Cardiovascular Pathologies Flashcards
What is Shock?
Any situation where there is not enough tissue perfusion.
Not adequate oxygen
ischemia—necrosis—-tissue failiure
shock is a progressive process (have stages)
SHOCK will lead to Low BP
Hypovolemic
Cardiogenic
Obstructive
Destributive (septic,Anaphylactic,Neurogenic)
what is Hypovolemic shock?
Losing of blood Volume
1) Blood loss
(GI Bleed due to perforated ulcers, Abdominal Aortic aneurysm, Trauma, Post partum Haemorrhages, Ectopic Pregnancy, Hemoptyisis/coughing blood)
2) Non-Blood fluid loss
(Third drgree Burns, Diarrhoea, Bowel obstruction, acute pancreatitis / protease damage tissue and fluid loss, vomitting, DKA//hyperglycemia, High urine output)
Body Compensation- Carotid bodies–> medulla—>constriction of muscularis layer of blood vessels and increase heart rate and contractility.
Kidney-renin-angiotensinogen-AT1-At2—–Vasoconstriction and aldosterone
release of ADH—increase thirst
Tachycardia seen (as a compensation mechanism)
CBC can show
high Hematocrit-> vody is losing a lot of plasma so RBC count wil be a false high (losing fluid)
low Hematocrit–> Losing RBC and plasma (blood loss)
Cyanosis (Lips tongue and extremities)
Hypoxia and ischemia
Necrosis
multisystem organ failiure
Why Increasing of the heart rate / contractility does not help in Hypovolemic shock?
Bod wants to compensate for low BP so ot increases the cardiac output and BP
BP = CO * SVR
CO= HR * Stroke volume
but Stroke volume depends on EDV and ESV
EDV= end diastolic voume (blood before contaction/blood during diastole or relaxation )
ESV= End systolic volume (blood remaining after contraction)
SV= EDV- ESV
but here we have very low EDV as de to loss of fluid and blood so even though we increase
Treatment for Hypovolemis shock?
Put them directly to fluids IV- crystaloids (saline or ringers solution) Albumins Hetastarch
Explain Cardiogenic shock.
Volume of blood is normal
Problem is with the heart which is not abke to generate sufficient power
Ventricles (pump) is failing
Causes-
Myocarditis
massive or multiple Mi’s
Valvular stenosis (Aortic stenosis/ Mitral stenosis)
Arrythmias (Tachy and Brady)
Dilated Cardiomyopathy (Weak and flabby ventricles)
Congenital heart diseases
decrease volume circulating —> BP low
compensation is the same.
Increase heart rate
increase rnein
increase constriction of blood vessels
If not treated cause ischemia, hypoxia, decrease ATP to tissues , lactic acid accumulation due to anaerobic respiration .—-> high H+ formation and causing of Metabolic Acidosis in body
Organ Failiure
Treatment–> treating the underlying cause
like in MI–> angioplasty and thrombolytic to the thrombotic vessel causing MI
Immediately put on Oxygen verry little fluid Give Vasopressors (epinephrine) Epinephrine increase HR as well as SVR Dobutamine incrase contractility Amrinone (PDE inhibitor)
What is tension pneumothorax?
When there’s damage to the pleura, either due to lung disease or trauma to the chest wall, air from the outside or from the lungs can flow freely into the pleural space, but cannot leave.
The accumulated air in the pleural space puts positive pressure on the lung and prevents it from expanding properly, which causes respiratory distress.
As the air continues to accumulate, the trachea and other structures of the chest can be pushed away from the pneumothorax, leading to increased difficulty breathing.
Mediastinal or tracheal shift to the contalateral side (opposite)
Additionally, the increased pressure inside the chest can compress the heart and lead to a collapse of the blood vessels that drain to the heart, in turn decreasing venous return and cardiac output. If left untreated, tension pneumothorax can rapidly progress to cardiovascular collapse, which ultimately leads to cardiac arrest.
Explain obstructive Pneumothorax?
Due to Tension Pneumothorax.
Compression of heart vesse;s, IVC, SVC, heart cannot ejeect blood out
hyperresonance sound on auscultation and percussion
Or Due to pericardial Tamponade
Increase pericardial fuid between peritoneum of heart
heart squeexing
cannot contract and dilate or fill heart with blood
triad– Becks triad for pericardial tamponade
High Jugular venous pressure
low Systemic BP
Muffle heart sounds (cannot hear clearly)
Or pulmonary Embolism
If there is a thrombus or embolous in the pulmonary artery very low amount of blood will go to the lungs and the blood amount returning to the LA wil also be low
EDV will be low Sv low BP decrease
Bronchioles wll constrict due to low perfusion to the alveoli due to not enough blood coming from the pulmonary artery so Respiratory distress is also seen
Hypoxemic Hypoxia
low O2 partial pressure
elevated lactic acid levels
multiple organ system failiure
Explain distributive Shock (septic)
In Hypovolemic, Cardiogenic and Obstructive shock the shock was due to not enough cardiac output by the heart and decreased tissue perfusion.
In distributive shock the shock is due to decreases SVR and that is the main reason for the decreased perfusion to organs.
