Acute Care Test1 Flashcards
Diastolic heart failure (DHF)
Impaired relaxation of heart
DHF is more common in females and HTN is a more common risk factor,
Although substantial proportion of patients w/ SHF have HTN
Calcium channel blockers
Selectively block Ca2+ entry into vascular smooth muscle cells
Mgmt of: HTN, angina, vasospasm
Reduce cardiac contractile force
Used to treat supraventricular arrhythmias
“dipine”
Most common: Amlodipine (Norvase), Diltiazem (Cardizem), Verapamil (Calan)
Limb leads
I: Right arm (-)(-) -> Left arm (+)(-)
II: Right arm (-)(-) -> Left leg (+)(+)
III: Left arm (-)(+) -> Left leg (+)(+)
A lead consists of 2 electrodes, 1(+) 1(-)
(Both listed above I-III to know where are)
Limb leads capture different regions of the heart.
“The vicious cycle”
Ventricular dysfunction->
Decreased CO ->
Compensations:
Increased SNS, RAS-Aldosterone, arginine vasopressin
->
Excessive vasoconstriction
Excessive Na+/H2O retention
->
Increased afterload
Excessive preload
->
Ventricular dysfunction
ST elevation
Indicates cell death
Most common cause: myocardial ischemia and infarction
Threshold values for ST- segment elevation consistent with STEMI are J-point elevation of > 2 mm in leads V2 and V3 or > 1 mm in all other leads
Heart valves- systole
Pulmonary and aortic valves open
Tricuspid and mitral valves closed
III
Area of heart?
Which coronary artery?
Inferior
PDA: posterior descending artery
(80% RCA- right coronary artery
20% LCx- left circumflex)
Nonischemic T wave
Hyperkalemia (elevated K+)
V4
Location of heart
Which Coronary artery
Septal / Anteroapical
LAD- left anterior descending
Dependent rubor
Blood pooling in maximally dilated capillary
Intermittent claudication pain
Cramping type, due to ischemia
Better with rest
Not typically burning
Pain increases with elevation and decreases with dependence arterial disease
Usually in calves, but can be thigh or butt
Cardiac remodeling -
MI / DCM
Myocardial infarction/ DCM ->
Cardiac dilation: Myocyte length increase >> width increase Extensive fibrosis Myocyte death Adv cardiac dysfunction
Wells score PE
+3
Clinically suspected DVT
Alternative diag less likely than PE
+1.5
HR > 100
Immobilization 3 or more days or Surgery in previous 4 weeks
History of DVT
+1
Hemoptysis
Malignancy or palliative
> 6 high probability
2-6 moderate probability
< 2 low probability
Score >4 PE likely - consider diag imaging
Score < 4 Pe unlikely- consider d-dimer to rule out
Left bundle branch block
R and L ventricules are not same- 1 side slower
Twin peaks
Complications of atherosclerotic plaque
Rupture or ulceration Calcification of atherosclerotic plaque Hemorrhage into plaque -> further narrowing Embolization Weakening of vessel wall -> aneurysm
Ventricular pacemakers
Used for abnormal rhythms
Like Type 2 or grade 3 AV node blocks, or significant A-fib
Wide QRS as pacemaker providing
“Pacer spikes”
Regulation of BP- slow
Renin-Angiotensin system (kidneys)
Natriuretic peptides (ANP and BNP)-heart Act as counter to RAAS
Systematic approach evaluating rhythm strip
Waveform configurations PR intervals QRS intervals RR intervals Rate to assess rhythm disturbance
Augmented leads
Termed unipolar leads because single (+) electrode that is referenced against combo of other electrodes
(Machine does calculations and designations)
Atrio-ventricular valves
Let side:
Bicuspid (Mitral) valve
Right side:
Tricuspid
Chordae tendinae and papillary muscles prevent inversion ic valves during ventricular systole
(Can become damaged from MI causing backflow “regurgitation”)
Mitral valve prolapse- what expect
Volume overload:
LA dilates (A-fib, thrombus formation, pulmonary congestion)
LVH for forward flow
Upon exertion:
Dyspnea
Auscultation:
Holosystolic murmur: regurgitation into LA
Pulse pressure
SBP - DBP: Normally ~ 40-60 mmHg
Low: < 40 mmHg may indicate pulse narrowing
Elevated: > 60 mmHg associated with higher CVD morbidity/mortality
Might be better predictor of CV risk than SBP
More reflective of microcirculation dysfunction
Mechanism may be due to endothelial damage from large oscillations in pressure each cardiac cycle
Mitral stenosis- expect
Pressure overload:
LA hypertrophy
Limited LV filling (LA thrombus breeding ground, A-fin, pulmonary congestion and HTN)
Upon exertion:
Dyspnea
Auscultation:
Opening snap, diastolic rumble
Composite score chest pain due to CAD
1 point each... Men > 55 yo/ Women > 65 yo Known vascular disease Pain worse with exercise Pain not elicited with palpation Patient assumes is cardiac origin
0-1
2-3
4-5 high probability
Mitral valve prolapse
2-6 % population
Valve snaps during systole
Mostly asymptomatic, cause unknown
Bigeminy
PVC occur every other beat
Premature ventricular contraction
Pericardial effusion
Accumulation of fluid in pericardial sac
Causes: similar to pericarditis
Symptoms: pressure pain in chest, dysphagia, dyspnea
Signs: muffled heart sounds, possibly JVD
May progress to a cardiac tamponade (not good)
Hypertrophic cardiomyopathy (HCOM)
Strong genetic link
55% familial relative
More common in African-Americans
Ejection murmur changes with position
Softens- sitting
Amplifies- standing/valsalva
Persistent Split S2 - no change w breath hold
Syncope or dyspnea during exercise
Persistent hypertrophy despite detraining
Rhythm: Wide QRS
Ventricular rhythm:
Below AV node (ventricles)
Rhythm/impulse generated below atria
V2
Unipolar Precordial (chest) lead
4th IC space to the L of sternum
Septal
QRS complex
Ventricular depolarization
(Atrial repolarization)
Normal:
0.06 - 0.10 seconds (1.5 - 2.5 small boxes)
Some patients may have wider QRS- absolute cutoff is 0.12 seconds
> 0.5 mV in at least 1 std lead (5 small boxes)
1.0 mV in at least 1 precordial lead (10 small boxes)
Upper limit 2.5 - 3.0 mV (25 small boxes)
Trans-cutaneous valve repairs
Typically older patients at high risk for open heart surgery
Promising early results comparing 4 ur clinical outcomes to open heart
V6
Area of heart?
Which coronary artery?
Lateral
LCx - left circumflex
Intermittent claudication
Pain in foot
Tibial Artery
Rhythm: Narrow QRS
Supraventricular:
AV node or above
(SA, AV, atria, nodal tracts)
ACC/AHA - Stage A
Patient at high risk for developing HF with no structural disorder of the heart
HTN, Atherosclerotic disease, DM, obesity, metabolic disorder
Anti-arrhythmics
Na+ channel blockers
Beta blockers
K+ channel blockers
Ca2+ blockers
Blanching
Pressure applied (to nail bed) until turns white. Indicates blood has been forced out of tissue
Late systole murmur
Mitral valve prolapse
Clicking sound hallmark
Factors that influence CO
Preload
The degree of myocardial distention prior to shortening
Largely depends on amt of ventricular filling
Afterload
Forced against which ventricles must act in order to eject blood
Largely dependent on arterial BP and vascular tone
Contractile state (contractility)
HR
Edema massage
Purpose and contraindications
Helps prevent putting edema, which increases likelihood of wounds
Contraindications: uncompensated CHF, untreated infection/cellulitis, active cancer, renal failure, severe pulmonary problems
HF: implications of an abnormal hemodynamic response to exercise
Associated pulmonary disorders impair breathing
Reduced gas diffusion in lungs
Increased work of breathing
Contribute to dyspnea and fatigue
Exaggerated redistribution of blood flow away from periphery and to respiratory muscles during exercise- May contribute to enhanced perception of fatigue
V1
Location of heart
Which Coronary artery
Anterior / Anteroseptal
LAD- left anterior descending
Clinical manifestations: Difference between Arterial and Venous disorders
Elevation
Arterial: worsens symptoms
Venous: lessens symptoms
Auscultation points
“All Physical Therapists Move” mnemonic
1. Aortic region
R 2nd intercostal space, parasternal
- Pulmonic region
L 2nd intercostal space, parasternal - Tricuspid region
L 4th intercostal space, parasternal - Mitral region
L 5th intercostal space, midclavicular
(There is also: Erb’s point
L 3rd intercostal space (LL sternal border) but n/a for this course)
Exercise testing
Cardiopulmonary stress test (gold standard)
6MWT (six minute walk test)
Alternative to CPXT to assess
Used extensively in HF studies 1
Predicts morbidity and mortality in patients with HF 2 (< 300 m)
Neuro-hormonal effects of heart failure
Kidney isn’t happy with decreased blood flow
Increases Na+/H2O retention to increase perfusion pressure
Increased E, renin, endothelin (all vasoconstrictors) and ANP (produced by heart for vasodilation)
Ventricular tachycardia
V-tach
4 or more PVCs (premature ventricular contraction) in a row
NSVT: non-sustained ventricular tachycardia
^ reading this in pt hy is not a contraindication for tx.
