Exam 1

MI

• Acute onset of myocardial ischemia that results in myocardial cell death 

• Infarction – occlusion in vessel that causes tissue death

MI Patho

• Plaque rupture ➡ platelet activation ➡ thrombus formation ➡ complete vessel occlusion 

• Necrosis of myocardial cells supplied by the occluded vessel 

  • Use of Aspirin  

  • Prevents the platelet aggregation 

  • Makes it harder for platelets to stick 

• Necrosis is irreversible 

  • Results in non-functional area of myocardium 

    • Can lead to HF 

  • Infarcted area can longer act as a pump or conduct electricity 

    • Increases risk of dysrhythmias 

• If the thrombus completely occludes the vessel, this will likely cause a STEMI. 

• If the clot partially occludes the vessel, then this is manifested as unstable angina/NSTEMI 

coronary arteries

• RCA goes to front and wraps around the back 

• LCA divides into two branches  

  • LAD goes down the front anterior wall 

  • Circumflex feeds the lateral wall and swings to the posterior wall 

• Widowmaker = occlusion in proximal LCA 

CAD patho

• Prolonged ischemia >20 minutes ->cellular death begins. 

• Ischemic tissue 

  • May not have normal contractility 

  • Has an increased risk of dysrhythmia formation 

• Infarction develops over minutes to hours 

• Death of cells- enzymes are released 

• Enzymes are: 

  • Troponin 

  • Creatine Phosphokinase (CPK) 

  • Myoglobin 

  • Lactic Dehydrogenase (LDH) 

type of mi based on ekg

ST elevation MI 

• STEMI 

• Transmural or full thickness 

Non-ST elevation MI 

• NSTEMI 

• Subendocardial – partial thickness 

acute MI symptoms

• Chest pain 

  • Sudden, severe, crushing, unrelieved by rest or nitroglycerin 

  • Often radiates to one or both arms, jaws, neck and back. 

  • No correlation between severity of pain and severity of infarction 

• New murmur, S3 or S4 heart sounds 

  • Infarctions can involve the papillary muscles 

  • S3 -> HF 

    • JVD and SOB 

    • Crackles 

  • S4 -> HTN 

• If heart failure is present – JVD, SOB 

• Dysrhythmias 

• BP ↑ or ↓ 

  • Pain and increased sympathetic reaction 

  • Large amount of damage can increase BP 

• EKG changes

MI clinical presentation

• Shortness of Breath/pulmonary edema 

• Diaphoresis 

• Palpitations 

• Nausea/vomiting 

  • Can be projectile 

• Anxiety, feeling of pending doom 

• Skin cool, clammy 

• Cardiac arrest 

• Shock 

• Dysrhythmias 

• Low grade fever – later sign 

  • 24-48 hours later 

• Cardiac enzyme elevation 

• EKG changes 

• Vital Signs 

brief exam

• ABC’s, vital signs, general observation 

• Neuro 

  • Stroke symptoms, restlessness, lightheaded, anxiety 

• Cardiac 

  • Chest pain, EKG changes, JVD, murmurs, S3, S4, pulses 

• Pulmonary 

  • Crackles, resp distress, tachypnea, pulmonary edema 

• Gastrointestinal 

  • Nausea/vomiting 

• Genitourinary 

  • Urine output 

• Skin 

  • Cool, clammy diaphoresis, pale 

• Psychosocial 

  • Feeling of impending doom, fear, denial 

causes of CP not related to ACS

• Aortic Dissection 

• Pulmonary Embolism 

• Esophageal Rupture 

• Pneumothorax 

atypical presentations

Women 

• Lethargy 

• Weakness 

• Nausea  

Elderly 

• May not feel the CP 

Diabetics 

• May not feel the CP 

Transplanted Heart 

• Will never have anginal CP 

• Get heart cath every year 

EKG diagnosis

Ischemia 

• ST segment depression 

• T wave inversion 

  • Nonspecific sign  

    • Antidysrhythmic drugs can cause this 

Injury 

• ST segment elevation 

• Injury = beginning of the MI 

  • Tissue is still viable 

Infarction 

• Pathologic Q waves develop permanently with STEMI 

• Irreversible damage 

cardiac enzymes

• Serum Enzymes 

• Enzymes are released as cellular necrosis occurs. 

• Troponin 

  • Very Specific for Cardiac Cellular Death 

  • Rises 3-6 hours after injury 

  • Peaks in 12-18 hours 

  • Stay elevated for 1-2 weeks 

• Other enzymes that rise: 

  • Creatine Phosphokinase CPK 

  • Lactic dehydrogenase LDH 

  • Myoglobin 

STEMI treatment

• Rapid transport to the hospital – activate EMS 

• 12 Lead EKG – to be read within 10 min 

• Obtain blood for cardiac biomarker – troponin 

• Routine medical interventions (MONA) 

• MONA is not definitive treatment but is for initiating treatment 

  • Morphine, Oxygen, Nitroglycerin, Aspirin

• Oxygen 

  • If O2 is < 94 

• Morphine

  • Pain and vasodilates 

• Aspirin – chewable 162mg to 325 mg 

  • antiplatelet 

• Nitroglycerin 

  • Check BP 

  • Sublingual 0.4 Q5 after checking BP if pain is unrelieved 

  • only give If SBP is > 100 

  • Slight burning is normal 

other STEMI tx

Beta blockers 

• IV 

• Decrease workload on the heart 

• Avoid v-fib 

• To slow HR 

• The slower the hr the more time in diastole 

• Diastole is when the heart is being perfused 

Anticoagulation 

• Clopidogrel, heparin, glycoprotein IIb/IIIa agents (Eptifibatide/Integrilin) 

reperfusion therapy

• Reperfusion – for eligible patients with symptoms within the past 12 hours 

  • PCI capable facility– door to balloon time 90 minutes 

    • Percutaneous coronary intervention in the cath lab 

  • Non-PCI capable facility – transfer to PCI capable facility if < 120 minutes to balloon time 

• If PCI cannot be done in < 120 minutes, administer fibrinolytics 

  • Dissolve the clot 

• If fibrinolytics are given, they should be administered within 30 minutes of arrival to hospital. (Door to needle time) 

MI nursing considerations

• IV access 

  • Administer meds 

• Monitoring vital signs/hemodynamic stability 

  • Enough blood to perfuse organs (brain, kidney, etc.) 

