Cardiac Flashcards
Cardiac output =
HR (beat/min) x Stroke volume (ml/beat) = cardiac output (ml/min)
Mediastinum
Space between lungs where heart lives
Cardiac cycle 5 steps
- Isovolumetric contraction: Ventricles are starting to contract and pressure is building. Tricuspid and mitral valves close (S1).
- Ventricular ejection: Pulmonic and aortic valves open: Blood is pushed out of the ventricles
- Isovolumetric relaxation: Pulmonic and aortic valves close (S2)
- Ventricular filling
- Atrial contraction “kick”
5 factors affecting cardiac rate
Sympathetic system
Parasympathetic system
Baroreceptors in carotids and aortic arch
Chemoreceptors
Electrolytes
Sympathetic effects on cardiac rate
Sympathetic system stimulates:
○ SA node and blood vessels to cause increased HR and vasoconstriction
○ Adrenal medulla to release epi and norepi
§ Beta1 receptors in the heart increase HR and contractility
§ Beta2 receptors cause bronchodilation and mild vasodilation in heart and lungs
§ Alpha receptors cause vasoconstriction in GI system and skin
Parasympathetic effects on cardiac rate
Parasymp system stimulates:
○ Vagal nerve stimulation causes decrease in HR by slowing SA node
§ E.g. valsalva maneuver, carotid sinus massage
Baroreceptors effect on cardiac rate
○ Sensitive to arterial pressure–increase in pressure will decrease HR and vice versa
Effects only temporary, will not mitigate chronic HTN
Chemoreceptors effect on cardiac rate
Respond to increased PaCO2, decreased PaO2 and/or decreased pH to increase cardiac activity
Electrolytes effect on cardiac rate
Affect cardiac muscle contraction
Imbalance of K+, Ca2+, or Mg2+ have strong effects on the heart
Dromotropic
something affecting conduction of the heart: positive/negative
Chronotropic
how fast/slow the heart is going
Inotropic
how strongly does the heart pump
Lusitropic
how well can the heart relax so it can fill
3 components of stroke volume
Preload
Contractility
Afterload
Preload
Volume of blood in ventricles before they contract at the end of diastole
Afterload
The pressure the ventricles are pumping against.
Systemic vascular resistance (SVR): the afterload of the left side of the heart–LV pumps against the pressure in the aorta
Right ventricle is pumping against the pressure in the lungs (PVR)
Ejection fraction
Stroke volume / End diastolic volume
The % of blood that actually gets pumped out with each beat
Defines difference between systolic and diastolic HF
Systolic HF ejection fraction
<40%
Weak ventricles cause heart to not pump well, reducing ejection fraction
Diastolic HF ejection fraction
> 50%
The heart can’t fill well due to stiff ventricle walls. Most of the blood in the ventricle gets pumped out so the ejection fraction is preserved, but it’s not a large amount of blood to begin with
Causes of systolic HF
HTN
CAD, ischemic heart disease
MI
Cardiomyopathy (blanket term for several myocardial diseases)
Valve disorders
Anemia
Causes of diastolic HF
HTN
Aging
Pericardial effusion
Pericarditis
Myocardial hypertrophy
Cardiomyopathy
Diabetes
Obesity
Onset and prone gender of systolic vs diastolic HF
Systolic: <65 males
Diastolic >65 females
Heart sounds systolic vs diastolic HF
Systolic: S3
Diastolic: S4
L sided HF backward effect
Blood starts backing up from the LV into the LA and the pulmonary veins and eventually the lungs become congested, and fluid starts coming out of the pulmonary capillaries.
L sided HF forward effect
Decreased cardiac output causes decreased tissue perfusion, which will activate RAAS in the kidneys
This causes increased BP, fluid retention, and vasoconstriction, which further increases the left ventricular preload and thus the backwards pooling of blood into the atria and pulmonary system. (the forward effect ends up contributing to the backward effect)
L sided HF backward effects CM
- Pulmonary congestion
- Dyspnea on exertion- Orthopnea
- Cough
- Paroxysmal (sudden) nocturnal dyspnea
- Cyanosis
- Basilar crackles
L sided HF forward effects CM
- Decreased perfusion>
- Fatigue- Oliguria
- Increased HR
- Faint pulses
- Restlessness, Confusion, Anxiety (poor perfusion to brain)
Causes of R sided HF
- Most common cause of right sided HF is left sided HF: When there is congestion in the lungs, the right side of the heart has to work harder due to the increased pressure. This can cause hypertrophy, which causes right sided HF.
