Week 3 Flashcards
What is the pathway of blood flow through the heart?
Returns from the periphery, enter through the vena cave, it empties 1st into the R atrium then it crosses the AV valves into the R ventricles, R ventricles pump through the pulmonic valve into the pulmonary trunk, which then splits into the R and L pulmonary arteries, which goes to the lungs, gets oxygen diffused at the capillary alveolar interphase, blood then returns through the 2 pulmonary veins which converges to the L atrium, blood then flows from the L atrium, across the bicuspid valve(mitral valve), into the L ventricle, which then pumps blood through the aortic semilunar valve, then into the aorta, then into the systemic circulation that perfuses our tissues
What happens during diastole in regards to the heart valves?
The semilunar valves(pulmonary and aortic valves) are closed, because the ventricles is relaxed due to less pressure behind the valves. The AV valves(mitral and tricuspid) are open as blood is entering into the chambers
What happens during systole in regards to the heart valves?
The mitral and tricuspid valves are closed, which allow for them to create a high pressure chamber, to egress blood across the pulmonic valve and aortic valve
What are heart valves?
Passive structures that respond to pressure.
What helps keeps the AV valves closed during systole?
Chordae tendinae
What causes a valve to open?
When contraction increases pressure within a given chamber greater than the downstream pressure. (more related to semilunar valves, especially the pulmonic and the aortic valve)
What causes a valve to close?
When contraction ends and pressure decreases below downstream pressure
What is the pressure across the aortic valve?
Anywhere between 80-100
What are the AV valves on the left side?
Bicuspid or mitral valve
What are the AV valves on the right side?
Tricuspid (3 leaflets)
What do the Chordae tendinae and Papillary muscles do during systole in the AV valves?
They become taut to prevent them from opening.
- Prevent inversion of valves during ventricular systole.
- Can become damaged from MI causing back flow “regurgitation”.
What are the semilunar valves?
Aortic and Pulmonic
What are the characteristics of the semilunar valves?
- Three leaflets on each
- No papillary muscles or chordae tendonae
- Do not lie back against the walls of the aorta or pulmonary artery
What are the general symptoms of Cardiac Valvular Disease?
- Easy Fatigue
- Dyspnea
- Palpitations
- Murmur
- Chest Pain
- Pitting Edema
- Orthopnea
- Dizziness
What is a murmur?
What we hear when there is turbulent flow across the valve.
Why do patients with a cardiac valvular disease get chest pain?
If we impair the pressure gradient, we impair the egress of blood out of the heart, and across the valves, we may impair myocardial performance, especially as we increase workload, if we can’t maintain demand, we may get transient ischemia and chest pain
Why do patients with a cardiac valvular disease get pitting edema?
If we have an impaired ability to get blood out of the heart, we can create backflow. Backflow on the right goes into the peripheral veins and back flow on the L, it will eventually go back to the lungs and eventually impair the R side
What is orthopnea?
Shortness of breath when laying flat, due to the fact that when you lay flat, blood shunts into the central part of the body, which increases pre-load/stilling, which is essential putting more fluid into a flooded system, which it can’t handle, causing backflow into the lungs
What is concentric remodeling?
Classified as an increased relative thickness, with a normal L ventricular mass
What is concentric hypertrophy?
Classified as an increased relative thickness, with an increased L ventricular mass
What is concentric remodeling and concentric hypertrophy typically in response to?
L pressure overload, with the earliest response typically being concentric remodeling
Why is concentric remodeling and concentric hypertrophy done?
In an attempt to limit wall stress and to allow for normal L ventricular systolic function and performance
How does concentric remodeling and concentric hypertrophy become a pathological change?
If we have sustained elevated pressures like we see in HTN, or an aortic stenosis,
What does concentric remodeling and concentric hypertrophy lead to when it becomes pathological?
L ventricular diastolic dysfunction, an impaired ability to relax, and potentially diastolic heart failure
What is eccentric hypertrophy?
When ventricles have an increased mass, with a dilated ventricular chamber, with normal to low relative wall thickness. EX: ischemic cardio myelopathy
What are the types of congenital valvular disease?
- Genetic
- Maternal exposure
What are the types of acquired valvular disease?
- Rheumatic fever
- Endocarditis
- Gradual fibrosis
In what population does mitral stenosis primarily occur in?
Females
What is the main cause of mitral stenosis?
Rheumatic heart disease
What is mitral stenosis?
Condition where valve Leaflets don’t opening easily or completely
What are the effects of mitral stenosis?
Decreases area and increases
resistance to flow between A-V
What is the most common type of valvular disease?
Aortic stenosis
What are the other less common causes of mitral stenosis?
Congenital mitral stenosis, such as parachute mitral valve; marked mitral annular calcification and infective
endocarditis with large vegetations (often fungal, why you get antibiotics before dental work)
What happens in a parachuted valve?
All of the chordae tendonae attach to one valve, which impairs its ability to open
What are the things that we see in a case of mitral stenosis?
Pressure overload
- L atrium hypertrophy
- Limited L ventricle filling
- LA thrombus breeding
ground
- A fib
- Pulmonary congestion and
HTN
Upon Exertion
- Dyspnea: back flow of fluid from L side into lungs
Auscultation
- Opening snap, diastolic rumbleWhat does mitral stenosis cause?
- 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 Left Atrium and increased turbulence
- Body may compensate early on with little or no symptoms
- May advance to right heart failure
What are the medical management methods for mitral stenosis?
Anti-coagulants and antiarrhythmics, surgery
What causes mitral regurgitation/incompetence?
Rheumatic heart disease, which affects the properties of connective tissue often seen rheumatic disease
How does mitral regurgitation/incompetence work?
Mitral valve does not close completely during
systole (Incompetence)
• Creates back flow (Regurgitation)
• Increase SV to compensate for back flow
• Upstream chamber (L Atrium) dilates out
• Eccentric hypertrophy to accommodate increased volume
What are the signs and symptoms of mitral regurgitation/incompetence?
Anxiety and palpitations w/ exercise
• Asymptomatic fine to exercise
• Symptomatic patients beta blockers
What is a mitral valve prolapse?
When the valve snaps open during systole. You would hear a click followed by a murmur
What are the characteristics of mitral valve prolapse?
Mostly asymptomatic, cause
unknown
What would you expect to see in mitral valve prolapse?
Volume overload - L atrium dilates - A - fib - Thrombus formation - Pulmonary congestion - LVH forward flow Upon exertion - Dyspnea Auscultation - Holosystolic murmur: regurgitation into L atrium
What are the most common types of aortic stenosis?
Calcific aortic stenosis and congenital bicuspid aortic valve stenosis
What is congenital bicuspid aortic valve stenosis?
A condition where there is only 2 instead of 3 leaflets in the aortic valve, which causes the resistance to flow to be a bit higher
What do we often see in aortic stenosis?
Mild thickening, calcification, or both of a tri-leaflet aortic valve without restricted leaflet motion
What would you expect to see in an aortic stenosis patient?
Volume overload - LV dilates out - LVH Upon exertion - Dyspnea Auscultation - Diastolic murmur "blowing"
What are the causes of Aortic Regurgitation/Incompetence?