• Continuous cardiac monitoring 

• Labs 

  • Troponin 

  • Electrolytes, BUN, Creat, CBC with platelet ct, INR, Magnesium, Glucose, Serum lipids, aPTT 

• Patient support and education 

PCI stent

• Invasive Procedures 

• Coronary stent placement 

• Done during the cardiac catherization 

• Permanent  

• Give Plavix/clopidogrel to avoid clotting in the stent 

PCI post care

• Monitor for dysrhythmias, chest pain, neurologic changes 

• Bedrest for at least 4 hours 

• HOB no higher than 30 degrees 

• Frequent VS checks every 15 min x’s 4, every 30 min x’s 4 and every hour x’s 4 

• Assess distal pulses with each VS check 

  • On the side of the pci 

• Assess for bleeding or hematoma with each VS check 

  • May not see the tachycardia bc of the meds 

• Monitor I/O 

  • Increase fluid intake or IV fluids to prevent contrast induced nephropathy 

  • Acetylcysteine – Mucomyst 

PCI complications

• Hematoma 

• Vascular complications 

• Embolism 

• Hypersensitivity to contrast dye 

  • Steroids, Benadryl, Pepcid to premedicate 

• Dysrhythmias 

• Bleeding 

• Restenosis 

  • CP 

• Stroke 

• Contrast induced nephropathy 

fibrinolytics

• Activate the body’s own fibrinolytic system to lyse coronary clots 

• Diagnosis of STEMI must be confirmed. 

• Not for an NSTEMI 

• Done if PCI cannot be done within 120 minutes 

• Damaged tissues, blood vessels or organs stimulate platelet aggregation 

• A platelet plug forms over damaged vessel 

• Clotting cascade is initiated 

• Vasoconstriction occurs 

• Fibrin surrounds platelets to form a clot 

• Fibrinolytics activate the body’s fibrinolytic system to lyse a blood clot 

• Dissolution of fibrin clot is done by plasmin. 

• Plasmin is circulating in the body in the inactive form of plasminogen. 

• Plasminogen is activated by tissue plasminogen activator (TPA) which converts the plasminogen into plasmin which digests the clot. 

• Early administration limits infarct size, reduces myocardial damage and improves outcomes 

absolute contraindications for fibronolytics

• Prior intracranial hemorrhage/hemorrhagic stroke 

• Known cerebral vascular lesion or neoplasm 

• Ischemic stroke with in the last 3 months 

• Suspected aortic dissection 

• Active bleeding 

• Recent major surgery or trauma 

• Severe uncontrolled hypertension (unresponsive to emergency therapy) 

• Known bleeding disorders 

• Pregnancy 

intracranial hemorrhage risk factors

Worst complication for fibrinolytics

• Age>65 years 

• Weight > 70kg 

• Female gender 

• HTN on admission 

evidence of reperfusion

• Reperfusion dysrhythmias (PVCs, accelerated idioventricular rhythm) 

  • Generally, not life threatening and not typically treated 

• Abrupt cessation of chest pain 

  • Though may not be a reliable indicator especially when morphine us used. 

  • Pain is subjective 

• Rapid return of ST segment to baseline 

• Very good indicator of reperfusion 

• Best predictor of reperfusion is the cessation of chest pain coupled with ST segment return to baseline 

post TPA infusion care

• Frequent assessment of VS 

• Continuous EKG monitoring 

• Observe for evidence of bleeding - ↓BP & ↑HR 

  • Assess body fluids for evidence of bleeding 

  • Flank pain/back pain – may indicate retroperitoneal bleeding 

  • Assess LOC – intracranial bleed 

    • Can be subtle like anxiety and restlessness 

  • Assess puncture sites for bleeding 

    • Anticipate the need to apply additional pressure at puncture sites 

• Evaluate response to therapy 

• Report manifestations of re-occlusion 

• Minimal handling of the patient 

  • Bedrest for 6 hours 

• Avoid injections 

• Best to insert 2 IVs prior to administration 

• Prophylactic H-2 blockers 

• Anticoagulation may be recommended after fibrin therapy to improve vessel patency and prevent re-occlusion. 

  • IV Heparin - monitor aPTT

  • Enoxaparin

indications for PCI capable facility post TPA

• Development of cardiogenic shock 

• Urgent transfer for failed reperfusion 

• In stable patients between 3 and 24 hours after successful fibrinolysis 

complications for acute MI

• Cardiogenic shock 

• Heart Failure 

• Dysrhythmias 

  • Ventricular 

  • Slow – Bradycardia, AV heart block 

• Pericarditis 

• Papillary muscle rupture 

• Wall rupture 

  • Septum 

  • Ventricular free wall 

• LV aneurysm 

• Bleeding 

• AKI 

• Anoxic brain injury if there was a cardiac arrest 

HF/pulm edema

• Infarcted tissue does not pump 

• Acutely may require vasopressor support and intubation 

• Treat with medications 

  • ACE Inhibitors 

  • Beta Blockers 

  • Diuretics 

  • Aldosterone Antagonists 

MI nursing care

Cardiac Assessment 

• Vital signs 

• Evaluation and relief of chest pain 

• Assessing for heart failure 

• Monitoring for dysrhythmias 

Evaluation of adequate perfusion 

• Level of consciousness 

• Adequate urine output 

• Most important 

• Gastrointestinal symptoms 

• Skin temperature 

• Capillary refill 

Nursing care for chest pain

• Assess and document CP 

• Vital signs including heart rhythm 

• Assess skin temp 

• 12L EKG 

• Decrease physical activity 

  • Priority if they do not need the oxygen 

• Oxygen, NTG, Morphine 

• Provide a restful environment 

• Small meals 

• Assist with ADLs 

• Avoid straining – stool softeners 

• Help patient to relax 

• Teach patients to recognize symptoms 

MI discharge meds

Statin therapy 

• Lowers cholesterol 

• Provide plaque stabilization 

• Stabilize their plaque 

• LFT, and Rhabdo 

Angiotensin converting enzyme inhibitors 

• If MI is anterior wall 

• HF and an EF < 40% 

Aldosterone antagonists 

• EF < 40% 

• Symptoms of HF 

• Diabetes 

• spironolactone 

Dual Antiplatelet Therapy (DAPT) 