- Cor pulmonale also can cause right sided HF
- Can be caused by cardiac cause like MI but this is less common
R sided HF backward effects
○ Hepatomegaly
○ Ascites
○ Splenomegaly
○ Anorexia
○ Subcut edema
○ JVD
- Renal congestion
R sided HF forward effects
Same as L sided forward effects
Manifestations and complications of HF
Fluid retention
Respiratory compromise
Renal insufficiency
Decreased GI function
Arrhythmias
Thrombi and emboli
Neuro impairment/fatigue/weakness
Cyanosis
Sudden cardiac death
P wave
Atrial depolarization
QRS complex
Ventricular depolarization
T wave
Ventricular repolarization
EKG vs echocardiogram
EKG finds conduction issues, echocardiogram finds structural issues
Right side heart valves
Tricuspid and pulmonary
Left side valves
Aortic and mitral
Valve issues are caused by
Aging
Calcification
Rheumatic heart disease
Rheumatoid arthritis
SLE (Lupus)
Congenital issues
Systemic inflammation
Chordae injury (the chords that control the valves)
Mitral regurgitation pathogenesis, onset, signs
LV works harder to pump blood to the body as some of it doesn’t go into the aorta
Leads to LA and LV hypertrophy and L sided failure
Slow/abrupt onset
Systolic murmur
Radial pulse may have a pronounced upstroke
Mitral stenosis pathogenesis, onset, signs
Blood will start backing up into the pulmonary vein, causing an increase in pulmonary vascular resistance (PVR)
This leads to RV hypertrophy and R sided heart failure as the RV is pumping against the increasing PVR
R sided HF impacts the SA and AV nodes leading to dysrhythmias like A-fib
The static blood may clot and create emboli
Pulmonary congestion
Fatigue, weakness
Low pitched diastolic murmur with an opening snap
Aortic stenosis pathogenesis, onset, signs
LV has to work harder and hypertrophies
Leads to ischemic angina (pain in the heart from lack of O2 to heart)
Syncope from lack of perfusion
L sided HF
This condition can lead to someone suddenly dying because the valve can suddenly cut off all blood flow, causing zero perfusion to tissues
Systolic murmur
Weak upstroke on radial pulse
Aortic regurgitation pathogenesis, onset, signs
Increases pressure in the LV and makes LV work harder
LV hypertrophy & failure
Dyspnea, pulmonary edema, arrhythmias
Widening pulse pressure (difference b/w systolic and diastolic)
Tachycardia, pounding heart, pulsing carotids, head bob on systole
Diastolic murmur
Fetal heart flow
Oxygenated blood from placenta through inferior vena cava to RA
Deoxygenated blood from body through superior vena cava to RA
From RA most blood goes through open foramen ovale to LA & some of it through tricuspid valve to RV
From RV minimal blood goes through pulmonary arteries to lungs (lots of pressure in lungs d/t them not expanding), most goes through open ductus arteriosus to aorta
Systemic vascular pressure (SVR) is pretty low because it is not a closed system–connected to umbilical arteries
○ At birth when the cord is clamped the SVR goes up dramatically
In a fetus the right side of the heart has a higher pressure than the left
After birth, the pressure on the left side overtakes the pressure on the right, which closes the foramen ovale and ductus arteriosus
Acyanotic vs cyanotic CHD
Acyanotic: Oxygenated blood is getting over to the R side of the heart directly
Cyanotic: Deoxygenated blood is leaving the R side and going over to the L side
Atrial septal defect
The foramen ovale did not close
Initially, L -> R sided shunt causing oxygenated blood to pour into RA - Acyanotic
Leading to more blood in RA and RV, causing the RV to pump harder
RV hypertrophy, pulmonary HTN
Eventually, RV hypertrophy increases RA pressure, causing a R -> L shunt - Cyanotic
Ventricular septal defect
There is a septum between the ventricles that should close off early in fetal development
If it doesn’t, it will cause a L -> R shunt from LV to RV (Acyanotic)
RV is getting too much blood and starts to hypertrophy, and eventually reverses the shunt from R -> L (Cyanotic)
Patent ductus arteriosus
Oxygenated blood spills out of the aorta and back into the pulmonary artery to the right side of the heart
L -> R shunt
Right side has to fight harder to get blood to the lungs against the flow spilling in from the aorta > RV hypertrophy
Once it is hypertrophied enough the flow reverses and the deoxygenated blood is going into the aorta in a R -> L shunt.
