chp 27

cardiac tamponade

• life-threatening condition where fluid or blood rapidly accumulates in the pericardial sac, increasing pressure and preventing the heart from filling during diastole

• risk factors: pericardial effusion, chest trauma, coagulation disorders, MI, drug reaction

• S/S: hypotension, JVD, muffled heart sounds, diaphoresis, decreased urine output, anxiety, weak and thready pulse, tachycardia

Diagnosis: echocardiogram, chest x-ray, ecg

Treatment: pericardiocentesis (needle aspiration), surgery (pericardial window), IVF, inotropic (dopamine)

CAD

• atherosclerotic plaque develops in a coronary artery

  • → narrowed arterial lumen

  • decreased coronary blood flow

  • reduced myocardial oxygen supply

  • myocardial ischemia

• complications:

  • angina, MI

  • dysrhythmias, HF

  • sudden cardiac death

• triggers

  • exercise or emotional stress

  • tachycardia, HTN

  • fever, cold exposure

classification of CAD

chronic ischemic heart disease

• fixed coronary narrowing → predictable reduction in blood flow during increased demand

• typical findings

  • stable angina with exertion or emotional stress

  • relief with rest or prescribed nitroglycerin

  • silent ischemia may occur in older adults or clients with DN

  • vasospastic (variant) angina may occur at rest because of temporary coronary artery spasm

acute coronary syndrome

• plaque disruption

  • → platelet adhesion

    • → thrombus formation

      • → sudden reduction in coronary blood flow

  • includes: unstable angina, NSTEMI, STEMi

evaluation coronary ischemia and MI

Electrocardiogram

• Detects ischemic changes

• ST-segment elevation may indicate STEMI

• ST-segment depression or T-wave inversion may indicate ischemia

• Abnormal Q waves may indicate new or old infarction

Cardiac biomarkers

• Troponin is the primary marker of myocardial injury

• Serial measurements help identify a changing pattern

• CK-MB may support evaluation of reinfarction

Echocardiogram

• Evaluates ventricular function

• Identifies wall-motion abnormalities

• Assesses valves and ejection fraction

Stress testing or myocardial perfusion imaging

• Used primarily to evaluate suspected stable ischemia

• Helps identify inducible ischemia

STEMI

Pathophysiology

Complete coronary artery occlusion
  → prolonged myocardial ischemia
  → myocardial cell injury and necrosis
  → ST-segment elevation on the ECG

Typical presentation

• Sudden, pressure-like or crushing substernal chest pain

• Pain may radiate to the arm, shoulder, neck, jaw, or back

• Pain may persist despite rest or prescribed nitroglycerin

• Diaphoresis, nausea, vomiting, dyspnea, or weakness

• Pale, cool, clammy skin

• Anxiety or a sense of impending doom

• Tachycardia or hypotension

Atypical presentation

• Women, older adults, and clients with DM may report à unexplained fatigue, SOB, indigestion-like discomfort, weakness, dizziness, nausea, minimal or no chest pain

factors determining the extent of MI

• Location of the blockage (proximal blockages = larger infarcts)

• Size of area supplied

• Duration of the occlusion (time = muscle)

• Metabolic needs of the affected tissue

• Collateral circulation (alternative blood supply pathways). Well-developed collaterals = smaller infarct size.

• Hemodynamic status (heart rate, blood pressure, and cardiac rhythm). Abnormal rhythm or low BP can worsen myocardial injury

complications of MI

• Heart failure- damaged myocardium cannot pump effectively

• Cardiogenic shock- severe pump failure; inadequate tissue perfusion

• Pericarditis- inflammation of the pericardium 2-3 days after MI

• Thromboembolism- blood clot forms in damaged ventricle

• Rupture of the heart- tear in ventricular wall, septum, or papillary muscle; w/in first week; often fatal

• Ventricular aneurysms- weakened, bulging area of ventricular wall

• Complications may occur immediately or days to weeks after an MI

medical management following MI

• Treatment goals: restore blood flow, reduce heart workload, prevent complications, improve long-term outcomes

• MONA

• Thrombolytic therapy (clot-busting drugs given if percutaneous coronary intervention [PCI] not available)

• Revascularization procedures

  • PCI- balloon angioplasty +/- stent, preferred for STEMI, goal door-to-ballon time < 90 min