• Aspirin 

• Clopidogrel (Plavix) 

MI discharge

• Call 911 for CP/SOB and associated symptoms 

• Seek immediate care for 

  • Unusual fatigue 

  • Rapid pulse 

  • Bleeding 

  • Urine, stool, nose,etc. 

  • Low urine output 

  • New or increased swelling in feet or ankle 

• Medications 

  • Take as prescribed 

  • Notify provider for side effects of medications 

• Education on medications 

  • Indications 

  • Side effects 

• Lifestyle modifications 

  • Heart healthy diet 

  • Smoking cessation 

  • Exercise – cardiac rehab 

  • Maintain ideal body weight 

    • BMI 18.5-24.9 

  • Manage stress 

  • annual flu shot

• Keep follow up appointments  

HF disparities

• African Americans have higher rates for HF 

• Ages 65-69 – 20/1000 have HF 

• Age >85 80/1000 have HF 

• LGBTQ adults have increased rates of smoking than heterosexual peers 

• Transgender adults have lower levels of physical activity than heterosexual peers 

• Lesbian and bisexual women have higher rates of obesity than heterosexual women 

HF

• a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood. 

• Characterized by 

  • Fluid volume overload 

  • Inadequate tissue perfusion 

  • Cardinal Manifestations are: 

  • Dyspnea and fatigue 

  • Exercise intolerance 

  • Fluid retention 

  • Peripheral edema 

ejection fraction

• percentage of blood that is ejected from the ventricles during systole 

• EF=SV/EDV 

  • 55-70% - Normal limits 

  • 40-55% - Below normal 

  • <35% - Increased risk of life-threatening arrhythmias 

• Cardiac Output = HR x SV 

preload and afterload

• Preload - the degree of stretch of the ventricular cardiac muscle fibers at the end of diastole 

  • The volume of blood in the ventricle at the end of diastole determines preload 

  • Diuresis decreases preload 

  • Fluid bolus increases preload 

• Afterload – the resistance to ejection of blood from the ventricle 

  • HTN and stenosis increase afterload 

• In heart failure both preload and afterload can be increased 

HF patho

• HF begins after an event produces a decline in the heart’s pumping capacity. 

  • Can have an abrupt onset or a gradual insidious onset 

  • Contractility decreases resulting in an increased end diastolic volume 

  • Causes increased stretching and dilation of the ventricular muscle tissue 

• Compensatory mechanisms are activated. 

  • The body’s attempt to maintain cardiac output 

  • Treatment for HF is aimed at blocking these compensatory mechanisms 

• Compensatory mechanisms 

  • Short term can restore cardiac function to a normal or near-normal range. 

  • Over time, compensatory mechanisms can lead to left ventricular remodeling and cardiac decompensation 

neurohormonal compensatory mechanisms

Baroreceptors 

• Decreased flow causes stimulation of the SNS 

Sympathetic nervous system (SNS) 

• Initially compensates by increasing heart rate and peripheral vascular resistance. 

• Over time, catecholamines cause toxic effects on the myocardium 

• Direct toxicity to the myocardium 

• Myocardial remodeling & facilitation of dysrhythmias 

Renin angiotensin aldosterone system 

• renal perfusion causes the kidneys to release renin. 

• Renin acts on angiotensinogen to form angiotensin I. 

• In the presence of angiotensin converting enzyme, angiotensin I is converted in the lungs into angiotensin II. 

• Angiotensin II causes vasoconstriction, sodium and water retention and pro-fibrotic and pro-inflammatory effects that contribute to cardiac remodeling. Also stimulates the release of aldosterone 

Aldosterone 

• Angiotensin II stimulates the release of aldosterone from the adrenal cortex which causes sodium and water retention. 

• Aldosterone is associated with cardiac fibrosis and ventricular remodeling 

causes of HF

• Hypertension 

• Diabetes Mellitus 

• Metabolic Syndrome 

• Atherosclerotic Disease – CAD, MI – CAD is found in the majority of those with heart failure 

• Cardiomyopathy 

  • Dilated, Ischemic, familial, alcohol-induced, cocaine, toxic, chemotherapy, tachycardia-induced, peripartum, iron overload, Stress (Takotsubo) 

• Valvular Disease 

• Thyroid Disease 

• Myocarditis 

• HIV 

• Rheumatologic/Connective Tissue Disorders 

• Amloidosis/Scarcoidosis 

natriuretic peptides

• Atrial natriuretic peptide 

• B-Type natriuretic peptide (BNP) 

  • Normal < 100 

  • Naturesis = sodium excretion 

• Beneficial but not sufficient to overcome other pathways 

• Hormones that are secreted due to myocardial wall stretching. 

• They have beneficial effects of natriuresis and vasodilation

systolic failure

• (HFrEF)

• Inability of the heart to generate adequate cardiac output to perfuse vital tissues. 

• Decreased contractility causes a decrease in stroke volume and an increase in left ventricular end-diastolic volume. 

