cardio pathophys

What is the primary function of the heart?

Pump blood through the pulmonary and systemic circulations.

What are the two pericardial layers?

Visceral pericardium is the serous inner layer on the myocardium; parietal pericardium is the fibrous outer layer.

How much fluid normally occupies the pericardial space?

About 40-50 mL of clear fluid, probably a plasma ultrafiltrate.

Where do the left main and right coronary arteries arise?

From the root of the aorta; they provide the principal blood supply to the heart.

Why is the normal QRS complex narrow?

Both ventricles depolarize almost simultaneously through specialized conduction tissue, usually within 60-100 ms.

What is cardiac output?

Cardiac output = heart rate × stroke volume.

What three factors determine stroke volume?

Contractility, afterload, and preload.

What does preload represent?

Ventricular filling/stretch before contraction.

What does afterload represent?

The pressure/resistance the ventricle must work against to eject blood.

What does contractility represent?

The intrinsic force of myocardial contraction.

A patient has a resting rate of 42 bpm. What broad dysrhythmia category is present?

Bradycardia: a heart rate that is too slow.

What are the two basic mechanisms of bradycardia?

Decreased sinus-node automaticity or blocked conduction preventing normal ventricular activation.

What happens when sinus-node pacemaker activity ceases?

Another cardiac pacemaker tissue can usually escape and activate the heart at a slower rate.

AV Block EKG

A patient has a PR interval >0.22 s but every P wave conducts to a QRS. Diagnosis and mechanism?

1st-degree AV block; AV conduction is prolonged, but atrial and ventricular activity remains 1:1.

Some atrial impulses fail to activate the ventricles. What diagnosis?

2nd-degree AV block; some, but not all, atrial impulses conduct to the ventricles.

A patient has no association between atrial and ventricular activity. What diagnosis?

3rd-degree AV block; atria and ventricles depolarize independently.

What factors are associated with AV block?

Aging, increased vagal input, drug side effects, and several congenital/acquired disorders.

Which congenital disorders are listed as associated with AV block?

Muscular dystrophy, tuberous sclerosis, and maternal systemic lupus erythematosus.

Which acquired disorders are listed as associated with AV block?

Sarcoidosis, gout, Lyme disease, SLE, ankylosing spondylitis, and CAD.

What is the management approach noted for AV-block bradycardia?

Evaluate reversible causes; permanent pacemaker implantation is often required.

What are the three cellular mechanisms of tachycardia?

Increased automaticity, delayed-repolarization triggered activity, and re-entry circuits.

How can delayed repolarization produce tachycardia?

Reactivation of sodium or calcium channels can cause spontaneous depolarizations after repolarization is delayed.

What is the most common cellular mechanism of tachycardia?

A re-entrant circuit involving parallel electrically separate regions with different conduction velocities.

What normally provides the only electrical connection between atria and ventricles?

The AV node.

A patient has short PR, wide QRS, and a slurred upstroke. What diagnosis?

Wolff-Parkinson-White syndrome due to an accessory AV pathway causing ventricular pre-excitation.

Why can hemoptysis occur in LV failure?

Increased pulmonary capillary pressure can place blood/fluid into alveoli.

How does WPW predispose to re-entrant tachycardia?

The accessory pathway creates two parallel atrioventricular connections, allowing a re-entry circuit.

How does reduced potassium-channel function cause long-QT triggered activity?

It prolongs the plateau, allowing sodium/calcium-channel reactivation and early afterdepolarizations.

Why can long-QT triggered activity be dangerous?

Triggered activity in the ventricles can produce potentially life-threatening ventricular arrhythmias.

What does a narrow QRS suggest during tachycardia?

Ventricular depolarization is occurring normally through specialized tissue; the origin is at/above the AV node.

What does a wide QRS suggest during tachycardia?

Ventricular activation is abnormal: ventricular origin or supraventricular tachycardia with aberrant/accessory-pathway conduction.

A Fib + Flutter

AV nodal re-enterant tachy + Atrioventricular re-enterant tachy

Atrial Tachy

What is heart failure?

Inadequate pump function causing congestion from fluid in the lungs and/or peripheral tissues.

Why can confusion occur in severe LV failure?

Impaired tissue oxygenation and reduced brain blood flow can contribute to confusion.

Why do rales occur in LV failure?

Increased pulmonary fluid in the alveolar/interstitial spaces produces crackling sounds.

Why can the lung bases be dull to percussion in LV failure?

Pulmonary congestion/pleural fluid increases density at the bases.

What four broad mechanisms can cause heart failure?

Inappropriate workload/volume or pressure overload, restricted filling, myocyte loss, and decreased myocyte contractility.

What are examples of myocyte loss mechanisms?

Genetic structural problems such as dystrophin-related disease and inflammatory injury after viral infection or another insult.

How can MI cause heart failure?

Myocyte injury/loss can be irreversible; fibrosis replaces contractile cells, producing systolic dysfunction.

How can ischemia cause diastolic dysfunction?

Ischemia decreases myocardial relaxation, impairing ventricular filling.

PV Loop

PV Loops

What is the immediate compensation after decreased pump function?

Neurohumoral and mechanical compensation temporarily supports cardiac output.

How does increased preload compensate for reduced cardiac output?

Greater filling/stretch increases sarcomere contraction through the Frank-Starling relationship.

How do catecholamines initially compensate for heart failure?

They increase heart rate and contractility, initially helping maintain cardiac output.

How does myocardial hypertrophy initially compensate?

Increased muscle mass and ventricular volume help support output, but chronic hypertrophy contributes to stiffness/remodeling.

Why can pulmonary edema cause a restrictive pattern?