  • Coronary artery bypass grafting (CABG)- surgical bypass of blocked artery

• Cardiac rehabilitation programs- Supervised exercise program w/ education on lifestyle modification

chronic ischemic heart disease

• Occurs when there is an imbalance between myocardial oxygen supply and oxygen demand over time

  • Decreased oxygen supply (less blood flow)

    • Atherosclerosis- plaque build up

    • Coronary vasospasm- sudden artery constriction

    • Thrombosis- blood clot blocking blood flow

  • Increased oxygen demand- stress, exercise, cold, tachycardia, hypertension

angina classification

• Angina occurs when the heart muscle does not receive enough oxygen (ischemia)

• Chronic stable angina- fixed narrowing of coronary arteries (atherosclerosis)

  • Occurs with exertion, stress, cold exposure; relief w/ rest, nitroglycerin; predictable pattern

• Silent myocardial ischemia- ischemia w/out chest pain

  • Common in pts w/ DM, older adults; detected by ECG changes, stress testing

• Variant (vasospastic or Prinzmetal) angina- coronary artery spasm

  • Often at rest, frequently at night/early morning; transient ST-segment elevation; tx CCB, nitrates

unstable angina

Atherosclerotic plaque ruptures
→ thrombogenic material is exposed
  → platelets adhere and aggregate
  → the coagulation cascade is activated
  → a thrombus forms
  → coronary blood flow ↓ suddenly

Clinical pattern:

• Unstable angina is part of acute coronary syndrome and may present with:

  • New-onset severe chest discomfort

  • Pain occurring at rest or with minimal exertion

  • Pain that is more frequent, intense, or prolonged than usual

  • Symptoms lasting longer than 20 minutes

  • Symptoms that are not fully relieved by rest or prescribed nitroglycerin

cardiomyopathies

Cardiomyopathies are a heterogeneous group of diseases of the myocardium associated with mechanical and/or electrical dysfunction

Primary Cardiomyopathies

• Confined to the myocardium

• Genetic- hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy (ARVC)

• Mixed (genetic & nongenetic origin)- dilated cardiomyopathy, primary restrictive cardiomyopathy

• Acquired- origin is inflammatory (myocarditis), stress (Takotsubo), or pregnancy (peripartum cardiomyopathy)

• Idiopathic cardiomyopathy- cause is unknown

Secondary Cardiomyopathies

• Conditions in which the cardiac abnormality results from another cardiovascular disease, such as myocardial infarction

hypertrophic cardiomyopathy HCM

• Genetic defects in contractile proteins

• Heart muscle thickens (hypertrophy), especially in the interventricular septum, left ventricular chamber becomes smaller

• Functional effects- impaired ventricular filling (diastolic dysfunction), possible left ventricular outflow obstruction, increased oxygen demand, reduced cardiac efficiency

• Clinical risks- syncope w/ exertion, dyspnea, CP, arrhythmias, sudden cardiac death (young athletes)

dilated cardiomyopathy

• A condition in which the ventricles enlarge and weaken, leading to poor systolic function

• Characteristics- enlarged (dilated) ventricles (often left first), thin myocardial walls, decreased contractility, reduced EF; big and weak pump

• Manifestations- fatigue, dyspnea on exertion, orthopnea, peripheral edema, S3 heart sound, arrhythmias, signs of heart failure

• Treatment- ACEi, ARBs, BB, diuretics, aldosterone antagonists, anticoagulation, implantable cardioverter device (ICD), heart transplant

aortic valve stenosis and regurgitation

• When heart valves malfunction blood flow becomes abnormal

• Stenosis: valve does not open fully

  • Narrowed valve opening, blood flow is obstructed, heart must work harder to push blood forward

  • Will hear murmur when valve is open, turbulent blood flow through a tight opening

  • Memory tip: stenosis = stiff & narrow

• Regurgitation (insufficiency): Valve does not close fully

  • Valve leaks backward, blood flows in the wrong direction, volume overload of heart chamber

  • Will hear a murmur when the valve should be closed, sound of blood leaking backward

  • Memory tip: regurgitation = reverse flow

• Atrioventricular (AV) valves (mitral & tricuspid) located between atria and ventricles

• Semilunar valves (aortic & pulmonary) are located between ventricles and great arteries

heart failure

• Can be classified based on:

  • Pump function: systolic (HFrEF) or diastolic (HFpEF) failure

    • Is the heart failing to pump out enough blood or failing to accept enough blood from the body/lungs?