IF seen while working with a patient STOP, check vitals and notify RN
PVD
Slow and progressive circulation disorder caused by narrowing, blockage or spasms in a blood vessel
Many involve any blood vessel outside heart
Arteries : PAD
Veins: CVI
Lymphatic vessels
Sternal precautious
No traction forces on sternum 6-8 weeks (longer if osteoporosis or on steroids)
No shoulder FLEX or ABD > 90*
Lifting restrictions 8-10 lbs 6 wks, then 30 lbs for 3 mo
Minimal push/pull (log roll to get out of bed, edge of chair before standing, use momentum and rocking, look up)
If sternal tissue fails, use rectus or pectoral flaps- severe ROM restriction of 20* FLEX and ABD, no lifting, push or pull
Monitor incision: 30% mortality of opens and becomes infected
Encourage splinting chest with pillow when coughing
Avoid valsalva
No driving (meds) initially- avoid 4-6 wks bc airbags
Exercise training
Acute Cardiovascular
Dose determined based on COX results
Moderate intensity aerobic 30-45 min
At least 3-5 x week is general recommendation
Low to mid resistance training recommended with aerobic training
Consider eccentrics !!(BP response)
Atherosclerosis characteristics
Slow, progressive Starts 20s-30s Often undetectable Initially plaques are sparsely distributed Increase in number and size over time Can affect any artery
Heart failure
Complications
Impaired exercise tolerance
Increased risk of ventricular arrhythmias
Shortened life expectancy
S/S essential to monitor to help determine the adequacy of mechanical pump function (LVAD)
Dizziness
Edema
Clinically apparent increase in interstitial fluid volumes
Develops when starling forces are altered so there is increased flow of fluid from vascular system into interstitium
R-R interval
Duration between subsequent heart beats
Duration used to calculate HR
Normal:
Should be regular and consistent, especially at rest
Will shorten during exercise as HR increases
____ pain not affected by workload but by posture
Neurogenic pain
ECG reviewed to identify 4 areas that require interpretation
HR
Heart rhythm
Hypertrophy
Infarction
Thoracotomy
Lobectomy
Lung transplant (bilateral AKA clamshell for COPD)
Splitting S1
The mitral (M1) and tricuspid (T1) valve sounds are slightly asynchronous
This is a normal finding as mitral closure may precede tricuspid closure by 20-30 msec (0.02-0.03 sec)
Produces 2 audible components
M1-T1 normal or “physiologic splitting” of S1
Wide splitting of 1st sound is almost always abnormal and warrants further medical attention
CVI
Chronic venous insufficiency
Vein wall and/or valves don’t work effectively
Impairs ability for blood to return to heart from legs, resulting in venous-stasis
Quadrigeminy
PVC (premature ventricular contraction) every 4 beats
Generally less concerning than Bigeminy or Trigeminy (bc within 6 per minute cutoff)
Inpatient PT implications
Getting patient moving:
Reduces risk of deconditioning, pulmonary complications (atelectasis and pneumonia), bed sores and DVT
Goals:
Determine stability for ambulation, transfers, stairs, ADLs, assistive device needs, tolerance to activity, return to PLOF or as close to possible
Discharge plans:
Ask if live alone/with family, floors in home, steps to needs
Neuro-hormonal effects of heart failure
Excess vasoconstriction Due to increased: Aldosterone Endothelin Angiotensin II Vasopressin Norepinephrine
(Not enough/enough effect from: NO, increased ANP, BNP)
Heart wall layers
(Inside-> outside) Endocardium Myocardium Visceral pericardium Pericardial cavity Parietal pericardium
NYHA - Class I
No limitation of physical activity
Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea (shortness of breath)
Nonischemic causes: ST depression
- RVH (Right precordial leads) or LVH (Left precordial leads, I, aVL)
- Digoxin effect on ECG
- Hypokalemia
- Mitral valve prolapse
- CNS disease
- 2ndary ST segment changes with conduction abnormalities (ex: RBBB, LBBB, WPW)
Presence of significant Q wave is diagnostic for ____, but ___ cannot be determined from ECG
Infarction
Date of infarction cannot be determined by ECG
aVF
Area of heart?
Which coronary artery?
Inferior
PDA: posterior descending artery
(80% RCA- right coronary artery
20% LCx- left circumflex)
HF Meds
Decrease preload: diuretic
Decrease afterload: ACEI
Control Sympathetic stimulation: beta blocker
Ca2+ blockers NOT used due to adverse effects with HF
Clinical implications for PAD
High risk individuals s/b examined for PAD and AAA
Important to monitor hemodynamics during exercise
Patients with intermittent claudication usu have some sort of walking impairments that significantly improves with exercise training
Exercise training as effective as surgical interventions in reducing symptoms and improve walking distances
Instruct in proper foot care, footwear and hygiene
Might improve nocturnal pain by elevating head of bed slightly
Spirolactone (Aldactone)
Aldosterone receptor antagonists: blocks aldosterone this interferes with Na-K+ exchange at distal tubule
AKA potassium sparing diuretic
Side effects: volume depletion, frequent voiding
Reduce BP by reducing blood volume via kidneys
Atenolol
Beta blocker - specific
Sympatholytic
Intermittent claudication
Pain in hip and butt
Aorto-iliac occulusion
Decompensated HF meds
Positive inotropes
Afterload reducers
Maintain MAP (IV NorE and E)
Heart failure
Mortality
1 in 9 deaths (2009)
5- year mortality is 50%
Most common cause of ED > 65 yo
NSR
Normal sinus rhythm
4 cell types of myocardium
Working/Mechanical cells
Nodal cells
Transitional cells
Purkinje cells
Endarterectomy
Surgical removal of any part of the inner lining of an artery, any obstructive deposits
Most often performed in carotid artery or femoral arteries
T-wave inversions
Sign of ischemia
Progresses to S-T segment changes (depression then to elevation)
S-T segment
Interval between ventricular depolarization and repolarization
Normal:
Discrete ST segment distinct from T wave is usually absent
(Should be in line with isoelectric line)
At higher HR (exercise) the ST-T segment is a smooth, continuous line beginning at the J-point (end of QRS) slowly rising to the peak of the T-wave
Sympatholytics
Beta blockers “olol”
Alpha 1-blockers “zosin”
Alpha 2-agonists
> 180/110 BP
What do you do?
Hold exam
Examine for organ damage
Contact PCP
Consider contacting EMS
PEA
Pulseless electrical activity
AKA electromechanical dissociation
(Ex: Sustained ventricular tachycardia… can go into v-fib)
QRS “normal” cutoff
0.12 seconds or 3 small boxes
T-wave
Ventricular repolarization
Normal:
Deflection should be same as largest component of QRS wave (usually R wave)
I.e. if R wave is (+) the T wave s/b (+)
Ex: in lead aVR it is normal for T wave to be (-); since QRS is also (-)
Role of endothelial cells (blood vessels)
Normally produce antithrombic molecules
Modulate immune response by resisting leukocyte adhesion and therefore inhibiting inflammation
Laminate shear stress favors:
NO production
KLF-2 mediates immune response, prevents deposition; SOD protects ROS
(Branch points subject to turbulent flow and tend to lack these effects)
Median sternotomy
CABG (coronary artery bypass graft)
Valve replacement or repair (Mitral MVR or Aortic AVR)
Heart transplant
One of the most frequent accesses in cardio-thoracic surgery
Vertical inline incision made along sternum
Chest wall is retracted, mediastinum exposed
Patients with nitroglycerin
Always have with during exercise sessions
Patients should report symptoms of chest pain and take NTG as directed
If symptoms persist 5 min after NTG, doe can be repeated 2 more times with 5 minute intervals between doses
If symptoms persist seek prompt medical attention
NTG can be used prophylactically 5-10 min before activity
Physiologic responses to activity s/b monitored (HR, BP, RPP)
S2
Dub
2nd heart sound
Closure of semilunar valves (aortic and pulmonic)
Marks beginning of ventricular relaxation and end of systole
Shorter duration and higher frequency than S1
Extra heart sounds
“Gallops”
S3:
occurs at beginning of diastole after S2.