Congenital, rheumatic, endocarditis, deterioration with age as well as long
standing HTN
What would you expect to see in an aortic regurgitation/incompetence patient?
Volume overload - LV dilates out - LV hypertrophy Upon exertion - Dyspnea Auscultation - Diastolic murmur "blowing"
- Eccentric hypertrophy
- Late stages maybe LA concentric hypertrophy?
- No pulmonary symptoms until very advanced stages
What are the exercise considerations for valvular stenosis?
- Close monitoring with RPE
- Low muscle perfusion may limit exercise
- Suppressed BP response to exercise, possibly exaggerated HR
- Low cardiac output
- Patients with symptomatic aortic stenosis clients are typically not candidates for exercise programs!
- Asymptomatic aortic stenosis: intensity should be low and progressed gradually
- Angina may be a symptom
What are the characteristics of valvular replacement and repair?
• Valves can be mechanical or biological
- Pig, cow, cadaver
- Typically requiring by-pass and a median sternotomy
• Mechanical typically bi-leaflet valve with 2 carbon
leaflets covered with polyester knit fabric
• Mechanical last a lifetime but require anticoagulant meds
• Biologic valves made of human, pig or cow tissue
(xenografts)
- Pig valves mounted on frames (stents) or can be stentless
• Young pts may be better candidate for mechanical due to limited life of biological valve
• Mechanical higher risk for infection, thrombus and
emboli.
- Will need life long anti-coagulation meds
What are the characteristics of the minimally invasive options for valvular replacement/repair?
- Da-Vinci Robot
- Becoming more and more common
- MIAVR is limited by the longer cross-clamp and cardiopulmonary bypass (CPB) times.
- They go through 3 or 4 ports in the body, allowing the surgeon to visualize the structure they are operating on, and replace the valve through that method
What are the pros of the minimally invasive options for valvular replacement/repair?
Reduced postoperative mortality and morbidity, shorter hospital stay and
better cosmetics
What are the characteristics of trans-cutaneous valve repairs?
- Transcutaneous Aortic Valve Repair/Implantation
- Typically reserved for patients at high risk for open heart surgery
- Usually Older patients, or those with significant compromise
- Promising early results comparing 4yr clinical outcomes to open heart
What are the layers of the pericardium?
- Fibrous
- Serous
- Pericardial Space
What is the fibrous layer of the pericardium?
Outermost layer, firmly bound to the central tendon of the diaphragm; sternum (sternopericardial ligaments) and mediastinal pleura
What is the serous layer of the pericardium?
Lines the inner surface of the fibrous pericardium (Parietal) and is reflected onto the heart as the visceral layer (Epidcardium), forms a closed sac
What is the pericardial space of the pericardium?
Potential space formed by the sac, filled with fluid that
lubricates the heart and reduces friction during movement
What is the epicardium?
Outer layer 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.
What is pericarditis?
Swelling and Irritation of the pericardium
What are the common causes of pericarditis?
- Viral infections, Bacterial infections (less common), Fungal infections (rare)
- May occur due to a heart attack, radiation therapy and post open heart surgery
What are the signs and symptoms of pericarditis?
• Sharp retrosternal pain with radiation to the back (lasting hours), fever
• Pain worsens with deep breathing or coughing
and when laying flat.
• Pain is improved while sitting up and leaning forward
• Friction rub on auscultation
What is pericardial effusion?
Accumulation of fluid in the pericardial sac, which then impairs the ability for the heart to contract and for it to expand and fill
What are the causes of pericardial effusion?
- Viral infections, Bacterial infections (less common), Fungal infections (rare)
- May occur due to a heart attack, radiation therapy and post open heart surgery
What are the signs and symptoms of pericardial effusion?
• Symptoms
- Pressure pain in chest, dysphagia, dyspnea,
• Signs
- Muffled heart sounds, possibly JVD
What may pericardial effusion progress to?
Cardiac tamponade…Not good
What are the rarer conditions that can cause Aortic Regurgitation/Incompetence?
Marfan syndrome, ankylosing spondylitis and certain STDs
How do trans-cutaneous valve repairs work?
They insert a tracer wire through a catheter to get to the aorta, then they will implant a valve over or within the damaged valve
How is pericardial effusion treated?
By drainage, through a process called pericardiocentesis, where they remove fluid from the pericardium
What happens in cardiac tamponade?
The heart has very little movement, because there is so much pressure on it and it can lead to death
What is auscultation?
The propagation of sound from the heart through the chest wall, which allows us to assess the function of valves
What should auscultation include?
The 4 primary auscultation areas of the heart using the
diaphragm, staring with the patient in the supine or seated position.
How do you start auscultations?
• Start by finding the angle of Louis (sternal angle aka manubriosternal junction)
located at the 2nd rib, which is easily felt as a small protuberance along the sternum.
• Auscultate each point starting with the Aortic region using the following Mnemonic: All – Physical – Therapists – Move (Aortic, pulmonic, tricuspid, mitral)
How do you differentiate between systole and diastole during auscultations?
When doing auscultations, palpate an artery and when you feel a pulsation is the beginning of systole(AV valves). During the period when we don’t feel a pulse but we hear an auscultation is beginning diastole(semilunar valves)
What are the regions we want to listen to during auscultation and where are they?
- Aortic Region: Right 2nd
intercostal space, parasternal (angle of louie) - Pulmonic Region: Left 2nd
intercostal space, parasternal (angle of louie) - Erb’s point: Left 3rd intercostal space aka Left Lower Sternal Border (not a major region)
- Triscupid Region: Left 4th
intercostal space, parasternal - Mitral Region: Left 4th or 5th
intercostal space, midclavicular
What is the 1st heart sound we hear during normal heart sounds?
S1 “Lub” The first heart sound • Closure of the AV valves • (Tricuspid and Mitral) • Occurs with ventricular contraction • Marks the approximate beginning of systole.
What is the 2nd heart sound we hear during normal heart sounds?
S2 “Dub” The second heart sound
• Closure of the Semilunar valves
- (Aortic and Pulmonic).
• Marks the beginning of ventricular relaxation and end of systole.
• The second heart sound is of shorter duration and higher frequency than the first heart sound.
In what region do we often appreciate subtle changes to the heart?
Mitral region
What is splitting S1( 1st heart sound)?
The mitral and triscupid valve sounds (M1 and T1) are slightly asychronous.
What are the characteristics of splitting S1( 1st heart sound)?
• This is a normal findings as
- the mitral closure may precede tricuspid closure by 20 to 30 msec (0.02 to 0.03 sec.).
• This produces two audible components
• (M1-T1) referred to as normal or physiologic splitting of the first heart sound (S1).
• Wide splitting of the first sound is almost always
abnormal and warrants further medical examination
What are the characteristics of splitting S2( 2nd heart sound)?
• (S2) is of shorter duration and higher frequency than S1.
• It has two audible components, the aortic closure sound (A2) and the pulmonic closure sound (P2)
• Normal or Physiologic splitting is demonstrated during inspiration in normal healthy individuals, since the
splitting interval widens primarily due to the delayed P2.
- Common in children and well condition athletes
When may persistent splitting S2 occur?
