cardiac conduction system, myocardial disease, heart failure, shock

the heart muscle generates…

electrical impulses (action potential) independently 

Specialized myocardial cells form the conduction system 

What is the Cardiac Conduction System 

• Sinoatrial Node (SA)

• Atrioventricular Node (AV)

• Bundle of His

• Purkinje Fibers

What is the pacemaker of the heart(60-100 bpm); generated impulse; controls atrial contraction 

Sinoatrial Node (SA)

What provides one-way conduction from atria to ventricles; joins atrial and ventricular conduction systems (40-60 BPM)

Atrioventricular Node (AV)

What conducts impulse from atria to ventricles 

bundle of His

What.. conduct impulse throughout entire tissue of ventricles; initiate ventricular contaction (15-40 bpm) 

Purkinje Fibers:

What is the…

• Flow of current associated with the passage of ions through ion channels (Na+, K+, Ca++) 

  • Potassium- intracellular 

  • Sodium- extracellular  

• Resting potential: selectively permeable to K+ & nearly impermeable to Na+; negatively charged 

• Depolarization: brief period in which polarity is reversed; cell membrane becomes selectively permeable to Na+ allowing it to move into the cell 

• Repolarization: reestablishment of membrane potential 

  • Using atp to pump sodium out and move potassium back in 

action potentials

What is the selectively permeable to K+ & nearly impermeable to Na+; negatively charged 

resting potential

What is the brief period in which polarity is reversed; cell membrane becomes selectively permeable to Na+ allowing it to move into the cell 

depolarization

What is the…

• reestablishment of membrane potential

  • Using atp to pump sodium out and move potassium back in 

repolarization

Electrocardiogram (ECG) 

• _P_: atrial depolarization 

• QRS: ventricular depolarization 

  • Ventricles are contracting  

• T: ventricular repolarization 

  • Ventricular diastole

What is the p wave

atrial depolarization

What is the QRS wave?

• ventricular depolarization

  • ventricles are contracting

What is the T wave

• ventricular repolarization 

  • Ventricular diastole  

Properties of Cardiac Cells 

• automaticity

• excitibility

• conductivity

• contractility

What is the ability of heart cells to spontaneously depolarize & generate action potential 

automaticity

What is the ease with which cardiac cells respond to and generate an action potential 

Excitability

What is the generation of electrical impulses and conduction throughout the muscle of the heart, stimulating the heart to contract and pump 

Conductivity

What is the the innate ability of the heart muscle to contract; the ability to produce changes in the force of contraction 

Contractility

Cardiac Dysrhythmias

causes…

“HISDEBS” 

H: Hypoxia

I: ischemia

S: SNS stimulation

D: drugs/toxins

E: electrolyte imbalances_

B: bradycardia_

S: stretch (enlargement of heart chambers)_

 

Cardiac Dysrhythmias..

Problematic if ..

impairs cardiac output and perfusion

• Normal Heart rate= 60-100 BPM 

• Bradycardias = HR < 60 

  • Orginated from SA node 

  • Slow heart rate 

• Tachycardias = HR > 100 

  • Orginated from SA node 

  • Fast heart rate 

  • Can decrease oxygen demand 

• Coronary arteries fill during diastole  

What is the normal Normal Heart rate=

60-100 bpm

Bradycardias= HR is …

<60

Orginated from SA node 

Tachycardias = HR is…

• > 100 

  • Orginated from SA node

TWO MAIN CATEGORIES OF CARDIAC DYSRHYTHMIAS 

• Atrial Dysrhythmias

• Ventricular Dysrhythmias

Atrial dysrhythmias

• Impulse originates in atria  

• Types 

  • Premature atrial contraction (PAC)

    • originate in atria and occur before the next expected SA node impulse; early beat 

      • Early unexpected beat  

  • Atrial flutter:

    • rapid atrial ectopic tachycardia from barriers to electrical conduction (scar tissue); saw-toothed EKG pattern with regular contraction; regular rhytym 

  • Atrial fibrillation:

    • rapid, disorganized atrial activation and uncontrolled atrial contraction; irregular contraction; Atria cannot repolarized for oncoming electrical impulse; irregular rhythm 

