Cardiovascular Notes 1 Flashcards
Cardiac Cycle
Process in which blood flows through the heart in one heartbeat.
Valves & Pressure in Systole
- Mitral & Tricuspid valves close (S1)
- Aortic & Pulmonic valves open
- Ventricles contract, ejecting blood through aortic & pulmonic valves
- Pressure in ventricles high
Valves & Pressure in Diastole
- Aortic & Pulmonic valves close (S2)
- Mitral & Tricuspid valves open
- Atria empty into the relaxed ventricles
- Pressure in ventricles low
Lub (heart sound)
T & M closing, S1, beginning of systole
Dub (heart sound)
A & P closing, S2, beginning of diastole
AV valves
Atrioventricular valves are the tricuspid valve & bicuspid (Mitral) valve.
- Tricuspid is on the right side, has three fibrous flaps anchored by chord tendinae to the papillary muscles (specialized extensions of the myocardium.)
- Chordae tendinae prevent valve prolapse
- Bicuspid (Mitral) valve is on the left & has 2 fibrous flaps.
Semilunar (SL) valves
Pulmonic valce & Aortic valve
SA (sinoatrial) node
- Near entry of superior vena cava in right atrium
- Pacemaker of heart that sets the rate & rhythm in normal hearts
Wave of Depolarization
- Spreads from SA node to the AV node where it is delayed shortly
- From AV node signal spreads to bundle of HIS and into the right & left bundle branches & into the muscle mass of the R & L ventricles
Normal sinus rhythm
- 60-100 bpm at rest in adults
- 110-150 in infants/children
Inherent rate of SA node, AV node, and Ventricles
SA node = 75 bpm
AV node = 60 bpm
Ventricles = 30-40 bpm
Emergency heart rates (tacky & brady)
Extreme tachycardia = 150-250 bpm
Extreme bradycardia = less than 30 bpm
Common Sx in Cardiovascular Dz (HPI)
-Pain/discomfort (Note location [chest, arm, back, jaw, neck] and whether they can point to it, radiation, mode of onset [rest or exertion], duration, alleviating factors, & associated sx) -Palpitation -Dyspnea/SOP/Orthopnea/PND -Fatigue -Edema -Syncope/lightheadedness/dizziness -Weakness
Past Medical Hx in cardiovascular pt
- Medications/allergies/and info pertaining to traditional CVD risk factors
- FLASHD
- CHADS2
- FHx (diabetes, HTN, hyperlipidemia, renal dz)
- Social habits & occupation
- Thoughtful ROS
- Might question pt’s partner regarding sleep-disordered breathing (loud snoring/sudden apnea)
How can PE be helpful?
- Determine cause of a sx
- Assess disease severity & progression
- Evaluate impact of therapies
PE - General appearance
- Observe pt age, posture, demeanor & health status
- Do they appear to be in pain, resting quietly, visibly diaphoretic w/foreboding sense of doom?
- Is their posture to avoid pain?
- How is their breathing?
- Pallor/cyanosis?
- Are they emaciated?
- Do they appear to have congenital syndromes: Down, Marfan, or Turners?
How to measure a standard blood pressure
Pt seated, appropriately sized cuff (err toward larger cuff), back supported, bare arm, legs uncrossed. Deflate at a rate of less than 3mmHg/sec
-Record in both arms
Orthostatic hypotension
BP falls more than 20 mmHg systolic &/or more than 10 mmHg diastolic in response to moving from supine to standing within 3 minutes.
May be accompanied by lack of compensatory tachycardia
Leg blood pressure
Can be measured at the calf with auscultation at the posterior tibial artery.
Changes in respiration rate
Increased - anxiety, hypoxic, pain
Decreased - moribund
Elevated temperature might be…
- rheumatic fever
- endocarditis
- post-MI
- hyperthyroid
Checking Pulses (peripheral & carotid)
Peripheral Pulses (arms & legs) for
- rate & rhythm
- intensity
- symmetry
- variations in pulse from beat to beat or with respiration
Carotid Pulse for
- Intensity & symmetry
- Auscultate to distinguish murmurs from carotid bruits
Checking Veins (peripheral & neck)
Peripheral - inspect for varicosities, inflammation, tenderness
Neck
- height, which is proportional to R. arterial pressure
- Jugular v is elevated w/pt reclining at 45 degree angle
- Identify highest point where pulsations can be detected & measure distance btwn this pt & sternal angle (normal is 1cm is significant
Chest Inspection
- Deformities or congenital abnormalities?