Persistent splitting S2 may occur in supine or recumbent
position however, the split should resolve on expiration
following sitting, standing, or a Valsalva maneuver.
• If splitting of S2 does not change with these measures or if found in adults warrants further medical examination
What are extra heart sounds (Gallops) that may be heard?
• S3 occurs at the beginning of diastole after S2 and is lower in pitch than S1 or S2 as it is not of valvular origin.
• Indicative of ventricular/heart failure.
-SLOSH’-ing-in SLOSH’-ing-in
S1 S2 S3 S1 S2 S3
• S4 Occurs prior to S1, produced by the sound of blood being forced into a stiff
or hypertrophic ventricle. (pressure overload)
• Indicative of LVH or HCOM
• a-STIFF’-wall a-STIFF’-wall
S4 S1 S2 S4 S1 S2
What is a murmur?
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 the myocardium.
• Onomatopoeia
What are the characteristics by which a murmur should be characterized?
• Shape - Crescendo (grows louder), decrescendo, crescendo-decrescendo, plateau • Location - Determined by the site where the murmur originates - A, P, T, M listening areas • Timing - Murmurs are longer than heart sounds - Systolic, diastolic, continuous • Intensity • Pitch • High, medium, low
What are the grades of intensity at which a murmur should be assessed?
• Graded on a 6 point scale
- Grade 1 = very faint
- Grade 2 = quiet but heard immediately
- Grade 3 = moderately loud
- Grade 4 = loud*
- Grade 5 = heard with stethoscope partly off the chest*
- Grade 6 = no stethoscope needed*
*Note: Thrills are assoc. with
murmurs of grades 4 – 6
What are the systolic murmurs we hear?
- Aortic stenosis - ejection type
- Mitral regurgitation - holosystolic
- Mitral valve prolapse - late systole
- HCOM-ejection type
- Ventral Septal Defect-holosystolic
What are the diastolic murmurs we hear?
- Aortic regurgitation - early diastole
2. Mitral stenosis - mid to late diastole
How should the sound of the murmur heard during aortic stenosis change with position?
When they stand it should decrease and when they sit it should increase
How should the sound of the murmur heard during hypertrophic cardiomyopathy change with position?
When they stand it should increase and when they sit it should decrease
What is heart failure (HF)?
A complex clinical syndrome that can result from any structural or functional cardiac disorder that results in the inability of the heart to eject blood to meet the demands of the body while maintaining
normal pressures in it’s chambers and the lungs. Cardiac pump dysfunction
What are the compensations that we see that helps manage reduced blood flow caused by heart failure?
Neurohormonal mechanisms (SNS & RAAS) to ↑ CO
(SV x HR); this is not good
natriuretic peptides
What are the symptoms of heart failure?
Shortness of breath, fluid retention, fatigue,
orthopnea, paroxysmal nocturnal dyspnea
What are the complications of heart failure?
Impaired exercise tolerance, increased risk of ventricular
arrhythmias, and shortened life expectancy
What is the etiology/cause of heart failure?
• Ischemic Heart Disease - (most common in the U.S.) • Hypertension* • Idiopathic Cardiomyopathy • Infections(e.g., viral myocarditis; Chagas disease) • Toxins (e.g., alcohol or cytotoxic drugs) • Valvular Disease • Prolonged Arrhythmias (Afib)
What are the neuro-hormonal Effects of HF?
• Kidney is not happy with
decreased blood flow, sets off the cascade of release of renin, which then converts to angiotensin and angiotensin 2, which leads to –>
• Increases Na+/H2O retention
to increase perfusion pressure
• Increased epi, renin, endothelin (all vasoconstrictors) and ANP (produced by heart for
vasodilation)
What are the factors that influence cardiac output?
- Pre load
- After load
- Contractile state (Contractility)
- Heart Rate
What are the components of preload that influences cardiac output?
• Preload is the degree of myocardial distension
prior to shortening.
• Largely depends on the amount of ventricular
filling
What are the components of after load that influences cardiac output?
- Force against which the ventricles must act in order to eject blood
- Largely dependent on the arterial blood pressure and vascular tone
What are the types of heart failure?
- Systolic
* Diastolic (DHF)
What are the characteristics of systolic heart failure?
- Impaired contractile function of the heart
* SHF most common etiology is ischemic heart disease, although many patients with DHF have coronary artery disease
What are the characteristics of Diastolic (DHF) heart failure?
- Impaired relaxation of the heart
- DHF more common in females and HTN is a more common risk factor, although substantial proportion of pts with SHF have HTN
What are the clinical outcomes of both types of heart failure?
• Clinical outcome is the same
- Patients usually have a combination of the two
What is paroxysmal nocturnal dyspnea?
Condition where patients, most often with heart failure will go to periods where they wake up from their sleep, most often because they are not breathing. They sleep with multiple pillows
What are the compensatory mechanism in heart failure as ti pertains to neurohormonal activation?
- Decreased cardiac output leads to
- Inc vascular resistance and renal sodium and water retention, which leads to
- Restoration of organ perfusion
What are the effects of neurohormonal activation in heart failure?
- Inc plasma norepinephrine
- Inc plasma renin activity
- Inc atrial natriuretic
- Inc Endothelin- 1
How does the Renin-Angiotensin System (RAAS) work?
Low perfusion of the juxtomedullary apparatus, which then releases renin, renin converts with angiotensinogens to form angiotensin 1, which travels to the lungs, interacts with angiotensin converting enzymes, which converts it to angiotensin 2, which has dramatic effects throughout the body like vasoconstriction, fluid retention, secretion of aldosterone(potent fluid retaining hormone), and increase sympathetic activity all with the goal of increasing BP to perfuse tissue
What is the cycle ignited by HF?
- Ventricular dysfunction –> dec cardiac output –> compensations(inc SNS, inc RAAS, inc arginine vasopressin) -> excessive vasoconstriction and inc Na/water retention -> increased afterload and excessive preload
What are the factors that the release of hormones in heart failure throw out of balance?
- NO
- BNP
- tANP
(all vasodilators)
What are the factors that influence cardiac output?
- Contractility
- Preload
- Afterload
- Stroke volume
- Heart rate
- Synergistic LV contraction, LV wall integrity, and valvular competence
Which of the types of heart failure is harder to treat?
Diastolic HF
What is the equation for Ejection Fraction?
EDV(end diastolic volume)-ESV(end systolic volume)/EDV
What is ejection fraction?
The total amount of blood we pump out after each heart beat to respect to how much blood was present in the heart previously. Poor relationship to VO2, so it has no relationship to tolerance of exercise
What is the normal value of ejection fraction?
55-75%
How does heart failure impact ejection fraction?
A reduction, we get pretty concerned if it drops below 50%
What is the NYHA classification?
A system used to classify the severity of HF
What is a class I on the NYHA classification?
No limitation of physical activity. Ordinary physical activity does not cause undue
fatigue, palpitation, dyspnea (shortness of breath)
What is a class II on the NYHA classification?
Slight limitation of physical activity. Comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea (shortness of breath).
What is a class III on the NYHA classification?
Marked limitation of physical activity. Comfortable at rest. Less than ordinary activity causes fatigue, palpitation, or dyspnea. Symptomatic with ADLs
What is a class IV on the NYHA classification?
