Decreased Cardiac Output Flashcards by Elias Cortez

What are manifestations of low cardiac output?

Skin:

Cool, Pale
Diaphoretic

Neuro:

Dizziness, Syncope,
Change in Level of Consciousness, Restlessness

Cardiovascular:

Chest Pain,
Low Blood Pressure,
Weak Peripheral Pulses, Decreased Capillary Refill

Respiratory:

Shortness of Breath, Tachypnea
Orthopnea

Renal:

Decreased Urine Output

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What is the order of medical interventions for a STEMI?

ASA
Clopidogrel (Plavix)- with or without perfusion
Oxygen
Nitroglycerine (NTG)
Morphine (Class 1 intervention)
D/C NSAIDS
Beta Blockers within 24 hours

ACE Inhibitors w/in 24 hrs in impaired Ejection Fraction, HTN, DM or Chronic Kidney disease
Anticoagulants (related to reperfusion strategy)
Heparin
Lovenox
IV Insulin indicated in 1st 24-48 hrs after STEMI to tightly control glucose
Fibrinolytics if time from onset of Sx •Goal is DOOR to NEEDLE is 30 minutes!!

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What can an intravascular ultrasound?

Evaluates coronary artery walls, stent placement and post PCI procedure for stent/angioplasty integrity
Used in conjunction with Cardiac Cath

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How do beta-blockers decrease myocardial oxygen demand?

(SLOW IVP Metoprolol, Labetalol)
Decreases myocardial oxygen consumption by lowering heart rate and contractility,
ALSO: Prevents ventricular remodeling

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What are some nursing interventions to decreased O2 demands during a cardiogenic shock?

vadminister analgesics & sedatives
position patient for comfort
limit patient activities
reduce anxiety
provide calm/quiet environment

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What are some medical treatments to restore perfusion and decrease O2 demands?

Oxygen: if SpO2
Aspirin: 160-325 mg- chew it, Blocks Thromboxane A2; Prevents clots at thrombus
Nitrates: Vasodilates coronaries à Increases perfusion through coronary arteries
- Not if pt has recently taken Phosphodiesterase Inhibitor (Viagra, Cialis, etc)=> DECREASED BP…
- “Nitrates should NOT be given to pts w/in 24 hrs of (Viagra) or (Levitra) adminis- tration or w/in 48 hrs of (Cialis)”
Beta Blockers:
- Decreases heart rate and extends diastoleà since coronary arteries fill during diastoleà Increases O2 supply to myocardium
Invasive Medical - Surgical / Technological Therapies:
- Percutaneous Interventions: Stents; Angioplasty; Atherectomy; etc..
- Intra-Aortic Balloon Pump
- Coronary Artery Bypass Graft
- Left Ventricular Device, Extracorporeal Mechanical Oxygenation (ECMO)

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How does ECMO work and when are the indications for it?

Extracorporeal Membrane Oxygenation (ECMO)

Blood is removed from venous end and oxygenated, by a membrane oxygenator
Blood is then delivered to the aorta or venous site, using an external mechanical pump

Indications:

Refractory cardiogenic shock w/ underlying potentially reversible heart condition,
Used as a bridge to a ventricular assist device or cardiac transplantation

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What causes cardiac tamponade, what are some complications and manifestations of it, and how would you treat it?

Causes:

This occurs from bleeding into pericardial sac (it is an Emergency)
Pericarditis, Myocardial rupture, Recent Cardiac surgery, End-stage renal disease (uremia), Metastatic cancer

Complications:

Obstructive shock, death
Pulseless electrical activity

Manifestations:

Associated with increased mediastinal drainage
Pulsus paradox= Exaggerated decrease of SBP during inspiration (> 10 mm Hg drop)
Beck’s Triad:
- Increased CVP
- Low BP
- Muffled heart sounds

Tx:

Pericardiocentesis
Pericardial window surgery

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What are some contraindications to the administration of fibrinolytics?

Prior intracranial hemorrhage
Known structural cerebral vascular lesion
Malignant intracranial neoplasm
Significant closed head injury within the last 3 months
Ischemic stroke within the last 3 months
Active bleeding
ST-segment depression

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What are factors that can decrease cardiac output?

Heart Rate:
- Excessive Increases and Decreases in HR due to Dysrhythmias
Preload:
- Decreased preload from Dehydration, Third spacing (Ex: Burns)
- Increased preload from Fluid Overload
Contractility:
- Altered conduction (Contractility) from specific Dysrhythmiasà decrease atrial kick à reducing contractility
- Decreased contractility (Ex: Myocardial Ischemia, Injury, Infarction- MI, Cardiogenic Shock)
Afterload:
- Excessively Increased afterload (Ex: HTN crisis)
- Decreased afterload -> less blood return to the heart, peripheral pooling 2o to vasodilation (Ex: Sepsis, Anaphylaxis)

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What are some complications associated with fibrinolytics?