• Over time the increased volume causes dilation of the heart 

 

diastolic failure

• (HFpEF) 

• The left ventricle loses the ability to relax normally and can’t properly fill with blood during diastole 

• There are no approved pharmacologic or device therapies for the management of patients with HF with preserved EF 

• Dyspnea should be treated with sodium restriction and gentle use of diuretics 

R vs L sided HF

Generally symptoms are seen together 

• Right 

  • LHF common cause of RHF 

  • Jugular venous distension 

  • Peripheral edema 

  • Ascites 

  • Hepatomegaly 

  • Jaundice 

    Weight gain 

• Left 

  • Problem with forward flow and blood backing up into lungs 

  • Pulmonary symptoms 

    • Pulmonary edema 

    • Pink frothy sputum 

  • Fatigue 

  • Exercise intolerance 

  • Cyanosis 

  • Orthopnea 

  • Paroxysmal nocturnal dyspnea (PND) 

  • Weak pulses 

  • Decreased perfusion to vital organs 

    • Decreased urine output (oliguria or anuria) 

    • LOC changes 

  • Cool clammy  

HF classes

NYHA

• I - Asymptomatic

• II - Minor Symptoms, onset with modest exertion

• III - Moderate symptoms, onset with minor exertion

• IV - Symptoms at rest

ACC/AHA

• A - at risk of HF but no structural disease

• B - Structural HF with no symptoms

• C - Structural HF with current or prior symptoms

• D - Symptoms at rest

HF manifestations

Neurological 

• Fatigue 

• Depression 

Cardiovascular 

• Laterally displaced PMI 

• S3 

  • Early diastolic heart sound 

  • Overfilling of ventricles creates a new sound 

• Jugular venous distention 

• Diminished pulse pressure 

  • Heart cannot create systolic pressure 

• Peripheral edema 

• Dysrhythmias 

Vital Signs 

• Tachycardia 

• Generally hypotensive 

Respiratory 

• Orthopnea 

• Paroxysmal nocturnal dyspnea 

• Acute pulmonary edema 

• Pulmonary crackles, wheezing 

• Cough 

• Pleural effusions 

Gastrointestinal 

• Hepatomegaly 

• Ascites 

• Jaundice 

• Cardiac cachexia 

• Weight gain 

Renal 

• Decreased urine output 

• Renal dysfunction 

HF diagnosis

• History and Physical Exam 

• Routine laboratory testing 

  • Electrolytes, BUN, creat, CBC, hepatic enzymes, BNP, Thyroid function testing 

• 12 Lead EKG 

  • Ischemia, ekg changes, past MI 

• CXR 

  • Cardiac enlargement 

  • Pulmonary arteries distended 

• Assessment of cardiac structure and function – transthoracic echocardiogram (TTE) 

• Ischemic work up to determine reversible causes 

• Want to ensure stents are not placed in already dead tissue 

HFrEF treatment

• Diuretics 

• ACEIs

• ARBs

• Beta Adrenergic Receptor Blockers 

• Aldosterone Antagonists 

• Nitrates and Hydralazine

• ARNI

• SGLT2i 

• Digoxin

• Inotropes

• Anticoagulation Antiplatelet Therapy 

diuretics

• The only pharmacologic agents that adequately control fluid retention 

• Loop diuretics - furosemide, bumetanide, torsemide 

  • Hypokalemia -> dysrhythmias  

  • Hypotension if already have a borderline BP 

• Thiazide diuretics – metolazone 

  • Increases potency of loop diuretic 

• Potassium sparing diuretics – spironolactone, eplerenone 

  • Aldosterone blockers 

• MOA

  • inhibiting the reabsorption of excretion of water and electrolytes, primarily sodium

• Preload and afterload

  • preload decreases with lower fluid volume

  • afterload decreases with decrease in BP

ACE inhibitors

• Decreases afterload 

• MOA

  • Prevent the conversion from angiotensin I into angiotensin II. 

• Check BP first 

• Drs like lisinopril because it's a once a day dose = more adherence 

• Stabilize LV remodeling 

• Improve symptoms 

• Reduce hospitalizations 

• Prolongs life 

• Adverse Effects – hypotension, cough, angioedema, renal dysfunction, hyperkalemia 

ARBs

• decrease afterload

• MOA

  • prevent angiotensin II from binding

• Used when patients are intolerant to ACE inhibitors. 

• Blocks the effects of angiotensin II on the angiotensin receptor. 

• Stabilize LV remodeling 

• Improves patient symptoms 

• Prevents hospitalization 

• Prolongs life 

• Not to be used with ACEI!!! 

• Adverse Effects – hypotension, azotemia, hyperkalemia 

Beta Adrenergic Receptor Blockers (beta blockers)

• Always check HR and BP 

• reduce afterload

• MOA

  • block epi and norepi → decreases HR

  • decrease contractility

  • slow conduction through AV node

• When given in combination with ACE inhibitors: 

  • Reverse LV remodeling 

  • Improve patient symptoms 

  • Prevent hospitalization 

  • Prolong life 

• Adverse Effects – Hypotension, bradycardia, heart blocks. Not for use in pts with active bronchospasm. Can mask hypoglycemia 

  • Most are cardio selective -> only affect b1 (heart) but can affect b2 (lungs) 

aldosterone antagonists

• MOA

  • reduce aldosterone which plays an important role in the pathophysiology of HF. 

• Diuretic effect 

• Prevents hospitalizations 

• Reduces mortality 

• Adverse effects – Hyperkalemia, gynecomastia, menstrual irregularities in spironolactone 

nitrates and hydralazine

• Used in African American patients with systolic dysfunction in addition to standard therapy. 

• Used for patients who are taking ACEI and BBL for symptomatic HF and who have persistent symptoms. 