Unable to carry on any physical activity without discomfort. Symptoms of heart
failure at rest. If any physical activity is undertaken, discomfort increases.
What is stage A in the ACC/AHA Guidelines for heart failure?
Patient at high risk for developing HF with no structural disorder of the heart
What is stage B in the ACC/AHA Guidelines for heart failure?
Patient with structural disorder without symptoms of HF
What is stage C in the ACC/AHA Guidelines for heart failure?
Patient with past or current symptoms of HF associated with underlying structural heart disease
What is stage D in the ACC/AHA Guidelines for heart failure?
Patient with end‐stage disease who requires specialized treatment strategies
What is the amount of METs that patients in the class I on the NYHA classification can tolerate?
At least 7 METs
What is the amount of METs that patients in the class II on the NYHA classification can tolerate?
5- 7 METS
What is the amount of METs that patients in the class III on the NYHA classification can tolerate?
Less than 5
What is the amount of METs that patients in the class IV on the NYHA classification can tolerate?
1 MET
What is the ejection fraction and description for patients that fall under the classification of I. Heart Failure with Reduced Ejection Fraction (HFrEF) on the Ejection Fraction Classification?
- Ejection Fraction: ≤40%
- Description: Also referred to as systolic HF. Randomized clinical trials have mainly enrolled patients with HFrEF and it is only in these patients
that efficacious therapies have been demonstrated to date
What is the ejection fraction and description for patients that fall under the classification of II. Heart Failure with Preserved Ejection Fraction (HFpEF) on the Ejection Fraction Classification?
- Ejection fraction: ≥50%
- Description: Also referred to as diastolic HF. Several different criteria have been
used to further define HFpEF. The diagnosis of HFpEF is
challenging because it is largely one of excluding other potential noncardiac causes of symptoms suggestive of HF. To date, efficacious therapies have not been identified.
What is the ejection fraction and description for patients that fall under the classification of HFpEF, Borderline on the Ejection Fraction Classification?
- Ejection fraction: 41% to 49%
- Description: These patients fall into a borderline or intermediate group. Their
characteristics, treatment patterns, and outcomes appear similar to those of patient with HFpEF.
What is the ejection fraction and description for patients that fall under the classification of HFpEF, Improved on the Ejection Fraction Classification?
- Ejection fraction: >40%
- Description: It has been recognized that a subset of patients with HFpEF previously had HFrEF. These patients with improvement or recovery in EF may be clinically distinct from those with persistently preserved or reduced EF. Further research is needed to better characterize these patients.
What are the types of medical exams for heart failure?
• CXR (chest x‐ray) - Fluid; cardiomegaly • EKG (electrocardiogram) - Wide QRS has higher mortality, dysrhythmias - Cardiac Resynchronization Therapy* • Echocardiogram - EF, chambers and valves, wall motion • Assess coronary arteries (underlying ischemia) - Cardiac cath - MRI - PET scan • Determine etiology • Interview (symptoms) • Physical exam (signs) • General chemistry labs: • BNP (B‐type natriuretic peptide)
What are the general chemistry labs for the medical examination of heart failure?
CBC, electrolytes (glucose, Mg, Na, K, Ca, BUN/Cr), thyroid panel, liver function tests (LFTs), lipid panel, cardiac enzymes, toxicology, coagulation studies
What are the characteristics of acute heart failure?
Immediately life threatening, in acute pulmonary edema and acute ischemia, medical emergency. End sequela of an MI
What are the characteristics of chronic heart failure?
Can exist in compensated failure for many years, cardiac dilation, poor pump quality, chronic peripheral edema and congestion
What is the time associated with acute HF?
- Instant, sudden
* Hr to days
What is the causal disease of acute HF?
- Acute MI
- Pulmonary Embolism
- Severe malignant HTN
What are the effects of acute HF?
- No time to compensate
- Acute Pulmonary edema
- Acute Ischemia
What is the time associated with chronic HF?
- Progressive
* Wks to months
What is the causal disease of chronic HF?
- Chronic HTN, valve dis
- Myocardial fibrosis
- Chronic lung disease
What are the effects of chronic HF?
- Full compensation
* Chronic edema, congestion
What kind of issue is Heart Failure with Reduced Ejection Fraction (HFrEF)?
Systolic issue
What kind of issue is Heart Failure with Preserved Ejection
Fraction (HFpEF)?
Diastolic issue
What kind of symptoms do we see L HF and why?
We see alot pf pulmonary symptoms, because the L ventricle pumps into the periphery, but it receives blood from the pulmonary veins, which come from the lungs, hence when there is a problem with the L ventricle, the blood is going to back up into the lungs and we get:
- Elevated respiratory rate
- Dyspnea
- Orthopnea
- Profound muscle weakness (skeletal muscle changes)
- Pulmonary edema
What kind of symptoms do we see R HF and why?
Pretty concerned about edema. The R heart receives blood from the vena cava and pumps into the R artery. If we can’t pump blood through the pulmonary and to the lungs, it is going to back flow into the periphery, the vena cava, the jugular vein, and then to the tissues, leading to:
- Bilateral swelling of the feet
- Ascites (swelling of the abdomen)
- Jaundice
- Weight gain
- Jugular vein distention
L ventricular failure can cause ____ and vice versa. Why?
L ventricular failure can cause R HF and vice versa. Because if we can’t pump blood out of the L side, we back flow into the lungs and the pulmonary vasculature which has elevated volumes and pressures that is going to load the R ventricle and we may eventually get R ventricular failure
What are the most relevant medical exams for heart failure?
• Echocardiogram - EF, chambers and valves, wall motion • Interview (symptoms) • Physical exam (signs) • BNP (B‐type natriuretic peptide) Most IMP
What are the physical exam signs we may see in patients with HF?
- S3 gallop, especially with systolic dysfunction
- S4 gallop with diastolic dysfunction
- Edema
- Persistent bilateral rales
What are the normal ranges for BNP (B‐type natriuretic peptide)?
0-100
What does a BNP of 100 mean?
HF may potentially be present
What does a BNP of over 300 mean?
Most definitely have HF
When do we have issues with patients that have chronic HF?
When they go into decomposition and balance is shifted
How can patients with chronic HF go to a state of acute HF?
- Sudden deterioration
- Natural or treatment failure
How can patients with acute HF go to a state of chronic HF?
Incomplete or partial recovery
What are the signs of retaining fluid in HF?
> 3lb weight gain overnight, >5lb weight gain over 1 week
What are the effects of after load on HF?
They will be unable to tolerate more load on the heart. Which is why vasodilator therapy for decreasing peripheral resistance though a bit counterintuitive is effective for patients with HF
What is the muscle hypothesis?
If we have HF, we go to a skeletal muscle hypo-perfusion state, which leads to skeletal muscle abnormalities, which then leads to ventilatory inefficiency.
-LV dysfunction leads to reduced peripheral blood flow, potentially leading to endothelial dysfunction, then deconditioning which leads to more issues
What are the effects of chronic HF on the O2 transport pathway?