Active bleeding
Hypersensitivity
Intracranial bleeding

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What are some complications associated with coronary artery bypass machine?

Bleeding d/t:

Mechanical damage to platelets and clotting factors, consumption coagulopathy,
Incomplete neutralization of heparin used to prime CBM
Thromboembolism d/t: Cannulation to CPM
Neurological deficits d/t:
Decreased systemic arterial pressure while on CP bypass
Embolus from cannulation to CBM
Inadequate renal blood flow associated w/ CBM

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Describe the Nursing Management with IABP & VAD Care

Monitor for dysrhythmias, peripheral ischemia, and bleeding
Monitor for balloon perforation
Monitor for migration (IABP), loss of L brachial /radial pulse, or renal damage. The ballon could have moved and blocked one of these
Monitor for device failure (VAD)
Prevent infection at insertion site
Prevent atelectasis or pneumonia

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What are some complications from getting a CABG

Hypovolemia and Vasodilation
Diuresis
Cardiac Tamponade

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How do ACE inhibitors/ARBs Decrease Myocardial Oxygen Demand?

Vasodilates and reduces workload of heart
ALSO: Prevents ventricular remodeling

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What are some drugs that increase cardiac output?

vamrinone, digoxin, dobutamine, dopamine, norepinephrine

Nitroglycerin

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What are some characteristics of a HTN emergency?

Same BP range as HTN Urgency (> 180/110-120 mmHg OR Diastolic BP > 120 mmHg)
Positive target organ damage present:
- Stroke, Cerebral hemorrhage, HTN encephalopathy
- Acute MI, Pulmonary Edema, Aortic dissection
- Acute Renal Failure
Manifestations:
- Severe HA, Neuro deficits, Vertigo
- Nausea and Vomiting
- Chest Pain
Others: based on target organ

Describe the pathophysiology associated with cardiogenic shock

Impaired ability of ventricle to pump blood forward leads to
- Decreased stroke volume (SV) &
- Increased blood in left ventricle @ end of systole
The decrease in stroke volume (SV) causes a decrease in cardiac output (CO) which leads to:
- decreased cellular O2 supply
- decreased tissue perfusion
An ineffective left ventricle results in increased end-systolic volume which pulmonary pressures increases & pulmonary edema
Pulmonary edema causes impaired gas exchange & decreases oxygenation which leads to further
- decreases cellular O2 supply
- decreases tissue perfusion

What are some characteristics of a unstable angina?

ST segment or T wave depression + Negative biomarker
- Absence of ST-segment elevation in NSTEMI is understood to involve less than full thickness (partial thickness) damage of heart muscle.
- No biomarkers because there is no damage being done to the heart yet

T wave inversion

What are the symptoms associated with successful reperfusion with fibrinolytics?

Relief of presenting symptoms
Reduction of atleast 50% of the intital st-segment elevation
Hemodynamic and electrical stability
Reperfusion arrhythmias such as PVCs or V tachy
Early peaking of the CKMB

What are the clinical manifestations of an MI?

•Chest discomfort (lasting longer than 20 minutes, but
Pressure, crushing, gripping
**Some may have silent MI: DM, Older adults, Women
Epigastric discomfort
Shortness of Breath
Nausea Vomiting -> with R. coronary artery
Excessive diaphoresis (ANS)
Pallor, Gray skin color (ANS)
Palpitations, Dysrhythmias
Anxiety, Sense of impending doom
S3, Rales (if MI complicated w/ CHF)
S4 (stiff ventricle from infarcted tissue)
Low grade temp (2o to inflammation, necrosis

What are some characteristics of a HTN urgency?

BP= > 180/110-120 mmHg OR Diastolic BP > 120 mmHg
No target organ damage
May be w/out symptoms OR
- HA
- Anxiety
- Epistaxis
- Dyspnea

What are some nursing implications with patients with LVAD?

Monitor Hemodynamics, Dysrhythmias,
Labs,
Anticoagulant therapies;
Ventilator management;
Sedation/Paralytics;
Psychosocial support;
Prevent infection

How would you treat a HTN emergency?

MEDICAL EMERGENCY
Admit To ICU
- Begin Anti-HTN Therapy: Bring BP down by 10% 1st hr; In 2-3 hr down by another 15%
  - Adrenergic Inhibitors- Esmolol, Labetalol, Metoprolol
  - Vasodilators- Nitroprusside, Nitroglycerine, Nicardipine
  - Diuretics- Furosemide (lasix)
Treat End Organ damage Problems
Symptom Management
- Nausea- Antiemetic
- Severe H/A- Analgesics

What are some clinical manifestations of cardiogenic shock?

* SBP * MAP * Decreased sensorium * Cool, pale, moist skin * UO * Chest pain * Tachycardia * Weak, thready pulse * Decreased S1 & S2 * **S3 heart sound** * Tachypnea, Crackles * Dysrhythmias * **Decreased cardiac output** * **Increased preload**

What are some manifestations of an MI seen in women?

