
Asynchronous modes deliver constant rate paced stimuli regardless of native rate of rhythm.
In asynchronous ventricle pacing there is a risk of pacemaker-induced ventricular tachycardia.
Note this differs from magnet application to an Implantable Cardioversion Defibrillator (ICD) which results in defibrillator deactivation.
In what circumstances should we consider placing a magnet over a pacemaker?
Sensor-induced tachycardia, pacemaker mediated tachycardia (PMT) (aka endless loop tachycardia), or runaway pacemaker
Treatment of Pacemaker-Induced Tachycardia
Occasionally pacemaker-induced tachycardia can self-resolve.
Additionally, some permanent pacemaker algorithms can sense and terminate this rhythm.
***However, if that does not occur we can keep it pretty basic:the causeis a circuit that needs to be disrupted. Options for this include:
Block the AV node, block the circuit
Vagal maneuvers (e.g. modifiedvalsalva [3])
Adenosine (other AV nodal blocking agents such asbeta blockersandcalcium channel blockers may also work)
Use a Magnet
Applying a magnet to the pacemaker converts it into asynchronous mode with no sensing (e.g. DOO = pacing both A and V).***This is more complicated ifthe patient’s pacemaker is combined with an implantable defibrillator (ICD).
Discuss differential diagnosis based on the above. Discuss differential diagnosis / underlying casues of vetnricular tachycardia
Common causes of monomorphic VT include:
ischemic heart disease
dilated cardiomyopathy
hypertrophic cardiomyopathy
Chaga’s disease
Discuss normal ICD function including firing, CXR features, and ECG features
Discuss normal ICD function including appropriate firing, CXR features, ECG features
implantable cardioverter-defibrillators or ICD’s are devices that can recognize ventricular tachycardia and fibrillation and terminate it by delivering an electrical shock.ICD’s are implanted in patients with cardiomyopathy and a low left ventricular ejection fraction because they are at risk of ventricular tachycardia, ventricular fibrillation and sudden cardiac death.
AICDs consist of various combinations of sensing and shocking electrodes. They are frequently combined with a pacemaker as a bundled system for the patient, treating both the patient’s established arrhythmia and also acting as a fail-safe system should ventricular fibrillation or ventricular tachycardia occur.
Device FunctionImplantable cardioverter-defibrillators are programmed to detect arrhythmia on the basis of rate. All such devices use the signal rate recorded by the right ventricular lead as the 1st detection criterion. For an arrhythmia to be declared, a specified number or percentage of sensed events must occur at a rate higher than the programmed cutoff rate. Once this criterion is met, the device will apply certain discriminators to differentiate between supraventricular tachycardia (SVT) or ventricular tachycardia (VT) and ventricular fibrillation (VF). If the device confirms VT or VF, either antitachycardia pacing (ATP) or shock is delivered. Conversely, if SVT is diagnosed by the device, all therapies are withheld.
When a patient presents with an ICD shock, a thorough but focused history and physical examination should be performed, along with device interrogation ( Typically, shocks (whether appropriate or inappropriate) cause symptoms of dizziness, lightheadedness, syncope, chest pain, or diaphoresis. In the event of inappropriate shocks, the patient might feel completely normal until the shock occurs.
Appropriate ShockIf the device interrogation reveals an episode of VT or VF that has resulted in appropriate therapy, the device function is within normal limits. In these cases, all efforts are directed towards treatment and towards prevention of more episodes of VT and VF. If a single episode of VT or VF has resulted in an ICD shock, no further treatment may be needed. In case of recurrent VT/VF or VT storm, treatment of underlying heart disease along with antiarrhythmic therapy to prevent more VT/VF will be required.
Discuss inappropriate ICD function
Inappropriate firing, failure to faire, misplacement issues
battery depletion
lead fracture or displacement (by surgery, defibrillation or CVL/PAC placement)
lead or box infection (e.g. due to bacteremia)
multiple shocks due to algorithm error, sensing failure, oversensing of physiological signals and lead failure
EMF interference from shaver, TV remote, MRI and also possible
ICD may be switched off intra-operatively because of interference from diathermy (need to turn back on!)
threshold may be changed by medications
Atrial fibrillation is the most common cause of inappropriate shock, followed by sinus tachycardia, atrial flutter, and atrial tachycardia.