- Visible precordial impulses/heaves?
Chest Palpation
- Begin w/pt in supine position at 30 degres.
- If heart is not palpable the pt should be examined in the left lateral decubitus position w/left arm above the head, or seated position leaning forward.
- PMI (point of maximal impulse) is normally over L ventricular apex in the midclavicular line @ 5th intercostal space. It’s less than 2cm diameter & best felt at end of expiration.
- -L ventricular enlargement displaces the apex beat leftward & downward.
- Palpate for thrills
Chest Auscultation
- Listen w/diaphragm (high pitched sounds) & bell (low pitched sounds)
- Use light pressure when listening w/bell
- If heart sounds are difficult to hear, or pt obese, listen in L lateral decubitus or seated & leaning forward
- Have pt exhale fully & hold the exhale *brings scope closer to chest wall.
Auscultation location: Aortic valve
Second intercostal space at R sternal border
Auscultation location: Pulmonic valve
Second intercostal space at L sternal border
Auscultation location: Erb’s point
Third intercostal space at L sternal border
Auscultation location: Tricuspid valve
Fourth intercostal space at L sternal border
Auscultation location: Mitral valve/L ventricle
Fifth intercostal space at L mid-clavicular line
The first heart sound
S1, comprises the mitral & tricuspid valves closing
It is high-pitched and can be split due to the valves closing at slightly different times.
Systolic Sounds - “clicks”
Abnormal, higher pitched than S1 & shorter duration
- Heard in mitral (MVP) or tricuspid prolapse (TVP) from abnormal tension of chord tendinae
- May come & go or vary from exam to exam
- Pearl~ With standing, ventricular preload decreases & the click moves closer to S1. With squatting, ventricular preload increases, prolapsing the valve later in systole & the click moves away from S1
Diastolic Sounds - S2, S3, S4, opening snap
- S2 is lower pitched than S1, and is due to closure of aortic & pulmonic valves. It is commonly split w/aortic closing first
- S3 occurs in early diastole due to a non-compliant dilated ventricle (might be normal in children, abnormal in adults)
- S4 occurs in late diastole from augmented ventricular filling, caused by atrial contraction. Abnormal, and more common than S3
- Opening snap (OS) occurs early in diastole & is high-pitched
Systolic Murmurs: Ejection sounds
- High-pitched and due to turbulent blood flow through the valve or outflow tract
- -Pulmonary or aortic stenosis/sclerosis (PS, AS) or normal semilunar valves w/dilation of the aortic or pulmonic root
- –Mid-systolic, gets louder as flow becomes more obstructed (crescendo)
- –Pearl~ Ejection sound accompanying pulmonic valve disease decreases in intensity w/inspiration. Is the only right-sided cardiac event to behave in this manner.
Systolic Murmurs: Regurgitant murmurs
- Due to retrograde or abnormal blood flow
- -Mitral or Tricuspid regurgitation/insufficiency
- –Holosystolic (longer duration than ejection murmurs)
Systolic Murmurs: Clicks
-Associated w/MVP or TVP, occur in late systole
Systolic Murmurs: Shunt murmurs
- Due to abnormal openings between vessels or heart chambers
- -Patent ductus arteriosis is a fetal structure that shunts blood slow from descending aorta to pulmonary artery.
- -Ventral septal defects (VSD)
- -Atrial septal defects (ASD)
Diastolic Murmurs: Ejection murmurs
- All diastolic murmurs are always abnormal & signify cardiac disease!
- Ejection murmurs, such as mitral stenosis & tricuspid stenosis occur mid-diastole & are high-pitched
Diastolic Murmurs: Regurgitant murmurs
**All diastolic murmurs are always abnormal & signify cardiac disease!
- Include aortic (AR) or pulmonic regurgitation (PR), occur in early diastole right after S2
- -Chronic AR causes a high-pitched decrescendo early to mid-diastolic murmur & is best heard along the L sternal border
- -PR is best heard along the L sternal border as well
Pericardial Friction Rub
- Caused by movement of inflamed visceral & pericardial layers
- High pitched squeaking found
- Best heard w/pt leaning forward or on hands & knees during held expiration
Pulmonary Assessment
Complete lung auscultation to assess for fluid accumulation, which may occur in various cardiac disorders including heart failure.
