Exam 2 Patho Master Set

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What are characteristics of an MI?

Irreversible myocardial necrosis due to prolonged ischemia (STEMI vs NSTEMI)

What is STEMI?

ST elevation MI, complete blockage of a coronary artery

What is a NSTEMI?

non-ST elevation myocardial infarction, from a Mural Thrombus with potential to Embolize.

(partial blockage of smaller area of ischemia)

What is the pathophysiology of a myocardial infarction?

• Atherosclerosis leads to plaque rupture and then thrombus formation.
• The coronary artery has occlusion (blockage of artery), leading to myocardial ischemia, which would lead into
• Cell injury, eventually necrosis, and then decreased cardiac function

What is the clinical manifestation of MI?

• Chest pain (angina)
• Dyspnea
• Diaphoresis
• Nausea
• Anxiety
• Fatigue

What do lab tests look for in Myocardial Infarction?

• Increased troponin
• Increased CK-MB
• ECG changes, ST elevation/depression
• Echo abnormalities

What are the risk factors for MI?

CAD, HTN, DM, Smoker, Hyperlididemia, PHx of CAD < 55 yo

• obesity, age, etc

What is troponin

a protein found in the heart muscle. It is released into the bloodstream when the heart muscle is damaged, such as during a heart attack

What is dyslipidemia?

abnormal amount of lipids in the blood

What do lipoproteins do?

they carry various lipid (triglycerides)/cholesterol components to tissues

What does LDL do?

transports cholesterol to cells

• LDL is absorbed by tissues and 70% is returned to the liver

What does HDL do?

HDL circulates to the tissues and takes up excess free cholesterol and takes it back to the liver

What are the two types of dyslipidemias?

Primary (genetics), and secondary (lifestyle, etc.)

What can secondary dyslipidemia stem from?

Diet, obesity, sedentary lifestyle, diabetes

What can contribute to atherosclerosis?

High LDL and low HDL

What is ventricular fibrillation?

Chaotic, disorganized ventricular electrical activity, which causes no effective contraction, and eventually no cardiac output

What are the causes of ventricular fibrillation?

• Acute myocardial Ischemia/Infarction
• Electrolyte imbalances (increase in potassium, decrease in magnesium)
• Heart failure, cardiomyopathy
• QT prolongation, drug toxicity, electrocution

What is the pathophysiology of Ventricular Fibrillation?

• Multiple ectopic foci in ventricles firing rapidly and asynchronouslyq
• No organized depolarization, causing no pulse or perfusion, leading to cardiac arrest

What is the ECG for Ventricular Fibrillation?

No P, QRS, or T waves

• Irregular, chaotic baseline ("bag of worms" appearance)

What is the treatment for ventricular fibrillation?

Immediate defibrillation + CPR

• Correct underlying cause after ROSC

What is ROSC?

Return of spontaneous circulation during arrest,
Revascularize and fix the electrolytes within the patient

What are the phases of MI with Ischemia on EKG?

(reversible) ST depression, T-wave inversion, due to transient O2 deprivation

What does an injury MI on an EKG look like?

(acute, potentially reversible), ST elevation with a STEMI pattern
this would indicate acute, transmural damage (blood vessel damage)

What does an infarction look like on an EKG?

(necrosis, irreversible) Pathologic Q waves, which would indicate dead myocardium, no depolarization

What does a 1st Degree AV Block consist of?

PR interval > 0.20s (constant), with a delay in AV nodal conduction

what does 2nd degree AV Block - Type I Mobitz I (Wenckeback) consist of?

Progressive PR lengthening leading to dropped QRS, due to fatigue of AV node

what does 2nd degree AV Block - Type II Mobitz II consist of?

Dropped QRS complexes without PR prolongation, with a block below AV node (His-Purkinje system) leading to a dangerous state

What does a 3rd degree AV block consist of?

Atria and ventricles beating independently (AV dissociation), with a ventricular escape rhythm present.

aka complete

What is CK-MB?

Creatinine Kinase - Myocardial Banding.
Byproduct of cell death specific to heart.

What's the difference between ischemia and infarction?

Ischemia: reversible, no necrosis, ST depression/T inversion, normal troponin

Infarction: Irreversible, necrosis present, ST elevation or Q waves, elevated troponin

Heart Failure

A complex clinical syndrome caused by reduced cardiac output that is insufficient to meet the body's metabolic needs.

Mechanisms of Heart Failure

Problems with pumping (impaired ejection of blood from ventricles) and filling (inadequate ventricular filling causing low output).

Common Ischemic Causes of Heart Failure

Ischemic heart disease such as angina or prior myocardial infarction.

Common Non-Ischemic Causes of Heart Failure

Valvular disease, arrhythmias, myocarditis, hypertrophy, inflammation, or obstruction.

Heart Failure Affected Sides

Both sides are usually involved, though one side may show predominant symptoms.

Types of Heart Failure

Left-sided heart failure and right-sided heart failure.

Left-Sided Heart Failure

Failure of the left ventricle to pump blood effectively into the systemic circulation.

