Cardiovascular Pathophysiology (heart failure, valve disease, cardiomyopathies, pericardial disease, arrhythmias, shock introduction)
# Lecture Summary
Subject: Cardiovascular Pathophysiology (heart failure, valve disease, cardiomyopathies, pericardial disease, arrhythmias, shock introduction)
## Key Learning Points
- Pericardial effusion = excess fluid between the two pericardial layers; severity depends on volume and rate of accumulation. Cardiac tamponade is the life-threatening extreme requiring urgent drainage.
- Cardiomyopathies: hypertrophic (septal/left ventricular wall thickening → outflow obstruction, risk in young athletes) and dilated (thin, floppy walls → poor squeeze, reduced cardiac output).
- Valve disorders: stenosis (narrowing) and regurgitation (incomplete closure) from ischemia, infection (Streptococcus → rheumatic heart disease), congenital defects, or degenerative calcification.
- Heart failure = heart's inability to pump adequate forward flow; key determinants are heart rate, stroke volume, preload, afterload, and contractility. Ejection fraction (EF) is a core measure.
- Distinguish left-sided vs right-sided heart failure by following the direction of backward flow to determine clinical signs (left → lungs; right → systemic venous congestion).
- Acute pulmonary edema is an emergent left-sided failure presentation (pink frothy sputum, severe hypoxia); treat with airway support, diuretics, inotropes, and volume/pressure management.
- BNP is a useful diagnostic/monitoring lab for volume overload (normal < 100 pg/mL; can be in the thousands in exacerbations).
- Electrical/conduction basics: SA node (60–100 bpm), AV node backup (40–60 bpm); EKG interpretation fundamentals (P, QRS, T waves), six-second strip method, and common arrhythmias including sinus brady/tach and atrial fibrillation (AFib).
- AFib: absent P waves, irregular rhythm, high thromboembolism risk → frequent need for anticoagulation (names mentioned in lecture: Coumadin, Xarelto, Eliquis, Exactaban [unclear]).
## Definitions
- Pericardial effusion: increased fluid in the pericardial space between visceral and parietal pericardium.
- Cardiac tamponade: severe compression of the heart due to rapid or large pericardial effusion causing impaired filling, decreased stroke volume, and potential cardiogenic shock.
- Cardiomyopathy: disease of the heart muscle; main types discussed:
- Hypertrophic cardiomyopathy: thickened interventricular septum/left ventricular wall causing outflow obstruction.
- Dilated cardiomyopathy: thinned, dilated ventricular walls with poor contractility.
- Valve stenosis: narrowing of a valve opening, restricting forward flow.
- Valve regurgitation (insufficiency): incomplete valve closure causing backward flow.
- Cardiac output: volume of blood pumped by the heart per minute; cardiac output = stroke volume × heart rate.
- Stroke volume: blood ejected by the left ventricle per beat.
- Preload: ventricular volume/pressure just before systole (venous return + residual volume left after previous beat).
- Afterload: pressure/resistance the heart must overcome to eject blood (systemic vascular resistance/PVR).
- Contractility (inotropy): intrinsic strength of cardiac muscle contraction; affected by myocardial health and medications (inotropes).
- Ejection fraction (EF): percentage of ventricular volume ejected per beat; normal ~60–70%. Lower EF indicates systolic dysfunction.
- BNP (B-type/Natriuretic Peptide): hormone released from atria/ventricles in response to volume/pressure overload; used diagnostically (desirable < 100 pg/mL).
- Orthopnea: shortness of breath when lying flat.
- Nocturnal dyspnea (paroxysmal nocturnal dyspnea): sudden nighttime breathlessness.
- Jugular venous distention (JVD): visible neck vein distention from increased central venous pressure.
- Pitting edema: peripheral edema that retains an indentation with pressure.
- Inotropes: medications that increase contractility (e.g., digoxin mentioned).
- Six-second strip: telemetry EKG recording of 6 seconds; count QRS complexes and multiply by 10 to estimate heart rate.
- Telemetry: continuous cardiac electrical monitoring.
- P wave: atrial depolarization on ECG.
- QRS complex: ventricular depolarization on ECG.
- T wave: ventricular repolarization on ECG.
- PR interval, QRS duration, QT interval: time measurements used to assess conduction timing (see values below).
## Detailed Topic Notes
Topics are presented in chronological order as in lecture.
### Pericardial Effusion and Cardiac Tamponade
- Anatomy review: heart has two pericardial layers (visceral adhering to heart; parietal forming an outer sac). Small amount of pericardial fluid is normal for lubrication.
- Pericardial effusion = increase of fluid between pericardial layers. Common causes: postoperative (especially after open-heart surgery), malignancy, infection, trauma.
- Severity depends on amount and rate of accumulation. Slow/routine effusions may be monitored; large or rapidly accumulating effusions may require drainage (pericardiocentesis or surgical drainage).
- Cardiac tamponade: life-threatening state when pericardial pressure limits diastolic filling → decreased stroke volume and cardiac output → potential cardiogenic shock. Common causes: post-surgical bleeding, blunt chest trauma.