Fluid replaces air and reduces vital capacity, producing restrictive physiology.

Why can pulmonary edema cause air trapping?

Small-airway closure increases, contributing to air trapping and increased work of breathing.

Why do heart-failure compensations eventually become harmful?

Persistent overload and neurohormonal activation increase preload/afterload and drive progressive remodeling and failure.

What happens to the isovolumic systolic pressure curve in systolic dysfunction?

It shifts downward, reflecting reduced effective contractile pump function.

What happens to the diastolic curve with hypertrophy/increased ventricular volume?

It shifts rightward in the pressure-volume framework.

What is the heart-failure sympathetic/RAAS sequence?

Heart injury → sympathetic/RAAS activation → initial perfusion support → chronic activation → increased preload/afterload → worsening HF.

What does chronic sympathetic activation do to veins?

Venoconstriction increases preload.

What does chronic sympathetic activation do to arteries?

Arteriolar vasoconstriction increases afterload.

How does reduced renal blood pressure activate RAAS?

Reduced renal pressure stimulates renin release, leading to angiotensin II formation.

How does angiotensin II help maintain GFR during low cardiac output?

Angiotensin II plus sympathetic activity constricts efferent glomerular arterioles.

What does angiotensin II stimulate that increases sodium retention?

Aldosterone.

What are the renal effects of aldosterone listed?

Increased sodium resorption and increased potassium excretion.

Why can chronic RAAS activation worsen heart failure?

Severe vasoconstriction raises afterload, further reducing cardiac output and renal perfusion in a vicious cycle.

Which other mediators are listed in heart failure?

Vasopressin, interleukins, TNF, and endothelin.

What is the role of TNF in remodeling?

TNF is linked to myocyte hypertrophy and apoptosis.

What is the role of endothelin?

It is a potent vasoconstrictor.

What cellular processes are altered during heart-failure remodeling?

Calcium handling, adrenergic receptors, contractile apparatus, and myocyte structure.

Why does cardiac myocyte loss have lasting effects?

Mature cardiac myocytes cannot proliferate; loss is replaced by remodeling/fibrosis rather than new contractile cells.

What is left-ventricular remodeling?

Changes in myocardial size and shape associated with heart failure.

How does apoptosis differ from necrosis in remodeling?

Apoptosis initially decreases cell volume without membrane disruption; eventual cell death leaves gaps in myocardium.

How does fibrosis develop in chronic heart failure?

Fibroblast activation plus myocyte death leads to collagen deposition in interstitial spaces.

How can ventricular dilation occur during remodeling?

Myocyte slippage can follow collagenase disruption of the collagen network.

connection between ACE inhibition and remodeling?

ACE inhibition an example of limiting/preventing adverse remodeling.

A patient has dyspnea, orthopnea, PND, rales, and pulmonary edema. Which failure pattern and mechanism?

LV failure; LV dysfunction raises pulmonary capillary pressure, driving fluid into lung interstitium/alveoli.

Why does left-sided HF cause orthopnea and PND?

Pulmonary fluid congestion increases when recumbent, producing dyspnea when lying down or awakening at night breathless.

Why can cardiac asthma cause wheezing?

Bronchial-wall edema obstructs small airways.

Cardiac Asthma Imaging

What is S3?

A low-pitched early-diastolic sound during rapid ventricular filling; in LV failure it is usually best heard at the apex.

How does S3 differ from S4 mechanistically?

S3 occurs during rapid ventricular filling; S4 occurs when atrial contraction fills a stiff ventricle.

S3 EKG

A patient has severe HF with alternating strong and weak peripheral pulses. What finding?

Pulsus alternans.

Why are severe-HF patients pale, cold, and sweaty?

Peripheral vasoconstriction redirects blood flow toward central organs/head.

What are key findings of right-ventricular failure?

Pedal edema, abdominal pain, elevated JVP, S3 at the sternal border, and a sustained systolic heave.

What can increase RV afterload?

Pulmonary arterial/capillary abnormalities, including pulmonary embolus and COPD.

What does JVP height estimate?

Right-atrial/central venous pressure.

Why can pleural effusion occur in LV failure?

Increased pulmonary capillary pressure promotes pleural fluid accumulation.

What causes the JVP a wave?

Atrial contraction.

What causes the JVP x descent?

Atrial relaxation and tricuspid-annulus descent.

JVP Image

What is S4?

A low-pitched end-diastolic sound caused by atrial contraction against a stiff ventricle; associated with diastolic dysfunction.

What causes the JVP v wave?

Right-atrial filling.

What causes the JVP y descent?

Tricuspid opening followed by right-ventricular filling.

A patient has elevated JVP, ascites, dependent edema, and hepatomegaly/RUQ pain. Mechanism?

Right-sided pressure raises systemic venous pressure → venous congestion → edema/ascites → hepatic congestion and capsule distention.

What is a positive hepatojugular reflux in RV failure?

Pressing the liver displaces blood into the vena cava; JVP rises when the RV cannot accommodate the added volume.

What is the most common cause of right-sided HF?

Left-sided heart failure.

Why can pulmonary edema lessen after severe RV failure from a left-sided lesion?

A lesion such as mitral stenosis may reduce LV preload/load when RV failure limits forward flow to the LV.

A patient has angina, syncope, HF, a delayed weak carotid pulse, and a systolic murmur at the base radiating to the neck. Diagnosis and mechanism?

Aortic stenosis; narrowed aortic valve obstructs LV outflow, causing reduced/ delayed ejection and LV pressure overload.

Murmurs Image 1

Murmurs Image 2

What is the typical aortic-stenosis murmur?

Mid-systolic, loudest at the base, often radiating to the sternal notch/neck.

Stenosis Image