Causes of Left-Sided Heart Failure

Ischemic heart disease, hypertension, or valvular disorders affecting the left heart.

Blood Flow in Left-Sided Heart Failure

Blood backs up into the lungs, leading to pulmonary congestion.

Common Symptoms of Left-Sided Heart Failure

Shortness of breath, orthopnea, paroxysmal nocturnal dyspnea, and fatigue.

Physical Exam Findings in Left-Sided Heart Failure

Pulmonary crackles, tachypnea, and signs of pulmonary edema.

Right-Sided Heart Failure

Failure of the right ventricle to pump blood effectively into the pulmonary circulation.

Causes of Right-Sided Heart Failure

Often secondary to left-sided heart failure or pulmonary hypertension.

Blood Flow in Right-Sided Heart Failure

Blood backs up into the systemic venous circulation.

Common Symptoms of Right-Sided Heart Failure

Leg swelling, abdominal distention, and weight gain.

Physical Exam Findings in Right-Sided Heart Failure

Peripheral edema, jugular venous distension, hepatomegaly, and ascites.

Specific Blood Test for Diagnosing Heart Failure

BNP or NT-proBNP, which are elevated in heart failure.

Electrolytes to Check in Heart Failure

Sodium, potassium, and magnesium.

Complete Blood Count (CBC) in Heart Failure

To check for anemia or infection that could worsen symptoms.

Lipid Profile in Heart Failure Evaluation

To assess cholesterol and triglycerides as risk factors for heart disease.

Thyroid Function Tests in Heart Failure

Hypothyroidism can worsen heart failure or mimic its symptoms.

Imaging Test for Heart Structure and Function

Echocardiogram.

Echocardiogram Measurements in Heart Failure

Ejection fraction and wall motion abnormalities.

Dissecting Aortic Aneurysm

A tear in the intimal layer of the aorta that allows blood to enter the medial layer and form a false lumen.

Most commonly affected by aortic dissection

Men aged 50-70 years, especially with hypertension or connective tissue disorders.

Major risk factors for aortic dissection

Chronic hypertension, atherosclerosis, Marfan syndrome, Ehlers-Danlos syndrome, bicuspid aortic valve, trauma, or iatrogenic injury.

Classification system for aortic dissection

The Stanford classification system.

Stanford Type A aortic dissection

Dissection involving the ascending aorta, with or without extension into the descending aorta.

Complications of Stanford Type A dissection

Aortic rupture, cardiac tamponade, aortic regurgitation, and coronary ischemia.

Management for Stanford Type A dissection

Urgent surgical repair.

Stanford Type B aortic dissection

Dissection confined to the descending aorta, distal to the left subclavian artery.

Complications of Stanford Type B dissection

Ischemia of abdominal organs, kidneys, or limbs.

Management for Stanford Type B dissection

Medical management with blood pressure control; endovascular repair if complications occur.

Cause of aortic dissection formation

A tear in the intima allows blood to dissect through the media, creating a false lumen.

Typical symptoms of aortic dissection

Sudden, severe, 'tearing' or 'ripping' chest or back pain that may migrate.

Additional clinical findings in aortic dissection

Pulse deficits, unequal blood pressure between limbs, neurological deficits, or shock.

Diagnostic test of choice for aortic dissection

CT angiography.

Preferred imaging test for unstable patients

Transesophageal echocardiography (TEE).

Gold standard test for aortic dissection

MRI angiography, though less used in emergencies.

Chest X-ray findings in aortic dissection

Widened mediastinum or pleural effusion.

ECG findings in aortic dissection

Nonspecific changes; helps rule out myocardial infarction.

Main goal of medical management in aortic dissection

Immediate blood pressure and heart rate control to reduce shear stress.

Initial medications used in aortic dissection

Beta-blockers for heart rate and blood pressure control.

Prognosis if an aortic dissection is untreated

Up to 50% mortality within 48 hours.

Prevention of aortic dissection

By controlling hypertension and monitoring patients with known aneurysms or connective tissue disorders.

What's Cardiogenic Shock?

Circulatory failure due to inadequate cardiac output, where the heart is unable to pump enough blood to meet the demands of tissue

Leads to systemic hypoperfusion and cellular oxygen deprivation

What are the causes of Cardiogenic Shock?

• Acute myocardial infarction (most common)
• Severe heart failure (systolic or diastolic)
• Cardiomyopathy
• Severe valvular disease (e.g., aortic stenosis, mitral regurgitation)
• Arrhythmias (tachyarrhythmias or brady arrhythmias)
• Mechanical complications (ventricular septal rupture, papillary muscle rupture)

What's the pathophysiology of Cardiogenic Shock?

• DECREASE in myocardial contractility leads to DECREASE in stroke volume & cardiac output
• INCREASE in left ventricular end-diastolic pressure leads to pulmonary congestion
• Systemic HYPOperfusion leads to activation of SNS & RAAS
• Further INCREASE afterload & myocardial oxygen demand leads to worsening dysfunction

What are the clinical symptoms of Cardiogenic Shock?