• For HF patients with are unable to tolerate ACEI and ARBs 

• nitrates

  • significantly decrease preload by dilating venous vessels → less volume in heart

• hydralazine

  • significantly decrease afterlaod by vasodilation

ARNI

• Sacubitril/valsartan (Entresto) 

• Used in place of an ACEI or ARB 

• Works by impairing neprilysin which degrades natriuretic peptides 

• Adverse effects – angioedema, hypotension, impaired renal function 

• reduces both preload and afterload

SGLT2i

• Sodium-glucose cotransporter-2 inhibitors (SGLT2i) 

• Dapagliflozin (Farxiga) 

• Reduces CV death and heart failure in those with and without heart failure and diabetes 

• MOA

  • increase glucose secretion by inhibiting SGLT2 → diuresis, decrease in BP, decrease in fluid volume

• reduces preload with diuresis

digoxin

• Indicated for use in patients with HF and atrial fibrillation

• MOA

  • inhibits the Na+/K+ ATPase pump in the cardiac myocytes → increase in intracellular sodium and increased calcium inside the cell

• Positive inotrope but drops HR 

• Considered for patients who have signs or symptoms of HF while receiving standard therapy. 

• Use of digoxin does not improve mortality 

• Toxicity can lead to dysrhythmias and hypokalemia increases toxicity

• minimal effects of preload and afterload

inotropes

• Affect contraction 

• Positive -> increase contraction 

• Negative -> decrease contraction 

• Dobutamine 

  • Stimulates beta 1 and 2 receptors 

  • Increases C.O. 

    • reduces afterload

  • Given as a continuous IV infusion 2-10 mcg/kg/min. 

• Milrinone 

  • Phosphodiesterase III inhibitor 

  • Increases Ca in the cardiac cells and vasodilates 

    • Decreases afterload 

  • Check BP frequently – typically Q2 vitals 

  • Increases cyclic AMP 

  • Increases C.O. and has vasodilator effects. 

  • Given as a continuous IV infusion 0.25 – 0.75mcg/kg/min 

anticoagulant therapy

• Patients with A fib or other risk factors for stroke should be anticoagulated 

• Aspirin – may be used in ischemic disease 

HF nursing care

• Daily Weights 

  • 2-3 pounds in a day or 4-5lbs in a week patient need to call a provider 

• I and O’s 

• Monitoring symptoms, 

  • electrolytes/renal fx 

  • Respiratory sx 

    • Especially important to know if SOB is infection, HF,  

    • If cough is infection or from ACEI 

• Monitoring medication effectiveness and side effects 

• Assessing support systems 

• Managing edema – thromboembolic hose, elevation of legs 

• Education 

  • Diet 

  • Medications 

  • Signs and symptoms 

  • Weight reduction 

  • Exercise 

  • Sexuality 

  • Depression 

  • Managing other comorbidities 

  • Smoking cessation 

device therapy

Internal Cardiac Defibrillators 

• Patients with an EF <35% are at risk for dysrhythmias and sudden cardiac death 

• Only for sudden arrest 

Biventricular Pacing (Cardiac Resynchronizing Therapy) 

• Benefits patients with left ventricular systolic dysfunction and a wide QRS complexes who are in NSR 

• Improves CO 

• Decreases mortality 

• Decreases hospitalization 

• Reverses LV remodeling 

HF preventative behaviors

• Routine hand washing 

• Dental health 

• Immunizations 

dysrhythmias

Definition 

• Disorders of the formation of electrical impulses in the heart 

• Disorders of conduction of electrical impulses in the heart 

• Both of the above 

Consequences – may have hemodynamic instability 

cardiac conduction system

• SA node is automatic pacemaker 

  • Spontaneously generates impulses because of permeability to sodium ions  (60-100)

• AV node 

  • Slow conduction 

  • Keeps SA node in check 

  • Allows diastole  

  • Back up pacemaker (40-60) 

• Purkinje fibers 

  • Backup backup pacemaker (20-40) 

dysrhythmia principles

• The EKG provides information only about electrical events in the heart 

  • It provides no information about contractile events 

  • Always assess the patient for any change in cardiac rhythm 

• Tachycardias 

  • Can be detrimental because 

  • Increase myocardial oxygen demand 

  • Decrease ventricular filling time 

  • Decrease coronary artery perfusion time 

• Bradycardias 

  • Can be detrimental because 

  • Decrease cardiac output 

  • Can cause syncope, chest pain

  • Remember CO=HR x SV 

Refractory periods

Absolute refractory period  

• QRS complex 

• The heart is being depolarized 

• Cannot respond to another impulse  

Relative Refractory Period 

• Part of ST and T wave 

• May or may not respond to a premature impulse 

• Can skew EKG 

Vulnerable period 

• Majority of T wave 

• Cells are still repolarizing 

• Premature impulses can be dangerous and can deteriorate patient into V-tach or V-fib (“R on T”) 

p wave

• Atrial depolarization 

• Symmetrical and rounded 

• Before QRS 

• increases with atrial hypertrophy 

QRS complex

• From the beginning of the QRS to the end 

• The composite of electricity in the ventricular septum and the right and left ventricles 

• Represents ventricular depolarization 

• Normal 0.06 to 0.10 seconds 

  • 1 ½ to 2 ½ boxes 

PR interval

• From the beginning of the P wave and goes to the first deflection of the QRS complex 

• Impulse activity in the heart before it gets to the ventricle 

• Normal 0.12 – 0.20 seconds 

  • 3-5 boxes 

• Represents the length of time required for SAN stimulation, atrial depolarization and conduction through the AVN before ventricular depolarization 

ST segment

• Represents early repolarization and lasts from the end of the QRS complex to the beginning of the T wave 

• The ST segment is normally isoelectric 

• At baseline 

• If it above or below the isoelectric line, it may be a sign of cardiac ischemia/infarction 

  • Below – ischemia 

  • Above - infarction 

T wave

• Represents ventricular repolarization 

• It follows the QRS complex and is usually the same direction as the QRS complex 

• T wave is asymmetric 

QT interval

• Beginning of the QRS to the end of the T wave – measures ventricular depolarization and repolarization 

• If the QT interval becomes prolonged, the patient may be at risk for a lethal ventricular dysrhythmia called torsades de pointes (V-tach) 