- Locomotor inefficiency due to reduced blood flow
- Back flow at the lungs may be impaired
- Impaired gas exchange
- Respiratory muscles have to work a lot harder which leads to dramatic increase of blood flow to the diaphragm, which in a sense steals blood to other muscles
What are exercise test to do for someone with HF?
• Cardiopulmonary stress test (gold standard)
- Assess VO2
• Six Minute Walk Test (6MWT)
- Alternative to CPXT to assess functional capacity
- Used extensively in HF studies 1
- Predicts morbidity and mortality in patients with HF (6MWD <300 m)
- Does not assess VO2
What are the implications of an abnormal hemodynamic response to exercise in patients with HF?
• Associated pulmonary disorders impair breathing
• Reduced gas diffusion in the lungs
• Increased work of breathing
• Contribute to dyspnea and fatigue
• Exaggerated redistribution of blood flow away from the periphery and to the respiratory muscles during Exercise
- May contribute to the enhance perception of
fatigue in HF patients
What are the medical management options for HF?
- Exercise
- Pharmacologic
- Surgical
What are the special exercise considerations for heart
failure?
• Avoid exercise after eating and vasodilator medications
• Use VO2max rather that HRmax
• Initial exercise intensity should be 10 beats below significant symptoms
• Signs of cardiac decompensation
- Pulse Narrowing, Arrhythmia, Fluid Changes 3lbs in 24hrs, 5lbs in a week
• Goal writing:
- Increased intensity/duration
- Functional activities and independence
What is the gold standard exercise intervention for patients with HF?
Aerobic Training (AT)
What are the parameters for Aerobic Training (AT) for patients with HF?
• Most often performed at “Moderate Intensities” (60-70% VO2Max).
• Most studies have used walking (treadmill/over-ground), or a recumbent bike/stepper
(NuStep)
- Easier for monitoring and allows for an objective method for progression
What are the improvements observed in patients with HF that do Aerobic Training (AT)?
VO2max, 6MWD, MLHFQ, LVEF, capillary density and peripheral artery diameter
What are the parameters for Resistance Training (RT) for patients with HF?
• Most often prescribed in the form of a PRE (progressive resistance exercise)
- 60-80% 1RM.
- Machines, free weights, body weight
- Most protocols emphasized lower extremity muscles.
What are the improvements observed in patients with HF that do Resistance Training (RT)?
“Muscle Hypothesis” Attenuated the loss of muscle mass, improved functional
mobility and ADLS, 6MWD and QoL (SF-36).
What are the effects of Aerobic Training (AT) and Resistance Training (RT) in patients with HF?
• Combined training improves muscle strength, body composition, aerobic capacity,
quality of life and vascular function in patients with severe heart failure when
• Greater effects than compared to just AT or RT alone.
What is the basic format for a HIIT program done for patients with HF?
- 10-min warm-up at 40–50 % of peak VO2 (& 60–70 % of peak heart rate)
- 3-min interval at 80–90 % of peak VO2 (& 85–95 % of peak heart rate)
- 3-min active recovery at & 40–50 % of peak VO2 (& 60–70 % of peak heart rate)
- Repeat intervals 4–6 times
- 5 min cool-down at 30–40 % of peak VO2 (50–60 % of peak heart rate)
What are the improvements seen in patients with HF when they do HIIT?
- 6MWD, VO2max, LV remodeling, BNP and SF-36.
* Often resulted in significantly better improvements when compared to AT.
What are the limitations seen in patients with HF when they do HIIT?
- May not be tolerated by all patients even if appropriate.
- Requires close and skilled supervision.
- As on 2013 out of all studies published only 100 subjects total.
- Some patients may benefit from beginning with conventional therapies before initiating HIIT.
What are the contraindications of HIIT in patients with HF?
Severely deconditioned patients or those susceptible to arrhythmias.
What is the parameters for HIIT in a patient with HF based on?
Their relative peak VO2
What is Inspiratory Muscle Training?
A tool we use often to in patients with HF to increase the efficiency of respiratory muscles in order to spare the blood flow that would normally go to the lungs during exercise and shift it to the muscles
What does Noninvasive positive-pressure ventilation (NPPV) do for patients with HF?
Provides patients with a higher fraction of inspired oxygen and increases interthoracic pressure; which decreases
dyspnea, and improves cardiac function.
What are the improvements seen in patients with HF using Noninvasive positive-pressure ventilation (NPPV)?
LVEF, FVC, FEV1, Plasma NorEp, 6MWD.
• Beneficial effects have been elicited with both nocturnal and acute delivery
What are the effects of NMES for patients with HF?
NMES can be used to help the muscles remain/become more active, attenuate some of the atrophy resulting from inactivity and provide low level strengthening.
What is the basic protocol for NMES in patients with HF?
10-25Hz, biphasic, variable “on and off” times totaling 20min-60min, 5- 7days/week.
• Targeted Muscles: Quadriceps, Soleus and Gluteals.
What are the improvements seen in patients with HF using NMES?
• 6MWD, BNP, QoL (KCCMQ, MLHFQ), Flow-Mediated Dilation
Safety
• No adverse reactions have been demonstrated thus far, even in patients with cardiac pacemakers.
What are the pharmacotherapy methods used in patients with HF?
• Angiotensin-converting enzyme inhibitors OR Angiotensin antagonists
- Vasodilate, dec Remodeling
• Beta Blockers *
- Dec HR, remodeling (block SNS), anti-arrhythmic
• Diuretic
- Dec Fluid volume, relieves dyspnea
• Aldosterone
- Dec Fibrosis, Na retention, Antagonists remodeling, aldosterone release
• Digoxin or Dobutamine or PD3
- Positive inotrope
What are the surgical management options of HF?
- Ventricular Assist Device (VAD)
* Heart Transplantation
What are the characteristics of Ventricular Assist Device (VAD) as a management option of HF?
- Limited organ availability
- Short term solution*
- Ability to sense preload
- Need Doppler to take pressure, may not have a true HR either (use RPE)
- Progressive exercise training is indicated
What are the characteristics of Heart Transplantation as a management option of HF?
- Native SA Node
- No longer innervated
- Different mechanisms for CO regulation during exercise
What are the characteristics of Imunosuppressive agents after transplant for HF?
- Prevent rejection
- Cyclosporine or Tacrolimus
- Prednisone
- Side effects: HTN, osteoporosis, muscle weakness, liver damage
What are the symptoms of an abnormal MI in women, elderly and diabetics?
- May not report chest pain (angina)
- SOB, Nausea, Emesis/Vomitting, Jaw Pain
- Altered Mental Status
What are the clinical findings of an acute myocardial infarction?
- Chest pain radiates to both arms
- Third heart sound on auscultation
- Hypotension
What are the clinical findings of chest wall pain?
At least 2 of the following:
- Localized muscle tension
- Stinging pain
- Pain reproducible by palpation
- Absence of cough
What are the clinical findings of gastroesophageal reflux disease?
- Burning retrosternal pain
- Acid regurgitation
- Sour or bitter taste in the mouth
- One week trial of high doe proton pump inhibitor relieves symptoms
What are the clinical findings of a panic disorder/anxiety state?
Single question: In the past 4 weeks, have you had an anxiety attack (suddenly feeling fear or panic)?
What are the clinical findings of pericarditis?