Increased cardiac workload can then lead to LV failure
Harsh, grinding systolic murmur
Systolic thrill can be felt
Coarctation of the aorta
Preductal (before ductus arteriosus) (more severe)
○ Blood backs up,
○ more blood to upper body and less to lower body
○ Aortic regurgitation
○ Intracranial hemorrhage
○ Aortic rupture
Postductal (less severe)
○ more blood to upper body and less to lower body
- Ductus arteriosus may open back up
Tetralogy of fallot
Four defects: pulmonary valve stenosis, RV hypertrophy, ventricular septal defect, overriding aorta
Starts as R -> L shunt
The strong RV pumps blood that ricochets off the stenosed pulmonary valve and the septal defect, into the aorta
Severity depends on level of stenosis
Leads to infective endocarditis and polycythemia
Transposition of great vessels
The great vessels switch place so the aorta is connected to the RV and the pulmonary artery to the LV
Leads to deoxygenated blood that never gets oxygenated, and oxygenated blood that never reaches the body
Can be lethal immediately upon birth
If baby is to survive there must be a septal defect that allows the blood to mix until it can be fixed by surgery
Etiology of dilated cardiomyopathy
○ Genetics (most common cause)
○ Alcohol use
○ Pregnancy
○ Post-viral infection in heart
- Reaction to chemo or radiation
Pathogenesis of dilated cardiomyopathy
Ventricles dilate -> increased cardiac workload -> myocardium degenerates and is replaced by fibrous tissue -> contractile failure -> slowly progressive CHF
○ May lead to emboli d/t static blood
CM of dilated cardiomyopathy
Same as CHF
Etiology of hypertrophic cardiomyopathy
○ Most likely genetic
Most common cause of death in young athletes
Hypertrophic cardiomyopathy CM
Sudden death, dyspnea, angina, can be asymptomatic, can lead to CVA, HF, a-fib
“You may go at any time, you may live until your 90”
Restrictive cardiomyopathy etiology
○ Diseases that increase fibrosis
○ Genetics
○ Virus
○ Malnutrition
○ Autoimmune
- Radiation
Restrictive cardiomyopathy CM
Exercise intolerance, dyspnea, paroxysmal noctural dyspnea, orthopnea, weakness, ascites, peripheral edema, hepatomegaly
Pericarditis etiology
○ Infection
○ Immune response
○ Uremia (nitrogen compounds build up in the blood)
○ Cardiac surgery
○ Neoplasm (cancer of the heart)
○ Trauma
Radiation
Pericarditis CM
○ Sharp, abrupt chest pain that radiates to back, neck abdomen or side. Worsens with deep breathing, cough, swallowing, position change. Relieved when sitting up and forward.
Dysphagia, fever, incr WBC, malaise, incr HR, friction rub, anxiety
Pericardial effusion etiology
○ CHF, hypoproteinemia (serous fluid),
○ blunt chest trauma, CPR (serosanguinous fluid),
○ obstructed lymph drainage (chylous fluid),
penetrating trauma to heart (blood)
Cardiac tamponade etiology
○ Effusion
○ Infection
○ Cancer
○ Tension pneumothorax
○ Trauma
MI
Cardiac tamponade CM
○ Reduced stroke volume, increased HR, venous congestion, distended neck veins, pulsus paradoxus, dull chest pain, EKC and chest Xray changes
Gradual, or rapid and deadly
Infective endocarditis pathogenesis
○ Pathogens clump onto surface, get enmeshed in fibrin, form vegetations and block valves, form thrombi and emboli.
Vegetations become fibrosed and calcified, valves can erode
Endocarditis risk factors
Rheumatic heart disease, IV drug use, CHD, prosthetic valves, implanted cardiac defibrillator (ICD), pacemakers, immunosuppressed
Endocarditis acute onset & CM
○ Abrupt onset, serious symptoms, virulent pathogen
○ Fever, chills, murmur, splinter hemorrhages in fingernails
Quickly turns to myocardial abscess, renal disease, emboli
Endocarditis subacute onset & CM
○ Insidious onset, vague symptoms, less virulent
Weight loss, fatigue, “flu”, low grade fever
Rheumatic heart disease etiology
- Group A throat Strep infection -> rheumatic fever -> rheumatic heart disease
Some people react to Strep A by directing antibodies against their own tissues as well as against the strep. Cross reactivity occurs between strep antigens and body tissues.
Rheumatic heart disease phases
- Acute phase: Infection, sore throat, inflammation of CT in heart, blood vessels, joints and subcut tissue.
- Recurrent phase: Heart inflames, carditis, valves swell and erode, platelets and fibrin clump on valve
Chronic phase: Permanent valve deformity (can show up after 10 years from initial infection)
- Recurrent phase: Heart inflames, carditis, valves swell and erode, platelets and fibrin clump on valve