Lower in pitch than S1/S2 b/c S3 not valvular
Indicative of ventricular/heart failure
SLOSH’-ing-in
S1 S2 S3
S4: Occurs prior to S1, produced by sound of blood being forced into stiff/hypertrophic ventricle Indicative of LVH or HCOM a—STIFF’-wall S4 S1 S2
AT (aerobic training) - HF
AT is gold standard exercise intervention
Most often “moderate intensity” (60-70% VO2 max)
Improvements: VO2 max, 6MWT, MLHFQ, LVEF, capillary density and peripheral artery diameter
Outer layer of connective tissue that covers heart
Epicardium
Angina- visceral pain fibers
Internal organs- such as heart or blood vessels, esophagus, visceral pleura- enter SC at multiple levels and map to parietal cortex corresponding to the cord levels shared with somatic fibers
Discomfort, heaviness, aching
Pain difficult to describe and imprecisely located
Medical exam- HF
BNP
ECG : wide QRS has higher mortality, dysrhythmias
Interview (symptoms)
Physical exam (signs)
Echocardiogram (EF, chambers and valves, wall motion)
CXR (chest x-ray: fluid, cardiomegaly)
Assess coronary arteries (underlying ischemia)
General chemistry labs
Chronic pain and hemodynamics
Diminished tolerance to painful stimuli
Reduced BP response and baroreflex to painful stimuli
Higher HR than heathy subjects at baseline and to painful stimuli
Lower parasympathetic and increased Sympathetic activity
Increased prevalence of HTN
Endothelial dysfunction
Increase: Adhesiveness of endothelium (adhesion molecules for leukocytes, T cells, platelets, permeability to oxidized LDL)
Macrophages engulf oxidized LDL and become foam cells
Endothelium becomes pro-coagulant and local adhesions associated with secretion of cytokines and growth factors
Transmigration of molecules (like leukocytes) into wall
Bipolar leads
Utilize a (-) and (+) electrode, and record the electrical activity between them
Limb: I, II, III
Mitral regurgitation/incompetence
Mitral valve does not close completely during systole (incompetence)
Creates back flow.
Increases to SV to compensate for back flow m
Upstream chamber (L atrium) dilates out
Eccentric hypertrophy to accommodate increased volume
20% >55 yo have some degree of mitral regurgitation (1/3 all cases caused by rheumatic heart disease)
Signs/Symptoms-anxiety and palpitations w/ exercise (if symptomatic- beta blockers)
II
Location of heart
Which Coronary artery
Inferior
PDA: posterior descending artery
(80% RCA- right coronary artery
20% LCx- left circumflex)
Pitting edema
1+
Barely detectable impression when finger pressed into skin
2+
Slight indentation; 15 sec to rebound
3+
Deeper indentation; 30 sec to rebound
4+
> 30 sec to rebound
ECG
Check PR intervals for…
AV blocks
Cardiac remodeling -
Chronic exercise/ Pregnancy
Chronic exercise / Pregnancy
Physiological hypertrophy:
Myocyte length increase > width increase
No fibrosis
No cardiac dysfunction
Medical management HF
Exercise
Pharmacological
Surgery
ECG systematic analysis
- Rate (fast or slow)
- Rhythm (regular or irregular)
- P wave and QRS complex w/ ea cycle
- Do P waves look alike
- Is there a P wave before every QRS
- Is PR interval w/in normal limits
Hydralazine
HTN med
Direct-acting smooth muscle relaxant, acts as vasodilator primarily in arteries and arterioles
Reduces BP by reducing TPR
Side effects: may increase Na+ retention and thus fluid retention, often used in conjunction with a diuretic
Chronic HF
Time, cause, effect
Time: progressive; weeks to months
Cause: chronic HTN, valve disease, myocardial disease, chronic lung disease
Effects: full compensation, chronic edema, congestion
Modifiable CVD risk factors
HTN Tobacco Elevated blood sugar Physical inactivity Overweight/Obesity Cholesterol/lipids (total <180 mg/dL optimal; HDL 40-60, LDL 100-129)
ACC/AHA - Stage B
Patient with structural disorder without symptoms of HF
Previous MI, LV remodeling including LVH and low EF, asymptomatic valvular disease
S1
Lub
1st heart sound
Closure of AV valves (tricuspid and mitral)
Occurs with ventricular contraction
Marks beginning of systole
Common end-organ damage associated with HTN emergencies
Acute pulmonary edema Acute left ventricular dysfunction Acute coronary syndrome (including acute myocardial infarction) Cerebral infarction HTN encephalopathy
ACC/AHA - Stage C
Patient with past or current symptoms of HF associated with underlying structural heart disease
Generalized edema
Heart failure Hypo-albumenia Nephrotic syndrome Cirrhosis Sepsis
A patient might be/become symptomatic with any AV node block due to ____.
A dropped or lost QRS indicates ____, which means ___.
Loss of CO (cardiac output)
Ventricles did not depolarize, which means
they don’t contract to push blood into systemic circulation for that time point
Ask if symptomatic and check BP
HCTZ (Esodrix)
1st drug of choice for essential HTN
Thiazide: block Na+ reabsorption in distal tune of nephron
Side effects: hypokalemia, hyponatremia, volume depletion, frequent voiding
Reduce BP by reducing blood volume via kidneys
ABI < 0.5
Indicates critical ischemia
Clinical manifestations: Difference between Arterial and Venous disorders
Skin appearance
Arterial: reduces hair, thick/brittle nails, shiny skin
Venous: cellulitis, dermatitis
Irregular rhythm
> 1 P wave per QRS
Causes of aortic regurgitation/incompetence
Congenital
Rheumatic
Endocarditis
Deterioration with age and long standing HTN
Rarer: Marfan syndrome, ankylosing spondylitis, certain STDs
Carotid bruit
Sound made by turbulent flow vibrating against arterial wall
Causes arterial wall to vibrate during systole
Indicates presence of arterial lesion/plaque
P wave
Atrial depolarization
Normal:
Duration < 0.12 sec (3 small boxes)
Amplitude < 2.5 mm (2.5 small boxes)
Right ventricular failure manifestations
Progressive failure Dependent edema (ankle or pretibial first) Jugular vein distention Abdominal pain and distention Weight gain R upper quadrant pain (liver congestion) Cardiac cirrhosis (ascites, jaundice) Anorexia, nausea Cyanosis (nail beds) Psychological disturbance
If patients on a beta blocker - use ___ for exercise
RPE
Because beta blocker means HR response won’t go up and thus can’t use HR
I
Area of heart?
Which coronary artery?
Lateral
LCx - left circumflex
Clinical manifestations: Difference between Arterial and Venous disorders
Skin color
Arterial: Cyanotic or pale, dependent rubor
Venous: hyperpigmented, often superior to medial malleolus-hemosiderin
Carotid sinus receptors respond to pressures
60-180 mmHg
patient feels like
“Heart skips a beat”
2nd degree AV node block
Type 2
Best anatomical place to hear S3 gallop
Apex of heart
5th intercostal space
Mid-clavicular line
Unipolar leads
Utilize a single (+) recording electrode, and a combination of other electrodes to serve as a composite (-) electrode
Precordial (chest): V1-V6
Unipolar (augmented): aVL, aVR, aVF
PAD findings
Intermittent claudication most common symptom but many asymptomatic or a have atypical lesions
Pallor on elevation
Dependent rubor
Impaired capillary refill
Impaired peripheral pulses
Types of aneurysms
Saccular AKA Berry
Small, spherical, 1-1.5 cm
Most common in brain tissue
Fusiform
Gradual more progressive
Dissecting
Blood filled channel within aortic wall
Surgical mgmt - HF
VAD- ventricular assist device (temp solution)
Heart transplant
In presence of acute injury, the ____, and gradually returns to the level of ___ over a period of 24-48 hours
ST segment elevated above isoelectric line
Gradually returns to level of isoelectric line over 24-48 hrs
Aortic incompetence
Failure of aortic valve to close tightly causing back flow of blood into L ventricle
Effects of afterload on HF
In normal heart, not much decrease in SV with increased afterload
However the effects are much more significant in patients with HF
Why vasodilator therapy- though counterintuitive - is effective with HF
Baroreceptors respond to _____.
___ loop with ___.
If arterial pressure suddenly rises…
If arterial pressure suddenly drops…
Stretching of arterial wall
Negative feedback loop with Vagus and Glossopharyngeal nerves
Pressure rises: walls passively expand, increases firing frequency
Pressure drops: decreased stretch of arterial walls, decreases receptor firing
Positive deflection on ECG means…
Going ABOVE isoelectric line
Acute HF
Time, cause, effects
Time: instant, sudden; hour to days
Cause: acute MI, PE, severe malignant HTN
Effects: no time to compensate, acute pulmonary edema, acute ischemia
Lead aVR
“Orphan lead”
Right
(Signal inverted)
VAD
Ventricular assist device
Surgical mgmt of HF
Limited organ availability Short term solution Ability to sense preload Need Doppler to take pressure- May not have a true HR (use RPE) Progressive exercise training indicated
QT interval corrected (QTc)
Since duration of QT varies with HR, raw QT interval often not used.