• 0.45 seconds is prolonged 

normal sinus rhythm

• Definition – the electrical impulse starts in the SA node 

• Regular rate and rhythm 

• Impulse travels through the normal conduction pathway 

• Rhythm: Regular 

• Rate: 60-100 bpm 

• Atrial conduction – 1 p wave before each QRS, consistent in shape 

• AV conduction – PR interval 0.12-0.20 seconds 

• Ventricular conduction – QRS 0.06-0.10 seconds 

sinus tachy

• Definition – occurs when the SAN creates an impulse at a faster than normal rate 

• Criteria: 

  • Rhythm - Regular 

  • Rate > 100 bpm 

  • AV conduction – PR interval 0.12-0.20 seconds 

  • Ventricular conduction – QRS 0.06-0.10 seconds 

• Causes: 

  • Physiologic or psychological stress, blood loss, anemia, shock, hypovolemia, heart failure, pain, hyper-metabolic states, fever, exercise, anxiety, hypoxia, hypotension, medications, infection, hyperthyroid, stimulants, illicit drugs 

• Treatments 

  • Treat the underlying cause 

  • monitor patient

sinus brady

• Definition – occurs when the SAN creates an impulse at a slower than normal rate 

• Criteria 

  • Rhythm - Regular 

  • Rate < 60 bpm 

  • AV conduction – PR interval 0.12-0.20 seconds 

  • Ventricular conduction – QRS 0.06-0.10 seconds 

• Causes – decreased metabolic needs, athletic training, hypothyroidism, vagal stimulation, medications, idiopathic SAN dysfunction, increased ICP, MI 

• Treatments 

  • Monitor the patient 

  • Treat only if symptomatic 

  • Treat underlying cause 

  • Atropine if caused by a vagal mechanism 

    • Blocks parasympathetic nervous system  

  • Unresponsive to Atropine 

    • Transcutaneous pacemaker, dopamine, epinephrine 

    • Transvenous pacemaker 

PAC

• Definition – a premature, ectopic electrical impulse discharges in the atrium before the next normal impulse of the SA node 

• Ectopic beat – a pacemaker site outside of the SAN 

  • Lots of ectopy = lots of irregularities  

• Complex comes in early 

• Criteria 

  • Rhythm – regular except where the premature beat occurs 

  • Rate – is the rate of the underlying rhythm 

• Atrial conduction – P wave before the ectopic beat is different from the p waves of the underlying rhythm 

• Causes – caffeine, alcohol, nicotine, stretched atrial myocardium, HF, anxiety, hypokalemia, hyper-metabolic states, atrial ischemia, medications 

• PACs are common in normal, healthy hearts 

• Treatment 

  • No treatment is generally needed 

  • Assess the patient 

  • Remove causing agent 

a flutter

• Definition – atria are depolarized at rates of 250-400 times per minute 

• Caused by a reentry circuit 

  • Not all the atrial impulses are conducted into the ventricle, causing a therapeutic block at the AV node 

• Criteria

  • Atrial rate is between 250-400 

  • Ventricular rate variable 

  • Atrial rhythm is regular 

  • Ventricular rhythm can be either regular or irregular, depending on the conduction pattern 

  • “P” waves produce a saw-tooth pattern called flutter waves 

• Causes 

  • Usually associated with underlying cardiac disease 

  • Long standing hypertension, cardiomyopathy, CAD, hypoxia, heart failure, valvular disease, SAN damage, post open heart surgery, digitalis toxicity 

• Blood stasis and thromboembolisms may occur due to lack of atrial contraction 

• Treatment 

  • Control heart rate

    • Diltiazem, beta blockers, digitalis 

  • Convert to NSR 

    • Amiodarone 

    • Cardioversion 

      • Onto the r wave because it is the absolute refractory period 

  • Vagal Maneuvers 

    • Carotid sinus massage, Cough 

  • Anticoagulation 

• when patient is unstable  

  • Restless  

  • Diaphoretic  

  • Low BP  

  • Chest pain  

  • SOB 

afib

• Definition – 

  • Uncoordinated atrial electrical activation from multiple areas in the atria 

  • Results in a rapid, disorganized, quivering, fibrillating atria 

• The ventricular rate is dependent on the ability of the AV node to conduct the atrial impulses 

• Lack of atrial contraction increases the risk of thromboembolism formation 

• Characteristics 

  • No P waves 

  • EKG baseline is irregular and undulating 

  • Ventricular rhythm is irregular and no pattern to the irregularity “Irregular, Irregularity” 

• Clinical Significance 

  • Loss of atrial systolic volume “atrial kick” 

  • The last bit of squeeze increases preload 

  • Loss of AV synchrony 

  • Reduced cardiac output 

  • Increased potential for thromboembolism 

• Causes 

  • Advanced heart disease, long standing hypertension, atherosclerosis, rheumatic heart disease, MI, HF, valve disease, pulmonary disease, after cardiac surgery, thyrotoxicosis, congenital heart disease 

• Rarely occurs in individuals with no functional heart disease 

• Goal 

  • Decrease ventricular rate 

  • Convert to NSR 

  • Prevent thromboembolism 

afib treatment and meds

Medications for rate control 

• Calcium channel blocker – diltiazem 

  • Continuous infusion 

• Beta blockers 

  • Just for rate control 

• Digoxin 

Medications for conversion 

• Amiodarone 

  • Loading dose and then PO 

• Dofetilide - Tikosyn 

• Flecanide – Tamboco

Thromboembolism in Afib 

• Origin is frequently the left atrial appendage 

  • Left atrial appendage closure 

  • Watchman 

• Most patients require some antithrombotic therapy 

• Antiplatelet agents - Aspirin 

• Antithrombotic medications 

• Anticoagulants 

  • Warfarin 

• Factor Xa inhibitors 

  • Dabigatran 

  • Rivaroxaban 

  • Apixaban 

Treatment 

• Cardioversion if unstable 

• Cardioversion – synchronized defibrillation 

  • Shock on the R because absolute refractory period 

• Invasive treatments 

  • Maze procedure 

  • Cut the atrial tissue to form scar tissue to stop the electrical impulses form forming 

