NUR 146 - WEEK 9 - Complications of MI Flashcards
Shock:
What is it?
Sympathetic Nervous Response
R-A-A-S Response
What is it:
- Situation where there is inadequate delivery of oxygen glucose to the body’s tissue
- Body responds by activating the sympathetic nervous system and RAAS
Sympathetic nervous:
- Vasoconstriction
- Tachycardia
- Increased cardiac contractility
RAAS Response:
-Vasoconstriction
- Increased sodium and fluid reabsorption
Shock:
Clinical manifestations
- Low blood pressure
- High heart rate
- Pale, sweaty skin
- Low urine output
- Loss of consciousness
Shock:
What are the types of shock?
Hypovolemic shock
Cardiogenic Shock
Distributive Shock
Septic Shock
Shock:
Hypovolemic Shock
What is it?
Examples of causes?
Treatment
Significant intravascular losses, caused by significant intravascular losses
- Most common type of shock
- Problem with preload
ex of causes: hemorrhage, dehydration, excessive diuresis
Treatment:
- Treat underlying cause of volume loss
- Fluid and blood replacement
- Medications as needed
Shock:
Distributive Shock
What is it?
What does it result in?
Intravascular volume is abnormally displaced within peripheral blood vessels, caused by massive vasodilation
Results in relative hypovolemia and inadequate tissue perfusion & reduced afterload
Subtypes:
- Septic shock
- Anaphylactic shock
- Neurogenic shock
Shock:
Cardiogenic Shock
What is it?
Cause?
Findings?
Heart cannot maintain sufficient output to meet the body’s demands d/t decreased cardiac output which leads to inadequate tissue perfusion
Cause:
- Severe left ventricular dysfunction
Findings:
- Decreased ejection fraction
- Decreased blood pressure
- Signs of decreased tissue perfusion
- Symptoms of heart failure
- Hypoxia
-
How do you know if a patient is in shock?
Blood pressure MUST be low
Cardiogenic Shock:
Goals
- Limit further myocardial damage
- Preserve healthy myocardium
- Improve cardiac function
- Increase oxygen supply to the heart and reduce oxygen demands
Cardiogenic Shcok:
Management
- Correct underlying causes
- Reduce preload and afterload –> less work for heart
- Improve oxygenation and restore tissue perfusion
- Hemodynamic monitoring
- Monitor fluid status
- Medications
Cardiogenic Shock:
Medications
Inotropic Agents:
- Work by increasing cardiac output, increase contractility
- Often in conjunction with vasodilators to decrease afterload
ex: Dobutamine, milrinone
Vasopressors:
- Work by stimulating sympathetic receptors
ex: norepinephrine, phenylephrine, neosynephrine
Cardiogenic Shock:
Intra-Arterial Balloon Pump
Temporarily used to improve heart’s ability to pump
- Threaded into the thoracic aorta via an artery
Function:
- Inflates at the beginning of diastole –> increases arterial blood flow through coronary arteries –> improved perfusion of myocardium
- Deflates at start of systole to allow blood to flow through the aorta
Heart failure:
What is it?
Risk factors?
How is it categorized?
The heart is unable to pump enough blood to meet the body’s metabolic demands
Risk factors:
- Age, ethnicity
- Smoking
- Obesity, diabetes
- Metabolic Syndrome
Categorized as:
- Left
- Right
- Systolic
- Diastolic
Heart failure:
Causes?