QTc = measured QT interval % square root of R-R interval
Normal < 0.44 seconds
CVI May result from
Vein wall degeneration
Post-thrombotic valvular damage
Chronic venous obstruction
Dysfunction of muscular pumps
Valvular replacement/repair
Can be mechanical or biological
Typically require by-pass and median sternotomy
Mechanical lasts lifetime but require lifelong anticoagulant meds.
Mechanical: higher risk for infection, thrombus or emboli
Younger pt may be better candidate for mechanical bc limited life of biological valve
V3
Unipolar precordial (chest) lead
Between V2 and V4
(Anterior wall)
75*
5 ECG mnemonic for electrode colors
“White on right”
“Snow over grass”
“Smoke over fire”
“Everyone loves chocolate”
RA- white RL- green LA- black LL- red V1- brown
V4
Unipolar precordial (chest) lead
Midclavicular line, 5th IC space
(Anterior wall)
60*
Murmur:
Decreases with standing
Increases with squatting
S1 sound
Aortic stenosis- ejection Type
R wave progression
Small R waves begin in V1/V2 and progress in size to V4/V5
The R in V6 is usually smaller than V5
In reverse, the S-waves begin in V6 or V5 and progress in size to V2
The S in V1 is usually smaller than V2
Transition from S>R to R>S usually occurs at leads V3 or V4
PVC
Premature ventricular contraction
Wide spontaneous funky QRS
Can be benign
Ectopic pacemakers/focus
Unifocal if similar
Multifocal if different
Cutoff 6 per minute
Check BP
ECG- what looking attire determine regular or irregular
P-P, R-R intervals
For every 10 bpm increment over a RHR of 75, mortality increases by…
All-cause 9%
Cardiovascular 8%
Especially if HR >90
Normal is 60-100 bpm
HTN crisis
76% urgencies
BP > 180/110
No signs of organ damage
24% emergencies
BP > 180/120
Showing signs/symptoms of organ damage
Wells score DVT
+ 1 points for each…
- Active cancer
- Calf swelling >= 3 cm
- Swollen unilateral superficial veins
- unilateral pitting edema
- Previous DVT
- Swelling of leg
- Local tenderness along deep venous system
- Paralysis, paresis or recent cast immobilization of LE
- Recently bedridden >=3 days, or major surgery in past 12 weeks
-2 for “alternative diag likely”
> 2 high probability
1-2 moderate probability
< 2 low probability
Venous network in LE commonly affected by CVI divided into …
Superficial (lesser and greater saphenous)
Deep (ant and post tibial, peroneal, popliteal, iliac, deep and superficial femoral)
Perforating or communicating veins
Normal HR
60-100 bpm
> 160/100 BP
What do you do?
Hold resistance exercise, consider aerobic exercise
Contact PCP
Monitor closely
Clinical manifestations: Difference between Arterial and Venous disorders
Symptoms
Arterial: aching, cramping that is predictable with activity or elevation
Venous: aching, burning, heaviness, fatigue while standing
NYHA class III
Marked limitation of physical activity
Comfortable at rest
Less than ordinary physical activity results in fatigue, palpitation, dyspnea (shortness of breath)
V3
Location of heart
Which Coronary artery
Septal / Anteroapical
LAD- left anterior descending
> 140/90 BP
What do you do?
Proceed with usual care
Contact PCP
Monitor closely
What BP range hold exam?
> 180/110
Clopidogrel (Plavix)
Anti-platelets
ADP inhibitor
V5
Unipolar precordial (chest) lead
Anterior Axillary line at level of V4
(Lateral wall)
30*
Blood lab to assess for MI
Cardiac enzymes: troponins and creatine kinase
Angina- stable
Discomfort gradually builds
Occurs with exercise at a predictable and consistent intensity
Gradually subsides with rest
Typically lasts 2-5 min, rarely more than 5-10
Improve with nitroglycerin
Pain and BP
Normal:
Systolic increase 15-25 mmHg
Diastolic increase 10-20 mmHg
Hyper-reactive if higher
Increased risk of developing HTN RR
Intermittent claudication
Pain in thigh
Iliofemoral occlusion
Most common leads for clinical setting
3-lead and 5-lead
3 lead ECG
3 electrodes: Right arm (white) Left arm (black) Left leg (red)
Bipolar limb leads (I, II, III)
Basic monitoring/research purposes
Mitral stenosis
Hypertrophy occurs in chamber upstream from stenosis, concentric type
Stretch of L atrium creates multiple foci causing arrhythmias
At risk for thrombus due to pooling in L atrium and increased turbulence
Body may compensate early on with little to no symptoms
May advance to R side heart failure
Medical mgmt: anticoagulant, anti-arrhythmics, surgery
Beta blockers
Primarily target Beta-1 receptor sites
Reduces: HR, BP primarily by reducing contractility, Sympathetic tone
Has anti-arrhythmic properties
In low doses actually function as anti-anxiety med
Limits adverse ventricular remodeling (dilation) after MI
Cautious with patients with kidney/renal dysfunction, pulmonary dysfunction or asthma
2 categories: specific and non-specific
P-R > 0.2 sec
AV block present
Trigeminy
PVC (premature ventricular contraction) every 3 beats
Generally less concerning than Bigeminy (bc within 6 per minute cutoff)
Splitting S2
S2 is shorter duration and higher frequency than S1
S2 has 2 audible components: aortic closure sound (A2) and pulmonic closure sound (P2)
Normal or physiologic splitting is demo during inspiration in normal healthy, since the splitting interval widens primarily due to the delayed P2 (common in kids and well conditioned athletes)
Persistent splitting S2 May occur in supine or recumbent position- however split should resolve on expiration following sitting, standing or valsalva
If splitting of S2 does not change w/ these are is in adults…further medical attention
Regulation of BP- fast
Baroreceptors (aortic arch and carotid sinus)
Effects of CHF in heart/blood
Decreased CO (SV, EF)
Cardiac remodeling; increased LVEDP
Increased systemic vasoconstriction (SNS, humoral, reflex, structure)
Impaired cardiac output distribution, pro-inflammatory state
Anemia -> decreased O2 content
HTN medications
Majority of patients will require 2 meds
Thiazide-Type diuretics usual initial med.
Depending on co-morbidities.., ACEI (ace inhibitor) ARB (aldosterone receptor blocker) BB (beta blocker) CCB (calcium channel blockers)
Aneurysms
Localized abnormal dilation by at least 50% compared to normal
Causes: atherosclerosis, congenital infections, Marfan’s
Risk factors: CVD and CVD risk factors (esp smoking), male, genetics (Marfan’s), 40-60 yo, HTN prevalent
Symptoms of cardiac valvular disease
Easy fatigue Dyspnea Palpitations Murmur Chest pain Putting edema Orthopnea Dizziness
Mean arterial pressure is normally regulated…
Within a narrow range
Mean arterial pressure typically 85-100 mmHg in adults
NYHA class IV
Unable to carry on any physical activity without discomfort
Symptoms of heart failure at rest
If any physical activity is undertaken, discomfort increases
ST depression types
Normal
Upsloping
Horizontal
Downsloping
Intermittent claudication
Pain in proximal 2/3 calf
Superficial femoral artery
Ischemia- causes of increased demand
Exercise
Cold weather (increased vascular resistance)
Mental/emotional stress
Spontaneous changes in HR and BP
Complications cardiac post surgery
DVT and/or PE Intra- or Peri-operative MI Pericarditis Infection Sternotomy failure Pulmonary complications Reduced bowel motility Deconditioning Neurocognitive decline Chest wall pain and mobility issues
___ receptors have high threshold pressure and are less sensitive that ____ receptors
Aortic arch receptors higher threshold and less sensitive than carotid sinus receptors
Intermittent claudication
Pain in distal 1/3 calf
Popliteal Artery
CVD defined by presence of ___.
3 major causes
Stenosis
Atherosclerosis
Thrombo-embolism
Vasculitis
Ejection fraction (EF)
EF = (EDV - ESV) % EDV
Normal value 55-75%
Mild 40-50.%
Moderate 30-40%
Severe < 30%
EF does NOT correlate with functional capacity
Blood lab to assess and track severity of heart failure
BNP
Brain natriuretic peptide
Presence of ___ in ____ indicates an anterior infarction and probable involvement of ___ Artery.