• Hypotension (systolic BP < 90 mmHg)
• Tachycardia
• Cold, clammy extremities
• Jugular venous distension, pulmonary crackles
• Oliguria (low urine output)
• Altered mental status

What is the treatment for cardiogenic shock?

Aspirin and IV fluids. NO NITRO IF LOW BP (oxygen and vent. support)

• Treat underlying cause (e.g. reperfusion in MI)
• Oxygen & Ventilatory Support
• Inotropes (e.g. DOBUTAMINE) to INCREASE contractility

What's the definitive therapy for Cardiogenic Shock?

Revascularization or Surgical Correction

What should you administer if there's persistent hypotension from Cardiogenic Shock?

Vasopressors

What should you administer if there's pulmonary congestion from Cardiogenic Shock?

Be careful of the use, but use diuretics

What should you use if the Cardiogenic Shock is refractory?

Mechanical support devices (IABP, ECMO, LVAD)

IABP

balloon helps circulate blood after heart failure, inflates with diastole and deflates with systole. Used to treat cardiogenic shock. Not for dissection, AAA, complications: site infection, bleeding, clot-general aortic dissection, perforation, thrombocytopenia, dysrhythmias, myocardial failure. Nursing: EKG, monitor LOC, pt should not bed leg w/ insertion

ECMO

Extracorporeal membrane oxygenation for severe respiratory failure.

LVAD

left ventricular assist device (bridge to cardiac transplantation)

What is Hypovolemic Shock?

• Circulatory Failure due to loss of intravascular volume
• Results in DECREASED venous return leading to REDUCED stroke volume and cardiac output
• Leads to systemic hypoperfusion and inadequate oxygen delivery to tissues

What are causes of hypovolemic shock?

• Hemorrhage (trauma, GI bleed, ruptured aneurysm)
• Severe dehydration (vomiting, diarrhea, excessive sweating)
• Burns (plasma loss)
• Third-spacing of fluids (pancreatitis, peritonitis, bowel obstruction)

What is the pathophysiology of hypovolemic shock?

• DECREASED circulating blood volume leads to DECREASED preload
• DECREASED stroke volume & cardiac output leads to systemic HYPOperfusion
• Compensatory SNS & RAAS activation leads to vasoconstriction, tachycardia, fluid retention

What happens if hypovolemic shock is untreated?

It will lead to impaired cellular metabolism, anaerobic metabolism, lactic acidosis, eventually ending in multi-organ failure

What are the clinical symptoms of hypovolemic shock?

• Hypotension
• Tachycardia
• Cold, clammy skin
• Weak, thready pulse
• Oliguria (low urine output)
• Altered mental status

What is the treatment for hypovolemic shock?

Preferred treatment is immediate fluid resuscitation (restoration of fluids)

• Treat underlying cause (e.g., stop bleeding, correct fluid loss)
• Volume replacement (IV fluids: crystalloids, blood products for hemorrhage)
• Oxygen therapy
• Trendelenburg position (temporarily)
• Monitor urine output and hemodynamics
• Prevent multi-organ failure with early recognition/correction

Trendelenburg position

The body is laid flat on the back (supine position) with the feet higher than the head by 15-30 degrees, A position in which the patient's feet and legs are higher than the head

What is septic shock?

A type of distributive shock, due to overwhelming infection and systemic inflammatory response

• Resulting from sepsis with profound circulatory and metabolic abnormalities
• Defined by persistent hypotension requiring vasopressors despite adequate fluids

HIGH MORTALITY

What is distributive shock?

Circulatory failure due to abnormal distribution of blood flow LEADING TO widespread vasodilation LEADING TO relative hypovolemia

results in decreased systemic vascular resistance and impaired tissue perfusion (your BP is too low man too low)

What are causes of septic shock?

• Bacterial infections (most common: Gram-negative & Gram-positive)
• Fungal Infections
• Severe infections (less common)
• Common sources: pneumonia, urinary tract infections, abdominal infections, blood stream infections

Immunosuppression
Significant bacteremia

What is the pathophysiology of septic shock?

Infection triggers systemic inflammatory response, leading to release of cytokines and mediators

• Widespread vasodilation leads to decrease in systemic vascular resistance & relative hypovolemia
• Capillary leak leads to tissue edema & hypoperfusion
• Cellular dysfunction leads to anaerobic metabolism, lactic acidosis, organ injury

What are clinical symptoms of septic shock?

• Hypotension
• Fever or hypothermia
• Tachycardia
• Tachypnea
• Altered mental status
• Warm-flushed skin (early) leading into cold-mottled skin (late)
• Oliguria

What is the treatment for septic shock?

Preferred treatment is: ICU admission, IV administration, antibiotics stewardship (ABS)

• Early recognition and rapid intervention crucial
• Broad-spectrum antibiotics (within 1 hr of recognition)
• Aggressive IV fluid resuscitation
• Vasopressors (norepinephrine first-line) for persistent hypotension
• Oxygen therapy & ventilatory support as needed
• Source control (drain abscess, remove infected device, surgery if needed)