      • Most common pathological one  

Premature atrial contraction (PAC):

• originate in atria and occur before the next expected SA node impulse; early beat 

  • Early unexpected beat  

Atrial flutter:

• : rapid atrial ectopic tachycardia from barriers to electrical conduction (scar tissue); saw-toothed EKG pattern with regular contraction; regular rhytym 

 

Atrial fibrillation:

• : rapid, disorganized atrial activation and uncontrolled atrial contraction; irregular contraction; Atria cannot repolarized for oncoming electrical impulse; irregular rhythm 

• Most common pathological one  

 

Ventricular arrhythmias: May be life threatening `

• Impulse originates in ventricle 

• Types 

  • Premature ventricular contractions (PVC)

  • Ventricular Tachycardia

  • Ventricular fibrillation

Premature ventricular contractions (PVC): 

  after PVC, ventricle unable to repolarize sufficiently to respond to next impulse from SA node; diastolic filling insufficient 

Ventricular Tachycardia: 

•  impulse originated in ventricles;  

• wide, bizarre QRS complexes; 

•  eliminates atrial kick, causes reduction in diastolic filling time—CO severely diminished or nonexistent 

Ventricular fibrillation 

• fatal within minutes;  

• ventricle quivers but does not contract;  

• no cardiac output;  

• no pulse 

What type of Ventricular dysrhythmias are life threatening

V-tach & V-fib due to decreased caridac output

What is a group of cardiac disorders that affect the heart msucle 

cardiomyopathy

What are types of cardiomyopathy

• Hypertrophic Cardiomyopathy 

• dilated cardiomyopathy (most common)

• myocarditis

What is Hypertrophic Cardiomyopathy 

• Genetic 

• Hypertrophy of left ventricle—decreased left ventricular chamber size  

• Manifestations:

  • Dyspnea 

  • Chest pain on exertion/exercise intolerance 

  • Syncope 

  • Arrythmias 

Manefestations of hypetrophic cardiomyopathy

• Dyspnea 

• Chest pain on exertion/exercise intolerance 

• Syncope 

• Arrythmias 

What is Dilated Cardiomyopathy (most common) 

• Most common cause of heart failure

• and Most common reason for heart transplant  

• Causes: 

  • Genetics

  • Infections

  • Toxins, Alcoholism

  • Chemo treatments

  • Metals

  • other disoeders  

• manefestiation:

  • Left Heart Failure  

cardiomyopathy:

Myocarditis

• “inflammation of heart muscle” 

• Related to infectious processes, inflammatory processes, autoimmune disorders, drug reactions 

What are Manifestations of myocarditis 

• Arthralgia 

  • Joint pain

• chills

• fever

• myalgia

  • muscle pain

• N/V

  • nausea

  • vomiting

• symptoms present in individuals a few weeks befroe diagnosis

What is Peripartum Cardiomyopathy (cardiomyopathy cont.) 

• Rare  

• Evident during last trimester of pregnancy or occurs sometime within the first 6 months after delivery  

• Causes: Infections, Immune Responses, Nutrition, Genetics, Drugs  

Heart failure

• Functional and structural disorder of the heart that results in risk of decreased cardiac output &/or pulmonary/systemic congestion 

• Reminder: Cardiac output= Heart rate X Stroke Volume 

• People with CHF often use cardiac reserve at rest 

Heart failure patho

• Any condition that reduces pumping ability of the heart: HTN, CAD, Cardiomyopathy, valvular disease 

Control of cardiac output

• SNS: increases HR and increases blood flow to the skeletal muscles 

• PNS: decreases HR 

• Preload: volume or loading conditions of the ventricle at the end of diastole (increased with aortic stenosis, decreased with hypovolemia); volume of blood stretching the heart muscle 

• Afterload: Force that the contracting heart muscle must generate to eject blood from filled heart—systemic vascular resistance and vascular wall tension 

• Myocardial Contractility: inotropy; contractile performance of the heart; increases cardiac output independent of preload and afterload 

how does SNS control cardiac output

increases HR and increases blood flow to the skeletal muscles 

how does PNS control cardiac output

decreases HR

Heart failure:

How does preload control cardiac output

volume or loading conditions of the ventricle at the end of diastole (increased with aortic stenosis, decreased with hypovolemia); volume of blood stretching the heart muscle 

Heart failure:

How does afterload control cardiac output

Force that the contracting heart muscle must generate to eject blood from filled heart—systemic vascular resistance and vascular wall tension 

Heart failure:

How does Myocardial Contractility control cardiac output

inotropy; contractile performance of the heart; increases cardiac output independent of preload and afterload 

What are the two main types of heart failure:

Systolic(pumping) versus Diastolic(filling) Failure 

• Systolic Dysfunction: impaired pumping; thin walls 

• Diastolic Dysfunction: impaired filling; thick walls 

impaired pumping; thin walls 

systolic dysfunction

impaired filling; thick walls 

Diastolic Dysfunction

What is the amount of blood ejected from the heart; normal ~ 65% 

ejection fraction

What is the

• Impaired ejection of blood from the heart during systole 

• Decreased contractility, causes decreased CO which, decreased EF  

• As EF decreases, preload ____increases_______—increases ventricle dilation—decreases contractility 

• Causes:

  • conditions that impair contractile performance

  • produce volume overload

    • (ex: hypervolemia, high blood pressure, valve disorders)

  • or generate pressure overload (from hypertension) 

Systolic heart failure/Heart Failure with Reduced Ejection Fraction (HFrEF): EF <40% 

What is..

• Abnormal relaxation of heart; impaired filling compromises cardiac output (CO); aggravated by tachycardia  

• Causes:  

• conditions that impede ventricle expansion (pericarditis), 

•  increase wall thickness, 

•  decrease chamber size,  

• delay cardiac relaxation 

Diastolic heart failure(filling problem)/Heart Failure with Preserved Ejection Fraction (HFpEF): EF >40% 

 

RIGHT-SIDED vs LEFT-SIDED heart failure

• Long term HF usually involves both sides 

• Right Ventricular dysfunction: impairment of ability to move deoxygenated blood from systemic circulation to the ____lungs ____  

  • Decrease in movement of blood to left side of heart (preload) 

  • Decrease of cardiac output 

• Causes:  

  • conditions that impede blood flow to the lungs or decrease pumping effectiveness of right ventricle 

  
  

What is….

• Impaired ability to move deoxygenated blood from the systemic circulation into the pulmonary circulation 

• Causes: left heart failure, valvular disease, pulmonary HTN 

right sided heart failure

Manefestations of right sided heart failure

• Peripheral edema (blood backs up into periphery) 

• Arms and feet 

• Ascites 

• JVD 

• GI tract congestion 

• Liver/spleen engorgement 

• Malnutrition 

What are causes of right sided heart failure?

left heart failure, valvular disease, pulmonary HTN 

What is..

• Decrease CO to system 

• Blood accumulates in left ventricle, atrium & pulmonary system 

• Pulmonary edema___—pressure inside capillaries exceeds pulmonary osmotic pressure(pushing pressure)

• Causes: HTN, MI, Valve disorders(valvular stenosis or regurgitation)

left sided heart failure

What are causes of left sided heart failure

HTN, MI, Valve disorders(valvular stenosis or regurgitation)

manefestations of left sided hear failure

• PULMONARY EDEMA  

• Activity intolerance 

• Cyanosis 

• Cough with pink frothy sputum 

• Dyspnea 

• Hypoxia 

• Orthopnea 

  • Difficutly breathing in certain positions

• SOB 

• Malnutrition 

• Nocturia 

NOTE:  Acute pulmonary edema is emergent life-threatening condition associated with left sided heart failure resulting in the decreased ability of the lungs to oxygenate the blood (poor gas exchange) and hemoglobin leaves the pulmonary circulation without being fully oxygenated. 

emergent life-threatening condition associated with left sided heart failure resulting in the decreased ability of the lungs to oxygenate the blood (poor gas exchange) and hemoglobin leaves the pulmonary circulation without being fully oxygenated. 

acute pulmomary edema

Manifestations of acute pulmonary edema:  