Significant Q waves in V1-V4
LAD (left anterior descending coronary artery)
HTN subdivided into…
Essential HTN-
Cause unknown, 95-99% of cases
Interaction between genetics and environment
Secondary HTN-
1-5%
Result of biochemical or mechanical pathology, potentially reversible
Regulation of arterial blood flow
Sympathetic: NE
(NE binds to alpha-1 causing vasoconstriction)
Circulating: E
Circulating hormone: angiotensin II
Local metabolites: prostaglandins
Mechanical: muscle contraction, vessel stretch (CA2+ influx)
4 groups most likely to benefit from statins
- Any form of ASCVD
- Primary LDL-C levels of 190 mg/dL or greater
- DM, 40-75 y/o, with LCL-C levels 70-189 mg/dL
- W/O DM, 40-75 y/o, with estimated 10-year ASCVD risk >= 7.5%
Depolarization of cell membrane allows influx of ___ into cell and efflux of __.
Na+ in
K+ out
Intermittent claudication- manifests
Predictable time and intensity, reproducible, doesn’t change with posture
Location of the diseased artery determines location of claudication
Walking test
Sinus rhythm
Normal
ARBs
Angiotensin 2 receptors “sartan”
Similar effects as ACEI, used when patients don’t tolerate ACEI (“coughing”)
Most common: Losartan (Cozar),Valsartan (Diovan)
Also used to treat patients with obstructive sleep apnea
Heart disease (CDC facts)
~ 610,000 Americans die annually (25% of deaths)
Coronary heart disease is most common (370k annually)
In US, heart attack every 43 seconds; death every minute from heart-related event
AKA: CAD (coronary artery disease); ASHD (atherosclerotic heart disease)
Aystole
Flat line
No electrical activity to heart
Special exercise considerations- HF
Avoid exercise after eating and vasodilator meds
Use VO2max instead of HRmax
Initial exercise intensity should be 10 beats below significant symptoms
Signs of cardiac decompensation: pulse narrowing, arrhythmia, fluid changes (3lbs on 24 hrs; 5lbs in a week)
Goal writing: increased intensity/duration; functional activities and independence
Pallor on elevation
Insufficient arterial pressure to perfuse when leg elevated above level of heart
Limb drains of blood, turns pale
Chronic HTN shifts baroreceptor curve to ____.
Right
(Mean arterial pressure increases x-axis; receptor firing y-axis)
Baroreceptor sensitivity decreases, the higher pressure is “new normal”
Couplet
2 PVCs (premature ventricular contraction) in a row
Concerning
Effects of CHF on gut/splanchnic organs
Hyperconstricted
When subjected to various stressors, endothelial cells can also produce….
Prothrombotic molecules
In response to injury or infection, secrete chemokines and produce cell surface adhesion molecules
Elevated BP
Systolic 120-129
Diastolic <80 (79 or less)
Irregularly irregular rhythm
RR interval and ectopy variable with no pattern- totally irregular
12-lead ECG is used primarily for ___. Single-lead monitoring is for ___.
12- lead: determining ischemia or infarction
Single-lead: evaluating heart rhythm
Stage 1 HTN
Systolic 130-139
Diastolic 80-89
Mitral valve prolapse sound
Click mid-systole (between S1 and S2)
Followed by a murmur
Heart failure with reduced ejection fracture (HFrEF)
EF = < 40%.
AKA systolic HF (SHF)
When contraction increases within a given chamber of the heart ___
When contraction ends …
Chamber pressure greater than downstream pressure, the valve opens
When contraction ends, pressure decreases below downstream pressure, the valve closed
Heart valves- diastole
Pulmonary and aortic valve closed
Tricuspid and Mitral valves open
On ECG, wave of depolarization is recorded as ___ when moving toward a (+) electrode on the skin
An upward deflection
Heart transplant
Native SA node
No longer innervated
Different mechanisms for CO regulation during exercise
Immunosuppressive agents needed-
Side effects HTN, osteoporosis, muscle weakness, liver damage
CHF etiology
Ischemic heart disease (most common in US) HTN Idiopathic cardiomyopathy Infections (viral myocarditis, Chagas) Toxins (alcohol or cytotoxic drugs) Valvular disease Prolonged arrhythmias (A-fib)
Lifetime risk is greater if BP remains > 160/90
Exercise considerations-
Valvular stenosis
Close monitoring with RPE
Low muscle perfusion may limit exercise
Suppressed BP response to exercise, possibly exaggerated HR
Low cardiac output
Pt with symptomatic aortic stenosis typically not candiofor exercise programs
Asymptomatic: intensity low and progressed gradually
Angina may be a symptom
Raynaud’s syndrome
Vasospasm causing reduced blood flow
Primary- more common in women (15-30 yo) more typical in cold climates, family history, no underlying disease
Secondary- less common, more serious. Usually appears around 40 (scelerodema, lupus, RA, repetitive trauma, smoking, atherosclerosis)
Severe- rare, could result in permanent hypoperfusion of digits
A significant Q wave is
1 mm wide
OR
1/3 size of QRS complex
P-R interval
The propagation of the cardiac AP from atria -> AV node -> ventricles
Normal:
0.12 - 0.2 seconds (3-5 small boxes)
(Will shorten during exercise as heart rate increases)
Hypertrophy is detected on a 12-lead ECG by looking at…
Waveforms- particularly P-wave and QRS complex for voltage (> 3 mV) or configuration
Pericarditis and ST elevation
Concave upwards ST elevation in most leads except aVR
No reciprocal ST segment depression (except maybe aVR)
T waves are usually low amplitude and HR usually increased
May see PR segment depression- a manifestation of atrial injury due to compression
Neuropathic ulcers
Plantar location
(Metatarsal heads- esp 2nd; sole of foot, balls of toes)
“Punched out” margins, usu correspond to pressure points
Insensate- often diabetic w/ peripheral neuropathy
May have arterial insufficiency signs/symptoms
Regular rhythm
1 P wave per QRS complex
RR interval constant
V2
Location of heart
Which Coronary artery
Anterior / Anteroseptal
LAD- left anterior descending
Mitral stenosis - etiology
Primarily females (66%)
Valve leaflets don’t open easily or completely
Decreases area and increases resistance to flow between A-V
Main cause: rheumatic heart disease
Other etiologies: congenital mitral stenosis such as parachute mitral valve; marked mitral annual calcification and infective endocarditis with large vegetations (often fungal)
Aortic stenosis
Calcific aortic stenosis and congenital bicuspid aortic valve stenosis account for majority of cases
Mild thickening, calcification, or both of a tri-leaflet aortic valve w/o restricted leaflet motion
~25% of the population older than 65 years
Q-T interval
Time taken for ventricular depolarization and repolarization
Shortens during faster HR,
Lengthens during slower HR
Normal:
Men: 0.4 - 0.44 sec (10-11 small boxes)
Women: 0.44 - 0.46 sec (11 - 11.5 small boxes)
Heart failure
Complex clinical syndrome from any structural/functional cardiac disorder that results in inability of heart to eject blood to meet the demands of the body while maintaining normal pressures in its chambers and lungs
Angiotensin-converting-enzyme inhibitors OR Angiotensin antagonists
Vasodilator
Decreases remodeling
Ectopic pacemakers/foci
Abnormal pacemaker sites located outside SA node that display automaticity
Normally their activity is suppressed via overdrive suppression- by the higher rate SA node
Can occur within atria or ventricles
ECG sinus rhythm
P wave followed by QRS
QRS preceded by P wave
P upright in leads I, II, III
PR interval > 0.12 sec (3 small boxes)
Murmurs classified on…
Shape (crescendo, decrescendo, plateau…)
Location (site where originates: A P T M)
Timing (murmurs longer than heart sounds. Systolic, diastolic, continuous)
Intensity (graded 1-6; 6 is so loud no stethoscope needed; “Thrills”associated w/ murmurs grade 4-6)
Pitch (high, med, low)
Aldosterone
Decrease fibrosis
Na retention
Antagonist remodeling
Aldosterone release
Polymorphic
2 different morphologies
Clinical manifestations: Difference between Arterial and Venous disorders
Pulses
Arterial: May be decreased or absent; bruits
Venous: normal but may be difficult to palpate
ECG
Rhythm
Check for…
P before each QRS
QRS after each P
PR intervals- for AV blocks
QRS intervals- for BBB
Typical post op progression and goals
Day 0: transfers to chair with RN in am
Day 1: transfer sit->stand, gets to doorway, pre-gait
Afternoon ambulation
Day 2-3: chest tubes and cardiac pacer d/c
Patient must be supine and remain still for 1 hr with d/c
Stairs and independent ambulation assessments
Ventricular rate vs Atrial rate
Should be 1:1
Phase 2
Cardiac AP
Influx of Ca2+ through L-Type Ca2+ channels
Electrically balanced by K+ efflux through delayed rectifier K+ channels
Angina- somatic fibers
Usually easily described, precisely located, and usually experienced as a sharp sensation
Effects of CHF on lungs
Increased: Pulmonary vascular pressure Stiffness VA/Q mismatch Alveolar- arterial O2 gradient Respiratory muscle work
Decreased:
Diffusing capacity
Aortic stenosis- what expect
Volume overload:
LV dilates out
LVH
Upon exertion:
Dyspnea
Auscultation:
Diastolic murmur “blowing”
Phase 0
Cardiac AP
Rapid Na+ influx
Through open fast Na+ channels
Statins
HMG-CoA reductase inhibitors
Blocks LDL synthesis
Increases HDL
Some anti-inflammatory properties
Common: Lovastatin (mevacor), Simvastatin (Zocor), Atorvastatin (Lipitor), Rosuvastatin (Crestor)
Heart failure
Compensation
Neurohormonal mechanisms (SNS and RAAS) to Increase CO (SV x HR); Natriuretic peptides
Digoxin or Dobutamine or PD3
Positive inotrope
The heart in general depolarizes and conducts from ….