CAD / Athersclerosis
MI
Hypertension
Cardiomyopathy
Valvular disease
Renal Dysfunction –> Fluid overload
Heart Failure:
Describe the “vicious cycle”
Underlying pathology results in declining heart function = decreased cardiac output
Body compensates for decreased cardiac output by activating compensatory mechanisms
- Compensatory mechanisms elevate blood pressure (afterload)
- Increased afterload = increased resistance on cardiac output
End result: Heart must work even harder to maintain cardiac output, resulting in worsening heart failure
- Decreased cardiac output = body compensates which increases BP (afterload) = increased resistance on cardiac outpt = heart must work harder = decreased cardiac output
Heart Failure:
Pathophysiology of Systolic Heart Failure
Underlying patho causes decreased blood to be ejected which = decreased flow sensed by baroreceptors which = activation of sympathetic NS to release epinephrine and norepinephrine
Epi and norepi cause systemic vasoconstriction which = reduced flow to kidneys
Kidneys respond by releasing renin (RAAS) which = angiotensin II which = vasoconstriction and release of aldosterone which = increased vasoconstriction and sodium retention
All of these mechanisms lead to more work for the heart
- low blood ejection = activation of catecholamines = vasoconstriction = less blood to kidneys = RAAS = vasoconstriction + higher blood pressure = more work for heart
-
Heart Failure:
Pathophysiology of Diastolic HF
Ventricular cells are fibrotic and stiff, so they resist filling with blood –> less blood enters the ventricles with each diastole
End result is decreased cardiac output
- Ejection fraction may be slightly decreased to around 50%, but not as low as with systolic HF
Heart Failure:
Left Side Heart Failure
Pathophysiology
What is it?
Risk factors?
Left ventricle does not pump blood efficiently
Blood backs up into left atrium –> blood backs up into lungs –> pressure builds up in pulmonary vessels and fluid is forced out of vessels into interstitial areas
Risk factors:
- Hypertension
- CAD, MI
- Valvular disease –> Increased afterload
Think: “Left = Lungs”
Heart Failure:
Left Side Heart Failure
Clinical Manifestations
Clinical manifestations r/t excess fluid in pulmonary tissues:
- Dyspnea
- Dry non-productive cough, may develop into a cough with pink frothy sputum
- Rales
Clinical manifestations r/t poor cardiac output:
- Altered digestion, dizziness, lightheadedness, confusion,
Heart Failure:
Pathophysiology of Right Side Heart Failure
What does it result in
Risk factors?
Blood backs up into right atrium –> blood backs up into vena cava and eventually into veins of the body –> pressure within the veins build up and fluid is forced out of blood vessels into the interstitial areas
Results in venous distention and systemic edema
Risk factors:
- Uncontrolled left sided heart failure
- Right ventricle MI
- Pulmonary disease
Heart Failure:
Right Side Heart Failure
Clinical Manifestations
Clinical Manifestations r/t excess fluid in venous system:
- Jugular Venous Distention (JVD)
- Hepatomegaly (and maybe secondary liver dysfunction)
- Ascites
- Weight gain
- Edema
Clinical manifestations r/t poor cardiac output:
- Generalized weakness
Congestive Heart Failure (CHF):
What is it?
Combination of left and right sided heart failure
Left side –> pulmonary congestion –> more work for right ventricle –> right sided heart failure
Manifestations:
- Includes those of both left and right side failure
Heart Failure:
Diagnostic Findings
Classification of HF:
- Classified using a staging system
-
Diagnostic tests:
- Echocardiogram to measure ejection
- Chest X Ray
- EKG
Labs: BNP, electrolytes, BUN/Cr, LFT, TSH, CBC, UA
Heart Failure:
Management
Treatment Goals:
- Improve cardiac function (Decrease preload & afterload)
- Reduce symptoms, improve functional status
- Stabilize condition and reduce risk of hospitalization
- Delay progression of HF to extend life expectancy
Treatment Options:
- Medications
- Lifestyle
- Modifications
- Supplemental oxygen
- Surgical interventions
Heart Failure:
Medications - Diuretics
Loop diuretics and thiazide diuretics:
- Furosemide (loop), hydrochlorothiazide
- “Less fluid in blood = less work on heart”
- Often first line treatment in patients with HF and severe volume overload
- Results in increased urine output
- Monitor for hypotension, electrolyte abnormalities (decreased K+), I&Os, daily weights
Aldosterone antagonists:
Spironolactone “Potassium-sparing diuretics
- Work by blocking effects of aldosterone –> results in excretion of sodium & water
- Monitor potassium & sodium