- Clinical triad of pleuritic chest pain (increases with inspiration or when reclining, and is lessened by leaning forward)
- Pericardial friction rub and electrocardiographic changes (diffuse ST segment elevation and PR interval depression without T wave inversion)
What are the clinical findings of pneumonia?
- Egophony
- Dullness to percussion
- Fever
- Clinical impression
What are the clinical findings of heart failure?
- Pulmonary edema on chest radiography
- Clinical impression/judgement
- History of heart failure
- History of acute myocardial infarction
What are the clinical findings of a pulmonary embolism?
- High pretest probability based on Wells criteria
- Moderate pretest probability based on Wells criteria
- Low pretest probability based on Wells criteria
What are the clinical findings of an acute thoracic aortic dissection?
Acute chest or back pain and a pulse differential in the upper extremities
What are some screening recommendations for all patients?
• At least take resting vitals on each patient • >140/90 proceed with usual care - Contact PCP - Monitor closely • >160/100mmHg Hold resistance exercise, consider aerobic exercise - Contact PCP - Monitor closely • >180/110mmHg; Hold Exam - Examine for organ damage - Contact PCP - Consider contacting EMS
What does Marfan’s syndrome result from?
A gene mutation overproduction of transforming growth factor beta (TGF-β)
What are the cardiovascular disorders found in those with Marfan’s syndrome?
• Aortic tear or rupture - Most often in ascending/thoracic aorta • Mitral valve prolapse • Aortic regurgitation • Arrhythmias (atrial & ventricular)
What are the interventions for Marfan’s syndrome?
- Close monitoring
- Medications for arrhythmias
- Surgery to correct defects
- Activity modification
What are the presentations of an abdominal aortic aneurysm?
• Dull, tearing ache/pain in low back, groin or mid abdominal left flank
- Pain may be sharper with greater dilations
• Chest Pain
• Weakness or transient paralysis of legs
• Width greater than 2 fingers widths
- >5cm concern for dissection, emergent case
• Palpable, pulsating (heart beat) abdominal mass
• Inter-arm systolic blood pressure difference >20 mm Hg was an
independent predictor of AAD, with a positive predictive value of 98%
• Absent or decreased peripheral pulses aka Pulse Deficit
• Tachycardia
What are the normal physical exam findings in athletes?
• Reversible!!!! Left Ventricular Hypertrophy - LV wall thickness (LVWT) and LV cavity size, permits enhanced filling. - Increased CO maintained at high HR • Bradycardia • Increased VO2max - >50ml/min/kg • Sinus Arrhythmia • Transient Split S2 - Changes with inspiration and expiration - Less common in adults
What are the symptoms of post exercise syncope in an athlete?
Exhaustion, Exercise-induced hyponatremia, heat illness, rapid reduction in preload and functional sympatholysis with elevated contractility and HR
What are the symptoms of syncope during exercise in an athlete?
More concerning; linked to HCOM, arrhythmogenic right ventricular cardiomyopathy
What are the screening recommendations of syncope in an athlete?
• Until diagnosis or pathologic causes excluded,
exercise is generally restricted.
• R/O post vs during; ask bystanders
• Screen for defects (Marfan’s, HCOM etc)
What are the presentations of hypertrophic cardiomyopathy?
• Strong genetic link to HCOM
- (55% of cases with familial relative)
- More common in Black/African Americans
• Ejection murmur changes with position
- Softens during sitting/squatting
- Amplifies during standing/Valsalva
• Persistent Split S2
- No change with breath holds
• S4 Gallop possible too
• Syncope or Dyspnea during exercise
• Persistent hypertrophy despite detraining
What are the screening recommendations for hypertrophic cardiomyopathy?
• Indicated for any athlete 12-25
• Yes to any of the 14 question warrants further examination
before participation in sports.
What are the 14 questions that are asked and could warrant further examination before participation in sports?
Personal history
1. Chest pain/discomfort/tightness/pressure related to exertion
2. Unexplained syncope or near syncope
3. Excessive and unexplained dyspnea/ fatigue or palpitations, associated with exercise
4. Prior recognition of a heart murmur
5. Elevated systemic blood pressure
6. Prior restriction from participation in sports
7. Prior testing for the heart, ordered by a physician
Family history
8. Premature death (sudden and unexpected or otherwise) before 50y of age attributable to heart disease in >/=1 relative
9. Disability from heart disease in close relative <50 yr of age
10. Hypertrophic or dilated cardiomyopathy, long QT syndrome, or other ion channelopathies, marfan syndrome, or clinically significant arrhythmias; specific knowledge of genetic cardiac conditions in family members
Physical examination
11. Heart murmur
12. Femoral pulses to exclude aortic coarctation
13. Physical stigmata of marfan syndrome
14. Brachial artery blood pressure (sitting position)
What are the symptoms of peripheral arterial disease?
- Bilateral calf pain
- Impaired distal pulses
- Delayed capillary refill in BLE
- Loss of hair on toes
- Dry, scaly skin
- Thickened toe nails
- Intermittent claudication
What are the characteristics of peripheral/chronic arterial disease?
• Older, smoker, sedentary
• Intermittent claudication most common symptom but many patients are
asymptomatic or have atypical symptoms
- Predictable time and intensity, reproducible, doesn’t change with posture,
- Walking test
• Pallor on Elevation
- Insufficient arterial pressure to perfuse when leg elevated above level of heart.
- Limb drains of blood.
• Dependent Rubor
- Blood pooling in maximally dilated capillary bed
What are some clinical pearls to keep in mind when doing differential diagnosis for cardiovascular conditions?
• Pain due to vascular causes increases with workload
• Neurogenic pain not affected by workload but by posture
• Edema typical with venous or lymph pathology not usuallu arterial
• Pain: ask about TYPE and LOCATION
• Intermittent claudication:
- Cramping type pain, due to ischemia, better with rest- not typically “burning”
- Usually in calves, although can be thigh or buttock
- Pain correlates with area of obstruction: hip and buttock= aorto-iliac occlusion, thigh
pain= iliofemoral occlusion, prox 2/3 calf- superficial femoral artery, distal 1/3calf=
popliteal artery, foot= tibial artery
• Pain increases with elevation and decreases with dependence arterial disease
What are the initial recommendations for treatment of heart disease?
Lifestyle Modifications • Following a healthy diet • Being physically active • Maintaining a healthy weight • Quitting smoking • Moderating alcohol consumption • Managing stress
What are medications used for in patients with heart disease?
- Lower LDL cholesterol
- Lower blood pressure
- Lower blood sugar level
- Prevent blood clots and/or inflammation
What is steady state?
The situation during chronic drug administration when the amount of drug administered per unit time equals drug eliminated per unit time.
What are the temporal characteristics of drug effect?
• A lag period is present before the plasma drug concentration (Cp) exceeds the minimum effective concentration (MEC) for the desired effect.
• Following onset of the response, the intensity of the effect increases as the drug
continues to be absorbed and distributed.
• This reaches a peak, after which drug elimination results in a decline in Cp and in the effect’s intensity.
• Effect disappears when the drug concentration falls below the MEC
What are the functions of agonist?
- Binds specifically
* Activates cell function
What are the functions of antagonist?