Right -> Left
Superior-> Inferior
Internal-> External
(Repolarizes in opposite direction)
V6
Unipolar precordial (chest) lead
Mid Axillary line at level of V4
(Lateral wall)
0* (left lateral)
HTN med considerations
Alpha blockers, Calcium channel blockers or vasodilating drugs may lead to sudden hypotension post-exercise
Avoid suddenly stopping exercise and undertake an extended cool down of light activity
Beta blockers and diuretics may impair thermoregulation
As cell becomes positive on interior, the myocardial cells …
Are stimulated to contract
Excitation coupling
Beta blockers
Decreased HR
Decreased remodeling (block SNS)
Anti-arrhythmic
Renin release stimulated by…
Sympathetic nerve activation (beta1 adrenoreceptors)
Renal Artery hypotension (caused by systemic hypotension or renal artery stenosis)
Decreased sodium delivery to distal tubules of kidney
Murmurs
Extra sounds during the cardiac cycle, such as whooshing or swishing made by turbulent blood flow often due to a faulty valve or structural changes in myocardium
V1
Unipolar precordial (chest) lead
4th IC space to R of sternum
Septal
aVL
Area of heart?
Which coronary artery?
Lateral
LCx - left circumflex
Afib vs Aflutter
Aflutter P-wave- distinct sawtooth
Afib P-waves- variable, hard to detect or not demonstrated at all
Aflutter Rhythm- usually fairly regular, Ltd R-R variability
Afib Rhythm- usually very irregular, high R-R variability, with isoelectric line variability
Aflutter usually has a fixed/consistent conduction block pattern
Infarction
ECG
Q waves
Inverted T waves
ST segment elevation or depression
Pericardium
Fibrous - outermost later, firmly bound to central tendon of diaphragm, sternum and mediastinal pleura
Serous - inner surface of fibrous pericardium (parietal) and reflected onto heart as visceral layer (epicardium)
Pericardial space - filled with fluid to lubricate/reduce friction
S3 occurs
At beginning of diastole
Ventricular fibrillation
Not pumping effectively
No pulse
Probably passed out
High risk of death (code blue)
Low-molecular weight heparin (LMWH)
Anti-coagulant
Fast acting (3-5 hrs) Used in patients with better kidneys
Often injected
Diuretic
Decreases fluid volume
Relives dyspnea
Acute HF
4 things
- Blood flow- vessels constrict, vital organs are not perfused with enough blood
- Kidney function- in response to insufficient blood feeding kidneys, their function deteriorates leading to fluid build-up
- Fluid buildup- fluid starts to leak out of vessels into surrounding tissues, causing body to swell and add weight
- Breathlessness- fluid builds up in lungs and alveoli, difficulty breathing and congestion (drowning in own body)
ST- depression
ST depression > 1 mm at J point
Significant for ischemia
Evolution of atherosclerotic plaques - developmental stage 2
Fibrous plaque
Lipoproteins transport/deposits LDL into arterial intima
Fatty streak covered by collagen and calcium deposits forming a fibrous plaque that appears grayish/whitish
Result = narrowing of lumen
Percutaneous coronary intervention (PCI)
Formerly known as angioplasty with stent
Non-surgical procedure
Catheter and balloon to place a stent to open up blood vessels in heart that have been narrowed by plaque buildup
2 types stents: bare metal and drug eluting
What must consider when monitoring the response to exercise for a patient with aortic stenosis
BP might not increase much during exercise
Furosemide (Lasix)
HF and patient’s with CAD with CKD
Loop diuretic: block Na+/K+/Cl- reabsorption
Side effects: hypokalemia, hyponatremia, volume depletion, frequent voiding
Reduce BP by reducing blood volume via kidneys
Exercise for claudication
Exertion to the point of leg pain is required for maximum benefits
For more severe cases: arm ergometry also improves walking performance
Leg strength training improves walking time- but not as much as treadmill
Interval training with short rest periods for relief is most effective
At least 3x week (for 12 weeks)
Intensity should induce claudication within 3-5 min; continue until pain is moderate (5/10)
Goal 30-35 min
NYHA- class II
Slight limitation of physical activity
Comfortable at rest
Ordinary physical activity results in fatigue, palpitation, dyspnea (shortness of breath)
AV node blocks
1st degree AV block PR > 0.20 seconds
2nd degree AV block: 2 types
Type 1: Mobitz I or Wenckeback
Increasing PR interval until a QRS complex is dropped (usually benign)
Type 2: Mobitz II
QRS dropped w/o any progressive increase in PR interval
TAVR/TAVI
Transcatheter aortic valve replacement
Accessed through femoral artery
Regularly irregular rhythm
RR interval variable but with s pattern
Normal and ectopic beats grouped together and repeating over and over
Nonischemic causes: ST elevation
- LVH (Left precordial leads, I, aVL)
- Conduction abnormalities (ex: LBB, WPW and non-specific intracardiac delay)
- Early repolarization pattern
- Aneurysm/old MI
- Pericarditis/myocarditis
- Brugada pattern
- Takotsubo (apical ballooning) syndrome
- Hyperkalemia
- Hypercalcemia
Clinical manifestations: Difference between Arterial and Venous disorders
Ulcers
Arterial: pale base, discrete borders, high-pressure sites like heel or toes
Venous: near medial malleolus, irregular border, pink base
Heart failure
Symptoms
Shortness of breath Fluid retention Fatigue Orthopnea Paroxysmal nocturnal dyspnea
Myopathy and statins
Myalgia up to 25%
Myagliga and weakness (7%)
Rhabdo assoc w statin possible but rare (<0.1% muscle pain, weakness, dark urine; more prominent muscle groups)
Murmur:
Increases with standing
Decreases with squatting
S1 sound
HCOM - ejection Type
Hypertrophic cardiomyopathy
Most common cause of HF in US?
