Cardiopulm Unit 4 VOPP only

Question 1

What happens after the first hours after Acute MI?

Answer 1

• Ischemia leads to necrosis of cardiac tissue in the affected area within minutes of coronary artery occlusion
• Initiation of an inflammation response that involves the release of various inflammation mediators and signals the recruitment of WBCs to the site of injury
• The overall pumping efficiency of the heart decreases as the affected part of the heart may become hypokinetic or akinetic

Question 2

What happens after the First days after Acute MI?

Answer 2

• The inflammatory response continues with the removal of dead cells and debris, preparing the groundwork for healing and scar formation.
• The area surrounding the necrotic tissue may become edematous and hemorrhagic due to the disruption of microvasculature.
• Fibroblasts begin to proliferate at the site of injury, laying down the extracellular matrix that will form the basis of the scar tissue.

Question 3

What happens after the First week after Acute MI?

Answer 3

• The development of a fibrous scar begins as granulation tissue and collagen deposition begins to form by about the end of the first week.
• This area remains vulnerable to mechanical stress due to the ongoing remodeling and relatively weak tensile strength of the new tissue.
• The shape and size of the ventricle begins changes through a remodeling process

Question 4

What happens after several weeks after an Acute MI?

Answer 4

• Over the next several weeks, the scar tissue continues to mature and strengthen, replacing the necrotic tissue.
• The collagen fibers reorganize, and the scar contracts. The process of ventricular remodeling can continue for months after an MI.
• This can involve hypertrophy (thickening) of the unaffected myocardium in an attempt to compensate for the lost muscle function

Question 5

What is Ventricular Remodeling? What is it influenced by?

Answer 5

• Process whereby the shape, size, and thickness of the myocardium changes in both infarcted and non-infarcted areas.
• It is influenced by the:
  -Size of infarct
  -Patency of artery that was infarcted (how healthy the artery is after the MI)
  -Ventricular load (via incr. pressure or volume)

Question 6

What can Adverse Ventricular Remodeling lead to?

Answer 6

Can lead to impaired systolic and diastolic dysfunction and arrythmias

Question 7

Ventricular Remodeling

What may cause a less favorable remodeling?

Answer 7

• Where there is increased size and load and decreased blood supply, there will be less favorable remodeling, possibly expansion of infarction, and higher risk of complications and mortality

Question 8

Ventricular Remodeling

What may promote a “reversal” or “positive ventricular remodeling?

Answer 8

• Medical therapies, lifestyle modification, and cardiac rehabilitation have the potential to promote “reversal” or “positive” ventricular remodeling to improve size, shape, and function of the heart’s chambers

Question 9

What are the Prognostic Factors for Mortality and Functional Status after an AMI?

(AMI = Acute Myocardial Infarction)

Answer 9

• Remaining Left Ventricular function (MOST IMPORTANT)
• Complications
• Infarction size
• Presence of disease in other coronary arteries which leave other parts of myocardium still at risk

Question 10

What are Complications after AMI?

Answer 10

Complications after an MI can stem from diverse mechanisms and can be considered mechanical, ischemic, arrhythmic, or a combination of those, and can influence an individual’s clinical progression and overall prognosis

Question 11

With AMI Complications, the severity and the type of complications depend on what factors?

Answer 11

• Factors like the extent of myocardial damage, the location of the infarct, the speed of medical intervention, and the overall health of the patient.

Increased levels of habitual physical activity before hospitalization for heart-related conditions are associated with better short-term cardiovascular outcomes

Question 12

With AMI, what is essential to minimize the risk of complications and reducing future risk?

Answer 12

Immediate and appropriate medical treatment(e.g., reperfusion therapy) is crucial to minimize the risk of these complications. Long-term management, including lifestyle changes and medication, is also essential for reducing future risks.

Patients with an “uncomplicated” profile will more often experience notably reduced rates of morbidity and mortality after their initial cardiac events

Question 13

What is the Criteria for Complicated Myocardial Infarction?
(9 items in chart)

Answer 13

Question 14

Complications after AMI

What happens if you have an occlusion of the L Main (L coronary) or LAD?

Answer 14

Most Common
- We will see pump dysfunction of failure

Question 15

Complications of the (L coronary or LAD)

If there is an occlusion of the L coronary or LAD. What happens when the Left Ventical is ~15% is compromised?

Answer 15

Decreased contractility -> hypotension -> decreased driving pressure/coronary perfusion -> increased ischemia -> decreased contractility

Question 16

If there is an occlusion of the L coronary or LAD. What happens when the Left Ventical is ~25% is compromised?

Answer 16

May see signs of heart failure (e.g., pulmonary edema)

Question 17

If there is an occlusion of the L coronary or LAD. What happens when the Left Ventical is ~40% is compromised?

Answer 17

Increased mortality due to ventricular tachycardia and fibrillation. Cardiogenic shock (SBP < 90 mm HG / MAP < 60-65) occurs around this range as well

Question 18

What happens if you have an occlusion of the RCA?