- Binds specifically
- Blocks agonist
- Does not influence cell function
When do patients get the most dramatic side effects with their meds?
At the beginning
Why can’t nitroglycerin be used orally?
It is completely extracted prior to reaching the systemic circulation.
• Thus it is usually administered via sublingual or transdermal routes, which bypass presystemic metabolism.
What is a non-competitive antagonist?
A drug that binds to an allosteric (non-agonist) site on
the receptor to prevent activation of the receptor
• Doesn’t compete for same site, but still prevents activation
What is a competitive antagonist?
A drug that binds to the same site as the agonist but does
not activate it, thus blocks the
agonist’s action.
• Competes for same site, but still prevents activation
What are the medications used for stage 1 HTN when indicated?
Thiazide- type diuretics when indicated
What are the medications used for stage 2 HTN when indicated?
2 drug combination: usually a diuretic and ACEI, or ARB or BB or CCB
What is the goal of diuretics?
To reduce blood pressure by reducing blood volume via kidneys
What are the types of diuretics?
- Loop
- Thiazide
- Aldosterone receptor antagonists
What is the most common type of loop diuretic?
Furosemide (Lasix), drug of choice for HF and patients with CAD w/CKD
What are the side effects of loop diuretics?
Hypokalemia, Hyponatremia, volume depletion, frequent voiding
What are the effects of loop diuretics?
Block the Na+/K+/2Cl resorption in the loop of Henle, high ceiling
What are the effects of thiazide diuretics?
Block Na+ reabsorption in the distal tubule of nephron
What is the most common type of Thiazide diuretic?
Hydrochlorothiazide “HCTZ”, (Esidrix), 1st drug of choice for essential HTN
What are the side effects of Thiazide diuretics?
Hypokalemia, Hyponatremia, volume depletion, frequent voiding
What are the effects of aldosterone receptor antagonists diuretics?
Blocks Aldosterone and thus Interferes with Na-K+ exchange at distal tubule ”aka Potassium Sparing Diuretic)
What is the most common type of aldosterone receptor antagonists diuretic?
Sprirolactone (Aldactone)
What are the side effects of aldosterone receptor antagonists diuretics?
Volume depletion, frequent voiding
What are the effects of sympatholytics: Beta Blockers –”olol”?
- Primarily target Beta-1 receptor cites, effects
- Reduces HR
- Reduces BP primarily by reducing contractility
- Reduces sympathetic tone
- Also has antiarrhythmic properties
- In low doses actually functions as an anti-anxiety medication
- Limits adverse ventricular remodeling (dilation) after MI
What is included in the specific categories of beta blockers?
Metroprolol (Lopressor), Atenolol
What is included in the non- specific categories of beta blockers?
Carvedilol, Propanolol
What are the cautions to take with beta blockers?
• Cautious use with patients with kidney or renal dysfunction
• Cautious with patients with pulmonary dysfunction or asthma
- Especially in non-selective beta blockers
- May block Beta-2 receptors and cause bronchoconstriction
• Suppresses sympathetic response to hypoglycemia in diabetics
- May not get tachycardia and shaky, may instead get sweaty and pale
What are the effects of sympatholytics: Alpha 1-Blockers “-zosin”?
- Block Alpha-1 receptors on vascular smooth muscle, thus reduce TPR and BP
- Often prescribed along with other medications
- Has been shown to be effective in treating Benign Prostate Hypertrophy
What is the most common types of Alpha 1-Blockers “-zosin”?
Doxazosin (Cardura), Prazosin (Minipress)
What are the effects of sympatholytics: Alpha 2-Agonists?
- Reduces vascular tone by central mediated methods by stimulating Alpha 2 receptors.
- Suppresses sympathetic outflow to vasomotor centers from the brainstem
- Not as commonly used
What is the most common types of Alpha 2-Agonists?
Clonidine (Catapres)
What are the effects of Angiotensin Converting Enzyme (ACE) Inhibitors “-pril”?
• Blocks the conversion of Ang 1 to Ang 2
- Lowers BP
- Few adverse side effects other than orthostasis
• Decreases afterload and improves survival in patients with HF
• Increases survival and prevents L ventricle dilatation post MI
What is the most common types of Angiotensin Converting Enzyme (ACE) Inhibitors “-pril”?
Lisinopril (Zestril), Captopril (Capoten) and Enalapril (Vasotec)
What are the effects of Angiotensin 2 Receptor Blockers (ARBs) “-sartan”?
• Blocks the conversion of Ang 1 to Ang 2
- Lowers BP
- Few adverse side effects other than orthostasis
• Decreases afterload and improves survival in patients with HF
• Increases survival and prevents L ventricle dilatation post MI
When is Angiotensin 2 Receptor Blockers (ARBs) “-sartan” used?
When patients don’t tolerate ACEI side effects “coughing”
• Also used to treat patients with Obstructive Sleep Apnea
What is the most common types of Angiotensin 2 Receptor Blockers (ARBs) “-sartan”?
Losartan (Cozar), Valsartan (Diovan)
What are the effects of Calcium Channel Blockers?
- Selectively block Ca2+ entry into vascular smooth muscle cells.
- Management of hypertension
- Management of angina
- Management ofvasospasm
- Reduce cardiac contractile force
- Used to treat supraventricular arrthymmias
What is the most common type of Calcium Channel Blockers?
Most common “-dipine)
• Amlodipine(Norvasc), Diltiazem (Cardizem), Verapamil (Calan)
What are the effects of other hypertensive meds: Hydralazine?
• A direct-acting smooth muscle relaxant used to treat hypertension by acting as a
vasodilator primarily in arteries and arterioles.
• Reduces BP by reducing TPR
What are the side effects of other hypertensive meds: Hydralazine?
May increase Na+ retention and thus fluid retention, often used in conjunction with a diuretic
What are the HTN Medication Considerations?
- Alpha blockers, calcium channel blockers or vasodilating drugs may lead to sudden excessive hypotension post exercise (also more common in elderly people)
- Avoid suddenly stopping exercise and undertake an extended cool down period of light activity.
- Beta blockers and diuretics may impair thermoregulation
What are the effects of HMG-CoA reductase inhibitors (Statin)?
Blocks LDL synthesis, Increases HDL, some antiinflammatory properties “-statin”
What are the side effects of HMG-CoA reductase inhibitors (Statin)?
Renal and liver damage, skeletal muscle myopathy
What are the common types of HMG-CoA reductase inhibitors (Statin)?
Lovastatin (Mevacor), Simvastatin (Zocor), Atorvastatin (Lipitor), Rosuvastatin (Crestor)
What type of medicine is HMG-CoA reductase inhibitors (Statin)?
Hyperlipidemia
What are the groups most likely to benefit from statin therapy?
- Patients with any form of clinical ASCVD
- Patients with primary LDL-C levels of 190 mg per dL or greater
- Patients with diabetes mellitus, 40 to 75 years of age, with LDL-C levels of 70 to 189 mg per dL
- Patients without diabetes, 40 to 75 years of age, with an estimated 10-year ASCVD risk ≥ 7.5%
What are the adverse symptoms of Statins?