Ischemic heart disease
MI
Myocardial infarction
Cell death in the heart muscle caused by complete and prolonged occlusion of a coronary artery
Phase 1
Cardiac AP
Transient K+ channels open
K+ efflux returns TMP to 0mV
Evolution of atherosclerotic plaques - developmental stage 1
fatty streaks
Lipid-filling smooth muscle cells
Potentially reversing
PAD findings
Affected limb may show signs of cyanosis
Feels cool to touch
Numbness or tingling reported in affected area
Skin may appear shiny, thin, pale and hairless
Nails become thickened and brittle
Semilunar valves
Aortic and pulmonary
3 leaflets of each side
NO papillary muscles or chordae tendinae
Do NOT lie back against walls of aorta or pulmonary artery
12 lead ECG
Diagnostic and stress testing
10 electrodes:
All 4 limbs (RA, LL, LA, RL)
6 Precordium (V1-V6)
Monitors 12 leads: V1-V6, I-III, aVR, aVF, aVL
Allows interpretation of specific areas of heart
You note elevated troponins in a patient chart and see comment “demand ischemia”- this can be due to…
Poor cardiac output and does not represent MI
Patient may be at risk for additional ischemia related to activity, so proceed cautiously
Composite score chest pain due to CAD
1 point each: Male > 55 / Female > 65 Known vascular disease Pain worse with exercise Pain not elicited with palpation Patient assumes pain is cardiac origin
4-5 high +LR
Unfractionated heparin
Anti-coagulant
Blocks clotting factors in blood, traditionally IV
24 hours to effect
Used post-op to prevent clots, DVT
Myocardial oxygen demand determinants
Wall stress
HR
Contractility
Systolic heart failure (SHF)
Impaired contractile function of heart
SHF most common etiology = ischemic heart disease, although many patients with DHF have CAD
Aortic regurgitation/incompetence
What expect
Eccentric hypertrophy
Late stages may include LA concentric hypertrophy
No pulmonary symptoms until very advanced
Volume overload:
LV dilates out
LVH
Exertion: dyspnea
Auscultation: diastolic murmur “blowing”
Clinical manifestations: Difference between Arterial and Venous disorders
Skin temp
Arterial: cool
Venous: normal
Left ventricular failure manifestations
Progressive dyspnea (exertions first) Paroxysmal nocturnal dyspnea Orthopnea Productive spasmodic cough Pulmonary edema: Extreme breathlessness, anxiety, frothy pink sputum, nasal flaring, accessory muscle use, rales, tachypnea, diaphoresis Cerebral hypoxia: irritability, restlessness, confusion, impaired memory, sleep disturbance Fatigue, exercise intolerance Muscular weakness Renal changes
Condition of imbalance between myocardial O2 supply and demand often caused by atherosclerosis of coronary arteries
Ischemia
Palpation of abdominal aorta
Relax abs- flex hips and support head and legs with pillow
Start left and superior to umbilicus
Apply first pressure with flattened fingers of both hands
Width > 2.5 cm (~2 finger widths) warrant further medical examination
Angina
Chest pain or discomfort due to cardiac ischemia
3 major types: stable, unstable, printzemental
Heaviness, tightness, pressure Discomfort gradually builds Gradually subsides Episode lasts 1-5 min Often confused with digestive disturbances
Stage 2 HTN
Systolic 140 or higher
Diastolic 90 or higher
Hemodynamics
Blood flow parallels CO
BF
CO = HR x SV
CO = driving pressure % resistance to flow…
or CO = (MAP - CVP) % TPR
Localized edema
MSK injury
DVT
CVD is
Disease and dysfunction to the myocardium and blood vessels, includes numerous problems, many of which are related to process of atherosclerosis
Arterial ulcers
Dorsal or distal location (toes)
Sharp margins
Painful
Pallor, loss of hair, nail dystrophy
Afib
Atrial fibrillation
Atrial activity poorly defined; may see course or fine undulations or no atrial activity at all
Cause by multiple ectopic pacemakers in atria
Ventricular response: irregularly irregular
Can be rapid, moderate or slow
Adequate control (HR < 110 bpm) Inadequate control (HR > 110 bpm)
PAC
Premature atrial contraction
Usually benign
ACE-Inhibitors
Angiotensin converting enzyme inhibitors “pril”
Blocks conversion of Ang 1 to Ang 2
Lowers BP
Few adverse side effects other than orthostasis
Decrease afterload and improves survival in HF
Increases survival and prevents LV dilation post-MI
Most common: Lisinopril (Zestril), Captopril (Capoten) and Enalapril (Vasotec)
EKG leads: the (+) terminal
The “eye”
Captures/receives the signal
Overlap of atherosclerotic disease
Coronary artery disease
Cerebrovascular disease
Peripheral artery disease
Patients with one often have coexistent disease in other vascular beds
HTN causes about 50% of ___ and increases risk of ___.
Ischemic CVA
Increased risk of hemorrhagic stroke
Ankle-Brachial Index (ABI)
Procedure
- Patient in supine
- Measure brachial artery pressure using Doppler US
- Apply same BP cuff to ankle on same side of body
- Palpate for posterior tibial artery- take SBP reading
- Palpate for dorsalis pedis artery- take pressure
- Repeat other side/arm-ankle
ABI = ankle pressure % brachial pressure
(Using highest value from L or R side)
Structure of artery walls
Intima: endothelial cells Internal elastic membrane Media: smooth muscle cells External elastic lamina Adventia
___ is due to increase in capillary pressure usually from an elevation of venous pressure caused by obstruction to venous and/or lymphatic drainage
Edema
Evolution of atherosclerotic plaques - developmental stage 3
Complicated lesion/Instable plaques
Continued inflammation can result in plaque instability, ulceration and rupture
Lipid core is exposed to blood stream, platelets accumulate, and thrombus forms
Result = narrowing of lumen or thrombo-embolotic event
Lead aVL
Lateral wall
ABI 0.5-0.8
Patients with claudication
Temporary epicardial pacer
Epicardial pacing wires common after open heart surgery, wires exit through mediastinal incision
Cardiac surgery makes myocardium irritable and prone to arrhythmia
Pacer used to control heart rate due and rhythm
ST-segment depression that develops during exercise is
An ischemic response to activity and following rest should return to baseline
ECG paper:
___ = 1 mV
10 mm
2 thick lined boxes; each thick box has 25 thin line boxes total, so 10 small boxes in a row is 1mV
Normal EF
> 55%
From echocardiogram
Is NOT related to functional capacity and tolerance to exercise
Coumadin (Warfarin)
Long-term Anti-coagulant
A-fib, chronic DVT
Blocks effect of Vit K-epoxide reductase
Effects of CHF - respiratory muscles
“Steal” blood from locomotor muscles
Lead =
Electrode =
Lead = signal Electrode = sticker placed on skin
___ is leading risk factor for CVD mortality.
Only __% are compliant with ___.
HTN
13% global deaths
Leading cause of CVD worldwide
Only about 50% compliant with medication
RT (resistance training) - HF
Once considered unsafe
Most often in form of a PRE (progressive resistance exercise)
60-80% 1RM
Most protocols emphasized LE muscles
Improvements: “muscle hypothesis” attenuated the loss of muscle mass, improved functional mobility and ADLs, 6MWT and WoL (SF-36)
3 types of ulcers
Atrial
Venous
Neuropathic
Capillary refill test
Blanch nail bed
Remove pressure
Count time until normal pink color returns
Normal refill fingers/toes is < 2 seconds
Ankle-Brachial Index (ABI)
Interpretation
ABI = ankle pressure % brachial pressure (Using highest value from L or R in equation)
Normally ABI = or > 1
ankle BP is as high as brachial
ABI = < 0.9 diagnostic of PAD
ABI 0.5-0.8 found in claudication
ABI < 0.5 critical ischemia
An ABI of 0.9 or lower has SpIN 83-99% and SnOUT 68-73% in detecting stenosis greater than 50%
(SnOUT of ABI less than 1.0 approaches 100%)
ECG paper:
Thin lines
Thick lines
thin:
1 mm intervals or 0.04 seconds
0.1 mV
Thick:
5 mm intervals or 0.2 seconds
0.5 mV
Aspirin
Anti-platelets
COX1 and COX2 inhibitor
Often used in low doses
Given larger doses during MI
V5
Area of heart?
Which coronary artery?
Lateral
LCx - left circumflex
Monitoring guidelines- 5 things “hold exercise”
- QRS widening > 0.12 sec
- > 6 PVC per min or couplet
- Glucose >250 or below 60
(Make sure they have a snack prior) - Resting 90mmHg > SBP > 180mmHg
OR DBP > 110 mmHg - RHR >100 or with A-fib > 110 bpm
Calculating HR on ECG paper- method 2
Count number of QRS complexes in a 6 second interval and multiply by 10 (30 thick lined boxes)
Ex: 8 QRS complexes x 10 = 80 bpm
(5 thick boxes = 1 sec)
Tissue plasminogen activators (TPA)
Thrombolytic
Facilitate breakdown of clots that have already formed by converting plasminogen to plasmin
Used in acute MI, if used w/in 1 hr of symptoms reduces mortality by 50%
Most common: Streptokinase (Streptase), UroKinase (Abbokinase)
Sustained ventricular tachycardia
Does not revert back to normal rhythm after ~30 sec
Left ventricular hypertrophy is present if
The depth of S-wave in V1 + height of R wave in V5
> 35 mm
Non-modifiable risk factors of CVD
Gender (male > female)
Age (male > 40; female >50)
Race (African-American or Asian)
Family history
Heart failure with preserved ejection fraction (HFpEF)
EF = > 50%
AKA DHF (diastolic heart failure)
41-49% borderline
> 40% improved
Pathophysiology - valvular disease
Congenital- genetic, maternal exposure
Acquired- rheumatic fever, endocarditis, gradual fibrosis
Phase 4
Cardiac AP
Na+ and Ca2+ channels closed
Open K+ rectifier channels keep TMP stable at -90mV
Factors that increase likelihood of MI (top 3)
Assoc with exertion
Radiation to L arm
Described as pressure
ST-segment depression at rest associated with chest pain may indicate…
Acute injury to subendocardial wall
Phase3
Cardiac AP
Ca2+ channels close
Delayed K+ rectifier channels remain open
Return TMP to -90mV
Venous ulcers
Maleolar location (usually medial)
Irregular margins
Hemosiderin staining (brown)
Varicose veins and pitting edema
Ischemic changes -ECG
Reduced blood flow ->
Reduced ability to conduct AP
Membrane potential changes
T-wave inversions
Progresses into S-T segment changes (depression then to elevation)
Pathologic Q waves
Scar tissue (prior tissue death)
J point
Initiation of ventricular repolarization
Junction between termination of QRS complex and beginning of ST segment
Normally, should be in line with isoelectric line
Presence of ___ in ____ indicates an inferior infarction and probable involvement of ___ Artery.