Abdominal Assessment
Palpate the abdomen, liver, and assess for splenomegaly. Assess for fluid wave/ascites. Assess for abdominal aortic aneurysm and for bruits.
Lower Extremities
Inspect for edema & signs of peripheral vascular dz. Palpate femoral, anterior tibial & dorsal pedal pulses. Assess for varicose veins & if present, assess for inflammation & tenderness. Inspect stasis dermatitis or ulcers.
Evaluating Chest Pain: Hx
*Men & women may manifest pain of cardiac origin differently!
Hx:
- Location, duration & quality of pain. Character, triggering & relieving factors, pattern of radiation.
- Past Medical Hx, risk factors for CAD: smoking, lipids, HTN, DM, obesity, mental stress/depression
Evaluating Chest Pain: Physical Exam
- General appearance
- Vitals + Pulse ox
- Chest exam/auscultation
- Abdominal exam
- Extremity exam
Evaluating Chest Pain: Testing
- Electrocardiogram (EKG or ECG)
- Chest x-ray (CXR)
- Cardiac enzymes
Evaluating Chest Pain: DDX
- MI, unstable angina, stable angina
- Dissecting aortic aneurism
- Pulmonary embolism, pneumothorax, pneumonia, pleurisy
- Pericarditis, Pancreatitis
- Malignancy
- GI Dz/ GERD
- Herpes zoster
- Musculoskeletal problems (costochondritis, joint dysfunction, etc.)
Palpitations
Any conscious sensation of heart activity.
Palpitations are associated with a wide range of arrhythmias.
Evaluating Palpitations: Hx
- Duration, character, triggers, onset/offset
- Ask pt to tap out the beat if possible
- Weakness, lightheadedness, syncope (indicates potentially serious arrhythmia!)
- Other concomitant sx
- Substance use/abuse
- Caffeine use
Evaluating Palpitations: PE
- Vitals & pulse ox
- Chest auscultation
- Thyroid exam
Evaluating Palpitations: Testing
- Resting 12 lead EKG w/rhythm strip
- Holter monitor
- Cardiac event monitor
- Serum electrolytes
- CBC
- Thyroid (TSH, free T4, maybe free T3)
- Maybe intracellular minerals, heavy metal screening, food allergy assessment
Evaluating Palpitations: DDX
Normal = w/exercise or emotion
w/arrhythmia is more likely cardiac dz
- extrasystoles
- tachyarrhythmias
- bradyarrhythmias
w/out arrhythmia is more likely non-cardiac
- anxiety, coffee, tobacco, panic disorder, drugs
- Anemia, hypoglycemia, phenochromocytoma
- Fever, allergy, migraine
- Thyrotozoxicosis
- Aortic aneurysm, diaphragm flutter
Orthostatic/Postural Hypotension
A fall in blood pressure more than 20 mmHg systolic and/or more than 10 mmHg diastolic in response to moving from supine to standing within 3 minutes.
Usually accompanied w/faintness, lightheadedness, dizziness, etc.
Evaluating Orthostatic Hypotension: Hx
- Triggers (drugs, bed rest, fluid loss)
- Sx of autonomic insufficiency (visual impairment, incontinence, constipation, heat intolerance, impotence)
- Sx of cardiovascular neurological, or malignant disorders
- May be asymptomatic or assoc. w/sx of orthostatic intolerance
Evaluating Orthostatic Hypotension: PE
After pt has remained supine for 5 min, have the stand & measure bp at 1 min & 3 min. If no increase in HR, consider autonomic impairment. And increase in HR beyond 100 bpm suggests hypovolemia.
Evaluating Orthostatic Hypotension: Testing
- EKG
- Serum electrolytes
- Glucose
- Consider adrenal testing or neurotransmitter urine test
Evaluating Orthostatic Hypotension: DDX
- Hypovolemia -> dehydration or blood loss
- Drug side effects, reaction to food, conditioning, ambient temp & humidity
- Autonomic unsufficiency as seen w/diabetes or Parkinson’s
Postural Tachycardia Syndrome (POTS)
- Exaggerated increase in HR w/postural change WITHOUT increase in BP
- Characterized by sx of orthostatic intolerance, increase or 28 bpm or more, and absence of significant BP change w/in 5 min of standing or upright tilt.