• EMERGENT – LIFE THREATENING  

• Air hunger 

• Crackles 

  • Air moves through fluid causing crackle 

• _Cough with pink frothy sputum 

• Cyanosis—lips/nailbeds 

• Diaphoresis/ cool clammy sking 

• Tachycardia 

• “drown in their secretions

Compensatory Mechanisms: Attempts to maintain cardiac reserve in heart failure

• Compensation for decreases in CO with heart failure worsen the disease state 

  • Frank-Starling 

  • SNS 

  • RAAS 

  • Neurohormones: ANP / BNP 

  • Ventricular hypertrophy and remodeling

   

What is the Frank Starling Mechanism 

• Normally: 

  • Operates through increase in preload 

  • Increased diastolic filling causes increase in stretching of myocardium 

  • Increased stretch causes increased contraction (inotropy(increased contraction))-- increased CO 

• In Heart failure (HF): 

  • Inotropy is ____decreased_______ from normal regardless of increase in preload 

  • Decrease in CO decreases perfusion to kidneys and increases Na+ and H2O retention—increasing vascular volume, further increasing preload 

  • Increased preload—Increased ventricle wall tension & myocardial oxygen consumption—can produce ischemia, further impairing inotropy—increased preload is worsening heart failure 

  
  

How does Frank Starling Mechanism work in heart failure

• Inotropy is ____decreased_______ from normal regardless of increase in preload 

• Decrease in CO decreases perfusion to kidneys and increases Na+ and H2O retention—increasing vascular volume, further increasing preload 

• Increased preload—Increased ventricle wall tension & myocardial oxygen consumption—can produce ischemia, further impairing inotropy—increased preload is worsening heart failure 

Sympathetic Nervous System, heart failure

• Maintains perfusion to organs 

• Increases HR, contractility, vascular tone, and Na+ & H2O retention 

• Can lead to tachycardia: 

  • increased_ O2 consumption

  • vasoconstriction

  • and cardiac arrythmias 

• Cardiac sympathetic tone and catecholamines (epinephrine & norepinephrine) elevated during late-stage HF 

• In severe HF, blood is diverted to cerebral and coronary flow—decreased flow to kidneys, skin, muscle, & abdomen: cardiogenic shock 

Renin-Angiotensin-Aldosterone, heart failure

• Reduction of renal blood flow and GFR leads to Na+ & H2O retention 

 

• Decreased___ renal blood flow causes ___increased______ in renin secretion, causing increased Angiotensin II production 

 

• Angiotensin II—potent ____vasoconstrictor______, facilitates release of norepinephrine & inhibits reuptake, increases aldosterone & ADH production 

 

• Aldosterone metabolized in liver—increased levels can lead to liver congestion 

 

• Increased ADH—inhibits water excretion and vasoconstricts 

 

• Angiotensin II and ADH regulate inflammatory & reparative processes that follow tissue injury—inappropriate remodeling of the heart 

Myocardial Hypertrophy & Remodeling (heart failure)

• Myocardium hypertrophies as result of increased workload 

• Inappropriate hypertrophy results in  

  • Structural changes: chamber dilation & increased mass 

  • Functional changes: impaired systolic or diastolic function 

• Ex: Uncontrolled fibroblast activity increases collagen fibers which increases ventricular wall stiffness—increases cardiac workload & electrical conduction abnormalities 

Heart failure:

• Myocardial Hypertrophy & Remodeling 

  • Inappropriate hypertrophy results in  

    • stuctural changes what are they

chamber dilation & increased mass

Heart failure:

• Myocardial Hypertrophy & Remodeling 

  • Inappropriate hypertrophy results in  

    • functional changes what are they

impaired systolic or diastolic function 

 

Natriuretic Peptide Hormones, heart failure

• Have potent diuretic and vascular smooth muscle effects 

• Inhibits Na+ & H2O reabsorption 

• Inhibits SNS, RAAS, endothelin inflammatory cytokines & vasopressin 

• Causes dilation of atrial and venous systems—___decreased _____ venous return—decrease preload & afterload 

  • Atrial natriuretic peptide (ANP): released from atrial cells in responses to pressure, stretch, or fluid overload 