  • Pulmonary vein ablation

• Some patients remain chronically in Afib 

PVC

• Definition 

  • Premature ectopic impulse that originates in the ventricle 

  • Conducted through the ventricles before the next normal sinus impulse 

• These can occur in healthy people 

• Characteristics 

  • Ventricular complex that comes in early 

  • QRS is wide, shape is bizarre and there are 

  • ST and T wave changes 

    • PVC’s make the rhythm irregular 

• Causes – caffeine, nicotine, alcohol, cardiac ischemia, heart failure, digitalis toxicity, hypoxia, acidosis, electrolyte imbalances, especially hypokalemia, obstructive sleep apnea 

• Multifocal  

  • More than one area firing prematurely 

  • PVC are asymmetric 

• Treatment 

  • Infrequent – no treatment needed 

  • Remove causing agent 

  • Amiodarone, lidocaine 

  • Amio is second line 

Vtach

• Definition 

  • 3 or more PVCs in a row, 

  • Rate exceeding 100 bpm 

  • This is an emergency and can be a life-threatening dysrhythmia 

• Characteristics 

  • Ventricular rate is >100 bpm 

  • Rhythm is usually regular 

  • QRS complexes are wide 

  • No P waves present 

• Causes – MI, ischemia, hypoxia, electrolyte imbalance, CAD, acidosis, digitalis toxicity, drug intoxications, HF, cardiomyopathy, valve disease 

• Treatment 

  • Pulse present 

    • Stable – antiarrhythmic drugs, amiodarone 

    • Unstable but conscious 

      • Sedate 

      • Cardioversion 

      • Antiarrhythmic drugs 

  • Pulseless – defibrillation 

    • Unsynched 

    • CPR 

vfib

• Definition 

  • Rapid, disorganized ventricular rhythm that causes ineffective quivering and pumping of the ventricles 

  • Life-threatening dysrhythmia 

• Characteristics 

  • No atrial activity seen 

  • Ventricular rhythm is extremely irregular and chaotic with no pattern 

  • QRS shape is irregular with undulating waves without recognizable QRS complexes 

• Causes 

  • The most common cause of cardiac arrest 

  • CAD, ischemia, MI, HF hypoxia, acidosis, electrolyte imbalances, valve disease 

• Treatment 

  • CPR, defibrillation, Epinephrine, amiodarone, vasopressin, lidocaine, sodium bicarbonate 

dysrhythmia symptoms

cardioversion and defribrillator

Cardioversion 

• Delivery of a timed or synchronized shock to terminate a tachy-dysrhythmia 

• Shock is synchronized with the “R” wave 

• Shock delivered during absolute refractory period 

Defibrillation 

• Unsynchronized electrical shock administered in an emergency situation to terminate a life-threatening dysrhythmia 

• Causes depolarization of a critical mass of myocardial cell all at once; 

• Sinus node will then recapture its role as the primary pacemake

causes of acquired valve disease

• Rheumatic heart disease 

  • caused by strep

• Infective endocarditis 

• Degenerative or age related 

• Myocardial infarction 

• Marfan’s syndrome 

• Trauma 

• Lupus 

• Scleroderma 

stenosis

• Restricts the forward flow of blood because the valve is unable to fully open 

Results in: 

• Increased the workload of the heart (increases afterload) 

• Hypertrophy of the of the chamber pumping against the stenotic valve 

• Level 1 murmur 

regurg

• Valve does not close completely and permits the backward flow of blood 

Results in: 

• Increased blood volume in the cardiac chamber receiving the backflow of blood 

• Over time, chamber receiving regurgitant blood flow will become dilated 

stenotic valve

Results in hypertrophy of atria -> Afib 

regurgitant/incompetent valve

• Ventricle contracts and blood flows backwards into atria resulting in hypertrophy -> afib and a flutter 

• Over time leads to ventricular hypertrophy as well  

Murmur grading

aortic stenosis

• Definition – an obstruction of blood flow from the left ventricle into the aorta during systole 

• Systolic murmur 

• Caused by a narrowing of the valve opening 

• AS causes an increase LV workload leading to LV hypertrophy 

• Over time, severe AS can cause: 

• A decrease in LV function 

• Resulting in heart failure (right sided and left sided) 

Risk factors 

• Congenital bicuspid valve 

• Degenerative stenosis 

• Age 

• Diabetes 

• Elevated cholesterol 

• Hypertension 

• Smokin 

Clinical Manifestations 

• Exertional dyspnea 

• Exercise intolerance 

• Fatigue 

• Angina 

• Syncope – fixed cardiac output

  • Cannot adjust CO 

• Systolic ejection murmur 

• Heart failure 

• Slower heart rate – takes longer for LV to eject blood 

aortic regurg

• Definition: 

• Backflow of blood from the aorta into the LV during diastole -> diastolic murmur 

• Due to ineffective closure of the aortic cusps 

• LVED volume increases 

• Over time causes dilation of the LV and subsequent heart failure 

• Lowers diastolic BP or widened pulse pressure because of backflow of blood 

Risk Factors 

• Infective or rheumatic endocarditis 

• Congenital malformations 

• Dissection aortic aneurysm 

• Chest trauma 

• Marfans 

Clinical Manifestations 

• Fatigue 

• Dyspnea on exertion 

• Palpitations 

• Dizziness 

• Sensation of a forceful heartbeat 

• Angina – due to drop in diastolic pressure – decreases coronary artery perfusion 