Significant Q-waves in II, III, aVF
Right coronary artery
Normal BP
Systolic <120 (91-119)
Diastolic <80 (61-79)
Turgor
Normally skin springs back to its resting position right away
In dehydrated patients this return to resting is delayed
May also observe hypotension, tachycardia, orthostasis, irregular HR and ECG
Myocardium oxygen supply determinants
O2 content
Coronary blood flow Coronary perfusion pressure Coronary vascular resistance: (External- compression Internal- intrinsic regulation: local metabolites, endothelial factors, neural innervation)
Cardiovascular diseases, including stroke and heart disease, account for ___% or ____ of all US deaths.
And ____.
1/3 or 33.6% deaths
Among leading causes of disability in US (nearly 4 million people)
5 lead ECG
- Right arm (WHITE- below clavicle)
- Right leg (GREEN- lower edge rib cage)
- Left arm (BLACK- below clavicle)
- Left leg (RED- lower edge rib cage)
- Chest (BROWN- V1)
Monitor displays bipolar leads (I, II, III) AND a single chest/precordial lead (can be V1-V6 depending on position)
Commonly used in acute care
Torsades de pointes
Code blue
Ventricular fibrillation
3rd degree AV node block
AKA Complete heart block
Atria and ventricles are electrically dissociated
P-waves and QRS complexes occur independent of each other
As always use QRS complexes to determine HR
S4 occurs
Late diastole
Ischemic contracture of myocardium
Insufficient or no ATP delivered to break cross myofilament cross-bridge
ECG paper:
Tick marks on rhythm strip = ?
3 seconds
Overview of pathophysiology of atherosclerosis
Endothelial dysfunction
Inflammatory process involving many cellular markers within the lesion
Deposits of fatty streaks initiating event
Lesions occur in large and medium sized vessels
May be present throughout lifetime
Angina- special populations
Elderly patients:
More likely to present with atypical symptoms (SOB, AMS)
Diabetics: may not be able to accurately sense or describe pain
Women: more commonly report nausea, emesis, jaw pain, neck pain, back pain
Presence of multiple RX, drugs and alcohol will also alter perception to perceive discomfort
Abdominal aortic aneurysm
Dull, tearing ache/pain in low back, groin or mid-abdominal left flank
Chest pain
Weakness or transient paralysis of legs
Palpable, pulsating abdominal mass (> 3cm)
Inter-arm systolic BP difference > 20 mmHg
Absent or decreased peripheral pulses (pulse deficit)
Tachycardia
Metoprolol (Lopressor)
Beta blocker - specific
Sympatholytic
Rhythm: No P wave but normal QRS
AV node
3 properties of cardiac muscle
Automaticity
Rhythmicity
Conductivity
Neurohumoral activation
Compensatory mechanisms in heart failure
Decreased CO ->
Renal sodium and water retention->
Restoration of organ perfusion
And/or
Decreased CO ->
Increase vascular resistance->
Restoration of organ perfusion
Factors that decrease likelihood of MI
Described as positional
Not associated with exertion
Reproducible with palpation
Described as sharp
Warning s/s of ltd exercise tolerance
- Resting tachycardia
- Lack of HR or BP increase with exertion (10 mmHg/MET)
- Exaggerated HR or BP response to exertion
- > = 10 mmHg fall in SBP with increased workload
- Low angina threshold
- Excessive dyspnea
- Slow HR recovery from activity
ACC/AHA - Stage D
Patients with end-stage disease who requires specialized treatment strategies
Coronary artery bypass graft
320k annually in US
1-2% mortality but 5-10% risk of MI during procedure
Graft vessels sewn to coronary arteries beyond blockage and attached to aorta
Triple, quadruple or quintuple bypasses are not routine
Most commonly used vessel for grafts is saphenous vein
Palpate pulse when auscultation:
When you feel pulse and hear a sound indicates ____
When
Systole (feel pulse and hear sound) - AV valves (M1, T1)
End of systole/beginning diastole (don’t feel pulse and hear a sound) - semilunar valves (A2, P2)
Types of Remodeling
Eccentric hypertrophy-Normal wall thickness with LV increased mass
Concentric hypertrophy- increased wall thickness and LV mass
Concentric remodeling- increased wall thickness, normal LV mass
Cardiac Remodeling - HTN
Chronic HTN->
Aortic valve stenosis
Pathological hypertrophy: Myocyte length increase < width increase Fibrosis Maybe cardiac dysfunction -> Cardiac dilation: Myocyte length increase >> width increase Extensive fibrosis Myocyte death Adv cardiac dysfunction
Calculating HR on ECG paper - method 1
60 % 0.2 = 300 bpm
(60 seconds per minute divided by thick line box of 0.2 seconds)
60 % 0.4 = 150 bpm
(60 sec % 2 thick line boxes)
60 % 0.6 = 100 bpm
(60 sec % 3 thick line boxes)
(Note: each thick line box = 0.2 sec)
Stage A patient
Therapy goals
Heart healthy lifestyle
Prevent vascular, coronary disease
Prevent LV structural abnormalities
Atrial flutter
Aflutter
Regular atrial activity with a saw-tooth appearances
Ventricular rate usually 60-100 bpm
Conduction ratio usually between 2:1 and 4:1
Supraventricular Rhythm
Not frequently encountered
In ventricular aneurysm… (ECG)
ST segment remains elevated and does not return to isoelectric line over time
Normal blood flow
5 L/min
Heart failure 3.5 L/min
Alpha-1 blockers
Block alpha-1 receptors on vascular smooth muscle, reducing TPR and BP
Effective treating: Benign prostate hypertrophy
Most common:
Doxazosin (cardura)
Prazosin (minipress)
Sympatholytics
Atherosclerosis
“Hardening of arteries”
Dynamic chronic inflammatory condition
Pathogenesis involves lipids, thrombosis, elements of vascular wall, and immune cells
ECG paper:
1 thick lined box
5 thick lined boxes
1 thick lined box (5 small boxes)
5 mm or 0.20 seconds
5 thick lined boxes (25 small boxes)
= 1 second
= 0.5 mV
Pericarditis
Swelling and inflammation of pericardium
Common causes: viral infections > bacterial infections > fungal infections
S/S:
Sharp retrosternal pain w/ radiation to back (lasting hours), fever
Pain worsens w/ deep breathing, coughing, laying flat
Pain improves sitting up and leaning forward
Friction rub on auscultation
HTN contributors
Diet (salt sensitivity) Inactivity Obesity Abnormalities of adrenal cortex Sleep apnea Sympathetic nervous system activity Kidney disease Congenital vascular disorders Recreational drugs and alcohol
Epicardium is outed later of connective tissue that covers heart, contains …
Variable amounts of adipose tissue that tends to aggregate along vessels and in the grooves on the surface of the heart
Effects of CHF in skeletal muscles
Decreased:
Blood flow, endothelial function, muscle pump, vasodilation, mitochondrial volume, capillary (% flow, RBC reflux), O2 diffusing capacity, micro vascular O2 pressure, intracellular O2 pressure, NO bioavailability (extracellular), glycogen
Increased:
Vasoconstriction, vascular stiffness, Atrophy Type 2 fibers, glycolytic stimulation/glycogen depletion, VO2 requirement
Clinical manifestations: Difference between Arterial and Venous disorders
Walking
Arterial: aching begins at specific time/distance; improves with rest
Venous: lessens symptoms
Angina- Unstable
Recent or acceleration of angina threshold
New onset < 2 months
Symptoms at rest > 15-20 min
Gradually worsens in a crescendo like pattern
May not respond to nitro or rest
Often precursor to MI
Acute vs Chronic HF
Acute:
Immediately life threatening, in acute pulmonary edema and acute ischemia, medical emergency. End sequela of an MI
Chronic:
Can exist in compensated failure for many years, cardiac dilation, poor pump quality, chronic peripheral edema and congestion
Clinical manifestations: Difference between Arterial and Venous disorders
Limb size
Arterial: decreased due to muscle wasting
Venous: swollen in chronic disease
For LVAD
RPE, HR or BP?
RPE
Bc continuous flow, no pulse and can’t take HR and BP
Lead aVF
Inferior wall
SVT
Supraventricular rhythm
Common ectopic pacemaker
No P wave
> 150 bpm
Alpha-2 Agonists
Reduces vascular tone by centrally mediated methods by stimulating Alpha 2 receptors
Suppresses Sympathetic outflow to vasomotor centers from brainstem
Not as commonly used
Most common: Clonidine (Catapres)
Sympatholytic