Modern ICDs are programmed to emit an audible tone or alert when they detect a change in certain measurable values. These values can range from battery voltage or lead impedance that pertain to device integrity, to the presence of atrial fibrillation or other measures that pertain to arrhythmia burden
Oversensing by a pacemaker or ICD may be classified as arising from oversensing of extrinsic (electrical signals other than myocardial) or intrinsic (myocardial) events. Oversensing in the ventricular channel may result in pre- syncope or syncope due to inhibition of ventricular pac-
ing. It may also result in inappropriate ICD detection or therapy delivery.
Discuss use of magnets in ICD-related presentations
Differentiate clinical features of ACS from prinzmetal angina and SCAD
Prinzmetal Angina:
CP at rest usually occurring between midnight and 0800
Recurrent episode of 5-15mins that usually form patterns
Usually relieved by medications
ECG changes are usually variable but present very similarly to ACS ECG changes
SCAD:
Very similar to typical ACS presentations
May have biomarkers present
Minor deviations in risk factors: Pregnant patients, emotional stress, ateriopathies and tissue disorders
ECG may show some changes related to the LAD coronary atery.
Patients are usually significantly younger and typically female.
Discuss coronary artery spasm and dissection including clinical presentation, diagnostic features etc
CAD vs CAS
CAD:
Clinical presentation is extremely similar to ACS. These patients will usually present with general ACS symptoms and chest pain. These patients may also have STEMI presentations as well. Patient’s Cardiac Biomarkers may be present but an absence of biomarkers does not prove there is no dissection. The presenting patients will typically be younger and female with scarcely any risk factors.
Diagnostic features:
On Coronary angiography, there is usually some form of mid-distal coronary artery dissection occurring most commonly affecting the Left Anterior Descending artery. These effects are commonly displayed as a lengthening and narrowing of the arteries affected.
CAS:
Clinical presentation:
May present asymptomatic and have a large variance in presentations with similarities to ACS presentations and occasionally sudden cardiac death. These symptoms occur regularly at rest and in the early morning. The symptoms are traditionally non exertional.
Diagnostic Features:
ECG:
The ECG may show evidence of Cardiac ischemia but the display of CAS on the ECG is variable. Transient ST Segment elevation occurs less often than ST segment depression. A peaking or amplification of the T-waves may be seen in addition to the aforementioned signs. ST segment depression usually occurs when the spasm of the artery is less severe. There have been times where SVT and other ventricular tachycardia have been present.
Discuss Pros and cons of standard ACS treatments in a patient with possible ACS
The treatment plan associated with ACS may exacerbate some previous conditions and encourage bleeding, specifically regarding the extensive risks associated with thrombolysis.
Medication interactions: A lot of the medications that we administer have potential to potentiate other home medications and/or home remedies.
Discuss receiving hospital considerations for a patient with suspected SCAD
Receiving hospital should have some Cardiac vascular surgery capabilities, preferably a center with ECMO.
Discuss causes of hypovolemic, non-hemorrhagic shock
Hypovolemic shock is characterized by decreased intravascular volume and increased systemic venous assistance (compensatory the mechanism to maintain perfusion in the early stages of shock). In the later stages of shock due to progressive volume depletion, cardiac output also decreases and manifest as hypotension.Hypovolemic shock divides into two broad subtypes: hemorrhagic and non-hemorrhagic.
Common causes of non-hemorrhagic hypovolemic shock include:
GI losses - the setting of vomiting, diarrhea, NG suction, or drains.
Renal losses - medication-induced diuresis, endocrine disorders such as hypoaldosteronism.
Skin losses/insensible losses - burns, Stevens-Johnson syndrome, Toxic epidermal necrolysis, heatstroke, pyrexia.
Third-space loss - in the setting of pancreatitis, cirrhosis, intestinal obstruction, trauma.