  • Brain Natriuretic Peptide (BNP): released from ventricle

    • Want less than 100 

What is released from atrial cells in responses to pressure, stretch, or fluid overload 

Atrial natriuretic peptide (ANP)

Clinical Manifestations of Heart Failure 

• Depend on extent and type of cardiac dysfunction & rapidity with which it develops 

• Reflect impaired pumping, decreased renal blood flow (RBF), & activation of SNS 

• Respiratory:

  • SOB (dyspnea, exertional dyspnea, orthopnea,paroxysmal nocturnal dyspnea)

  • Chronic dry nonproductive cough (cardiac asthma) 

• Fatigue, weakness, & mental confusion: decreased output 

• Fluid retention & edema: increased hydrostatic pressures—hydrothorax, ascites; nocturia, oliguria 

• Cachexia & malnutrition 

• Cyanosis 

• Arrythmias & sudden cardiac death: atrial fibrillation most common 

Heart Failure in Elderly  

• Common cause of disability 

• Common reason for admissions in age 65 and older 

• Elderly may have a decreased reaction to SNS  

• Heart becomes stiffer and has decreased compliance 

• Aging increases vascular stiffness which affects afterload  

SHOCK

• Impaired tissue PERFUSION

 

• Acute emergency in which tissues are deprived of oxygen and cellular nutrients or are unable to use these to meet their metabolic demand 

• Critical decrease in SYSTEMIC TISSUE PERFUSION 

  • Regardless of the cause, there is _DECREASE in Cardiac Output,  

    • compensatory mechanisms are activated(for ex: RAAS system)  

    •  failure of compensatory mechanisms if underlying problem not resolved, hypoxic cell injury & death

• Acute failure of circulatory system to adequately supply peripheral tissues and organs resulting in cellular hypoxia—shock exerts effect at cellular level—not enough oxygen & nutrients for production of ATP 

Stages of shock:

• initial stage

• compensatory

• progressive

• refractory

Initial stage of shock

Cardiac output is ___decreased___ and there is decreased perfusion of organs

Compensatory stage of shock

almost immediately, mechanisms kick in to maintain homeostasis; maintain CO, BP, & tissue perfusion (SNS, RAAS, etc.) 

• SNS: release of epinephrine and norepinephrine increase HR & contractility to increase cardiac output and perfusion 

• RAAS: Renin released—Angiotensin II (vasocontraction)-- Aldosterone (increase Na+ & H2O retention) 

• Compensatory mechanisms detrimental if shock state is prolonged:

  • Vasoconstriction ultimately leads to decreased tissue perfusion—inflammatory mediators released (histamine), cellular metabolism impaired, lactic acid build up 

• Compensatory mechanisms detrimental if shock state is prolonged:

Vasoconstriction ultimately leads to decreased tissue perfusion—inflammatory mediators released (histamine), cellular metabolism impaired, lactic acid build up 

Progressive stage of shock:

compensatory mechanisms begin failing to meet metabolic demands, and the shock cycle is perpetuated  

refractory stage of shock:

shock becomes unresponsive to therapy and is considered irreversible 

Types of shock:

• Cardiogenic Shock

• Hypovolemic Shock

• obstructive: cardiac tamponade, pulmonary embolism

• Disrubutive: septic shock anaphylaxis,neurogenic shock

What kind of shock is being described?

MI, Acute valve damage 

• Failure of heart to pump to meet body's demands 

• Decreased Cardiac output, hypotension, hypoperfusion, & tissue injury despite adequate intravascular volume 

• Decreased CO d/t  

  • poor contractility,  

  • increased_____ afterload (compensatory mechanisms) 

  •  & ____excessive___ preload (blood returning is added to blood that was not pumped adequately) 

• Most common cause is Myocardial infarction (MI)

Cardiogenic Shock

Manefestations of cardiogenic shock  

• Hypoperfusion 

• Hypotension 

• Cyanosis 

• MAP & SBP decrease with narrow pulse pressure and near normal DBP 

• Decrease urine output 

• Changes in level of consciousness (LOC), cognition 

What kind of shock is being described?

significant loss of volume (blood loss or dehydration) 