  • Side affected: right-sided or left-sided failure

    • Is the right or left side of the heart failing?

  • Cardiac output: high-output versus low-output failure

    • Is cardiac output high or low?

systolic vs diastolic function in HF

Systolic dysfunction

• Heart cannot pump effectively

• Decreased ejection fraction less than 40%, weak contraction, blood remains in ventricle, forward flow decreases

• Think “weak squeeze”

• Common causes- MI, dilated cardiomyopathy

Diastolic dysfunction

• Heart cannot relax and fill properly

• Normal ejection fraction, stiff ventricle, impaired filling, increased filling pressures

• Think “stiff ventricle”

• Common causes- HTN, left ventricle hypertrophy, aging

HR right vs left

Right-Sided Heart Failure: Right ventricle cannot pump blood forward to the lungs.

• Systolic: RV cannot pump effectively → ↓ blood to lungs

• Diastolic: RV cannot relax/fill → ↓ forward flow

• What Happens? Blood backs up into the systemic circulation. Right heart → veins → body

• Memory tip: Right = Rest of body

Left-Sided Heart Failure: Left ventricle cannot pump blood forward to the body.

• Systolic: LV cannot pump enough blood to body

• Diastolic: LV cannot relax/fill properly

• What Happens? Blood backs up into the pulmonary circulation.

• Left heart → lungs

• Memory tip: Left = Lungs

 

heart failure output: high vs low

High Output: The heart pumps normally or even excessively, but the body’s demand is too high. Cardiac output may be normal or elevated. Peripheral vasodilation. Persistent demand exceeds supply.

• Causes: severe anemia, hyperthyroidism, sepsis, pregnancy, AV fistula

• Clinical Signs: warm extremities, bounding pulses, tachycardia, signs of fluid overload

• Think: demand problem

Low Output (most common): The heart cannot pump enough blood to meet the body's needs. Decreased cardiac output. Poor tissue perfusion. Compensatory vasoconstriction

• Causes: myocardial infarction, cardiomyopathy, severe valve disease, advanced hypertension

• Clinical Signs: cold, pale extremities, weak pulses, fatigue, confusion, possible cyanosis

• Think: pump failure

manifestations of heart failure

Impaired pumping →

• ↓ CO: fatigue, weakness, exercise intolerance, confusion (late)

• Blood back-up: Left-sided leads to pulmonary congestion. Right-sided leads to systemic congestion.

• ↓ renal blood flow à RAA pathway à

  • Fluid overload, edema, increased preload, worsening heart failure. Body tries to compensate but makes it worse.

• SNS à Tachycardia, ↑ contractility (initially) vasoconstriction, ↑ afterload. Overtime leads to ↑ myocardial oxygen demand, ventricular remodeling, further pump failure.

heart failure diagnosis

• Stages of Heart Failure (ACC/AHA)

  • Stage A: At risk (HTN, CAD, diabetes). No structural disease yet

  • Stage B: Structural heart disease. No symptoms

  • Stage C: Structural disease. Current or prior symptoms

  • Stage D: End-stage heart failure. Refractory symptoms

• Blood Tests: BNP or NT-proBNP (elevated in HF). Electrolytes. BUN/Creatinine. Troponin (if acute).

• Diagnostic Tests: Echocardiogram (EF measurement). Chest X-ray (cardiomegaly, congestion). ECG. Cardiac MRI (if needed)

heart failure treatment

• Non-Pharmacologic: Sodium restriction, fluid restriction (if severe), daily weights, smoking cessation, cardiac rehab, monitor for worsening symptoms

• First-Line (Guideline-Directed Therapy): ACE inhibitors or ARBs, beta blockers, aldosterone antagonists, SGLT2 inhibitors

• Symptom Relief

  • Diuretics (Furosemide/Lasix)