Discuss crystalloids vs colloids for volume administration in resuscitation and non-resucitation situations
Crystalloids have small molecules, are cheap, easy to use, and provide immediate fluid resuscitation, but may increase oedema. Colloids have larger molecules, cost more, and may provide swifter volume expansion in the intravascular space, but may induce allergic reactions, blood clotting disorders, and kidney failure.
Using starches, dextrans, albumin or FFP (moderate‐certainty evidence), or gelatins (low‐certainty evidence), versus crystalloids probably makes little or no difference to mortality. Starches probably slightly increase the need for blood transfusion and RRT (moderate‐certainty evidence), and albumin or FFP may make little or no difference to the need for renal replacement therapy (low‐certainty evidence).
Discuss the general management of hemorrhagic shock
Stop hemorrhage when possible
Replace blood loss with balanced transfusion approach (also when possible)
TXA
Mitigate lethal diamond – coagulopathy, hypothermia, acidosis, and hypocalcemia
Review anticoagulant medication and consider reversal
Discuss the concept of a massive transfusion protocol (MTP)
Patients with severe hemorrhage may developrefractory hemorrhagedue to a collection of factors:
Dilution of clotting factors (including platelets and fibrinogen).
Hypothermia from transfusion of cold products.
Hypocalcemia-induced coagulopathy (due to citrate in blood products).
Acidosis.
Massive transfusion protocols involve the use of balanced transfusion (including PRBCs and clotting factors), in efforts to avoid dilutional coagulopathy. Traditional labs generally won’t return fast enough to guide the use of clotting factors
The hemoglobin level takes hours to fall after bleeding. Consequently, checking the hemoglobin has little role in determining need for MTP.
Hypotension is usually alatemanifestation of hemorrhage.
On physical exam, the patient is cool, pale, and edematous with moderate mottling in his extremities. GCS 15, RR 36, HR 128, BP 88/65, SpO2 92%, Temp 36.4.
Labs: WBC 18.8, TnI 143 ng/L. pH 7.21(v), pCO2 34, HCO3 17.
Discuss resuscitation goals/end points
Continuous pulse oximetry should be used to monitor for respiratory compromise. Oxygen goals vary depending on patient comorbidities, but in the acute care setting blood oxygen saturations of >90% are acceptable.
For a patient with decompensated heart failure, the blood pressure needs to be high enough to perfuse the organs. However, if the pressure istoo high, this will increase the workload on the heart (excessive afterload). Often an ideal blood pressure will be in the low-normal range (e.g., MAP 60-65 mm) with evidence of organ perfusion
Urine output 0.05-0.1cc/kg/hr
Normal mentation
Serial ECGs
Serial labs – looking for trends and evidence of improved perfusion and organ function
Optimize volume status
Consider giving a fluid challenge if the following conditions are met:
(1) There is insufficient end-organ perfusion (e.g., acute kidney injury).
(2) No evidence of pulmonary congestion (e.g., no B-lines on lung ultrasonography).
(3) Overall assessment suggests true hypovolemia (e.g., no systemic congestion).
Fluid should be given in boluses of 500-1000 ml fluid challenges, with careful determination of the effect on the patient. If fluid isn’t causing clinical improvement, don’t give more.
Be careful – static hemodynamic parameters (e.g., CVP, pulmonary capillary wedge pressure) do not predict fluid-responsiveness and should not be used as the primary determinant of fluid administration
onsider diuresis if the following conditions are met:
(1) There is significant pulmonary and/or systemic congestion.
(2) Overall assessment suggests total body fluid overload.
For patients who aren’t responding adequately to furosemide, consider adding a thiazide diuretic (e.g., metolazone 5 mg q12hr-q24hr). This may enhance sodium excretion, with improved clearance of extravascular edema fluid.Patients with severe systemic congestion may have reduced absorption of some diuretics, so they may require IV diuretics (e.g., IV furosemide plus IV chlorothiazide). More on diuresis:.
Patients with substantially elevated central venous pressure can experience animprovementin renal function with diuresis, because decreasing venous congestion will increase blood flow through the kidney. The driving pressure through the kidneys is equal to the MAP minus the CVP, so lowering the CVP may increase renal perfusion.
Study diagram