• Diminished blood volume—inadequate filling of vascular compartment 

• Acute loss of 15%-20% of circulating volume 

  • Hemorrhage 

    • Ex: gunshot wound 

  • Severe burns (plasma loss) 

  
  

  • Severe dehydration 

  
  

  • Vomiting/diarrhea 

  
  

  • Third spacing (shifting of fluids from vascular compartment to interstitial space) 

  
  

  • Can lose 10% (500mL) with no adverse effects 

  
  

  • Increasing blood loss decreases stroke volume but arterial pressure remains constant d/t compensation(compensatory mechanisms) & vasoconstriction 

    • Within seconds: tachycardia, vasoconstriction and increased contractility occur

    • Mobilization of blood stored in venous side of circulation (~350 mL stored in liver) 

    • Increase intravascular volume through absorption of interstitial fluid, conservation of H2O & Na+, & thirst 

• cardiac output and tissue perfusion decrease before BP beings to fall 

• Cardiac output & arterial pressure decrease to zero when 30-40% of blood is removed 

hypovolemic shock

manefestations of hypovolemic shock

• Thirst 

• Tachycardia 

• Cool clammy skin (vasoconstriction) 

• Decreased arterial pressure—moderate to severe shock 

• Decreased urine output—blood diverted to heart & brain 

• Tachypnea—increase availability of O2 

• Changes in mentation—restlessness(key indicator of hypoxia) then lethargy/coma 

What kind of shock is being described?

•  Results from mechanical obstruction in flow of blood through central circulation (great veins, heart, or lungs) 

• Something blocking blood flow  

• Manifestations: right-sided heart failure 

• Causes:

  • Dissecting AAA 

  • Cardiac tamponade 

  • Pneumothorax 

  • PE 

Obstructive: Cardiac tamponade, pulmonary embolism 

What kind of schock is being described

Sepsis, Anaphylaxis, or Neurogenic: loss of blood vessel tone, enlargement of vascular compartment & displacement of volume away from the heart & central circulation; decrease of SNS control or release of excessive vasoactive substances 

 

Distributive(most common)

What kind of shock is being described?

• Severe systemic allergic reaction; immunological reaction that releases vasodilator substances (histamine, its going to dialate every vessel in your body) 

• Results in massive vasodilation & increases in capillary permeability 

• Often develops suddenly and death can occur in minutes 

• Causes: Tree nuts, Medications, Latex, Shellfish, Insect venom (bees) 

Anaphylactic Shock 

Manefestations of Anaphylactic Shock 

• vary based on sensitivity and rate & quantity of exposure 

• Laryngeal edema 

  • Swelling in throat (larynx) 

• Urticaria

  • hives 

• Smooth muscle contraction 

• Angioedema  

• Circulatory collapse  

What kind of shock is being described?

• Associated with severe infection and systemic response 

• Activated neutrophils kill microorganisms but also injury endothelium by releasing substances that increase capillary permeability & increase vasodilation 

septic shock

What are manefestations of septic shock?

• Hypotension 

• Warm, flushed skin 

• Hypovolemia (arterial & venous dilation) 

• Cognitive changes (decreased cerebral blood flow) 

what kind of shock is being described?

Loss of sympathetic control due to defect in vasomotor area of the brain 

• spinal cord injury, depressant drugs/ anesthesia, hypoxia, lack of glucose 

neurogenic shock

Complications of shock

• Acute respiratory distress syndrome (ARDS):  

• Acute renal failure (ARF):  

• Disseminated intravascular Coagulation (DIC): 

• GI complications:  

• Multiple organ dysfunction syndrome (MODS): 

Shock complication:

Acute respiratory distress syndrome (ARDS):  

• Rapid onset of profound dyspnea that occurs 12 to 48 hours after the initiating event 

  • Lungs get stiff and you dont oxygenate as well 

Shock complication:

• Acute renal failure (ARF)

due to impaired renal perfusion or direct kidney injury; ATN most common 

Shock complication:

Disseminated intravascular Coagulation (DIC):

 widespread activation of coagulation; small clots cause occlusion of small & midsized arteries; depletion of platelet & coagulation factors increase risk for bleeding