Answer 18

• Right Ventricular Dysfunction, SA/AV nodal dysfunction, and arrythmias
• The pt may experience bradycardia, AV block, Atrial Fibrillation and Atrial Flutter

Question 19

Complications after AMI

What is Persistent Sinus Tachycardia?

Answer 19

Elevated HR originating from the SA node

Question 20

Complications after MI

After an MI, how can this affect the patient HR?

Answer 20

• After an MI, the heart may become less efficient at pumping blood due to damage to the myocardial tissue. The body compensates by increasing the HR to maintain adequate cardiac output and perfusion to vital organs. This compensatory mechanism can result in persistent sinus tachycardia

Question 21

After an MI, what would happen if the patients HR is too high? What S/S should we look for?

Answer 21

• Cardiac output may fall due to the markedly reduced ventricular filling time (affecting pre-load)

In these cases, look for signs of:
- Hypotension
- Acute Altered Mental Status (AMS)
- Ischemic chest discomfort due to increasing myocardial oxygen demand but reduced coronary blood flow
- Acute Heart Failure (e.g., fluid back up with pulmonary edema, dyspnea)

Question 22

Complications after MI

With Persistent Sinus Tachycardia, what should PTs do when screening and managing the pt?

Answer 22

PTs should monitor the heart rate before, during, and after physical activity to ensure it remains within safe limits.
- Physical activity intensity may need to be adjusted based on heart rate responses, and adequate rest periods should be incorporated to prevent excessive cardiac strain

Question 23

Complications after MI

Following an MI, what is Systolic Hypotension a Result from?

Answer 23

Results from diminished heart pumping capacity due to muscle damage, reducing stroke volume and systolic blood pressure, and potentially compromising organ blood flow.

Question 24

Complications after MI

With Systolic Hypotension, what should PTs do when screening and managing the pt?

Answer 24

PTs should monitor the blood pressure before, during, and after physical activity to ensure it remains within safe limits.
- It’s important to observe for signs of hypotension, such as dizziness, lightheadedness, or fainting.
- Physical activity protocols may need to be modified to prevent sudden changes in blood pressure and ensure patient safety.

Question 25

# Complications after MI What is a useful method to assess arterial blood flow and ensuring there is sufficient organ perfusion?

Answer 25

Monitoring Mean Arterial Pressure (MAP) - MAP = [(2 x DBP) + SBP] / 3 - **Normal Values 70-110 mm Hg** - A MAP **less than 60 mmHg** may indicate inadequate tissue perfusion and should, in a majority of circumstances, lead the clinician to modify the pt’s position and/or activity to increase MAP right away

Question 26

After an MI, how can low-level activity affect the heart?

Answer 26

After an MI, the heart's ability to increase blood flow in response to activity can be compromised. - Even low-level activities may demand more oxygen and blood than the heart can supply, leading to ischemia.

Question 27

# Complications after MI With Ischemia with Low-Level Activity, what should PTs do when screening and managing the pt?

Answer 27

While some degree of transient ischemia can be expected following an MI and revascularization procedures - PTs should be vigilant for signs of persistent ischemia during rest or activity which could be due to incomplete revascularization, re-occlusion, or other complications

Question 28

# Complications after MI With a patient that has Ischemia with Low-Level Activity, what happens once they are medically cleared to exercise?

Answer 28

- Once medically cleared, the use of graded exercise testing can help in establishing safe exercise intensities following MI. - Physical activity should be paced and gradually progressed over time toward guideline-based parameters. - Patient education on recognizing symptoms and appropriate actions is also crucial for patient safety

Question 29

What is Pulmonary Edema?

Answer 29

Abnormal accumulation of fluid in the alveoli and interstitial spaces of the lungs

Question 30

How does Pulmonary Edema result from an MI?

Answer 30

- Cases where the left ventricle is affected, the heart's ability to effectively pump blood can be significantly compromised. - This leads to an increase in pressure in the left atrium and subsequently in the pulmonary veins and capillaries. - The elevated pulmonary capillary pressure forces fluid out of the capillaries and into the alveolar spaces, resulting in pulmonary edema. - This fluid accumulation interferes with gas exchange, leading to decreased oxygenation of the blood and respiratory distress.

Question 31

# Complications after MI With patients with Pulmonary Edema, during the screening process, what should PT look out for?

Answer 31

- Shortness of breath, especially when lying flat - Rapid, shallow breathing - Coughing, noting any presence of frothy sputum that may be tinged with blood - Audible “crackles” or wheezing upon auscultation of the lungs ## Footnote Continuous monitoring of respiratory rate, oxygen saturation, and subjective reports of dyspnea during therapy sessions is critical for any patient who has pulmonary edema. Immediate action should be taken if signs of worsening pulmonary edema are observed.

Question 32

With patients with Pulmonary Edema, how should these patients be managed in terms of activities?

Answer 32

- Activities should be tailored to the patient's tolerance, avoiding excessive exertion that might exacerbate respiratory distress. - Positioning strategies can be employed to facilitate breathing and optimize oxygenation, avoiding positions the increase dyspnea or work of breathing. - Coordinate with the medical team regarding the use of supplemental oxygen during therapy sessions if indicated.