- Imaging example discussed: axial CT showing large circumferential fluid collection around heart; heart compression reduces effective contraction and filling; such cases often require drainage.
- Clinical implication: monitor post-cardiac surgery patients for effusion/tamponade; evaluate hemodynamics and imaging.
### Cardiomyopathies
- Hypertrophic cardiomyopathy (HCM):
- Pathology: asymmetric septal hypertrophy (thickened septum/left ventricular wall).
- Physiology: dynamic obstruction of left ventricular outflow, worse with exertion → decreased forward flow; predisposes to arrhythmias and sudden cardiac death (noted risk in athletes).
- Clinical: may be detected in younger individuals; important reason for thorough sports physicals.
- Dilated cardiomyopathy (DCM):
- Pathology: ventricular dilation and thin, floppy walls → poor contractility and low stroke volume.
- Clinical: progressive heart failure; many patients become candidates for transplant.
- Note on causes: cardiomyopathies can be genetic, post-infectious, ischemic, toxin-related, or idiopathic.
### Valve Disorders
- Review of valves: four valves ensure unidirectional flow; atrioventricular valves (tricuspid, mitral) and semilunar (pulmonic, aortic).
- Common etiologies of valve disease:
- Ischemia/MI causing papillary muscle dysfunction or valve leaflet damage.
- Infection/endocarditis (Streptococcus commonly implicated; untreated strep → rheumatic heart disease).
- Congenital malformations.
- Degenerative calcification with aging (calcium deposition stiffens leaflets → stenosis).
- Types of valve dysfunction:
- Stenosis: narrowed opening; valve may open incompletely (reduces forward flow). Example: aortic stenosis from calcification → increased afterload and left ventricular hypertrophy.
- Regurgitation: valve does not close properly → backflow (e.g., mitral regurgitation → left atrial pressure increase → pulmonary congestion).
- Mixed presentation possible (stenosis + regurgitation).
- Diagnosis: auscultation for murmurs; echocardiography for leaflet/flow assessment.
- Treatment: medical management, valve repair/replacement (aortic valve replacement common and often successful).
### Heart Failure: Fundamentals
- Cardiac output = stroke volume × heart rate. Normal heart rate: 60–100 bpm.
- Stroke volume determinants: preload, afterload, contractility.
- Preload: volume in ventricle before systole. Practically includes residual blood left after previous beat (20–30% of volume remains normally) plus venous return. Preload sets the initial stretch and filling.
- Afterload: pressure/resistance the ventricle must overcome to eject blood (systemic vascular resistance/PVR); high afterload (e.g., hypertension) increases ventricular work.
- Contractility: intrinsic strength of myocardial contraction. Can be increased by inotropic drugs (digoxin mentioned) or decreased deliberately to rest the heart in certain post-MI settings.
- Ejection fraction (EF): normal ~60–70% (heart ejects ~60–70% of volume each beat). In heart failure EF drops (examples given: EF 40% or 30% signifies significant systolic dysfunction).
- Compensatory mechanisms: SNS activation, RAA (renin-angiotensin-aldosterone) system activation, ventricular remodeling (hypertrophy), which initially maintain output but later worsen heart function.
- Clinical points:
- Athletic individuals may have lower resting HR due to increased stroke volume and better contractility.
- Hypertension → chronic increased afterload → concentric hypertrophy (thicker wall) → eventual reduced contractility and heart failure.
- Digoxin increases inotropy; some medications reduce contractility briefly to rest the heart after infarction.
- Mechanical supports: intra-aortic balloon pump (balloon pump), ventricular assist devices (VADs), and ultimately heart transplantation in selected patients.
- Fluid-volume facts:
- Normal ejection fraction concept reiterated: heart normally ejects 60–70% and retains remainder to start next cycle.
- 1 liter of retained fluid ≈ 2.2 pounds weight gain.
- BNP is released in response to volume overload; useful for diagnosis and monitoring (goal < 100 pg/mL).
### Left-Sided vs Right-Sided Heart Failure (etiology vs signs/symptoms)
- Important teaching point: differentiate etiology (cause) from backward-flow signs/symptoms. Students often confuse which side causes which symptoms.
- Left-sided heart failure:
- Common etiologies: myocardial infarction (ischemia) or long-standing hypertension.
- Pathophysiology: left ventricle fails → blood backs up into left atrium → pulmonary veins → pulmonary circulation.
- Clinical manifestations (follow backward flow → lungs): pulmonary congestion, crackles (rales) especially at lung bases, orthopnea (needs multiple pillows), paroxysmal nocturnal dyspnea, hypoxia, possible pink frothy sputum in acute edema.
- Right-sided heart failure:
- Common etiologies: primary lung disease (COPD, pulmonary pathology) or secondary to left-sided failure.
- Pathophysiology: right ventricle fails → blood backs up into right atrium → systemic venous system.
- Clinical manifestations (follow backward flow → systemic venous): peripheral edema (legs/ankles), pitting edema, jugular venous distention (JVD), hepatomegaly, ascites, generalized fluid retention and weight gain.
- Practical mnemonic: left → lungs (L and L); right → rest of the body (systemic venous signs).
