Cardiac Pathophysiology: HTN, CAD, HF, Arrhythmia 10/12

3 functions of heart

electrical conduction, pumping, blood supply

2 types of myocytes

electrical: non-contractile, generate electrical signal

contractile: mechanical/pumping, most of atrial/ventricular tissue

both are excitable (responds to electrical stimulus)

Conduction System

Automaticity

what has highest autmatic rate

SA node, AV node, bundle of His, bundle branches, purkinje fibers

ability to spontaneously initiate electrical signals

SA node has highest (60-100), AV node is the generate (40-60), ventricular conduction is candle light (25-40)

Electrocardiogram

PQRST

P wave: atrial depolarization

QRS complex: ventricular depolarization

T wave: ventricular repolarization

PR interval: time between atrial+ventricular depolarization

QT interval: time between ventricular depolarization+repolarization

Chronotropic

Ionotropic

Heart rate vs. Pulse

affecting HR (+, -, incompetence)

+ionotropy: increase Ca= increase contractility

electrical activity vs. circulation

Excitation-Contraction Coupling

action potential to myocyte contraction

primary ion is Ca2+, Na+, K+

Cardiac Output

What is SV

how much blood is pumped to body per minute, nl is 5-6 L
Co=SV times HR

SV: how much blood is ejected in each heart beat from left ventricle

Preload

Contractility

Afterload

stretch of ventricles prior to systole
relate to amount of blood present in heart at end of diastole

myocardial ability to contract in response to preload
depends on contractile proteins, availability of ATP/Ca2+

resistance that left ventricle faces to pump blood out to body
primary determinant of aortic BP
increase afterload: HTN, aortic valve stenosis (stiffening/tightness)

why does blood pressure matter

too low? we dont perfuse the organs

too high? we damage our organs, damages eyes, kidneys, brain, blood vessels

How is it sensed if our BP is low?

RAAS

blood leaves heart, baroreceptors (reads bp), medulla vasomotor center

BP high? parasympathetic

BP low? sympathetic

Blood travels through kidneys, low BP (detected through nephron), juxtaglomerular cells release renin, reacts with angiotensinogen, produces angiotensin 1, ace, angiotensin 2, vasoconstriction + aldosterone release (retain sodium, water)

HTN definitions

Normal: 120/80

Stage 1: 130/80

Stage 2: 140/90

HTN

Etiology, pathogenesis, clinical manifestations, treatment implications

E: primary (unknown causes), secondary (result of some other condition), malignant (HTN with end organ damage)

P: heart works harder (requires more O2), arteries gets damaged, plaque develops

CM: moderate (headache, confusion). malignant (LOC, coma, MI)

TI: lifestyle therapy, BP lowering medication

Coronary Artery Disease Risk Factors

genetics, age, smoking, HTN, obesity

Hyperlipidemia

Serum cholesterol sources

Contributes to atheroscleroses and coronary disease

diet, endogenous production, genetic tendency

Atherosclerosis Development

endothelial injury: bp increase, stress on artery walls. increase permeability/thrombosis

deposition of serum lipoproteins in vessel walls, progress to blockage

CAD definitions

ischemia, infarction, stable angina, acute coronary syndrome

inadequate blood supply/organ

tissue necrosis

myocardial ischemia. supply/demand mismatch, when active

unstable angina, NSTEMI, STEMI

Supply vs Demand

HR, oxygen content of blood, coronary perfusion

contractility, heart rate, afterload, preload

Acute coronary syndrome: Unstable Angina

ischemia without infarction (non-necrotic), no elevation of cardiac biomarkers

supply demand mismatch without infarction

Cardiac Biomarkers

NSTEMI

STEMI

released by damaged myocytes, troponin (most accurate, peak at 2 hours, still shows as elevated even a day later)

no ST segment elevation, elevated cardiac biomarkers

ST segment elevated, elevated cardiac biomarkers

Non-atherosclerotic MI

Types

Clinical Manifestations

Long term Complications

Treatment Implications

Type 1: artery blocked
Type 2: caused by increase O2 demand or reduced supply (COPD, lung disease)

chest pain, difficult breathing, GI upset, diaphoresis

wall rupture, valve dysfunction, cardiogenic shock, HF

improve blood flow (CABG, anti-platelets), decrease O2 (Beta blockers, Ca2+ channel blockers), lifestyle factors

Arrhythmias

Risk factors and etiology

Pathogenesis

any abnormality in heart rate or rhythm

genetic (family mutations), structural and ischemic heart disease (MI, HTN, history of heart disease), endogenous + exogenous triggers (metabolic imbalances, certain infections)

normal/enhanced automaticity: physiological response, increase HR
electrophysiologic mechanisms: abnormal impulse formation or conduction

Structural Remodeling

scar/fibrosis can be ischemic or non-ischemic, structural changes can lead to functional changes

Normal sinus rhythm

Sinus bradycardia

Sinus tachycardia

60-100 bpm

automatic/physiological, reduced automaticity (athlete)

automatic/physiological, abormal automaticity

Arrhythmia symptoms

syncope, sudden cardiac arrest

usually asymptomatic at first

Junctional Bradycardia

AV node is primary pacemaker, partial/complete heart block

congenital: muscular dystrophy

latrogenic: medication side effect

Typical Atrial Flutter (Pre-Afib)

etiology: remodeling of Cavo-tricuspid isthmus region

clinical manifestations: regularly irregular rhythm, sawtooth pattern

treatment: ablation, medications to slow or prevent

Atrial Fibrillation (AFib)

etiology: structural remodeling/genetics

clinal manifestations: irregularly irregular, no p wave, risk of thromboembolism

treatment: prevent blood clots, slow symptoms

Cardiomyopathy

Dilated

Hypertrophic

Restrictive

group of diseases of myocardium

sometimes genetic, ischemic (bc of MI) or nonischemic (everything else, genetic, viral, alcohol)

ventricles dilated, most common, ischemic, impaired contraction of ventricles

genetic/familial condition. obstruct aortic outflow

rare, stiff, happen with cardiac amyloid

Heart Failure

Complex syndrome

not same as cardiomyopathy, but leads to HF

results from structural/functional impairment of ventricular filling/ejection (insufficient CO to meet bodies needs)

Systolic HF

Diastolic HF

Stroke volume

Ejection Fraction

failure of contraction, decrease left ventricular ejection fraction

failure of ventricle to adequately relax bc of thicker wall, decrease CO

colume of blood ejected by left ventricle each beat

fraction of blood ejected by left ventricle with each beat

B-type natiuretic peptide (BNP)

released in response to changes in pressure within the heart

agonist to angiotensin 2 and aldosterone

can be used for intial HF diagnosis

Left sided HF

Right sided HF

etiology: ischemic heart disease, HTN, valvular disease
clinical manifestations: dyspnea w/ lying down, cough

etiology: left heart failure

clinical manifestations: hypertrophy, peripheral edema, JVD