Low BP= Low CO or Low SVR
1) Septic
Gram negative bacteria—-> endotoxins—–> Damage tissues
Tissue releases prostaglandins and leukotrines that activate mast cells (macrophages of tissues)
Mast cell–> Histamine, PG, Leukotrines,——>
Blood vessel dilation and leaky BV Increased permeability—–>decreasd blood pressure
Chemotactic agents also attaract complements and leuckocytes.
Enhancement of inflammatory reactions
WBC releases
IL-1 —-> Hypothalamus—> PGE2—–> High body temp (Fever)
IL-6—–> Liver—–> Acute phase reactants protiens generation
IL-8—> Make other WBC to increase phagocytic activity
Endotoxins can also increase expression of PAI1 tissue plasminogen inactivator
Microvascular thrombus formation in small vasculature’’
Also increase the expression of Tissue factor on the endothelium—-> increase in coagulation activity
If these happen in various part of the body then it could lead to DIC
Bleeding because your body has already used up almost all the clotting factor and materials in forming various thrombus that now it is bleeding.
Can bleed from orifices
ROS formation by Wbc that leads to further damage of endotheliums
Compensation
In early stages there is a high CO
decrease SVR
Treatment –
IV antibiotics
crystalloids and vasopressors
Explain anaphylactic shock( distributive)
Severe Systemic Allergic reaction
bee sting,
food and drug allergies
IV cntrast
Alergen—> processed by macrophages—>Presentation on MHC II molecule—-> Thelper —–> chemical mediators—–>stimulate b cell—–> Plasma cell—–> IgE Antibody
Mast cell+IgE—-> Histamine and other mediators
Anaphylactic shock and vasodilation
Respiratory distress
itching rashes and hives
tratment –> epinephrine
Explain Neurogenic shock
Acute Spinal cord injury
if between ti to l2—-> autonomic bloavkade of SNS
unaopposed vagal sysem
high PNS
high vasodilation and bradycardia
What is Congestive Heart Failiure?
Congestive heart failure (CHF) is a chronic progressive condition that affects the pumping power of your heart muscle. While often referred to simply as heart failure, CHF specifically refers to the stage in which fluid builds up within the heart and causes it to pump inefficiently
Systolic heart Failiure
Diastolic Heart failiure
Pathophysioogy of Congestive Heart Failiure?
Systolic heart failure
DECREASED EJECTION FRACTION
1) systolic Heart failiure Ventricles Cannot generate enough stroke volume (volume of blood ejected per beat) so cardiac output is also decreased CO= HR*SV SV depends on= Preload = contractility and 1/Afterload
……..decreases contractility–
low contractility, low SV, low CO
diseases include-
Myocadial Infarction (anterior and lateral)
Dilated Cardiomyopathy
……..increased preload with decreased contractility-
Even if preload is increased but contractility is compromized then also SV will be decreases
the blood will keep sitting in the heart as preload will keep accumulating and heart is not strong enough to contract and push all blood out
this can happen in conditions such as
Mitral regurgitation and aortic regurgitation
Tachyarrythmia
Bradyarrythmia
Pathophysiology of CHF (DIAStolic HF)
DECREASED FILLING ACTIVITY
DECREASED VENOUS RETURN AND PRLEOAD
Daistolic HF
heart is stiff and fibrotic and does not want to stretch.
………..Decreases preload (venous return)
Conditions can include ischemic heart disease or MI (Fibrosis) Restrictive Cardiomyopathy (amyloidosis) Constrictive Pericarditis Cardiac Tamponade
……….Afterload increase (ncreases resistance that does not allow the blood to flow from ventricle to arteries)
Hypertension (ventricle work harder and hyprtrophy of ventricles in acute phase)
inchronic phase of hypertehnsion the hypertrophic ventricle becomes weak and flabby and thus can lead to systolic Heart failiure
Aortic stenosis (leads to hypertrophy of ventricles)
Coarctation of aorta (narrowinf)
WE take afterload in case of diastolic HF as with increase in afterload the ventricles undergo hypertrophy causing less filling of ventricles due to less space
decreasing the cardiac output and preload
so basically if any condition is causing increased afterload, it will eventually lead to decrease in preload and this decrease in preload is Diastolic HF
name diff in systolic and diastolic hf?
Systolic is contraction so prolem with heart contraction
here we will see the contracility as this relates with systole of heart.
Decreased contractility will lead to decrease Stroke vplume any how doesn’t matter if preload is high or low
usulay preload is not affected and venous return is normal but preload can accumulate
in diastolic HF there is a problem with heart dilation that LEADS to DECREASED PRELOAD
here the reason for the Diastolic HF is increased afterload (a cause per se) that furthur causes hypertrophy and diastolic HF and then causes decreased preload
(all connected)
Explain Right sided Heart Failiure (CHF)
Not commonly occurs on its own
usually due to L side HF
Increased Afterload
- pulmonary stenosis
- pulmonary hypertension
- pulmonary thrombus
- Cor Pulmonale (due to COPD)
increased Preload
- Tricuspid Regurgitation
- Pulmonary regurgitaion
Decreased Contractility
- Inferior Mi(only damage right ventricle)
- Myocarditis