- Oft diagnosed in younger pts w/postural intolerance
- More common in women 5:1
- Precise pathophysiologic basis not well defined
Synocpe
Transient loss of consciousness (LOC) from transient global cerebral hypoperfusion. Characterized by rapid onset, short duration, & spontaneous recovery. LOC results from reduced blood flow to reticular activating system in brainstem.
Evaluating Syncope: Hx
- Current medications
- Drugs
- Details of syncope & pre-syncope event w/associated sx
Evaluating Syncope: PE
- General appearance (pallor, diaphoresis)
- Vitals/pulse ox
- Orthostatic BP
- Cardiac auscultation
Evaluating Syncope: Testing
- Resting EKG
- HCT
- Serum electrolytes
- Cardiac enzymes
Evaluating Syncope: DDX - Vascular
Autonomic: Vascular steal syndromes (subclavian steal syndrome)
Orthostatic: Autonomic insufficiency, Idiopathic, Volume depletion, Drug/alcohol induced
Reflex Mediated: Carotid sinus hypersensitivity, Vasovagal
Evaluating Syncope: DDX - Cardiac
-Autonomic: Obstructive cardiac valve dz, aortic dissection, atrial myxoma, pericardial dz, tamponade, hypertrophic obstructive cardiomyopathy, myocardial ischemia, infarction, pulmonary embolism, pulmonary hypertension
-Arrhythmias:
Bradyarrhythmias (atrioventricular block, sinus node dysfunction, bradycardia),
Tachyarrhythmias (Supra Ventricular Tachycardia [atrial fibrillation, paroxysmal supraventricular tachycardia], Ventricular Tachycardia [structural heart dz, inherited syndromes])
-Implanted pacemaker or ICD malfunction
Edema
Increase in volume of interstitial fluid w/ or w/out increase in blood volume. May appear as unexplained wt gain, tight rings or shoes, facial puffiness, swollen extremities, ascites or pitting edema. May be localized or general.
Evaluating Edema: DDX
- CHF (dependent edema)
- Liver dz
- Myxedema
- Pericardial dz
- Nephrotic syndrome (low albumin)
- Hemiplegia
- Lymphedema (more localized)
- Idiopathic
ECG is used to…
Assess for arrhythmias, myocardial ischemia, and enlarged chambers.
Echocardiography is used to…
Assess valvular disorders, chamber hypertrophy or dilation, cardiomyopathies, heart failure, and pericarditis.
EBCT is used to…
Assess coronary arteries, Quantify calcifications, assess atherosclerosis.
(now MSCT or MDCT are used more. These are computer tomography. EB is electron beam, MS is multislice and MD is multi detector.)
MRI/MRA is used to…
Evaluate mediastinum, aorta.
PET is used to…
Assess myocardial perfusion
Radionuclide Imaging is used to..
Do myocardial perfusion studies
Stress testing is used to…
Screen CAD
Invasive Procedures/tests
Cardiac Catheterization, CABG. For more intensive artery assessment.
Etiology of Primary Arterial Hypertension
Multifactorial, poorly understood. Genetics, lifestyle.
Etiology of Secondary Arterial Hypertension
Secondary to another pathology, excessive alcohol use, OCP use, sympathomimetics, corticosteroids, or cocaine.
S/Sx of Arterial HTN
Usually asymptomatic. Sx: Dizziness, facial flushing, HA, fatigue, epistaxis, nervousness. Sometimes a 4th heart sound. Can be emergent.
Dx of Arterial Hypertension
Sphygmomanometry*, dx made with 2 BP readings: supine/seated, then standing, on 3 separate days. The average of those readings used to dx.
Malignant HTN
HTN w/retinal hemorrhage, exudates, or papilledema. Usually diastolic greater or equal to 120mmHg, but can be as low as 100mmHg if BP increase is rapid.
Hypertensive Urgency
Severe HTN, diastolic greater or equal to 120mmHg in asx pts.
HTN: Hx
Known duration, previous levels, Risk factors: CAD, HF, stroke, renal dz, dyslipidemia, DM, gout, fam hx, smoking, meds, drugs, ETOH, salt & stimulant use, sx of end organ damage, sx that suggest secondary cause of HTN
HTN: PE
Ht, Wt, waist circumference, fundoscopic, auscultation for neck & abdominal bruits, full CVP & neuro exam.