* Chest Pain: most commonly reported acute symptom among men & women, **but more women than men report non–chest pain** * Atypical * Fatigue, * Upper back and neck pain, * Nausea

What are some risk factors for CAD?

* Smoking\* * Hypertension\* (\>140/90) * Age (M \> 45; F \> 55) * Dyslipidemia\* * Low HDL * Elevated LDL / TG * Family Hx of premature CHD in 1st degree relative (M Chronic conditions: * Diabetes Mellitus * Chronic Kidney Disease * Obesity * Lack of regular physical activity * Lack of diet rich in fruit, veggies, fiber

What are some characteristics of a STEMI?

* ST elevation + Pathological Q waves * Becuase when an atheromatous plaque ruptures in a coronary vessel and the clot which forms completely obliterates the vascular lumen, **_the entire thickness of the myocardial wall supplied by that vessel becomes ischaemic and is at risk of infarction_**. This process evolves over a series of hours and is associated with characteristic ECG changes at different time-points during its evolution. * Positive Biomarkers * ↑ CPK-MB - **Rises within 4-6 hrs of _damage_**; Peaks at 18-24 hrs, Stays elevated for **3-4days** * ↑ Detected in blood w/in **2-4 hrs after ischemia starts**; peaks 18-24 hours, stays elevated for **5-9 days**

What are some complications with an LVAD?

•Bleeding, Coagulation, Disconnection, Emboli, Drive line Infection

What is primary PCI and what is it used for?

Primary PCI: * **Procedure of choice for STEMI** * **DOOR to BALLOON time goal = 90 minutes** * Especially elder pt who may not be eligible for Thrombolytics Early Tx for Unstable NSTEMI: * V-Tachy, Hemodynamics poor, Heart Failure, ST deviations, Refractory chest pain

How would you treat a HTN urgency?

* Give Oral anti-HTN meds to decrease BP gradually over 12-24 hours to a lower BP Target * This will decrease chance of ischemia from a rapid BP change * Manage any other symptoms * Alleviate Pain, Anxiety * Monitor for escalation of BP and movement into HTN Emergency * If OK, can go home with good medical follow-up

How do calcium channel blockers Decrease Myocardial Oxygen Demand?

* (Cardizem, Cardene) * Decreases Heart Rate and contractility à decreases workload

What are the indcations for using an intra-aortic balloon pump?

**Indications:** * Acute MI, * Cardiogenic Shock refractory to meds * Ejection Fraction **Function:** * Catheter inserted through femoral until tip located in Descending Aorta * **Balloon inflates on diastole→ ↑Myocardial O2 supply** * **Balloon deflates on systole →↓LV afterload (decreases myocardial O2 demand)**

When would you start a patient on oxygen?

If SpO2

How do analgesics Decrease Myocardial Oxygen Demand?

* Morphine 2-4 mg IVP q 5 min prn) * Provides relief of pain * Reduces anxiety * Opioids will venodilate like NTG with same good effects

How do nitrates (nitroglycerine) work to Decrease Myocardial Oxygen Demands by?

Dilates peripheral veins --\> decreases Preload & Afterload thereby, decreases O2 demand

What is the pathogenesis of a HTN crisis?

* Elevated BP itself * Mechanical stress and vessel wall damage * Increased vascular permeability, activation of clotting cascade * Endothelieal damage -\> Release of vasoconstrictors * RAAS activation -\> * Angiotensin II -\> Vasoconstriction + release of Proinflammatory cytokines * Oxidative Stress -\> * Decreased Nitric Oxide (vasoconstriction)-\> Increased BP * Increased reactive Oxygen free radicals (H2O2, etc..)-\> cellular damage * Endothelial dysfunction -\> * Activated Common Final Pathway * Activated platelet adhesion * Decreased vasodilation

What can echocardiography be used for?

* Evaluates **heart structural function and heart wall movement** * Determines pt’s ejection fraction after MI to detect cardiac contractility changes * Can detect post ACS- MI complications such as: * Valvular dysfunction * Ventricular aneurysm * Akinesis or Hypokinesis (No or Decreased heart wall movement)

What are some characteristics of a NSTEMI?

* ST segment or T wave depression + Positive biomarker * Absence of ST-segment elevation in NSTEMI is understood to involve less than full thickness (partial thickness) damage of heart muscle. * There is a positive biomarker because the heart muscle is getting ischemic ST depression

What is the order of medical interventions for a NSTEMI?

* 1. ASA * 2. Oxygen (1st 6 hours) for SpO2 * 3. NTG * IV in first 48 hrs for persistent ischemia, HTN, Heart Failure * Should NOT interfere with mortality reducing beta blockers and ACE inhibitors * 4. Morphine * If NTG is unsuccessful AND other anti-ischemic meds on board) * 5. Beta Blockers (within 24 hrs) * Start PO when hemodynamically stable * May use if HTN * 6. ACE Inhibitors (within 24 hrs) * Used mostly in select patients (HFailure or LVEF