• Rhabdomyolysis associated with statin treatment is very rare (<0.1%)
- Classic triad is muscle pain, weakness, and dark urine
- More prominent in proximal muscle groups, such as the thighs and shoulders
- Other less common symptoms: Limb swelling, cramps and stiffness
• Myagliga and weakness are more frequent adverse symptoms
What are the characteristics of anti- coagulants: Unfractionated Heparin (check aPTT)?
- Blocks clotting factors in blood, traditionally IV med, time to effect 24Hrs
- Used to post operatively to prevent clots, DVT
What are the characteristics of anti- coagulants: Low-Molecular weight heparin (LMWH)?
- Blocks clotting factors in blood, traditionally IV med, time to effect 24Hrs, faster effect time (3-5hrs),
- Used in patients with better kidneys
- Often given as SC injections Enoxoparin (Lovenox)
What are the characteristics of anti- coagulants: Coumadin (Warfarin) (check INR)?
- Blocks effect of Vitamin K-epoxide reductase
* Used for long term anticoagulation (Afib, Afib, Chronic DVT)
What are the characteristics of anti-platelets: Aspirin?
- COX1 and COX2 inhibitor, prevents platelet aggregation
- Often used in low doses, chronically
- Given in larger doses during MI
What are the characteristics of anti-platelets: Clopidogrel (Plavix)?
ADP inhibitor, prevents platelet aggregation
What are the characteristics of Thrombolytic: Tissue Plasminogen Activators (TPA)-clot busters “-kinase)?
- Facilitate breakdown of clots that have already formed by converting plasminogen to plasmin
- Used in Acute MI, if used within 1hr of symptoms reduces mortality by 50%
- Most common: Streptokinase (Streptase), UroKinase (Abbokinase)
What are the effects of Anti-arrhythmic: Class 1-Na+ Channel Blockers: Lidocane, Flecanide?
Used to treat Vtach, Vfib
What are the effects of Anti-arrhythmic: Class 2-Beta Blockers: (Propanolol)?
Used to treat atrial arrhythmias (Afib) and SVT
What are the effects of Anti-arrhythmic: Class 3-K+ Channel Blockers : Sotalol, Amiodarone?
- Slows repolarization phase, used in acute coronary syndromes
- SVT, Vtach, Vfib
What are the effects of Anti-arrhythmic: Class 4-Ca2+ Blockers (Verapamil, Diltiazem)?
Used to treat SVT
What are the effects of Anti-arrhythmic: Adenosine?
Used to treat SVT, Atropine used for Bradycardia
What are the characteristics of Anti-anginals used to treat Acute Coronary Syndrome and what are their effects?
- Sublingual Nitroglycerin (NTG)
- Rapid acting vasodilator, takes 2min (veins>arteries)
- Reduces preload and afterload, reduces angina
- Taken under tongue, every 5minutes, 3max, have patient sit when taking.
What are the characteristics of aspirin used to treat Acute Coronary Syndrome and what are their effects?
Prevent platelet aggregation and some pain relief
What are the characteristics of Morphine (IV) used to treat Acute Coronary Syndrome and what are their effects?
Acts as a vasodilator, and helps reduces pain and anxiety
What are the characteristics of Beta-Blockers (IV) used to treat Acute Coronary Syndrome and what are their effects?
Given to reduce mVO2 and to prevent deadly arrhythmias
What are the characteristics of Supplemental 02 used to treat Acute Coronary Syndrome and what are their effects?
Improve coronary 02 sat, Prevent respiratory failure
What are the characteristics of Anticoagulation (Heparin/LMWH) used to treat Acute Coronary Syndrome and what are their effects?
Given if patient is to get PCI
What are the characteristics of ACE Inhibitors used to treat Acute Coronary Syndrome and what are their effects?
Used post MI, prevents long term mortality and remodeling
What are the characteristics of Statin Therapy used to treat Acute Coronary Syndrome and what are their effects?
Used post MI, risk reduction
What are the goals of treatment for the used of meds when treating HF?
- Decrease preload (Diuretic)-Lasix or Spironlactone
- Decrease afterload (Ace-Inhibitor)-Lisinopril
- Control sympathetic stimulation (Beta Blocker)-Carvedilol or Metoprolol
Ca2+ blockers not used due to adverse effects in patients with HF
What are the effects of Angiotensin-converting enzyme inhibitors OR Angiotensin antagonists?
Vasodilate, dec Remodeling
What are the effects of Beta Blockers?
Dec HR, remodeling (block SNS), anti-arrhythmic
What are the effects of Diuretics?
Dec Fluid volume, relieves dyspnea
What are the effects of Aldosterone?
Dec Fibrosis, Na retention, Antagonists remodeling, aldosterone release
What are the effects of Digoxin or Dobutamine or PD3?
Positive inotrope
What are the characteristics of Positive Inotropes used for Decompensated HF?
Usually administered via IV
• Dobutamine (sympathomimetic, stimulates B1 receptors in heart)
• IV dopamine (B1 adrenergic; precursor of NorEpH)
• PDE Inhibitors (Milrinione) and Amrinone (inocor) IV or infusion
What are the characteristics of Afterload reducers used for Decompensated HF?
Usually administered via IV
• (Hydralazine)-Arterial: Afterload reduction, to improve LV output
• (Long acting nitrates)-Venous: – reduces filling pressures and preload
• (Isosorbide dinitrate)-Non-selective – treats both elevated filling pressures and low LV output
What is used to maintain MAP in Decompensated HF?
IV Norepinephrine and Epinephrine
What are the characteristics of Digitals (Digoxin) used for Cardiac Glycoside?
• Comes from the foxglove plant
• Effects
- Positive Inotrope w/o increasing mVO2
- Anti-arrhythmic (HF w/ Afib)
- Controls sympathetic tone
• However can also cause arrhythmias and prolong QT interval.
• Beginning to be phased out
What is used to find ejection fraction?
Echocardiogram
Where is the best place to hear an S3 gallop?
Apex of the heart. 5th intercostal space, mid clavicular line on the L
What is the best way to monitor a patient with HF’s exercise response if the patient is using a beta blocker?
RPE, if they are not using a beta blocker then do HR and RPE
What are the Warning S/S of Limited 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 an increase in workload- STOP
- Low anginal threshold
- Excessive dyspnea
- Slow HR recovery from activity
When do you hold exercise for patients when looking at their blood glucose?
When blood glucose levels are higher than 250
What is the most common cause of heart failure in the United States?
Ischemic Heart Disease
Do patients with an LVAD have a pulse?
NO, especially those with a continuous flow type. So use mean arterial pressure to find BP
What best applies to a patient’s
pharmacologic management s/p LVAD implantation?
Cardiac medications are necessary to help augment native cardiac pump function and prevent mechanical pump dysfunction
What signs or symptoms is essential to monitor to
help determine the adequacy of mechanical pump function
Dizziness, because this is a sign that perfusion is low
What clinical exam procedure can be used to distinguish between an aortic stenosis ejection murmur and hypertrophic cardiomyopathy ejection murmur?
- Auscultation during squatting vs standing
- Auscultation during Valsalva (decrease
What must you consider when monitoring the response to exercise for a patient with aortic stenosis?
Their blood pressure might not increase much during exercise