Palpate abdomen for masses, liver & kidney enlargement.
Evaluate periph. pulses & extremities, brachial & femoral pulsas palpated simultaneously screen for coarctation of aorta.
HTN: Tests
If new dx: UA, resting ECG, blood creatinine, BUN, K, Na, Mg, Ca, glucose, lipids, TSH. Consider homocysteine, CRP, fribrinogen, fractionated lipids. Limited echo for LVH.
Suspect secondary cause of HTN if…
Onset prior to puberty, acute rise in someone well controlled, severe & non responsive to therapy (3 drugs, including diuretic), age
Renal tests for evaluating HTN
BUN, creatinine, UA & urine micro, IV pyelogram, MRA w/gadolinium or angiography for renal artery stenosis
Endocrine tests for evaluating HTN
Electrolytes, glucose, Ca, UA, 24hr urine K, VMA, metanephrine
Neurological tests for evaluating HTN
No good screen. Use hx & PE
Metabolic & drug tests for evaluating HTN
Hx & chem screen
Scleroderma, SLE, polymyositis in HTN
May be 2ndary causes of HTN. Use Hx, PE, and other sx.
Etiology/Risk factors in Atherosclerosis & CAD (coronary artery dz)
Obesity, dyslipidemia, HTN, insulin resistance, prothrombic states, pro-inflammatory states, smoking, hyperhomocysteinemia, elevated CRP. Oxidized LDL->pro inflammatory cytokines->Angiotensin II makes more of those. Diabetes enhances cell injury & pro-infl. cytokines.
S/Sx of Atherosclerosis/CAD
Can be asx for decades. Sx depend on location of plaque, include angina, TIAs, IC, unstable angina, stroke, limb pain at rest, and SUDDEN DEATH!
Dx/Screening for Atherosclerosis/CAD
Hx, risk factor screening (lipid profile, blood sugar, fibrinogen, platelets, lots of others), Exercise or nuclear stress testing. Imaging (CT [w/angiogram?], carotid artery ultrasound, cardiac catheterization.)
Angina Pectoris
A sx of CAD (coronary artery dz). Chest pain from ischemia.
Angina Pectoris: Etiology
Leading cause of death in industrialized countries, usu from atherosclerosis. Insidious. Mjr complications are angina, MI, and sudden death.
Angina Pectoris: HPI
PQRST, other sx, provoking factors
Angina Pectoris: S/Sx
Transient pain/discomfort usually with exertion, relieved by rest. Feel substernal heaviness/pressure, may radiate to jaw, teeth, neck, L shoulder, sub scapular areas, down L arm. Lasts 2-5min, worse in cold, after eating, w/anxiety. HR & BP elevate. If it happens at night/rest MI is more likely.
Unstable Angina S/Sx
Changes in a person’s usual sx. Heart sounds distant, diffuse apical pulse. SOB, belching, nausea, indigestion, diaphoresis, dizziness, lighteadedness, clamminess, fatigue. Possible S4 gallop. Woman can have different experience from men.
Variant angina (Prinzmental’s angina)
Due to coronary artery spasm, occurs at rest. ST elevation on EKG rather than depression. Tends to occur at the same time each day.
Silent ischemia
CAD without sx, most often in diabetics. Thus, it’s important to screen diabetics for CAD!
Angina Pectoris: PE
Gain clues for the likelihood of CAD in a person w/chest pain. -> Decreased peripheral pulses or bruits in femoral or carotid a’s, Xanthomas, point tenderness over chest wall (pain is unlikely to be CAD).
Most common findings: tachycardia, new mitral regurg murmur, elevated BP, S4
EKG in Angina
EKG is usually normal between attacks. During episode there may be visible Q or T wave inversion. ST depression may be noted. Could see smaller R wave & bundle branch disturbances.
Angina: DDX
cervicothorac spine abnormalities, nonspecific chest wall pain, GI dz, pulmonary dz, pericarditis, psychological, costochondral separation, costochondritis, dyspnea, aortic dissection, mitral valve prolapse, radiculopathy
Acute Coronary Syndromes
Unstable angina, NSTEMI, STEMI
Acute obstruction of an artery, usually dt thrombus in coronary artery.