- Management overlaps but targets the underlying cause (control blood pressure and treat ischemia for left; treat lung disease or manage left failure if secondary for right).
### Acute Pulmonary Edema (emergent presentation)
- Occurs with sudden severe left ventricular failure (e.g., massive MI leading to abrupt loss of forward flow).
- Pathophysiology: rapid pulmonary capillary hydrostatic pressure increase → massive transudation of fluid into alveoli.
- Classic sign: pink frothy sputum (blood-tinged, foamy sputum) — emphasized as a test-relevant finding.
- Clinical picture: sudden severe hypoxia, cyanosis, respiratory distress. Often need intubation/ventilation and aggressive management.
- Acute management priorities:
- Airway protection (intubation if needed).
- Rapid diuresis (e.g., intravenous furosemide/Lasix) to remove intravascular volume.
- Inotropes and vasodilators as indicated to support cardiac output and reduce afterload.
- Albumin may be used to shift fluid back into the vascular space in some contexts.
- Consider mechanical support (IABP, VAD) in refractory cases.
- Diagnostics: chest X-ray (pulmonary edema, enlarged cardiac silhouette), BNP elevation, echocardiography or TEE for function and structural assessment.
### Heart Failure Monitoring and Outpatient Management
- Frequent monitoring strategies: daily weights, blood pressure checks, medication adjustment (Lasix dosing is commonly titrated — described as a "Lasix game").
- Heart failure clinics and programs may include daily phone follow-up, home monitoring devices, and close outpatient adjustments to prevent hospital readmissions.
- Lifestyle: sodium restriction (low-salt diet) and adherence to medications are emphasized to prevent fluid overload.
- Devices: implantable defibrillators; mention of a wearable vest called "Zolvest" in lecture (term presented as "Zolvest" — [unclear]); vest used as temporary external defibrillator prior to permanent device.
- Advanced options: valve replacements, VADs, and heart transplantation in select patients (younger candidates more likely).
### Electrical Conduction and Arrhythmias (intro)
- Conduction system review:
- SA node: primary pacemaker, 60–100 bpm.
- AV node: secondary pacemaker, 40–60 bpm.
- Bundle of His and Purkinje system conduct to ventricles.
- ECG basics:
- P wave = atrial depolarization.
- QRS = ventricular depolarization.
- T wave = ventricular repolarization.
- Small square on ECG paper = 0.04 seconds; large square = 0.2 seconds.
- Typical QRS duration ≈ 0.12 seconds; QT interval ~0.44 seconds (values given in lecture; students not required to memorize all in detail but useful for practice).
- Heart rate estimation:
- Six-second strip method: count QRS complexes in 6-second strip and multiply by 10 for bpm (used for telemetry strips).
- Eyeballing regularity: assess if spacing between complexes is consistent (regular) or variable (irregular).
- Interval measurements:
- PR interval measures atrial to ventricular conduction time.
- QRS duration measures ventricular depolarization time.
- QT interval measures total ventricular depolarization + repolarization time. Some drugs can prolong QT and increase arrhythmia risk.
### Common Rhythms Covered
- Sinus bradycardia:
- Rhythm: sinus with all waves present but HR < 60 bpm.
- Clinical context: may be normal in athletes; may be symptomatic in others (dizziness, syncope). Assess for medication effects (e.g., digoxin).
- Sinus tachycardia:
- Rhythm: sinus with HR > 100 bpm.
- Causes: fever, pain, anxiety, hyperthyroidism (e.g., Graves' disease example), caffeine, nicotine, exercise, etc.
- Atrial fibrillation (AFib):
- ECG features: absence of distinct P waves, irregularly irregular rhythm, variable R–R intervals.
- Physiology: chaotic atrial electrical activity → ineffective atrial contraction → stasis of blood in atria (especially left atrial appendage).
- Clinical consequence: high risk of thrombus formation and embolic stroke; many AFib patients require anticoagulation.
- Anticoagulants mentioned in lecture: Coumadin (warfarin), Xarelto, Eliquis, Exactaban [unclear]. Also mentioned mechanical options (filters) to reduce embolic risk.
- Rate/rhythm control and anticoagulation selection depend on patient context.
### Telemetry Strip Examples (brief)
- Example six-second strips were shown and interpreted:
- Counting QRS complexes and multiplying ×10 for approximate heart rate (e.g., 8 QRS ×10 = ~80 bpm).
- Examples of bradycardic strip (~40 bpm) and tachycardic strip (~130 bpm) illustrated.
- Importance of correlating rhythm with symptoms and clinical context (athlete, medications, fever, thyroid disease).
## Exam Callouts
- Key exam focus: distinguishing left-sided versus right-sided heart failure (etiology vs signs/symptoms). Follow the backward flow of blood to predict clinical manifestations (left → pulmonary; right → systemic).
- Acute pulmonary edema: classic test finding — pink frothy sputum; recognize as emergent left-sided failure.
- Importance of understanding preload, afterload, contractility, cardiac output, and ejection fraction for exam scenarios.
- Practical telemetry skills: six-second strip heart rate estimation and recognition of AFib vs sinus rhythms may be tested.