• Heart failure 

• Diastolic murmur – high pitched blowing sound 

aortic valve disorder treatments

Aortic Stenosis 

• Echo surveillance 

• Medications 

  • ACE inhibitors – reduce afterload 

  • Statins – some evidence to suggest they slow disease progression 

• Surgery – Aortic valve replacement 

  • Aortic balloon valvuloplasty 

    • High mortality 

  • TAVR – trans catheter aortic valve replacement 

    • Worry about hemorrhage with arterial stick 

    • Contrast dye can damage kidneys 

Aortic Regurgitation 

• Echo surveillance 

• Medications – afterload reduction 

  • Vasodilators, - ACE inhibitors, calcium channel blockers 

• Sodium restriction 

• Surgery – Aortic valve replacement 

  • Surgery should be done before symptoms develop 

  • Operative mortality is 3% 

  • Patient with marked cardiac enlargement and LV dysfunction - mortality rate 10% 

mitral stenosis

Definition 

• Obstruction of LV filling due to a narrowing/incomplete opening of the orifice of the mitral valve 

• MV is open during diastole to allow blood to flow from the left atrium to the left ventricle 

Patho

• Increased work of the left atrial causes hypertrophy 

• Left atrial hypertrophy increases the risk of developing A fib 

• Patients who develop A fib can become very symptomatic because they rely on atrial systolic volume to contribute to left ventricular end-diastolic volume 

• Atrial systolic volume contributes to 10 % of EDV 

• Blood backs up into the lungs 

Risk Factors 

• Streptococcal infections 

• Congenital valve abnormality 

Clinical Manifestations 

• Dyspnea on exertion 

• Fatigue 

• Palpitations and chest pain 

• Left atrial enlargement - increases risk of A fib and thrombus formation 

• Orthopnea, paroxysmal nocturnal dyspnea 

• Pulmonary edema 

• Heart failure 

• Diastolic murmur – low frequency rumble 

mitral regurg

Definition – backflow of blood from the LV to the LA during systole due to incomplete closure of MV 

• Can be acute or chronic 

• Volume overload leads to ventricular dilation 

• Causes progressive LA dilation and RV dysfunction and pulmonary hypertension 

Risk Factors – HF, endocarditis, mitral valve prolapse, acute MI 

Volume overload occurs in the 

• Left atrium 

• Left ventricle 

• Leads to ventricular dilation 

Causes progressive 

• LA dilation 

• RV dysfunction and 

• Pulmonary hypertension 

Clinical Manifestations 

• Tachycardia 

• Fatigue, weakness 

• Exertional dyspnea 

• Orthopnea 

• Increased risk of atrial fibrillation 

• Signs of left sided heart failure 

• Pulmonary edema and congestion 

• Later - right sided heart failure 

• Pansystolic or holosystolic murmur 

  • The entire time during systole 

treatments for mitral disorders

Mitral Stenosis 

• Echo surveillance 

• Control HR – beta blockers 

• Treat A fib 

• Anticoagulate for A fib 

• Mitral valvuloplasty 

  • Highly successful with low rate of restenosis 

• Surgery 

  • Repair or replace valve 

Mitral Regurgitation 

• Echo surveillance 

• Medications 

  • Vasodilators – hydralazine, ACEI 

  • Rate control for A fib – beta blockers, calcium channel blockers 

  • Anticoagulate for a fib/a flutter 

  • Diuretics for volume overload 

• Surgery 

  • Valve repair 

  • Valve replacement 

types of valves

Tissue Valves 

• Don’t last as long as mechanical valves 

• Don’t require lifelong anticoagulation 

Mechanical Valves 

• Require lifelong anticoagulation 

• Generally last longer than tissue valves 

valve selection criteria

• Patient’s age 

• Patient’s size 

• Medical history 

• Ability to comply with a medical regime 

  • Warfarin 

  • If young female -> tissue because of pregnancy

  • If young in general -> mechanical bc lasts longer  

prosthetic valve complications

• Thrombus formation 

  • Especially in the mitral position 

• Leaking around valve 

• Infective Endocarditis 

  • Antibiotic prophylaxis prior to any dental procedures; 

  • 1 large dose of an antibiotic 1 hour before procedure (i.e. amoxicillin 2 grams 1 hour before procedure) 

• Degenerative changes in tissue valves 

• Complications associated with prolonged anticoagulation therapy

mitral valve prolapse

• Definition – a type of mitral valve insufficiency that occurs when one or both of the mitral valve cusps billow into the atrium during systole 

Physical Signs 

• Mid or late systolic click 

Diagnosis 

• Echocardiogram TTE and/or TEE 

Treatment 

• Beta blockers for palpitations 

• Avoid stimulants 

• If symptomatic, valve repair or replacement 

 

 

infective endocarditis

• Definition – an infection of the endocardial surface of the heart which may include one or more heart valves, the endocardium or a septal defect. Requires: 

  • Endocardial injury 

  • Bacteremia 

• Endocardial injury attracts platelets and fibrin 

• Bacteria adheres to the injured surface and produces a vegetation 

• Vegetation enlarges as the pathogen, more platelets and more fibrins are attracted to the site 

• Vegetation can breakoff and travel via the bloodstream to other organs 

• May cause stroke, sepsis, pericarditis, infarction of the lung, spleen, liver kidney and myocardium 

Risk Factors 

• Recent dental procedures, poor dental health, 

• History of congenital heart disease or valvular disease 

• Long-term indwelling IV-line, hemodialysis 

• IVDA, indwelling urinary catheters prosthetic valves, implanted hardware 

Diagnosis 

• Patient history and physical 

• Blood Cultures 

• Echocardiogram 

IE manifestations and treatment

Manifestations 

• Fever, elevated WBC 

• Heart murmur 

• Roth spots - hemorrhages in the fundi of the eyes caused by emboli 

• Symptoms of heart failure due to valve malfunction 

• Stroke symptoms 

• Skin manifestations 

  • Janeway lesions –small hemorrhages on palms or soles of feet 

  • Osler nodes – small tender lesions on fingers or toe pads 

  • Splinter hemorrhages -1-2 mm red-brown streaks on the nail bed due to small emboli 

Treatment 

• 6-week course of antibiotic therapy 

• Supportive Therapy 

• May require valve replacement surgery