Unstable Angina
Prolonged rest angina, new onset angina of at least class III, increasing angina
Non-ST segment elevation MI (NSTEMI)
Myocardial necrosis WITHOUT acute ST elevation of Q waves, increased cardiac enzymes
ST-segment elevation MI (STEMI)
Myocardial necrosis with ST elevation of ECG (may show Q waves)
Acute Coronary Syndromes: Dx
ECG & presence of serologic cardiac markers (CK-MB & Troponin 1) are diagnostic for NSTEMI & STEMI
PE: cold, clammy person, BP elevated unless in shock. May see basilar rales, murmurs, S4 gallop, split S2, tachy/cradycardia, cyanosis, elevated temp, thready pulse, papillary murmur, and shock or pulmonary edema.
Ventricular arrhythmias are common.
CHF - Congestive Heart Failure
Syndrome of ventricular dysfunction w/reduction in the pumping action of the heart. Can be caused by structural abnormalities/cardiomyopathies, valve dz, MI, ischemia, CAD, HTN, PDA, VSD, arrhythmias. *Left sided CHF causes Right sided CHF, renal insufficiency, liver dz, all aggravating the initial problem. Volume overload (PV, renal failure) causes HTN & CHF.
Classifications of Heart Failure (NY Heart Association)
Class I-IV
Class I: no physical activity limitations, no dyspnea, fatigue or palpitations.
Class II: slight limitation with dyspnea on ordinary physical activity
Class III: Moderate limitation of activity w/sx during less than ordinary activity
Class IV: severe limitation w/dyspnea at rest
Congestive Heart Failure: Dx
CXR - enlarged silhouette, Kerly-B lines, pleural effusion
Echocardiography - LV hypertrophy
BNP > 100
May also see high BUN/creatinine/protinurea, liver enzymes, etc.
Cor Pulmonale
Enlargement of R ventricle secondary to lund dz. If chronic, sx might be slight dyspnea at rest, syncope, chest pain, and abnormal heart sounds. R
Cardiomyopathies
Structural or functional abnormality of the myocardium. Caused by drug/chemical sensitivity, radiation, serum reactions, connective tissue dz, viruses, bacteria, aging, thyroid dz, anemia, and nutritional disorders.
When to consider Cardiomyopathies?
When valve dz, hypertensive dz, and lung dz have been ruled out as causes of sx and there is no other explanation for ventricular failure, heart enlargement, or other evidence of heart dz.
Classes of Cardiomyopathy
Dilated C, Hypertrophic C, Restrictive C.
Dilated Cardiomyopathy
Ventricular dilation & systolic dysfunction. Sx - dyspnea, fatigue or peripheral edema. 25% have atypical chest pain. Atrial or ventricular tacyarrhythmias. Poor prognosis w/out transplant.
Hypertrophic Cardiomyopathy
Ventricular hypertrophy w/diastolic dysfunction. Mostly inherited, abnormal myocardium. 20-40 yo on exertion sxs of chest pain, dyspnea, palpitations, syncope & increased risk of death. *Young athletes that die suddenly on the field.
Restrictive Cardiomyopathy
Non-compliant ventricles resist filling. Least prevalent form of cardiomyopathy. Results in pulmonary HTN, Sx - exertional dyspnea, orthopnea, peripheral edema in RV dysfunction. Angina & syncope are UNcommon. See quiet heart sounds, rapid pulse, lung crackles, pronounced neck vein distention.
Arrhythmias
Rhythm disturbances resulting from abnormal electrical impulse FORMATION, CONDUCTION, or both. Can be asx, or experience palpitations, hemodynamic compromise (dyspnea, chest discomfort, pre syncope, syncope) or cardiac arrest.
Sinus Rhythms
Normal P wave precedes every QRS complex in a 1:1 ratio
Sinus Bradycardia: 100/min in adults.
Sinus Arrhythmia: normal increase in HR w/inspiration, more pronounced in children. (Common, non-pathological)
Bradyarrhythmias
Rate less than 60bpm. Decreased intrinsic pacemaker function or blocks in conduction (usu AV node or His-Purkinje system)
Tachyarrythmias
Rate greater than 100bpm. Usu due to reentry phenomenon enhanced by shortened tissue refractoriness, lengthened conduction pathway (hypertrophy), or slowed impulse conduction (ischemia).