• Reduce fluid overload

• Decrease edema

• Improve breathing

circulatory failure

• Inadequate tissue perfusion

  • → insufficient oxygen and nutrients to cells

  • → anaerobic metabolism

  • → lactic acid build up

  • → metabolic acidosis

  • → cell death & organ dysfunction

Types

• Hypovolemic

• Cardiogenic

• Obstructive

• Distributive

• Neurogenic

• Anaphylactic

• Sepsis

hypovolemic shock

• Acute loss of 15% or more of circulating blood volume- results in decreased preload, decreased cardiac output, and decreased tissue perfusion

• Cause is loss of volume- hemorrhage, fluid loss (dehydration), third spacing

• Compensatory mechanisms- SNS & RAAS activation

Manifestations

• Early- tachycardia, cool/clammy skin, delayed cap refill, restlessness/anxiety, decreased urine output

• Late- hypotension, altered LOC, weak/absent pulses, metabolic acidosis

cardiogenic shock

• Heart fails to pump blood effectively leading to decreased cardiac output and inadequate tissue perfusion

• Causes- acute MI (most common), severe HF, cardiomyopathy, dysrhythmias, valve failure

• SNS & RAAS activation

• Vasoconstriction increases resistance to blood flow

• Increased workload on the heart worsens heart failure

obstructive shock

• Shock caused by a mechanical obstruction to blood flow → Prevents adequate cardiac filling or ejection
  → Leads to ↓ cardiac output and ↓ tissue perfusion

• Causes- pulmonary embolism, cardiac tamponade, tension pneumothorax, aortic dissection, evisceration (increased right heart pressure)

distributive shock

• Shock caused by widespread vasodilation
  → Severe ↓ systemic vascular resistance (SVR)
  → Relative hypovolemia
  → ↓ Tissue perfusion

• The blood vessels are too dilated. The volume may be normal, but the vascular container is too large.

• Types- septic (infection), anaphylactic (allergy), & neurogenic (spinal cord injury)

• Memory tip = container is too big

sepsis (SIRS)

Infection → Immune system overactivation → Bacteria release endotoxins → Immune cells release inflammatory mediators:

• Tumor Necrosis Factor (TNF-α), interleukin-1 (IL-1), other cytokines

What Do These Mediators Do?

• Increase Metabolic Demand- Tissues require more oxygen. ↑ Cellular metabolism. ↑ Oxygen consumption

• Cause Widespread Vasodilation- ↓ Systemic vascular resistance (SVR). Warm, flushed skin (early). ↓ Blood pressure

• Increase Capillary Permeability- Fluid leaks into tissues. Relative hypovolemia. Edema.

• Activate Coagulation Pathways- Microclots form in small vessels. Impaired microcirculation. Risk for DIC (disseminated intravascular coagulation)

treatment to correct and reverse shock

Treatment Goals- Restore tissue perfusion, improve oxygen delivery, correct the underlying cause, prevent organ failure

Restore Circulating Volume- Fluid resuscitation (IVF), blood products (if indicated), used primarily in hypovolemic and septic shock

Control the Cause- Stop bleeding (hypovolemic), antibiotics (septic), remove obstruction (PE, tamponade),  revascularization (cardiogenic, MI)

Improve Oxygen Delivery- Supplemental oxygen, mechanical ventilation if needed, maintain adequate hemoglobin levels, goal is to increase oxygen available to hypoxic tissues

Support Hemodynamics- Vasopressors if fluids insufficient (norepinephrine, epinephrine, dopamine). Inotropes for cardiogenic shock (dobutamine), goal is MAP >65 mmHg and ensure organ perfusion

complications of shock

• Acute lung injury (acute respiratory distress syndrome - ARDS)

• Acute renal failure

• Gastrointestinal complications

• Disseminated intravascular coagulation (DIC)

• Multiple organ dysfunction syndrome (MODS)

GI complications

• Shock → widespread vasoconstriction → redistribution of blood to brain & heart → severe ↓ mucosal perfusion → ischemia of stomach & intestines → cellular ATP depletion → mucosal breakdown & ulcer formation

• GI tract is vulnerable because: high metabolic demand, dependent on constant blood flow, protective mucous barrier ↓ during shock, intolerance to enteral nutrition worsens hypoperfusion

Manifestations:

• Early: loss of appetite, nausea, vomiting

• Within hours (trauma, sepsis, burns): superficial gastric & duodenal lesions

• 2–10 days after insult: sudden GI hemorrhage, bowel obstruction, occult or overt bleeding